lederr

Archive for the ‘Fitness/Health’ Category

The 6 Most Shockingly Irresponsible “Fitspiration” Photos

In Fitness/Health on Thursday, 12 September 2013 at 05:40

The 6 Most Shockingly Irresponsible “Fitspiration” Photos.

Advertisements

22 Things Happy People Do Differently

In Fitness/Health, Happiness, Meditation on Saturday, 23 March 2013 at 15:58

22 Things Happy People Do Differently.

Large study shows substance abuse rates higher in teenagers with ADHD

In ADHD, ADHD Adult, ADHD child/adolescent, Fitness/Health, Psychiatry, School Psychology on Sunday, 24 February 2013 at 10:03

Large study shows substance abuse rates higher in teenagers with ADHD.

Consequential Growth

In Fitness/Health, General Psychology, Happiness, Mindfulness, Well-being on Thursday, 14 February 2013 at 11:12

Consequential Growth

By: Timothy J. Wachtel

Written for the Texas Association for Adult Development & Aging

I’m older now. A little more pale, a little more frail, but I got my wits. The ebbs and flows of life have taken their course and have strewn me all over the place. It didn’t seem fair then and it doesn’t seem fair now. What do I have to show for it? I still try to keep my head held high and I smile a lot. Boy, life sure has a way of serving up its fair share of bumps and bruises . . . kinda glad in a way.

*****************************************

Have you ever found yourself in this reflective space? Have you ever not found yourself in this place? I think that everyone can agree that any individual who reaches the midpoint of adulthood and beyond is never immune to the trials and tribulations of life. It comes with the travel package. There always tend to be those pinnacle times of life; the times where the emotions get bruised, the spirit gets suffocated, the isolation looms large, the mind runs wild, and the rug from underneath you is no longer there. These life events and novel experiences come in many forms, as you very well know. Divorce, death of a family member, religious conversion, relocation, job transfer, job loss, injury or disease, natural disasters, kids move out, spouse goes off to war, traumatic stress, conflict; the list seems forever endless.

Is there a silver lining to all of this? I believe the answer is emphatically YES! We oftentimes don’t realize the goodness in these types of life events while we’re a part of the process. And it is a process; these situations, events, and experiences have a necessary starting point and oftentimes tend to be phases or stages throughout the process. Some people reach the productive end to the process, while others don’t quite reach the same successful terminal point. Today, science is doing more than ever before to inform us of these types of processes. More and more research is demonstrating evidence of the fact that many of these types of inexplicable occurrences in life result in very positive outcomes.

Research has found that individuals going through “troubled waters” over the course of a significant period of their lives tend to develop a greater sense of altruism and resilience, many experience more satisfaction or well-being in their life, and still others are finally able to come to terms with the meaning of their life. Scientists and practitioners use a battery of different terms to identify some of these events, some of which include: critical life eventsposttraumatic growthstress-related growthspiritual emergencytransformational crisisposttraumatic positive adjustmentgrowth through adversity, and the positive outcomes of one’s battle with Post-Traumatic Stress Disorder (PTSD).

I recently came up with a term that I believe helps to encapsulate the upsides to many of the downsides of life. “Consequential Growth” is the term I use to describe the results of these processes. Consequential Growth seems to semantically emphasize the necessary consequences we oftentimes experience throughout the growth process. The term broadly identifies the “dark nights” and the cognitive, spiritual, and emotional hardships we face during these times of duress.

Many books have been written on the positive results of these types of experiences in one’s life. Notably, the individual and collective works of Calhoun, Tedeschi, and Joseph talk much to these processes; especially in terms of Posttraumatic Growth. Moreover, many naturalistic and experimental research studies have found conclusive evidence of consequential growth. They inform us that those who are able to grow through their perceived negative experiences oftentimes maintain a more positive orientation toward life, are generally more optimistic, and tap into healthy coping strategies to get through the hardship(s). These individuals often have strong social circles and are seen by others as stronger and wiser as a result of going throughthe consequential growth process, even though they never signed-up for the turbulence.

The aging process is indeed complex. Life situations can catapult us right off our comfortable life. This is the stuff of character, wisdom, virtue, transformation, transcendence, higher consciousness, emotional resiliency, generativity and care for your fellow human beings. I wish you well on your next tumble.

References:

Tedeschi, Richard G.; Lawrence G. Calhoun (1995). Trauma and Transformation: Growing in the Aftermath of Suffering. SAGE Publications, Inc.
Joseph, Stephen (2011). What Doesn’t Kill Us: The New Psychology of Posttraumatic Growth. Basic Books
Timothy “Tim” J. Wachtel

Executive Director

The Center for Optimal Adult Development

www.optimaladult.org

Retrieved from: http://www.optimaladult.org/index.cfm/knowledge-center/coad-news-notes/consequential-growth/

 

stressed is just “desserts” spelled backwards!

In Fitness/Health, Mindfulness, Well-being on Monday, 4 February 2013 at 12:14

ignore the drama. anger is deathly. practice gratitude. view with compassion. do unto others…

http://www.huffingtonpost.com/2013/02/04/stress-health-effects-cancer-immune-system_n_2599551.html?ir=healthy-living&utm_campaign=020413&utm_medium=email&utm_source=Alert-healthy-living&utm_content=Title

is you are sick, please stay home!

In Fitness/Health on Monday, 4 February 2013 at 09:42

Sick Persons’ Germs Spread to Half

of Commonly Touched Office Surfaces, Study Finds

If you thought you could avoid your sick coworkers’ germs by just covering your nose and mouth when they sneeze, we have some bad news to deliver — you probably won’t be able to escape their germs because they get EVERYWHERE.

New yet-to-be-published research conducted by scientists at the University of Arizona shows that half of the most commonly touched surfaces in the office (like the coffee pot handle, tabletops, doorknobs and phones) can become infected with a sick person’s germs — all by lunchtime.

The study, conducted by public health professor Kelly Reynolds and germ expert Charles Gerba, involved having 80 people go about their regular work-day business in an office at the university. Most of the study participants received droplets of water on their hands at the beginning of the day, but one of the participants got droplets of fake viruses, which acted like the cold, flu and stomach flu viruses, that researchers were able to test for in the office environment later on.

The researchers found that after just four hours, more than half of the office surfaces had traces of the fake viruses. And by the end of the day, 70 percent of the tested surfaces had traces of the fake stomach flu viruses (cold and flu viruses have a shorter survival time, so had largely dissipated by the end of the day).

The findings were surprising because the office setting wasn’t one where people were milling about constantly.

“They basically go in their offices, sit in their chairs and are on their computers. They may go to the bathroom, and they have a common kitchen area they share and a photocopy machine, but that’s about it,” Reynolds said in a statement.

Researchers said that the risk of getting sick from one of these fake viruses was between 40 and 90 percent.

“Most people think it’s coughing and sneezing that spreads germs, but the number of objects you touch is incredible, especially in this push-button generation. We push more buttons than any other generation in history,” Gerba said in the statement.

The researchers then conducted a second study where free tissues, hand sanitizer and disinfecting wipes were offered to the employees. The risk of becoming infected with one of the fake viruses went down to 10 perfect.

But what if the sick person is living in your homeClick here for our tips for staying healthy when you’re caring for a flu patient.

Retrieved from: http://www.huffingtonpost.com/2013/02/03/sick-person-germs-office-surfaces-contaminate_n_2583589.html?ncid=edlinkusaolp00000003

four questions to ask…

In Fitness/Health, Mindfulness, Well-being on Wednesday, 23 January 2013 at 07:56

http://www.johnclarkiii.com/Notable-Quotes-11-from-John-Clark-III.html

2013…a healthy pup and a healthy you!

In Animal Rescue, Animal Welfare, Fitness/Health on Friday, 11 January 2013 at 07:30
 


Exercising With Your Dog in 2013

Is exercise on your list of New Year’s Resolutions for 2013? Man’s best friend can be your best exercise partner.

 

With your dog as your workout companion, you’ll get a loyal and eager exercise partner in return. Research has shown that you’re more likely to stick to your fitness program if you exercise with your furry friend.

Here are a few tips for exercising with your dog:

Walk or jog your way to fitness 
Ready to turn your dog walks into short exercise routines? It’s the easiest way to start and a brisk walk can be great exercise for both you and your doggie. Start slowly (10 to 15 minutes) and work your way up to longer walks or jogs. Up to 20 or 30 minutes should be OK for most dogs, depending on their breed and health.

Beyond the walk

While walking and jogging can be great activities, why stop there? Add more variety with dog-friendly activities like…

Swimming – Water dogs like Labradors, Retrievers and Poodles enjoy swimming, especially during hot weather. Keep it short, fun and safe.
Obstacle course – Set up a homemade obstacle course in your backyard or visit a dog park with a course. While your dog runs the course, sprint with him to get your own exercise.
Fetch or tag – Take the average game of fetch or tag even further. Throw a ball or toy and race him to it or play tag where you’re “it.”
Canine dancing – Choreographed dancing with your dog is a sport called musical freestyle. Create a dance routine to upbeat music and burn some calories! Here’s an example on video.
Dog frisbee – This fun outdoor game can turn into a competitive sport for you and your pet. Keep it casual or join a“Disc Dog” club for more motivation.
Doggie soccer – Can your pooch kick it like a canine Beckham? Find out if he can push a large dog ball with his nose or paws for a game of soccer. It’s OK to use a soccer ball too, just avoid kicking it at his nose or body.

Check with the vet (and your doctor) first 
Make a vet visit your first priority. During the vet check, learn of any breed-specific limitations that could affect Fido’s workout. You should get checked by your own doctor as well, before any new exercise routine is started.

Make the workout work for your dog
You may push your own limits in a workout, but don’t do the same with your dog. A Chihuahua, for example, can’t do a mile-long run, but he may be up for a brisk 20- to 30-minute walk. Be careful with smaller breeds in general and be extra careful with short-nosed breeds (pugs, boxers, chow chows, mastiffs, etc.). They can have problems breathing and cooling down effectively.

Mind the signs of health and safety
In his eagerness to keep up, your dog may overdo it, so it’s up to you to watch for signs of exhaustion or overheating. Heavy panting, pale gums, walking unevenly or lagging behind you are all signs that it’s time to stop. To stay safe, exercise in the mornings or evenings when there’s less heat and take a water bottle for you and him on long sessions.

Retrieved from: http://blog.petsupermarket.com/

you don’t have to bypass treats…tips for holiday eating

In Fitness/Health, Mindfulness on Tuesday, 18 December 2012 at 06:52

Holiday Eating: 17 Things To Consider When You’re Obsessing About Food And Weight

The Huffington Post  |  By Margaret Wheeler Johnson Posted: 12/17/2012 12:55 pm EST  |  Updated: 12/17/2012 5:02 pm EST

Every year I tell myself it will be fine, and every year it is not fine.

After over a decade of dealing with my eating issues, I’ve come to think of my relationship with food as my mind’s other track — the ticker tape of thoughts and anxieties that streams constantly at the edge of my life.

Did I eat too much? Too little? Am I hungry? How hungry? Should I eat now? Will I regret it if I don’t, or if I do? What if I gain weight endlessly? What if I’m just not equipped to feed myself? What kind of person can’t feed herself? If I were smarter/better/healthier/saner, I would be better at this…

Some days I can nearly tune it out, like news of unrest in a far-off country whose name and capital I used to know but now can barely recall. Sometimes I can almost pretend it doesn’t concern me. I can choose not to see it. I can go about my day.

Except now. From Thanksgiving through New Year’s, I’m forced to tune in. Festive brownies and cookies and bark and nog are everywhere. There are enormous meals with relatives who leave me questioning all of my food and life choices. There is way too much booze. There are little black dresses and glittery miniskirts that do not look like I hoped they would, and there are multiple opportunities, also known as holiday parties, to feel sized up by everyone in the room. Oh, and it’ll all be on Instagram very, very soon.

This year, I haven’t pretended that it’s fine. Mainly because I had this piece to write, I decided to feel it and think about it and recognize the ways in which this still really sucks. At the same time, I mulled over the things I’ve learned in the years since I made it through the initial throes of an eating disorder, the ones I’ve spent physically healthy but still trying to figure out how to feel okay about eating. And I thought about the maddening divide between all that hard-won knowledge and actually putting it into practice.

This is not a list of things I know because I’ve figured this eating thing out — far from it. It’s a list of the things I know because of some rare moments of clarity that I remember because they felt different from everything else on the ticker tape.

17 Things To Think About When You’re Obsessing About Food And Weight

BEFORE YOU EAT

1. You aren’t what you eat. 
Physically and long-term, you are. But experts have also noted that overeating once — even really, really overeating — won’t make you gain weight instantly.

More important, how much you eat at a single meal has absolutely nothing to do with whether or not you’re a good friend, daughter, mother, sister, aunt, thinker, worker, citizen or overall human. Nothing you consume will diminish how valuable you are in those areas that count so much more.

2. You’re not wrong to want what you want. 
It was an amazing moment when I realized that most healthy people like to eat and don’t feel bad about that. People who aren’t overweight and never will be like to eat. They want cupcakes just like overweight people want cupcakes. Goodness and wanting an enormous piece of chocolate cake aren’t mutually exclusive — despite thehundreds of millions of dollars spent annually to convince us that food and the people who eat it are virtuous or evil, clean or dirty, indulgent or guilt-free.

You’re not wrong or bad to want the cake. Who in their right mind wouldn’t?

3. Why you tend to eat more than your body wants.
And what puts you into overeating mode. Stressful conversation? A food that represents escape for you? Eating while you watch TV or read? Certain restaurants?

There are two reasons to think about this. For one, identifying your triggers can help you recognize when you’re vulnerable and protect yourself (more on that later). And the other reason is that thinking about what sets you off can tell you a lot about what you really want.

Geneen Roth, the author whose insights into emotional eating I find to be spot-on every time, wrote, “There is a whole universe to discover between ‘I’m feeling empty’ and turning to food to make it go away.”

Although I resist creating food rules for myself because they remind me of the deprivation of anorexia, when I’m having an especially hard time, I throw out anything that doesn’t have to be cooked before it’s consumed. If I have to cook it, I have to think about it and why I want it and what desire I might be trying to displace because fulfilling that other hunger or even acknowledging it feels too difficult or inconvenient or painful.

WHILE YOU’RE EATING

4. How amazing the food tastes. 
I am somehow stunned every Thanksgiving and Christmas by how good it all is. It makes sense — I’ve had a whole year to forget — but that means the flavors and textures amaze me every time. How good is cranberry sauce? It’s like jam, but earthier, drier and less sweet. And can we talk about mashed potatoes, which really are god’s gift, and stuffing — lord, I love stuffing — and the taste of real butter in food? What’s a life where you don’t let yourself taste real butter? Not any life I’m interested in.

5. When you stop tasting it. 
If you’re no longer into the flavor of what you’re eating, why are you still eating it? Waste isn’t ideal, but you may need to put off worrying about that until eating becomes less stressful. I’ve learned that if I’m not allowing myself to say no to what’s on my plate, that’s probably an expression of other things in my life I don’t feel like I can say no to. Saying no to food I don’t want right at that moment can help me begin to say no to the bigger things I need to refuse or contain.

6. It’s just food. 
Sure, holiday food is special, particularly if your family has its own recipes and traditions of preparing certain dishes together. And for anyone who struggles with food and weight issues, food is never — and may never be — “just food.” That said, remember that the traditional nature of holiday food means you’ve had it before and will have the opportunity to have it again. It’s much, much more important for you to feel good now, in the moment, and later in the day than it is for you to have a second or third helping you don’t really want. Remember that you’re more powerful than the food on your plate, and you matter more. Hear that? You are more powerful than the food on your plate. It’s just food.

7. If you’ve hit any of your triggers and how you can change the situation. 
Now that you know what your triggers are, consciously watch for them. When you hit one, do whatever it takes to keep it from leading to behavior that you know will make you feel terrible. I’ve found that focusing on one action helps. “All you have to do is leave the table,” I tell myself. Or, “All you have to do is throw it away.” I don’t think about how I might feel after I do it. I shut off the list of potential consequences (“What if I’m hungry later? What if the host is insulted? What if people wonder why I left or where I went?”).

Get up. Go to the bathroom. Make a phone call. Invent a work emergency. Do whatever it takes to get away from the food for at least a little while to remind yourself that you’re in control, that it’s just food and that you can take or, literally, leave it.

8. Whether you’re into the people you’re eating with.
If not, think about how you feel about the people you’re eating with. In a 2011Glamour essay on not drinking during the holidays, Sarah Hepola observed, “When you’re sober, you see with utter clarity which friends you feel comfortable around and which make you itch for an open bar.” Apply the same test to the role food plays in your friendships. If you have any friends you wouldn’t hang out with if food weren’t involved, they could be part of the problem.
AFTER YOU EAT

9. Shame doesn’t motivate.
You’ve already started doing the thing. You know what I’m talking about. You think you ate too much, so you spend the next 12 to 36 hours berating yourself for the undisciplined, disgusting, worthless, fat (etc. etc.) waste of genetic material you think you are. You begin to plan how you’ll make up for your “sins” — you’ll exercise for three hours every day, you’ll restrict your calories for the rest of the week, you’ll go on a cleanse.

When I spoke to Geneen Roth about this last year, she emphasized, “Shame, guilt, punishment, fear has never led anyone to change,” and yet people remain convinced that it will. In her books, Roth has always advised that the day after you overeat is the time when it is most important to be kind to yourself. “Recognize the inner critic or the judge … for what it is,” she urged. “It’s not your friend.”

10. Bingeing isn’t “for ladies.”
One of the mantras that hindered my recovery from the worst of my eating disorder was a tagline I came across in (I think) a yogurt ad. The page demanded of the female consumer, “Why are you still eating like a frat boy?” That would never be me, I vowed, and I put the same question to myself every time I reached for “frat boy” foods. Smart, sophisticated, ambitious, successful women didn’t eat pizza or onion rings, I told myself — it didn’t even occur to them to want those things. I extended this made-on-Madison-Avenue logic to cookies and cake, then bread, then carbs of any kind. Then I was careful not to “need” carrots or anything with fat in it, then breakfast, then lunch, then ever finishing a serving of anything.

Here’s the confusing thing: As much as women are encouraged to subsist on yogurt and aspartame, romantic comedies regularly show women sobbing into pints of ice cream. Ads encourage ladies to binge, too.

No wonder women have an especially f-ed up relationship with food (and there aresigns that men are catching up). But there’s another reason women are prone to emotional eating, which Caitlin Moran summarized brilliantly in her book “How to Be a Woman,” excerpted in the Wall Street Journal in June 2012:

by choosing food as your drug — sugar highs, or the deep, soporific calm of carbs — you can still make the packed lunches, do the school run, look after the baby, stop in on your parents and then stay up all night with an ill 5-year-old…

Overeating is the addiction of choice of “carers,” … It’s a way of screwing yourself up while still remaining fully functional, because you have to… slowly self-destructing in a way that doesn’t inconvenience anyone. And that is why it’s so often a woman’s addiction of choice.

So the next time you overeat or have a full-on binge, think about the following:

A) It wasn’t heroin.
B) There’s stuff in your life you’re having trouble coping with. That stuff probably deserves your attention. You, in the meantime, deserve compassion.
C) There is actually no rule condemning women to starve or binge, just lots of unhelpful suggestions that we should. Work toward being a woman who doesn’t obey the insanity.

11. How big you are. 
Bear with me. “Big” is an adjective most of us learn early on is something you never, ever want to be called. It’s the opposite of being contained and in control. And in a culture that only puts very, very thin women on screens and in ads, big equals un-special, unworthy of attention, unseen.

After a lot of years of thinking about how much being “big” scared me, I realized the thing I feared the most wasn’t my own physical size, it was the huge, seeping, unnamed emptiness that no one sees. That was the mass I was really trying to shrink or fill through various eating behaviors. I think of it as a black hole located somewhere in my stomach/chest region, the center of my body. It’s freezing, ugly, abandoned, condemned, and for a long time I believed that emptiness would always be my starting point, where I was from.

But then on an ordinary afternoon when I was wondering for the nth time how I’ve let that emptiness motivate so much of my behavior throughout my life, a different explanation occurred to me. What if the cavity inside could be a place, not an emptiness? What if it was light and inhabitable? What if all along the space I’d been trying to fill and not feel was somewhere I wanted to live? And what if that space inside made me bigger than this war I’ve waged against myself as long as I remember, with food always my weapon of choice?

The moment didn’t last. Of course it didn’t. The impulse to fill that place, to cancel it out, returned. But now I know that it isn’t vacant and doesn’t need to be fixed, and I’m curious about what else is there. And that is huge.

12. The small space. 
If you don’t like thinking about any part of yourself as even metaphorically big, here’s something small you can explore. I’m not a fan of appropriating another faith’s scripture for secular Western self-coddling, but a Catholic nun originally pointed me to this quote from the Hindu Upanishads, so that boundary’s already been crossed. Here it is:

In the centre of … our own body, there is a small shrine …, and within can be found a small space. We should find who dwells there, and we should want to know him.

No matter how much you ate, the small space remains, undamaged, and so does the person inside. She is — you are — still there, and we should want to know her.

THE REST OF THE TIME (WHEN YOU DON’T HAVE FOOD IN FRONT OF YOU AND AREN’T STARVING OR STUFFED)

13. How you would feel if no one, including you, could see your body.
Here’s one of the simplest, most illuminating exercises I know: One weekend day, don’t wear makeup or do anything to your hair. Wear the most comfortable clothes you own, which may involve some very ratty sweats. Go through a whole day like that and notice that how you look in no way inhibits your ability to operate in the world. I do this a couple of times a month and feel better about everything listed above every time I do.

14. The fact that you do have a body and how amazing that is. 
For long periods of my life, I didn’t want a body. I remember wishing in my teens that I could just live as a brain floating around. I resented the maintenance a female body required. I didn’t mind so much the plucking and shaving and blow-drying and makeup — some of that was fun. I resented not being able to eat what I wanted — the women I grew up around dieted constantly, so I thought it was required of adult female humans. I resented that my body wasn’t good enough as it was. I resented that, through no fault of my own, my postpubescent body required serious management.

Years later, I’ve finally started thinking about my body in terms of what it can do. I learned, for instance, that exercise can be not about a countdown on the elliptical machine but about health and technique and spending more time outside. To my great astonishment, the body I punished for years can run five miles. If a calorie counter were involved, I’m not sure I ever would have discovered that.

15. If you want to lose weight, why.
Is it because you’re not a healthy weight (per your doctor)? Or is it because you look in the mirror and think, “I’m disgusting,” because you fantasize about slicing off parts of your body (which has never done anything to you except bear witness to your actions). If the latter, you don’t need to lose weight, you need to get angry at whatever made you feel like you deserve to be treated that way. No one does. And per #9, talking to yourself like that isn’t going to change your eating.

16. Pretending your issues aren’t your issues won’t make them go away. 
At some point in an episode of obsessing about how much I’ve eaten and how much I’m going to eat and worrying that food will always, always control my life, that I will never escape the ticker tape, I get so fed up that I swing to the opposite extreme. “I’ll just shut it off,” I tell myself. “Why don’t I just wing it? Everyone else manages to feed themselves,” I think, then add, in near-demented contradiction of all eating experiences in my life up to this point, “How hard can it be?”

Let me save us all a lot of trouble by reporting that much like shame, this has not ever, once, resolved anything for me.

17. This is hard. 
Eating sanely — I can’t say normally because emotional and intellectualized eating seem to be the norm in American culture — is an incredibly ambitious proposition. Eat when you’re hungry, stop when you’re full: so much easier said than done.

How sanely you eat is relative, but when I’m berating myself for the fact that I’m still struggling to do that, I try to think about how far I’ve come. One reason eating in December is especially hard for me has nothing to do with sparkly miniskirts and everything to do with the fact that 12 years ago at this time of year I weighed 30 pounds fewer than I do now. I was 18 and looked 11, I was freezing all the time because I had so little body fat and sometimes I brushed my teeth multiple times a day because toothpaste almost felt like food. I remember one night sitting curled up, gaunt and silent, against my mother at my university’s holiday service — she had come to take me home and put me in a hospital — and recognizing that the way I was living wouldn’t sustain me but being unable to imagine any other way of being. I remember the point when, surrounded by the music and warmth, I thought very clearly that it would be so much easier if that moment were my last.

The truth is that it would have been easier — for me, though not my family. If I’ve learned anything in the aftermath of an eating disorder, it’s that the day-to-day business of feeding and inhabiting an adult female body is harder than starving it ever was.

Twelve years later, there are still times when I eat until I’m ill in order not to feel, and there are times when I look in the mirror and think, “Look what you’ve let yourself become.” So far the best thing I know to do about all of that is remind myself that I stuck around for the hard part, that I would have missed so much if I hadn’t and that I’m doing the best I can.

Retrived from: http://www.huffingtonpost.com/2012/12/17/holiday-eating-what-to-think-when-you-obsess_n_2315545.html?ir=women&utm_campaign=121712&utm_medium=email&utm_source=Alert-women&utm_content=Photo

Breakthrough in biosensing: New virus detection method under development

In Fitness/Health, Medication, Medicine on Sunday, 16 December 2012 at 16:05

Breakthrough in biosensing: New virus detection method under development.

are you getting enough???

In Fitness/Health on Thursday, 6 December 2012 at 09:02

sleep quiz:

http://www.webmd.com/sleep-disorders/rm-quiz-sleep?ecd=soc_tw_120612-am_rmq_sleep

ease the symptoms of depression with one easy step!

In Fitness/Health, Mood Disorders on Saturday, 1 December 2012 at 10:31

Physical Exercise Eases the Symptoms of Depression in Children Growing Up in Unsafe Neighborhoods

26 November 2012

Living in unsafe neighborhoods may impact children’s mental health. However, physical activity has been found to be related to lower levels of depressive symptoms among children. A recent study of 89 children aged 9-12 found that physical activity may buffer the relationship between unsafe neighborhoods and child depressive symptoms.

Children living in unsafe neighborhoods are more likely to be depressed. Improving neighborhood safety is perhaps the clearest way to improve the situation, but it’s not always easy to make quick community changes that will benefit children. Given that many neighborhoods will continue to be unsafe, recent research has focused on understanding factors that help break the link between neighborhood safety and depression and therefore inform intervention efforts.

One of these factors is physical activity. Activities such as aerobic exercise and competitive sports teams have benefits for child development – and lower levels of depressive symptoms are just one of these.

One of the challenges is that children who live in unsafe neighborhoods tend be less in engaged in physical activity compared to those in living safer neighborhoods. This is largely due to the lack safe areas for exercise.

Physical activity as a buffer

Child psychologists Sonia L. Rubens and Paula J. Fite from the University of Kansas decided to look at data on depressive symptoms, physical activity and neighborhood safety. They examined whether physical activity acts as a moderator between neighborhood safety and depressive symptoms in school-age children.

They expected children who were physically more active to report fewer depressive symptoms than those who lived in similar areas but weren’t physically active.

The study included 50 boys and 39 girls aged 9-12 from a metropolitan US community with approximately half a million residents. Participants and their caregivers were recruited from neighborhoods that varied in socioeconomic status. The majority of children were Caucasian, and about 27% of the sample received public assistance. Both children and caregivers were asked questions about neighborhood, delinquency, after-school activities, parenting, and peers.

Not surprisingly, there was a significant relationship between living in an unsafe neighborhood and high levels of depressive symptoms. Further, depressive symptoms were more serious for minority (non-Caucasian) youth.

The relationship between neighborhood safety and physical activity was different for children who were physically active and those who weren’t. Among those who participated in any sort of physical activity – whether school sports or other games – living in an unsafe neighborhood did not make depression more likely. However, among those who didn’t participate in any physical activity, children who lived in unsafe neighborhoods were more likely to be depressed than those who lived in safer areas.

The implications for intervention

The study implies that engaging in some physical activity may ease the effect of unsafe neighborhood on child mental health. Providing better options for physical activity for children living in such neighborhoods may be an important next step in prevention and intervention efforts. It may also be a cost-effective way to improve outcomes, as other research suggests.

Meeting this challenge will require practical assistance as well as encouragement, given the lack of safe spaces to play in some of these neighborhoods.

It is likely that physical activity is a buffering factor that is more relevant for children growing up in unsafe neighborhoods that to those living in safer neighborhoods. Namely, the children living in safer neighborhoods reported the lowest levels of depressive symptoms even when they were not engaged in physical activity. That may indicate that these children benefit from other protective factors that are not available to children living in less safe neighborhoods.

Any caveats?

This study comes with several limitations that affect the generalizability of the findings. The sample was small, and the study was based on a questionnaire at a single point in time rather than following children and their families across time. It is not possible to tell from this study, for example, whether a lack of exercise led to depression for children in unsafe neighborhoods, or whether their depression came first and caused them to avoid sports and games – or both.

Either way, establishing that physical activity changes the nature of the link between depression and neighborhood safety may help program designers and commissioners consider community-based interventions for children who live in unsafe neighborhoods.

**********

Reference
Rubens, S. L., & Fite, P. J. (2012). The influence of physical activity in the relation between neighborhood safety and depressive symptoms among school-age children. Child Indicators Research, 2. DOI 10.1007/s12187-012-9155-5.

Retrieved from: http://www.preventionaction.org/research/physical-exercise-eases-symptoms-depression-children-growing-unsafe-neighborhoods/5908

age really might be “just a number”

In Fitness/Health, Happiness, Well-being on Wednesday, 21 November 2012 at 09:30

You’re Only As Old As You Feel

By: Jennifer Warren

Nov. 20, 2012 — The old saying “You’re only as old as you feel” has new life, backed up by a new study.

Researchers found older people with positive views on aging were 44% more likely to recover fully after severe disability than those with negative views on aging.

People with positive attitudes about aging also had a slower decline in their ability to do daily tasks such as dressing and bathing.

“It may be something worth considering that might help people’s recovery,” says researcher Becca Levy, PhD, associate professor at the Yale School of Public Health.

Upside to a Positive Attitude

Until now, experts say, most of the research on attitudes about aging and health has looked at the health risks and losses linked to a negative outlook.

But this study suggests there may be tangible health benefits to having a more positive view about aging.

“It’s not just about reducing the losses associated with aging, but also about making gains in one’s health or disability status and regaining what might have been lost,” says Tara L. Stewart, PhD, assistant professor ofpsychology at Idaho State University.

“These people with positive stereotypes about aging experienced health gains and better recovery, not just a reduction of health losses,” Stewart says.

Views on Aging Affect Recovery

In the study, researchers periodically surveyed 598 people aged 70 or older about their views on aging over a period of about 11 years.

None were disabled when the study started, but later on, all of them had at least one month when they needed help with daily tasks such as bathing, dressing, or walking. In some cases, their disability was severe; other cases were mild.

They were asked for the first five words or phrases that come to mind when they think of old people. The researchers rated their responses on a five-point scale as most positive, like “spry,” or most negative, like “decrepit.”

The results appear in the Journal of the American Medical Association.

The findings were strongest for older people with the most severe types of disability.

They were 44% more likely to fully recover from severe disability than those with negative age stereotypes.

Also, older people with positive views on aging were more likely to progress from severe disability to mild disability or mild disability to no disability.

Older people with positive age stereotypes also had a slower rate of decline in their ability to perform daily activities as they got older.

Of course, many factors affect whether or to what extent a person recovers from disability. This study does not prove that a positive attitude about aging made a difference. But it showed the strongest relationship between age stereotypes and recovery was among those people with positive age stereotypes and the most severe type of disability.

Attitude and Aging

Positive views on aging may help people bounce back from disability and promote independent living in a variety of ways, the researchers say.

One of the biggest ways may be psychological. Stewart says a person’s attitudes about aging say a lot about how much they believe their health is under their own control.

For example, people who view seniors as spry rather than decrepit may be more likely to live a healthy lifestyle, keep up on their doctor appointments, and take their medicines as prescribed.

“Holding a negative stereotype about aging, like believing illness is caused by aging, would cause them to feel less in control and responsible for their health and lead to different sorts of strategies,” Stewart says.

Levy also says there may be a physiological side to it.

“People who have more positive age stereotypes tend to have the advantage in experiencing stress,” says Levy. “They tend to suffer from less cardiovascular stress.”

Researchers say the next step is to look at how people can upgrade their attitudes about aging.

“We need to emphasize some of the positive as we get older instead of focusing on the developmental losses that may happen with aging,” Stewart says.

Retrieved from: http://www.webmd.com/healthy-aging/news/20121120/old-as-you-feel?ecd_tw_112112-am_new_nofeelold

find your grit…

In Fitness/Health, Happiness, Inspiration, Mindfulness, Well-being on Thursday, 15 November 2012 at 16:55

http://positivepsychologynews.com/news/renee-jain/2012110824569

The disastrous behaviour of the memory

In Fitness/Health, Mindfulness, Well-being on Tuesday, 6 November 2012 at 16:32

The disastrous behaviour of the memory (Click the photo to enlarge).

and i bet you thought this was another neuro article…

mental weight lifting…

In Brain imaging, Brain studies, Fitness/Health on Monday, 5 November 2012 at 13:45

Mental strain helps maintain a healthy brain

Posted By Daniel Pendick On November 5, 2012

When it comes to keeping healthy and fit, living a mentally active life is as important as regular physical exercise. Just as your muscles grow stronger with use, mental exercise keeps your mental skills and memory in tone.

Are certain kinds of “brain work” more effective than others? I put that question to Dr. Anne Fabiny, chief of geriatrics at Cambridge Health Alliance and an assistant professor of medicine at Harvard Medical School.

Any brain exercise is better than being a total mental couch potato. But the activities with the most impact are those that require you to work beyond what is easy and comfortable. Playing endless rounds of solitaire and watching the latest documentary marathon on the History Channel may not be enough. “If it’s too easy,” Dr. Fabiny says, “it’s not helping you.”

Four brain-health strategies

As I write in the November 2012 Harvard Men’s Health WatchDr. Fabiny recommends four complementary strategies for keeping your brain healthy.

Be a lifelong learner: You spend the first half of your life building dense networks of connections between brain cells. Scientists call that “cognitive reserve.” Continuing to learn new things builds and maintains these connections.

Strain your brain: Think of all mental activities as a continuum. Watching a TV documentary would be on the passive, mildly challenging end of the spectrum, while learning how to converse in a new language would be on the active, very challenging end. When it comes to cognitive reserve, mentally challenging tasks have the biggest impact. “Be open to new experiences that cause you to see the world and do things differently,” Dr. Fabiny says.

Get uncomfortable: One stereotype of aging is that young people are bold explorers but older people are timid homebodies who “know what they like.” Stereotype though it may be, it is easy to get in a rut. Getting out of your comfort zone from time to time challenges your mental skills. An example of this would be traveling to a city that you haven’t been to before, which forces you to navigate unfamiliar surroundings.

Be social: Social isolation, aging researchers have discovered, puts people at risk of losing some of the brain reserves they have built up over a lifetime. There are many ways to be social. One good way is working as a volunteer in a social setting, which allows you to have contact with a variety of people and puts you in new situations.

Don’t forget your body

Healthy brain aging should involve the rest of the body, too. There is abundant evidence that physical activity that gets your pulse thumping helps the mind as well as the heart.

And if that exercise involves mental skill and balance, like racquet sports or a walking round of golf, it’s even better. As you vanquish your opponents on the court or green, you might also notice an improved ability to keep score in your head.

Related Information: Improving Memory: Understanding age-related memory loss

Retrieved from: http://www.health.harvard.edu/blog/mental-strain-helps-maintain-a-healthy-brain-201211055495?utm_source=twitter&utm_medium=socialmedia&utm_campaign=110512-pjs1_tw

 

more on exercise…

In Fitness/Health on Monday, 5 November 2012 at 13:01

Declining Fitness Over a Decade Doubles Risks of AMI, Death

By: Shelley Wood

LOS ANGELES — Finnish men who lost more than 15% of their cardiorespiratory fitness over a 10-year period faced a near doubling of their risk of acute MI over the subsequent decade and more than twice the risk of dying of any cause, a new study shows.

Dr Jari A Laukkanen (University of Eastern Finland, Rovaniemi, Finland) presented 10-year results from the ongoing Kuopio Ischemic Heart Disease Risk Factor Studyhere at the American Heart Association 2012 Scientific Sessions.

In clinical practice, physicians “usually measure the risk factors that are easy to treat,” Laukkanen told heartwire . “But even after taking into account the usual risk factors–lipids, BMI, smoking, BP, diabetes, and alcohol consumption–still there was a risk related only to fitness, and it should be [given] more importance.”

The Kuopio study enrolled an unselected population of 2682 men between the ages of 42 and 60 that Laukkanen described as a mix reflective of the broader population–most of the men had no CVD at baseline, but some had preexisting CAD.

All men participated in a baseline exam in the late 1980s that included a respiratory gas analyses and electrocardiogram during exercise testing. Of the original cohort, 585 men underwent repeat testing 11 years later. During this initial study period, fitness levels declined, on average, by 5.2 mL per kg/minute of VO2max (equal to 1.9 METs change). Previous studies have suggested that levels of cardiorespiratory fitness typically decline at a rate of 5% to 15% per decade between the ages of 20 and 80 years, Laukkanen noted.

Staying Fit, Staying Alive

In the Kuopio study, the average follow-up time beyond the second exercise test was 10.9 years. During this follow-up period, study subjects had a total of 81 acute MIs, and 92 subjects died. When analyzed according to change in fitness levels, a loss of more than 15% of baseline cardiorespiratory fitness over 10 years was associated with an 88% increased risk of AMI and a 122% increased risk of total mortality, after adjustment for age and other risk factors. The results remained statistically significant after taking baseline VO2max into account.

The investigators also showed a dose-response with declining exercise: for every 1-MET decrease in VO2max, the risk of all-cause death increased “by a constant proportion,” Laukkanen said.

“VO2max can be used as a very powerful predictor of AMI and all-cause death beyond that predicted by many conventional risk factors.” Laukkanen and colleagues concluded. “The main public-health message is that it is very important to maintain the level of cardiorespiratory fitness to prevent a premature death from all-causes.”

What’s Good for the Gym . . . 

To heartwire , Laukkanen said that he does not routinely measure VO2max in clinical practice unless there is a reason for performing exercise testing, and current guidelines do not support routine measurement of cardiorespiratory fitness in healthy patients. But his study provides some rationale for performing more exercise tests in the future: it is inexpensive, noninvasive, and easy to perform in the clinic, he said.

“I think many of us are interested in measuring our fitness level–for example, you can go to a gym and take the test, and it’s quite easy to measure. But for some reason, it is a different topic to talk about measuring your fitness level in the gym than [measuring it] at the doctor’s office.”

Other studies have suggested that people–even doctors–tend to overestimate their fitness level.

His study also provides an oft-repeated reminder to physicians that urging their patients to become fit or maintain their fitness does have measurable benefits on cardiovascular health and longevity. And taking the time to measure fitness in practice, even just to establish a benchmark, may prove helpful in preventing future disease, he added.

Heartwire © 2012  Medscape, LLC

Citation: Declining Fitness Over a Decade Doubles Risks of AMI, Death. Medscape. Nov 04, 2012.

Retrieved from: http://www.medscape.com/viewarticle/773882

teach happy!

In Education, Fitness/Health, Mindfulness, Pedagogy, Well-being on Saturday, 3 November 2012 at 11:57

Why We Need to Add Happiness to the School Curriculum

By: OLGArythm

http://olgarythm.blogspot.com/2012/10/why-we-need-to-add-happiness-to-school.html

Young people graduate from school equipped to solve mathematical equations, arrange chemical experiments, and write essays. But often they graduate to the adult life not equipped with skills that will help them deal with everyday struggles, emotions, and difficulties. They are not equipped to be happy individuals.

Happiness is arguably the ultimate meaning of our life. Is there anything we want more for our kids than to be happy? If given a choice, would a parent prefer that her child knows capital cities of all countries or knows how to be a happy person? The ultimate purpose of the traditional academic education is to instill children with knowledge needed for for their future careers. But it does not teach kids the good attitude to deal with the many future personal experiences that make up our life. Inner well-being and peace are as crucial and necessary as the academic skills. It does not make sense to pay no attention to the development of happiness skills.

In 2011, United Kingdom published a report that confirms that lots of kids face serious emotional problems by the time they graduate school. Based on UK statistics, which probably does not differ too much from the situation in the USA, by the time an average class of 30 young people reach their 16th birthdays:

  • 10 of them will have witnessed their parents separate
  • 3 will have suffered from mental health problems
  • 8 will have experienced severe physical violence, sexual abuse or neglect
  • 3 will be living in a step family
  • 1 will have experienced the death of a parent
  • 7 will report having been bullied.

Relate (a leading provider of counseling, therapy, and education in UK)  cites research evidence which shows that emotional and mental health problems developed in childhood and adolescence go on to affect adults later in life. The resulting problems with poor emotional adjustment and general feelings of unhappiness are bad enough. But that is not all the consequences our kids are facing. Unhappiness and emotional imbalance can cause young people to do badly in exams or drop out of education altogether, with consequent damage to their long-term employment prospects and health. For more on the report, see http://www.optimus-education.com/can-schools-promote-happiness.

I agree with Relate’s specialist that schools are the best places to reach young people, and early intervention is effective. But I believe that the most effective solution is prevention. Adding the subject of happiness to school curriculum can help children better deal with their issues, and develop coping mechanisms for the future.

Usually, the kids get emotional guidance and character building from interacting with families and friends. As parents, we always try our hardest to raise good people: continuously pass our wisdom to our kids, indoctrinate our values to them, tell them what is good and what is bad, teach them manners, help them with the choice of profession and life partner (if they let us). But do we teach them how to be happy, joyful, grateful, peaceful? Do we live our lives with contentment and moderation, leading our children by example? Parents are people too, and not all of us are happy ourselves. Unfortunately, we do not always have the time, the vision or the skills to instill the basics of happiness into our children. So both the adults and the kids go about the pursuit of happiness by the trial and error method.

There are more and more politicians, organizations and individuals who believe that happiness skills can be learned and should be included in traditional educations. On his Facebook page, the Dalai Lama says that education is the proper way to promote compassion, piece of mind and tolerance in society, which bring a sense of confidence and reduce stress and anxiety (https://www.facebook.com/DalaiLama) . England requested that schools and colleges promote wellbeing to students (http://www.optimus-education.com/can-schools-promote-happiness). The US army uses classes developed by the “Authentic Happiness” program at the University of Pennsylvania to increase resilience levels of the troops (http://www.authentichappiness.sas.upenn.edu/newsletter.aspx?id=1552).

School is the place where our kids grow up, and where they are formed as individuals as much as they are at home. The school system has the infrastructure for influencing entire generations, letting out better adjusted and happier people. Unfortunately, schools spend most of their efforts on achieving high test results and good rankings. There is little emphasis on personal or emotional development. I believe happiness skills are among some of the most important skills a person possesses. To me it is obvious that the school system must help develop happiness skills as much as literacy skills in all children. I would like to see USA schools and schools all over the world to add happiness lessons to their curricula and deliver it to every kid. It will make for better adults and for better societies, and ultimately, for better world.

To see this happen, I plan to open an organization to raise public support, develop happiness curriculum and promote it to schools and departments of education in the US and possibly, worldwide.

If you think this idea is important and worthwhile, and you would like to help, please contact me. I am looking for anyone who can contribute their skills, knowledge, and advice in the fields of not-for-profit organizations, school curricula, marketing, public relations, legal aspects and more!

Retrieved from: http://olgarythm.blogspot.com/2012/10/why-we-need-to-add-happiness-to-school.html

recipe for a younger brain…

In Brain imaging, Brain studies, Fitness/Health on Friday, 2 November 2012 at 07:11

Two Things Needed for a Younger Brain

Henry S. Lodge, M.D.

When I was in medical school, we were taught that you got all your brain cells by the time you were two years old. And by age 30, you start to lose them. Cognitive aging was simply the slow, steady loss of brain cells that occurred as you age. Well, it turns out this was wrong! Scientists around the world have demonstrated that your brain can continue to grow throughout your life — growing new cells, forming new connections, and rewiring existing ones. But this only happens if you use it. An idle brain will wither and decay, which leads to the decline in cognitive function that we once accepted as being part of the normal aging process.

There are two great roads to rejuvenating your brain, and they might surprise you:
 Exercise. MRI studies show marked growth in new brain tissue after three months of regular exercise. This growth is not just in the parts of the brain that control movement. It’s also evident in the areas responsible for memory, decision-making, and judgment.

 Social Connectedness. Your brain grows and thrives in direct proportion with the meaningful social connections you have — meaning your engagement with friends, family, and your community. People who are lonely and depressed actually lose brain tissue overtime and show marked reductions in cognitive function. But people who stay connected with others and give back to their communities improve their chances of staying vibrant and sharp well into their later years.

There’s a wonderful scientific study going on that’s a great example of the power of staying connected. A program called Experience Corps is putting older people in schools as reading tutors for young kids. The kids are doing better, of course. But the tutors are doing better too — a lot better! All markers of health are improving — blood pressure and weight are going down, and mood and energy are going up. What’s also interesting is that a wide range of blood tests that measure inflammation (linked to long-term risks of heart attack, stroke, and common cancers) also show improvement with social connection and emotional involvement!

Are you surprised at the control we can have over our brain health? Could this prompt you to make different lifestyle choices?

Retrieved from: http://forums.webmd.com/3/mens-health-community/forum/818?ecd=soc_tw_110112_am_community_youngerbrain

adhd and exercise…more positive evidence of benefits

In ADHD, ADHD Adult, ADHD child/adolescent, Education, Fitness/Health, School Psychology on Friday, 2 November 2012 at 06:49

A Little Exercise May Help Kids With ADHD to Focus

Published November 01, 2012

Reuters

Twenty minutes of exercise may help kids with attention-deficit hyperactivity disorder (ADHD) settle in to read or solve a math problem, new research suggests.

The small study, of 40 eight- to 10-year-olds, looked only at the short-term effects of a single bout of exercise. And researchers caution that they are not saying exercise is the answer to ADHD.

But it seems that exercise may at least do no harm to kids’ ability to focus, they say. And further studies should look into whether it’s a good option for managing some children’s ADHD.

“This is only a first study,” said lead researcher Matthew B. Pontifex, of Michigan State University in East Lansing.

“We need to learn how long the effects last, and how exercise might combine with or compare to traditional ADHD treatments” like stimulant medications, Pontifex explained.

He noted that there’s been a lot of research into the relationship between habitual exercise and adults’ thinking and memory, particularly older adults’. But little is known about kids, even though some parents, teachers and doctors have advocated exercise for helping children with ADHD.

So for their study, Pontifex and his colleagues recruited 20 children with diagnosed or suspected ADHD, and 20 ADHD-free kids of the same age and family-income level.

All of the children took a standard test of their ability to ignore distractions and stay focused on a simple task at hand – the main “aspect of cognition” that troubles kids with ADHD, Pontifex noted. The kids also took standard tests of reading, spelling and math skills.

Each child took the tests after either 20 minutes of treadmill exercise or 20 minutes of quiet reading (on separate days).

Overall, the study found, both groups of children performed better after exercise than after reading.

On the test of focusing ability, the ADHD group was correct on about 80 percent of responses after reading, versus about 84 percent after exercise. Kids without ADHD performed better – reaching about a 90 percent correct rate after exercise.

Similarly, both groups of kids scored higher on their reading and math tests after exercise, versus post-reading.

It’s hard to say what those higher one-time scores could mean in real life, according to Pontifex, who published his results in The Journal of Pediatrics.

One of the big questions is whether regular exercise would have lasting effects on kids’ ability to focus or their school performance, he said.

And why would exercise help children, with or without ADHD, focus? “We really don’t know the mechanisms right now,” Pontifex said.

But there is a theory that the attention problems of ADHD are related to an “underarousal” of the central nervous system. It’s possible that a bout of exercise helps kids zero in on a specific task, at least in the short term.

Parents and experts alike are becoming more and more interested in alternatives to drugs for ADHD, Pontifex noted. It’s estimated that 44 percent of U.S. children with the disorder are not on any medication for it.

And even when kids are using medication, additional treatments may help them cut down their doses. Pontifex said future studies should look at whether exercise fits that bill.

“We’re not suggesting that exercise is a replacement, or that parents should pull their kids off of their medication,” Pontifex said.

But, he added, they could encourage their child to be active for the overall health benefits, and talk with their doctor about whether exercise could help manage ADHD specifically.

“Exercise is beneficial for all children,” Pontifex noted. “We’re providing some evidence that there’s an additional benefit on cognition.”

Retrieved from: http://www.foxnews.com/health/2012/11/01/little-exercise-may-help-kids-with-adhd-focus/?utm_source=twitterfeed&utm_medium=twitter#ixzz2B3qU8bOp

what are you grateful for? practice gratitude.

In Alternative Health, Fitness/Health, Mindfulness on Friday, 2 November 2012 at 06:25

The Year In Gratitude: Introducing the virtual Gratitude Visit

By DANIEL TOMASULO, PH.D.

“You have to take risks. We will only understand the miracle of life fully when we allow the unexpected to happen.” — Paulo Coelho

Each year is a transition.  We let go of relationships, connections to places, jobs and ways of being.  But this opens us to new people, new associations and different ways of relating.  Through death or circumstance or choice we move away from those we loved, or cared for, or knew: The unknown, the surprise, the unexpected takes their place.  This is life.

Too often the losses weigh us down with a centrifugal sadness that keeps us pinned to the passing.  Our energy is invested in the mourning, often for longer than what may be healthy or helpful.

But the loss we experience is directly proportional to the joy and love and engagement we’ve had.  We feel the pain because we knew the joy.  So the grieving must honor the connection as well.

The research on gratitude keeps demonstrating how powerful a positive intervention of having gratitude in our lives can be.  To acknowledge someone for being in your life is one of the most dynamic ways to increase your well-being and the well-being of others.  This exercise works best if you write it down, and even better if you can deliver a letter of gratitude to the person involved.  Here’s how it works.

Think of a person who has been a positive person in your life, but with whom you are no longer involved.  Write out a letter of gratitude for the positive features of your relationship.

If it is possible and appropriate, meaning that it would not cause harm, embarrassment or upset to the other person, find them.  Track them down and read them the letter.  This is the famous gratitude visit exercise researched by Martin Seligman, the positive psychology researcher.

If they are unavailable or have died, read the letter out loud to an empty chair.  Let them know how much you appreciate who they are (were) and the joy and gratitude you have for them being (or have been) in your life.

Now for the interesting part: Reverse roles. Sit in the empty chair and become them for the role play. As them, respond to the letter that was just read to you.

Finally, come back into your own chair and say the final things you wish to say.  Notice how you feel.  Yes, they may no longer be in your life, but honoring the joys they brought you can help them if they are available, and you feel better if it is done through an empty chair.  I call this second method the Virtual Gratitude Visit (VGV).

There may be others you would like to share your gratitude with.  New research has show that gratitude toward God is perhaps one of the most powerful ways to evoke feelings of well-being.  With a VGV you may want to express your gratitude toward God.  Yes, it is okay to reverse roles and become him, but don’t forget to come back to your own chair.  Otherwise you are going to find a lot of prayer requests in your email inbox.

Last but not least, as we transition into the New Year, perform a VGV toward the people we haven’t met.  When I think back to last January and the people I said goodbye to over the year, literally several dozen new people came into my life who have filled me with unexpected joy and hope and wonderment.  Gratitude can be used to open us up to the future.  Try a VGV with a person you haven’t met yet but know you are scheduled to meet, or to the unknown, unexpected encounters you are bound to have. You may even want to express your gratitude toward a future self, the person you are becoming over the next year.

Finally, when the dust from the VGVs settles down, take a moment and review the year. Notice your breath.  Just like people and events in our life, our breath is drawn in and released.  We don’t hold on or just breathe out: we take in and let go.  What we are left with is the stuff of life.

We began with the words of the brilliant Brazilian lyricist and novelist, Paulo Coelho.  I don’t think anyone could say it more clearly than him, so it seems fitting to end with his thoughts as well. “When someone leaves, it’s because someone else is about to arrive.” 

References

Rosmarin, D.H., Pirutinsky, S., Cohen. A., Galler, Y., & Krumrei, E.J. (2011). Grateful to God or just plain grateful? A study of religious and non-religious gratitude. Journal of Positive Psychology, 6(5), 389-396.

Seligman, M. E. P., Steen, T. A., Park, N., & Peterson, C. (2005). Positive psychology progress: Empirical validation of interventions. American Psychologist, 60(5), 410.

Tomasulo, D. (2011). Can God and Gratitude Help Your Mental Health?. Psych Central. Retrieved on December 27, 2011, from http://psychcentral.com/blog/archives /2011/12/11/can-god-and-gratitude-help-your-mental-health/

Retrieved from: http://psychcentral.com/blog/archives/2012/01/03/the-year-in-gratitude-introducing-the-virtual-gratitude-visit/

Gratitude Research Delivered: Diagnosis, Part Two

By DANIEL TOMASULO, PH.D.

Jen Cunningham Butler uses a highly proactive and inspiring approach in dealing with the anniversary of her cancer diagnosis. At once it was corrective and intuitive; courageous and simple; heartfelt and effective.  Jen prepares for the day by honoring her health and recovery. She actively demonstrates her gratitude toward the physicians, nurses  and support staff involved in her treatment. Her story is detailed in Part One.

Part One chronicles Butler’s ongoing effort to demonstrate gratitude to all those who helped during her treatment.  These are simple acts of gratitude such as writing notes, bringing a tray of goodies into the treatment center, and even lollipops to the parking attendants.

Although these offerings of gratitude are modest, these actions undid the anxiety of recalling the day, while activating a positive sense of self and affecting others.  Instead of anxiety and depression, she was able to instill joy, feelings of well-being, and hope — because some of the goodies were delivered personally to women currently undergoing radiation.

We could leave this as a beautiful example of a human interest story, knowing that the tale alone will inspire others to approach their diagnosis day, divorce day, or whatever their “D” Day is in a different manner.  But there is something more to this story that intrigued me.

What Jen had done intuitively was to follow some foundational research in gratitude.  In fact, the cornerstone of what she did is an exact representation of one of the original positive interventions offered by Martin Seligman, former president of the American Psychological Association and the man introduced at conferences now as the “Father of Positive Psychology.”

In a seminal 2005 article, Seligman and his colleagues (Seligman, Steen, Park, & Peterson, 2005) reported on studies with five positive interventions.  One of these they simply called the gratitude visit.  The Internet-based study engaged participants to write a letter of gratitude to someone who had been particularly kind to them in the past, but who had never been properly thanked.  Then the participants had to deliver the letter personally.

Sound familiar?

What made this study so unique in the field of positive psychology was that it was a randomized control study. The gold standard of research designs, it randomly assigns participants to the condition(s) being studied, one of which is a placebo.  The placebo condition for this experiment was to ask participants to write about their early memories every night for a week. These folks were then compared to people delivering the gratitude visit.  Those participants were given a week to write and deliver a letter of gratitude as described above.

The researchers used results from 411 participants and measured them on two scales, the Center for Epidemiological Studies–Depression Scale (CES-D), and the Steen Happiness Index (SHI).

The results?  One week after the study, people taking part in the gratitude visit were happier and less depressed, and this lasted for one month after they had completed the visit.  Of the five interventions studied, those taking part in the gratitude visit demonstrated the greatest positive change.

There are two interesting features of this study.  First, it demonstrates that a gratitude visit isn’t merely an act of kindness, it is a proven method of improving well-being by increasing happiness and reducing symptoms of depression.  Second, a six-month followup of all participants found that those who continued their particular exercise on their own continued to experience long-term benefits.

Jen thinks about her gratitude visits all year long.  Her benefits are ongoing.

Thank you, Jen, for giving us inspiration and encouragement with your ongoing examples of turning lemons into lemon trees.  For the rest of us there is only one question left: Who are we going to write our gratitude letter to?

For more information and another gratitude intervention check here.

References

Seligman, M. E. P., Steen, T. A., Park, N., & Peterson, C. (2005). Positive psychology progress: Empirical validation of interventions. American Psychologist, 60(5), 410.

Tomasulo, D. (2012). The Year in Gratitude: Introducing the Virtual Gratitude VisitPsych Central. Retrieved on October 28, 2012, from http://psychcentral.com/blog/archives/2012/01/03/the-year-in-gratitude-introducing-the-virtual-gratitude-visit/

Retrieved from: http://psychcentral.com/blog/archives/2012/11/01/gratitude-research-delivered-diagnosis-day-part-two/

 

the workplace blahs…

In Fitness/Health on Friday, 2 November 2012 at 05:31

What to Do When You Feel Blah About Your Job

By MARGARITA TARTAKOVSKY, M.S.

You open your eyes, and a feeling of dread washes over you. It’s a weekday, which means it’s a

workday, which makes work one of the last places you’d like to be.

Or maybe you don’t feel dread, exactly. Instead, it’s a vague feeling. Something between despair and

delight – perhaps indifference. You’re not particularly excited about your job. But you’re also not running

for the hills.

Either way, your job isn’t doing it for you: You’re feeling blah.

And you’re not alone. According to a 2011 survey by consulting company Accenture, 57 percent of

women and 59 percent of men were dissatisfied with their jobs.

Blah feelings can mean many things. The key is to dig deeper, and see how you can improve your work

situation — and ultimately your life. Below, two seasoned coaches share their wisdom on what to do.

Excavating Your Blah Feelings

For starters, consider if the blahs follow you after work. “Check in and see if you feel blah when on vacation, over the weekend, and when

doing things outside of work that are restorative or fun,” said Rachel W. Cole, a life coach and retreat leader.

Let’s say they don’t. Let’s say your blah feelings are isolated to your work. But is it your profession as a whole or something about your

particular job that’s the problem?

“Is it the people, the tasks, the subject matter, the hours, the pressure of a tight deadline, the too-much-time-glued-to-a-computerscreen?” said Michelle Ward, the When I Grow Up Coach, who’s helped hundreds of people create the career they think they can’t have —

or discover in the first place.

For instance, Ward worked with a teacher who wanted her help in finding a new career path. After six sessions, however, she realized that

she didn’t need to switch careers; she needed to switch jobs. Today, Ward’s client is working at “another school where the staff [is] kind

and open to new ideas,” Ward said.

If you’re not sure which parts of your job are problematic, for several days, keep a notebook close by as you work, she said. Any time

you’re feeling blah, jot down precisely what you’re doing. “Get as specific as you can,” Ward said.

Identifying Your Hungers and Values

Determining your true values and desires is an important step toward realizing a fulfilling career and life. Does your current job align with

your deepest values or desires?

Cole works with clients to identify their hungers so they can lead well-fed lives. “Practice noticing what doesn’t feel good [or] right,

[which] usually points to a hunger,” she said. She also suggested answering these journal prompts:

“I’m afraid I can’t/won’t get it, but what I really desire is…”

“No one in my life knows I secretly hunger for…”

“If I’m honest with myself, I’m deeply and truly hungry for…”

Ward asks her clients to complete a “Values Game” at this site. “[It] helps you hone in — and then prioritize — what your values are,” she

said.

She also suggested readers reflect on meaningful moments in their lives. “If they get clear on why those moments felt that way to them,

then their values aren’t far behind,” she said.

Switching Careers or Pursuing Passions on the Side

Should you stay with your current career – or should you switch professions altogether? “It boils down to what’s meaningful to [you],

what feels enough,” Ward said.

Some people are perfectly happy doing work they’re good at – and then volunteering, sewing or styling on the side, she said.

However, others yearn to do things they’re passionate about as their profession, she said. For these individuals a side gig simply isn’t

enough.

But, of course, switching careers isn’t simple. So “don’t do it unless you really just have to,” Ward said. “You need that ache, that sense

of regret if you don’t go for it.”

Again, self-reflection can help you in making this difficult decision. Cole suggested asking yourself these questions:

  • “How does work make me feel?”
  • “Is it my specific workplace that doesn’t work for me or is it the career itself?”
  • “Does the job leave me enough time and energy to pursue my passion after work?”
  • “Are there ways to change my current job to meet some or all of my needs [such as] delegating to others, asking to telecommute, etc.?”
  • “If I had a year to live, and I still needed to employed, would I stay here or leave?”

If you’re still stumped, hiring a coach can be incredibly helpful. (Also, check out Ward’s series with inspiring stories of people who’ve found new jobs or started their own businesses since 2008.)

Remember that “It’s never ever too late in life to change your mind, switch paths, try something new, change our mind again, do a U-turn or take a sharp left,” Cole said. Linear career paths are rare, she said.

“Switch up your life to match who you are now and what you know about yourself,” she said.

Retrieved from: http://psychcentral.com/blog/archives/2012/11/01/what-to-do-when-you-feel-blah-about-your-job/

sex and the smartphone…

In Fitness/Health on Thursday, 1 November 2012 at 08:23

Teens Who Use Smartphones May Engage in More Sex

By Rachael Rettner
MyHealthNewsDaily

Teens who own a smartphone may be at increased risk for engaging in risky sex behavior, a new study suggests.

In the study, teens who had access to the Internet on their cellphones were more than twice as likely to engage in sex with a person they met online compared with those without access to the Internet on their phones. Teens with smartphones were also more likely to be sexually active in general, and more likely to say they had been approached for sex online.

The results held even after the researchers accounted for factors that could affect sexual behavior and cellphone use, such as age, gender, race and sexual orientation.

The study was presented here today (Oct. 30) at the annual meeting of the America PublicHealth Association.

Smartphones likely aren’t directly causing risky teen sex, said study researcher Eric Rice, of the University of Southern California’s School of Social Work in Los Angeles. Rather, smartphones may make it easier for teens to arrange sexual encounters, Rice said.

“It’s a tool through which this sort of behavior can happen,” Rice said.

While parents have come up with strategies to monitor the online behavior of their kids on computers, “I don’t know that we’ve thought through quite as clearly what it means for teens to have the Internet on their phones 24 hours a day,” Rice said.

Rice said sex education programs should start to include discussions regarding the risks of seeking sex online. In addition, parents should use this as an opportunity to begin a discussion with their teen about sexual health and use of technology, he said.

“I don’t want parents to freak out,” Rice said.

The study involved about 1,840 high-school students in the Los Angeles Unified School District who were surveyed in the 2010 to 2011 school year. The majority (71 percent) identified as Hispanic or Latino.

About one-third said they had a smartphone, 5 percent said they used the Internet to seek sex partners, and 17 percent said they had been approached for sex online. For comparison, a Nielson survey released in September found about 58 percent of 13- to 17-year-olds now own a smartphone. Differences in demographic factors may have also played a role in smartphone ownership.

Forty-seven percent of teens who owned a smartphone said they were sexually active, compared with 35 percent of those who did not own a smartphone.

The researchers plan to submit their study for publication in a scientific journal.

Follow Rachael Rettner on Twitter @RachaelRettner, or MyHealthNewsDaily @MyHealth_MHND.We’re also on Facebook & Google+.

Retrieved from: http://vitals.nbcnews.com/_news/2012/10/30/14810390-teens-who-use-smartphones-may-engage-in-more-sex?lite

this won’t hurt a bit…and it’s the truth!

In Fitness/Health on Thursday, 1 November 2012 at 06:48

article regarding children, pain, anxiety, and a good doctor.

http://commonhealth.wbur.org/2012/09/doctor-says-it-wont-hurt

obesity statistics for students in a philadelphia school…

In Education, Fitness/Health on Wednesday, 31 October 2012 at 15:06

Prevalence, Disparities, and Trends in Obesity and Severe Obesity Among Students in the Philadelphia, Pennsylvania, School District

Jessica M. Robbins, PhD, Giridhar Mallya, MD, MSHP, Marcia Polansky, ScD, MS, MSW, Donald F. Schwarz, MD, MPH

Prev Chronic Dis. 2012;9 © 2012 Centers for Disease Control and Prevention (CDC)

Abstract

Introduction Epidemic increases in obesity negatively affect the health of US children, individually and at the population level. Although surveillance of childhood obesity at the local level is challenging, height and weight data routinely collected by school districts are valuable and often underused public health resources.
Methods We analyzed data from the School District of Philadelphia for 4 school years (2006–2007 through 2009–2010) to assess the prevalence of and trends in obesity and severe obesity among public school children.
Results The prevalence of obesity decreased from 21.5% in 2006–2007 to 20.5% in 2009–2010, and the prevalence of severe obesity decreased from 8.5% to 7.9%. Both obesity and severe obesity were more common among students in grades 6 through 8 than among children in lower grades or among high school students. Hispanic boys and African American girls had the highest prevalence of obesity and severe obesity; Asian girls had much lower rates of obesity and severe obesity than any other group. Although obesity and severe obesity declined during the 4-year period in almost all demographic groups, the decreases were generally smaller in the groups with the highest prevalence, including high school students, Hispanic males, and African American females.
Conclusion Although these data suggest that the epidemic of childhood obesity may have begun to recede in Philadelphia, unacceptably high rates of obesity and severe obesity continue to threaten the health and futures of many school children.

Introduction

Childhood obesity increased dramatically in the latter part of the 20th century, making it a leading public health issue.[1] In 2009–2010, 18.2% of US children aged 6 through 19 years were obese, although national data suggest that the prevalence of childhood obesity is plateauing.[2] Arkansas data support this trend, while recent New York City data indicate that childhood obesity is decreasing;[3–7] however, the long-term trends and applicability to other parts of the United States are uncertain.

Recent efforts have been made to assess the epidemic increases in childhood obesity in the United States through public health surveillance methods. An important context in which such surveillance can take place is the school, because most children aged 5 through 18 years are enrolled in school and 90% of these students attend public schools.[8] Many schools have nurses or other trained health personnel on site, and increasing numbers of school districts have mandated routine weight screening for students. The Centers for Disease Control and Prevention commissioned a report to provide guidance for school-based body mass index (BMI) measurement programs;[9] Arkansas mandated school statewide BMI screening beginning in 2003, and as of 2009, a dozen other states had followed suit.[9] Nonetheless, few communities have obtained and analyzed their data to track childhood obesity at the local level.[10]

To identify the baseline prevalence and trends in childhood obesity locally, we analyzed height and weight data for students in kindergarten through grade 12 in the School District of Philadelphia. The school district includes approximately 300 public and charter schools, educating approximately 200,000 students. More than 80% of students are of racial/ethnic minorities, and more than 50% are eligible for free or reduced-price meals based on family income.

Our primary goals were to assess the prevalence of obesity and severe obesity among children in the School District of Philadelphia and to determine whether the prevalence of obesity and severe obesity changed between 2006–2007 and 2009–2010, the most recent school year for which data were available.

Methods

School District of Philadelphia records cover all students enrolled in Philadelphia public schools at any point during the year, a number that varied from 189,913 in 2006–2007 to 177,499 in 2009–2010 (T. Williams, written communication, April 2012). Students who attended charter schools exclusively were not included. Analyses were limited to students aged 5 through 18 for whom valid height and weight measurements were recorded. These students represented an increasing percentage of the total school population over the 4 school years included, from 61.6% in 2006–2007 to 70.4% in 2009–2010. The demographics of the total school population are presented in the Appendix.

Students’ heights and weights were measured by school nurses. Pennsylvania mandates that all children in kindergarten through grade 12 have their height and weight measured annually by a nurse or teacher. The Pennsylvania Department of Health’s Division of Chronic Disease Intervention and Division of School Health have developed a manual to provide guidance to school districts and other educational entities on best practices in measuring and reporting these data.[11] The measured heights and weights were entered into a secure school district database with the date of the examination. BMI measurements for girls whose records indicated a pregnancy were excluded from these analyses.

BMI was calculated as weight (kg)/height (m2) and compared with sex and age-specific norms from CDC growth charts[12] to determine BMI percentile. Obesity was defined as a BMI at or above the 95th percentile. Severe obesity was defined as a BMI of 35 or higher or 120% or greater of the threshold for obesity, based on the recommendation of Flegal et al.[13] The validity of the 99th percentile estimates that have been commonly used to characterize severe obesity among children is questionable; these estimates do not match well to the empirical data on which the CDC growth charts were based.[13] We conducted a secondary analysis of BMI values above the 99th percentile criterion to assess the sensitivity of the results to the differences in definition of severe obesity.

The demographic variables examined were sex; race/ethnicity; socioeconomic status, using eligibility for free or reduced-price school meals as a proxy; and grade. Race/ethnicity patterns were different for boys and girls and are therefore presented separately by sex. Data were weighted for nonresponse so that the measured population would more accurately represent the entire school population. Weights were calculated by grade and racial/ethnic group.

Although no intentional sampling was conducted, we conducted significance tests using SAS version 9.2 (SAS Institute, Inc, Cary, North Carolina) to assess the likelihood that changes over time represented chance findings. We assessed the significance of changes across time by testing a linear variable for school year in multivariable models that included a race/ethnicity–sex term, age in years, grade, and eligibility for free or reduced-price meals, adjusted for clustering within schools. Separate models were also conducted for each demographic group to assess time trends within groups.

To assess the possibility of bias associated with missing data, we identified a subsample of schools in which missing data were minimized (defined as at least 75% of all enrolled students having been measured during the school year), calculated the prevalence of obesity in this high-response sample, and compared the results with those of the total study population.

Results

Valid height and weight measurements were obtained for 61.6% of all students in 2006–2007, 66.4% in 2007–2008, 69.1% in 2008–2009, and 70.4% in 2009–2010. These figures exclude girls whose records indicated a pregnancy during the school year (n = 1,134 during all 4 school years, 0.48% of all measured female students).

The demographics of the study population were similar to those of the entire student population, except that a larger proportion of the total population was in grades 9 through 12 (31.5% in 2009–2010, compared with 26.4% of the measured population) and a smaller proportion was in kindergarten through grade 5 (46.7% compared with 51.0%) (Table 1). The demographic characteristics of the population were generally similar for all 4 years. Boys comprised approximately 51% of the student population throughout the study period. African Americans were the largest racial/ethnic group (60.1% of all students and 59.3% of those measured in 2009–2010), followed by Hispanics (17.6% of all students, 16.7% of those measured), non-Hispanic whites (13.6% of all students, 14.2% of those measured), and Asians (6.3% of all students, 7.2% of those measured). The most notable change over time was the increase in the proportion of students who were eligible for free or reduced-price meals (from 48.9% to 57.4% among all students and from 50.8% to 59.5% among those measured), a change that occurred primarily between the 2007–2008 school year and the 2008–2009 school year.

In 2009–2010, the prevalence of obesity among Philadelphia’s public school students was 20.5% (Table 2). The prevalence was higher among students in grades 6 through 8 (23.0%), compared with both kindergarten through fifth grade (19.1%) and high school students (20.8%). Among boys in 2009–2010, Hispanics had the highest prevalence of obesity (25.6%), followed by whites (20.7%); among girls in 2009–2010, African Americans had the highest prevalence (22.7%), followed by Hispanics (20.6%). The lowest prevalence by far—less than half that of any other group—was among Asian females, at 8.9% in 2009–2010.

Obesity declined slightly from 21.5% in 2006–2007 to 20.5% in 2009–2010, representing a 4.8% decrease (Table 2). Most of the decrease was between 2006–2007 and 2008–2009, followed by a leveling off in 2009–2010. This pattern varied by demographic group. At the beginning of the period, the prevalence of obesity was slightly higher among boys than girls (21.7% vs 21.3%); in the most recent school year this was reversed (20.4% among boys vs 20.6% among girls). Among high school students, the small decline in obesity was not significant. Trends within racial/ethnic–sex groups were significant for African American, non-Hispanic white, and Asian boys and for Hispanic girls. None of the subgroup changes between 2008–2009 and 2009–2010 was significant.

The prevalence of severe obesity in 2009–2010 was 7.9% (Table 3). Patterns of disparities in severe obesity were similar to those for obesity. Severe obesity was most prevalent among students in grades 6 through 8 (9.1% in 2009–2010), and the prevalence of severe obesity exceeded 9% among Hispanic boys and African American girls in 2009–2010. Trends over time in severe obesity were similar overall to those for obesity (Table 3). For the overall population, severe obesity prevalence decreased from 8.5% to 7.9% from 2006–2007 to 2009–2010, representing a 7.7% decrease. The largest significant changes were seen among African American boys and Hispanic girls. Results using the 99th percentile of BMI as a threshold (not shown) showed similar patterns, with slightly lower overall prevalence and somewhat larger declines over time (from 6.3% in 2006–2007 to 5.6% in 2009–2010).

Some groups that had shown declines in obesity, severe obesity, or both, including those with the highest prevalence of severe obesity, experienced small nonsignificant increases during the 2009–2010 school year. Most schools contributed at least 1 school year to the high-response subset with measurements for 75% or more of enrolled students. Analyses limited to this subset did not differ substantially from results for the complete data.

Discussion

Analyses of annually collected height and weight data on more than 100,000 public school children in Philadelphia from 2006–2007 to 2009–2010 demonstrated that the prevalence of obesity may be decreasing in small but potentially meaningful ways. However, trends were not consistent across subgroups, and obesity remains alarmingly high, particularly among some racial and ethnic minorities. Severe obesity, which confers the greatest short- and long-term risks to physical and emotional health, affects nearly 1 in 12 children in Philadelphia.

Some of these findings are consistent with national statistics on child overweight and obesity from the National Health and Nutrition Examination Surveys (NHANES),[2] although national rates of obesity in 2009–2010 were lower than those found among Philadelphia public school children. The differences were greatest for non-Hispanic whites, among whom 17.2% of boys and 13.0% of girls aged 6 to 19 years were obese nationally, compared with 20.7% of boys and 17.3% of girls aged 5 through 18 years in the School District of Philadelphia. This finding may reflect differences in socioeconomic status between whites in Philadelphia public schools and the US population overall. African Americans in the School District of Philadelphia had lower rates of obesity than those in the national data (19.1% for boys and 22.7% for girls in Philadelphia vs 25.4% for boys and 26.1% for girls nationally). In both the NHANES and School District of Philadelphia data, African American girls had higher rates of obesity than non-Hispanic white girls. In the NHANES data, African American boys also had higher rates of obesity than non-Hispanic white boys, although the opposite was true among Philadelphia public school children. This may again reflect the lower socioeconomic status of whites in the Philadelphia public schools compared with those in the national NHANES sample.

The NHANES study did not find evidence of any noticeable trends in obesity prevalence from 2007–2008 through 2009–2010. The differences seen between the School District of Philadelphia and NHANES data may reflect the different age ranges (5 through 18 in Philadelphia vs 6 through 19 in NHANES), different periods (2006–2010 vs 2007–2010), differences in measurement and methods, or genuine differences between Philadelphia public school children and national averages. The small size of the NHANES study population, which yielded 80% power to detect changes in obesity prevalence of 5% or more,[14] may have precluded detecting declines in obesity over this period.

Routinely collected BMI data for public school children have been published only for a few jurisdictions, including New York City and Arkansas. The prevalence, disparities, and trends in obesity among public school children in New York City were similar to those seen here, with generally consistent small declines in obesity, including an apparent leveling off in both cities in 2009–2010. Among students in kindergarten through eighth grade, the prevalence of obesity in Philadelphia public school children was between 0.2% and 0.7% lower than among those in New York City in the same period. In 2009–2010, the prevalence of obesity in these grades was 20.3% in Philadelphia and 21.0% in New York City.[7]

The prevalence of obesity found in Philadelphia public school children is also similar to statewide findings for public school children in Arkansas. The prevalence in the 2009–2010 school year was 21% in Arkansas and 20% in Philadelphia.[3] Trends were generally declining or flat during the last several years. Many of the specific racial/ethnic differences noted, such as the marked sex disparity among Asian students, are consistent.[3–6] Arkansas has not, however, reported the recent decline in obesity among African Americans noted in both Philadelphia and New York City.

Children affected by severe obesity face even greater health risks than obese children. Among children examined in the NHANES survey, those who were above the 99th percentile of BMI had higher mean blood pressures and insulin levels, lower mean high-density lipoprotein (HDL) cholesterol levels, and higher prevalence of metabolic syndrome than those who had BMI percentiles in the 95th to 97th range, putting them at greater risk of cardiovascular disease.[15] In the HEALTHY study, a survey of primarily low-income and minority sixth-graders, students with BMI at or above the 99th percentile had higher blood pressure and insulin levels, lower HDL cholesterol levels, and larger waist circumferences than those who were moderately obese.[16] Psychosocial comorbidities are also more severe among children and youth with severe obesity.[17] Although the prevalence and consequences of severe obesity in children have prompted widespread interest in various interventions, including bariatric surgery for adolescents[18] and child welfare involvement,[19] trends in severe obesity have been less widely studied or reported than those for overweight and obesity. Madsen et al, using different definitions of severe obesity (BMI ≥97th or ≥99th percentile), reported differing trends among subgroups of California students.[20] Some of the patterns they found, such as continuing increases in severe obesity among African American girls, are not consistent with those found from analysis of School District of Philadelphia data. This inconsistency could reflect regional differences; our secondary analysis indicated that using BMI at or above the 99th percentile to define severe obesity would not affect these trends.

Many of the strengths and limitations of these data originate from the routine screening assessments of student populations conducted by school nurses. The data represent large, unselected populations and were collected by experienced clinical professionals; conversely, they were not collected under rigorous protocols or with consistent equipment, nor were they validated. Research on the accuracy of measurements taken in schools suggests that measurements taken by school nurses are of reasonably high quality.[21] The substantial proportions of students that were not measured, especially in the higher grades, leave potential for selection bias, although our secondary analyses suggest that such bias is limited. Children who did not attend public schools during the school year, including those who attended private, parochial, and charter schools, were not included, and obesity prevalence and trends could differ in these groups. The similarities seen in both trends over time and disparities between racial/ethnic–sex groups when comparing the Philadelphia data with data from New York City and Arkansas strengthen our confidence in their accuracy.

Although these data do not allow us to say what is responsible for the apparent reversal of the trend toward increasing childhood obesity, greater attention has been paid to improving school health environments both nationally and in the School District of Philadelphia. Since 1999, the EAT.RIGHT.NOW. Pennsylvania Nutrition Education TRACKS program has provided nutrition education to all students and parents who are eligible for SNAP (the federal Supplemental Nutrition Assistance Program) and is now in more than 270 district schools (T.E. Wolford, written communication, March 2012). In 2004, the district beverage policy mandated the removal of all sodas and sugar-sweetened drinks from vending machines, and in 2006 snack standards were developed for á la carte and vending items. In 2006, the Philadelphia School Reform Commission passed a comprehensive School Wellness Policy with provisions for competitive foods, physical activity, and nutrition education. Finally, from 2009–2010, School Food Services began offering “universal” or free breakfast to all students, discontinued the use of fryers, and switched from 2% to 1% low-fat milk. In 2010, the Philadelphia Department of Public Health (PDPH) launched the Get Healthy Philly (www.foodfitphilly.org) initiative to improve nutrition and physical activity through citywide policy and systems changes. PDPH has partnered with public and private sector organizations, including the School District of Philadelphia, to decrease the population-level burden of obesity and related diseases, particularly among children. Such comprehensive efforts may help accelerate the decreases in BMI found in the study reported here.

The inconsistency of findings between subgroups and the small increases in obesity, severe obesity or both in some groups in the most recent year of data indicate that it is not yet certain that the epidemic increases in child obesity are over. Continued surveillance is required to clarify whether we are seeing minor inconsistencies in a continuing crisis or a true change in the epidemic.

In either case, the prevalence of unhealthy weight remains unacceptably high among public school children in Philadelphia, and the evidence that some groups are facing exceptionally high health risks associated with obesity is sobering. When almost 9% of all teenage students are severely obese, identifying effective means of preventing obesity in our children, helping those already affected to attain a healthier weight, and preventing the serious chronic health problems associated with obesity remain urgent public health responsibilities.

Appendix:

Appendix.  Demographic Characteristics of All Students Aged 5 Through 18 Years, Philadelphia School District, 2006–2010a

Characteristic School Year, n (%)  
2006–2007 2007–2008 2008–2009 2009–2010  
Total% 186,224 (100.0)% 180,479 (100.0)% 175,632 (100.0)% 172,975 (100.0)  
Grade  
K-5% 83,155 (44.7)% 81,395 (45.1)% 80,417 (45.8)% 80,723 (46.7)  
6–8% 43,591 (23.4)% 40,679 (22.5)% 38,288 (21.8)% 36,967 (21.4)  
9–12% 58,711 (31.5)% 57,677 (32.0)% 56,197 (32.0)% 54,533 (31.5)  
Ungraded% 728 (0.4)% 728 (0.4)% 730 (0.4)% 752 (0.4)  
Age, y  
5% 7,960 (4.3)% 7,819 (4.3)% 7,889 (4.5)% 7,904 (4.6)  
6–8% 40,298 (21.6)% 39,384 (21.8)% 39,720 (22.6)% 39,718 (23.0)  
9–12% 54,123 (29.1)% 52,048 (28.8)% 50,581 (28.8)% 50,435 (29.2)  
13–15% 47,144 (25.3)% 43,872 (24.3)% 40,576 (23.1)% 39,098 (22.6)  
16–18% 36,699 (19.7)% 37,356 (20.7)% 36,866 (21.0)% 35,820 (20.7)  
Sex  
Male% 96,119 (51.6)% 93,092 (51.6)% 90,583 (51.6)% 89,046 (51.5)  
Female% 90,105 (48.4)% 87,387 (48.4)% 85,049 (48.4)% 83,929 (48.5)  
Race/ethnicity  
African American% 117,064 (62.9)% 111,813 (62.0)% 107,887 (61.4)% 104,007 (60.1)  
Hispanic% 30,878 (16.6)% 30,948 (17.1)% 30,225 (17.2)% 30,536 (17.7)  
Non-Hispanic white% 25,502 (13.7)% 24,558 (13.6)% 23,830 (13.6)% 23,459 (13.6)  
Asian% 10,548 (5.7)% 10,539 (5.8)% 10,606 (6.0)% 10,901 (6.3)  
Other% 2,232 (1.2)% 2,621 (1.5)% 3,084 (1.8)% 4,072 (2.4)  
Eligibility for free/reduced-price meals  
Eligible% 91,016 (48.9)% 86,666 (48.0)% 99,829 (56.8)% 99,333 (57.4)  
Not eligible% 95,208 (51.1)% 93,813 (52.0)% 75,803 (43.2)% 73,642 (42.6)  

Abbreviation: K, kindergarten.
a Values may not sum to total due to missing data.

References

  1. Ogden CL, Flegal KM, Carroll MD, Johnson CL. Prevalence and trends in overweight among US children and adolescents, 1999–2000. JAMA 2002;288(14):1728–32.
  2. Ogden CL, Carroll MD, Kit BK, Flegal KM. Prevalence of obesity and trends in body mass index among US children and adolescents, 1999–2010. JAMA 2012;307(5):483–90.
  3. Year eight assessment of childhood and adolescent obesity in Arkansas (fall 2010 – spring 2011). Little Rock (AK): Arkansas Center for Health Improvement; February 2012.
  4. Year seven assessment of childhood and adolescent obesity in Arkansas (fall 2009-spring 2010). Little Rock (AK): Arkansas Center for Health Improvement; December 2010.
  5. Year six assessment of childhood and adolescent obesity in Arkansas (fall 2008-spring 2009). Little Rock (AK): Arkansas Center for Health Improvement; December 2009.
  6. Year five assessment of childhood and adolescent obesity in Arkansas (fall 2007–spring 2008). Little Rock (AK): Arkansas Center for Health Improvement; September 2008.
  7. Centers for Disease Control and Prevention. Obesity in K-8 students — New York City, 2006–07 to 2010–11 school years. MMWR Morb Mortal Wkly Rep 2011;60(49):1673–8.
  8. Strizek GA, Pittsonberger JL, Riordan KE, Lyter DM, Orlofsky GF. Characteristics of schools, districts, teachers, principals, and school libraries in the United States: 2003–04 Schools and Staffing Survey (NCES 2006–313). Washington (DC): US Government Printing Office, US Department of Education, National Center for Education Statistics; 2006.
  9. Nihiser AJ, Lee SM, Wechsler H, McKenna M, Odom E, Reinold C, et al. BMI measurement in schools. Pediatrics 2009;124(Suppl 1):S89–S97.
  10. Sheon A, Katta V, Costello B, Longjohn M, Mantinan K. Registry-Based BMI Surveillance: A Guide to System Preparation, Design, and Implementation. Altarum Institute, June 2011. http://www.altarum.org/files/imce/Chomp_BMI_FINAL_060811lr.pdf.
  11. Johnson CB, Huff MK, Gray A. Procedures for the growth screening program for Pennsylvania’s school-age population. Harrisburg (PA): Pennsylvania Department of Health; 2004.
  12. Kuczmarski RJ, Ogden CL, Guo SS, Grummer-Strawn LM, Flegal KM, Mei Z, et al. CDC growth charts for the United States: methods and development. Vital Health Stat 11 2002;(246):1–190.
  13. Flegal KM, Wei R, Ogden CL, Freedman DS, Johnson CL, Curtin LR. Characterizing extreme values of body mass index–for-age by using the 2000 Centers for Disease Control and Prevention growth charts. Am J Clin Nutr 2009;90(5):1314–20.
  14. Ogden CL, Carroll MD, Curtin LR, Lamb MM, Flegal KM. Prevalence of high body mass index in US children and adolescents, 2007–2008. JAMA 2010;303(3):242–9.
  15. Skelton JA, Cook SR, Auinger P, Klein JD, Barlow SE. Prevalence and trends of severe obesity among US children and adolescents. Acad Pediatr 2009;9(5):322–9.
  16. Marcus MD, Baranowski T, DeBar LL, Edelstein S, Kaufman FR, Schneider M, et al. Severe obesity and selected risk factors in a sixth grade multiracial cohort: the HEALTHY study. J Adolesc Health 2010;47(6):604–7.
  17. Zeller MH, Modi AC. Predictors of health-related quality of life in obese youth. Obesity (Silver Spring) 2006;14(1):122–30.
  18. Brandt ML, Harmon CM, Helmrath MA, Inge TH, McKay SV, Michalsky MP. Morbid obesity in pediatric diabetes mellitus: surgical options and outcomes. Nat Rev Endocrinol 2010;6(11):637–45.
  19. Murtagh L, Ludwig DL. State intervention in life-threatening childhood obesity. JAMA 2011;306(2):206–7.
  20. Madsen KA, Weed AE, Crawford PB. Disparities in peaks, plateaus, and declines in prevalence of high BMI among adolescents. Pediatrics 2010;126(3):434–42.
  21. Stoddard SA, Kubik MY, Skay C. Is school-based height and weight screening of elementary students private and reliable? J Sch Nurs 2008;24(1):43–8.

Retrieved from: http://www.medscape.com/viewarticle/771896?src=nl_topic

 

if you want to make lasting memories, get moving!

In Fitness/Health, Neuroscience on Tuesday, 30 October 2012 at 08:04

How Exercise Can Help You Master New Skills

By: Dr. Mercola

Just as your mind forms intellectual memories, it also forms what are known as muscle or “motor” memories.

Have you ever marveled at how well you can still ride a bike, even if you haven’t been on one in 20 years?

This is an example of motor memory at its best; while your muscles don’t actually “remember” how to ride a bike, your brain does, and sends a complex, though seemingly effortless, array of signals to your muscles instructing them how to perform the proper movements to keep you upright and pedaling.

Motor memory is obviously extremely important for everyday tasks like walking and climbing stairs, but it’s also crucial for more specialized skills – like mastering your golf swing or tennis serve.

If you’re in the process of mastering a new skill, research has revealed a novel way to “cement” that knowledge into your brain for later recollection – so you can remember how to get that “hole-in-one” the same way you remember how to ride a bike…

Exercising Right After Learning Makes Long-Term Memories Stronger

Researchers at the University of Copenhagen asked men to learn a tracking skill on a computer, which required them to use a joystick to trace a red line as it squiggled across the screen. A portion of the men exercised before learning the new task, some of the men did not exercise at all, and another group exercised just after learning the new skill.

At follow-up testing an hour later, the men performed basically the same, but as time went on, those who exercised gained a clear advantage. Those who fared the best belonged to the group who exercised just after learning the task. At testing sessions one day, and then one week, later, they traced the line more accurately and with greater agility. The group that exercised before learning the new skill also performed better than those who didn’t exercise (though not as well as the group that exercised after).

It appears, then, that if you want to help strengthen your memories, and be sure new information you’re receiving is successfully imprinted into your brain for later use and recall, a workout just after the learning may be very beneficial. The researchers concluded:1

“These findings indicate that one bout of intense exercise performed immediately before or after practicing a motor task is sufficient to improve the long-term retention of a motor skill. The positive effects of acute exercise on motor memory are maximized when exercise is performed immediately after practice, during the early stages of memory consolidation.”

Exercise Even Builds New Brain Cells

The hippocampus is a major component of your brain. It belongs to the more ancient part of your brain known as the limbic system and plays an important role in the consolidation of information from your short-term memory to long-term memory and spatial navigation. An animal study found that not only does mild exercise activate hippocampal neurons, it actually promotes their growth. In the brain, this also, in turn, helps with the creation of new brain cells.2

Another study, for instance, revealed that when mice exercised, they grew an average of 6,000 new brain cells in every cubic millimeter of tissue sampled.3 The growth occurred in the hippocampus, which, as mentioned, is considered the memory center of your brain, and the mice showed significant improvements in the ability to recall memories without any confusion.

During exercise, nerve cells in your brain also release proteins known as neurotrophic factors. One in particular, called brain-derived neurotrophic factor (BDNF), triggers numerous other chemicals that promote neural health, and has a direct benefit on cognitive functions, including memory consolidation and enhanced learning.

So while the featured study focused on exercise to benefit motor memory, research also supports its benefit for intellectual memories as well. If you want to have a memory like an elephant’s… it’s time to hit the gym. Some of the research highlights include:4

  • Among elementary school students, 40 minutes of daily exercise increased IQ by an average of nearly 4 points
  • Among 6th graders, the fittest students scored 30 percent higher than average students, and the less fit students scored 20 percent lower
  • Among older students, those who play vigorous sports have a 20 percent improvement in Math, Science, English and Social Studies
  • Fit 18-year-olds are more likely to go on to higher education and get full-time jobs
  • Students who exercise before class improved test scores 17 percent, and those who worked out for 40 minutes improved an entire letter grade

Even once you’re in the workforce, exercise can be an invaluable tool to increase your performance and productivity. Research shows an employee who exercises regularly is 15 percent more efficient than those who do not, which means a fit employee only needs to work 42.5 hours in a week to do the same work as an average employee does in 50.5

Think You Don’t Have Enough Time to Exercise?

I understand that you are busy, but if you take time out of your day to eat and sleep, it is equally important in the long term to make time to exercise (and not in lieu of sleeping, either!). If you neglect to exercise, you are literally passing up dozens of benefits to your health, the value of which simply cannot be measured. Do you want to slow down your aging process? Lower your risk of heart disease, diabetes and cancer? Relieve pain? Fight depression? Cure insomnia?

Exercise may be the answer you’ve been searching for.

As for the time element, it does take some practice to make exercise part of your routine. It’s generally said that it takes 3-4 weeks to turn an action into a habit, but some estimates put it at closer to 66 days, or just over two months. I find that it’s easiest to schedule exercise into my day the way I would any other important event or meeting. Write it down on your calendar, add it to your smartphone reminders… do whatever you need to do to set aside the time, and then stick with it.

The time you need to devote may actually be far less than you think, too, as short periods of intense exercise, such as Peak Fitness, are proving to be even better for you than longer sessions of traditional cardio. Here’s a summary of what a typical high-intensity Peak Fitness routine might look like:

  • Warm up for three minutes
  • Exercise as hard and fast as you can for 30 seconds. You should feel like you couldn’t possibly go on another few seconds
  • Recover at a slow to moderate pace for 90 seconds
  • Repeat the high intensity exercise and recovery 7 more times

As you can see, the entire workout is only 20 minutes. That really is a beautiful thing. And within those 20 minutes, 75 percent of that time is warming up, recovering or cooling down. You’re really only working out intensely for four minutes. If you have never done this, it’s hard to believe that you can actually get that much benefit from only four minutes of intense exercise, but that’s all it is. You can see a demonstration in the video below.

Since it’s so intense, you only need to do Peak Fitness two or three times a week. Then, round out your exercise program with strength training, core exercises and stretching to give your brain, and body, a wonderful, healthy boost.

Retrieved from: http://fitness.mercola.com/sites/fitness/archive/2012/10/12/exercise-improves-memory.aspx

New York Times and Wall Street Journal Warns That Hospitals Are Killing Us

In Fitness/Health on Sunday, 28 October 2012 at 09:16

New York Times and Wall Street Journal Warns That Hospitals Are Killing Us

By Dr. Mercola

If medical errors were a disease, they would be the sixth leading cause of death in America, writes surgeon Dr. Marty Makary in the Wall Street Journal.1

By some estimates, they may actually be the leading cause… These errors kill the equivalent of four jumbo jets’ worth of passengers… every week, Dr. Makary says, and this is likely a conservative estimate.

According to the 2011 Health Grades Hospital Quality in America Study, the incidence rate of medical harm occurring in the United States is estimated to beover 40,000 harmful and/or lethal errors each and EVERY day.2

What’s most shocking is that the harm often is preventable.

Shocking Medical Errors are All Too Common

Dr. Andrew Saul, co-author of Hospitals and Health: Your Orthomolecular Guide to a Shorter Hospital Stay (which is available on Amazon), recently explained that the lowest estimate makes hospitals one of the top 10 causes of deaths in the United States… and the highest estimate makes hospital and drugs the number one cause of death in the United States. Some of the top 10, and most lethal, medical mishaps are mistakes that should be extremely rare, but happen with shocking regularity:

1. Preventable Adverse Drug Reactions

An estimated 450,000 preventable medication-related adverse events of mostly correctly prescribed drugs occur in the U.S. every year. A large part of the problem is simply because so many drugs are used and prescribed – and many patients receive multiple prescriptions at varying strengths, some of which may counteract each other or cause more severe reactions when combined. Dosage errors, medication mix-ups and even giving the wrong medication to the wrong person are all too common.

2. Avoidable Infections

Hospital-acquired infections are alarmingly common, and sadly they’re often deadly. In the United States, more than 2 million people are affected byhospital-acquired infections each year, and a whopping 100,000 people die as a result. According to the 2011 Health Grades Hospital Quality in America report,3 analysis of approximately 40 million Medicare patients’ records from 2007 through 2009 showed that 1 in 9 patients developed such hospital-acquired infections!

The saddest part is, most of these cases could likely have been easily prevented with better infection control in hospitals – simple routines such as doctors and nurses washing their hands between each patient, for example.

3. Surgical Souvenirs

Surgical tools or other objects are left inside people after surgery far more often than you’d like to think. This is often the result of surgical staff failing to count, or miscounting, equipment during the procedure. Unexpected pain, fever and swelling after surgery are all indications that you could have a surgical tool or piece of a tool still inside you.

Just how often does this occur? One study in the New England Journal of Medicine found that about 1,500 Americans have objects left inside of them following surgery every year.4

Overtreatment is Taking its Toll

Too many medications, unnecessary surgeries, inappropriate medical screening… there is perhaps no other society that is subjected to as much excessive medical care, and often the “treatment” ends up being worse than the disease.

It’s estimated that up to 30 percent of all medical procedures, tests and medications may be unnecessary5 – at a cost of at least $210 billion a year6 (plus the cost of emotional suffering and related complications and even death – which are impossible to put numbers on). The New York Times recently highlighted several examples of this epidemic of overtreatment, including:7

  • A woman who received a CT scan and an MRI for a black eye (and was told she might have a brain tumor as a result, which resulted in an agonizing two-week wait for the results… she was fine and had no tumor)
  • An elderly man who was put on two antidepressants after having a stroke, and subsequently began suffering from dementia and hallucinations (the drugs are associated with cognitive problems); after his son persuaded doctors to change the medications, the man’s mental health quickly improved
  • A new mom who said she felt “bullied” by doctors to perform a battery of tests on her 3-month-old daughter, who was born premature – even though her prior doctor had ruled her symptoms as normal

In her book, Overtreated: Why Too Much Medicine Is Making Us Sicker and Poorer, Shannon Brownlee also explained that as much as a third of the medical care received in hospitals does nothing to improve your health! What happens is that you often get certain medical tests because of what your physician’s specialty is, not because that’s necessarily the test you need. For example if you have low back pain and see different specialists you will get different tests: rheumatologists will order blood tests, neurologists will order nerve impulse tests, and surgeons will order MRIs and CT scans.

But no matter what tests you get, you’ll probably end up with a spinal fusion because it’s one of the “more lucrative procedures in medicine,” Brownlee says – even though the best success rate for spinal fusions is only 25 percent!

Angioplasties and certain types of chemotherapy with similar low success rates are just as prone to be ordered, Brownlee says, because that’s where hospitals’ investments lie. You see, they have all this equipment and they need to use it to get a return on it – but they also need to get you out of there as quickly as possible, so they can get the next patient in. What ensues is a type of aggressive patient therapy where an unacceptable number of people will be harmed every year as a result of the medical treatments they received in the hospital.

5 Ways to Stop the Madness…

In the Wall Street Journal, Dr. Makary went on to explain five simple reforms that could make health care much safer:

  1. Online “Informational” Dashboards: This would include easily accessible hospital ratings for people to check out prior to choosing where to receive care. Information on rates of infection, readmission, surgical complications and “never events” (mistakes that should “never” happen, such as operating on the wrong body part), as well as annual volume for each type of surgery it performs, and patient satisfaction scores, would be available.

By being held publically accountable, it would prompt hospitals with low scores to make changes – or business would suffer.

  1. Safety Culture Scores: Anonymous surveys of hospital employees (including doctors, nurses, technicians, etc.) can reveal valuable information that correlates with better patient care, such as whether teamwork is good or bad, or whether employees feel they can speak up if they see a medical error in progress. These scores should be readily available to the public.
  2. Cameras: If health care workers know they’re being filmed, it greatly improves compliance with established safety practices, such as hand washing, and even has been found to improve the quality of medical procedures. It also provides a way for doctors to review, critique and improve their surgical skills.
  3. Open Notes: Certain hospitals have begun using “open notes,” which gives patients online access to their doctors’ notes. Not only does this allow patients to correct any inaccurate information, it also sometimes prompts people to remember a crucial piece of their health care history that they left out during the appointment.
  4. No More Gagging: If you’re a victim of a medical mistake, you will likely be ordered to not speak about it publicly as part of any settlement you receive. Some doctors are even asking patients to sign forms promising not to post anything negative online regarding their care before their first appointment. In hospitals, many health care workers feel they cannot speak up about medical errors, for fear of putting their jobs in jeopardy or suffering retaliations from co-workers.

But as Dr. Makary said, “We need more open dialogue about medical mistakes, not less.”

You’re Being Admitted to the Hospital: Tips for Staying Safe

In my recent interview (above) with Dr. Saul, he shared potentially life-saving tips in the event you find yourself in a hospital. Knowing how to prevent disease so you can avoid hospitals in the first place is clearly your best bet. But knowing what to do to make your hospital stay as safe as possible is equally important. Understand that you, the patient, are the most powerful entity within the entire hospital system. However, the system works on the assumption that the patient will not claim that power. Knowing your rights and responsibilities can help ensure your hospital stay is a safe and healing one.

One of the reasons I am so passionate about sharing the information on this site about healthy eating, exercise, and stress management with you is because it can help keep you OUT of the hospital. But if you do have to go there, you need to know how to play the game.

Many believe training hospitals will provide them with the latest and greatest care, but they can actually be far more dangerous.

As a general rule, avoid elective surgeries and procedures during the month of July because this is when brand new residents begin their training. According to a 2010 report in the Journal of General Internal Medicine,8 lethal medication errors consistently spike by about 10 percent each July, particularly in teaching hospitals, due to the inexperience of new residents. Also be cautious of weekends.

My primary suggestion is to avoid hospitals unless it’s an absolute emergency and you need life-saving medical attention. In such cases, it’s worth taking one of Dr. Saul’s recommendations, which is to bring a personal advocate – a relative or friend who can speak up for you and ensure you’re given proper care if you can’t do so yourself. If you’re having an elective medical procedure done, remember that this gives you greater leeway and personal choice – use it!

The other KEY is to be proactive and start pursuing a healthy lifestyle today so you don’t become a victim. I have compiled my best tips in a customized 100-page report on how you can Take Control of Your Health. It is customized to three different levels and you can start at any level, but be sure and read from the beginning, as reviewing the basics is the best way to reinforce healthy patterns.

Download Interview Transcript

Retrieved from: http://articles.mercola.com/sites/articles/archive/2012/10/27/medical-errors-kill.aspx?utm_source=dlvr.it&utm_medium=linkedin

 

exercise and adhd…

In ADHD, ADHD Adult, ADHD child/adolescent, Fitness/Health, Neuropsychology, Psychiatry, School Psychology, Special Education on Sunday, 21 October 2012 at 09:43

Exercise May Lead to Better School Performance for Kids with ADHD

ScienceDaily (Oct. 16, 2012)

A few minutes of exercise can help children with attention deficit hyperactivity disorder perform better academically, according to a new study led by a Michigan State University researcher.

The study, published in the current issue of the Journal of Pediatrics, shows for the first time that kids with ADHD can better drown out distractions and focus on a task after a single bout of exercise. Scientists say such “inhibitory control” is the main challenge faced by people with the disorder.

“This provides some very early evidence that exercise might be a tool in our nonpharmaceutical treatment of ADHD,” said Matthew Pontifex, MSU assistant professor of kinesiology, who led the study. “Maybe our first course of action that we would recommend to developmental psychologists would be to increase children’s physical activity.”

While drugs have proven largely effective in treating many of the 2.5 million school-aged American children with ADHD, a growing number of parents and physicians worry about the side effects and costs of medication.

In the study, Pontifex and colleagues asked 40 children aged 8 to 10, half of whom had ADHD, to spend 20 minutes either walking briskly on a treadmill or reading while seated. The children then took a brief reading comprehension and math exam similar to longer standardized tests. They also played a simple computer game in which they had to ignore visual stimuli to quickly determine which direction a cartoon fish was swimming.

The results showed all of the children performed better on both tests after exercising. In the computer game, those with ADHD also were better able to slow down after making an error to avoid repeat mistakes — a particular challenge for those with the disorder.

Pontifex said the findings support calls for more physical activity during the school day. Other researchers have found that children with ADHD are less likely to be physically active or play organized sports. Meanwhile, many schools have cut recess and physical education programs in response to shrinking budgets.

“To date there really isn’t a whole lot of evidence that schools can pull from to justify why these physical education programs should be in existence,” he said. “So what we’re trying to do is target our research to provide that type of evidence.”

Pontifex conducted the study for his doctoral dissertation at the University of Illinois before joining the MSU faculty. His co-investigators included his adviser, kinesiology professor Charles Hillman, and Daniel Picchietti, a pediatrician at the Carle Foundation Hospital in Champaign, Ill. The research was funded by the National Institute of Child Health and Human Development.

Michigan State University (2012, October 16). Exercise may lead to better school performance for kids with ADHD. ScienceDaily. Retrieved October 21, 2012, from http://www.sciencedaily.com­ /releases/2012/10/121016132109.htm

Retrieved from: http://www.sciencedaily.com/releases/2012/10/121016132109.htm

STOP…and be happy!

In Fitness/Health, Inspiration, Mindfulness, Well-being on Saturday, 20 October 2012 at 07:50

Be Happier: Ten Things to Stop Doing Right Now

Jeff Haden

Sometimes the route to happiness depends more on what you don’t do.

Happiness–in your business life and your personal life–is often a matter of subtraction, not addition.

Consider, for example, what happens when you stop doing the following 10 things:

1. Blaming.

People make mistakes. Employees don’t meet your expectations. Vendors don’t deliver on time.

So you blame them for your problems.

But you’re also to blame. Maybe you didn’t provide enough training. Maybe you didn’t build in enough of a buffer. Maybe you asked too much, too soon.

Taking responsibility when things go wrong instead of blaming others isn’t masochistic, it’s empowering–because then you focus on doing things better or smarter next time.

And when you get better or smarter, you also get happier.

2. Impressing.

No one likes you for your clothes, your car, your possessions, your title, or your accomplishments. Those are all “things.” People may like your things–but that doesn’t mean they like you.

Sure, superficially they might seem to, but superficial is also insubstantial, and a relationship that is not based on substance is not a real relationship.

Genuine relationships make you happier, and you’ll only form genuine relationships when you stop trying to impress and start trying to just be yourself.

3. Clinging.

When you’re afraid or insecure, you hold on tightly to what you know, even if what you know isn’t particularly good for you.

An absence of fear or insecurity isn’t happiness: It’s just an absence of fear or insecurity.

Holding on to what you think you need won’t make you happier; letting go so you can reach for and try to earn what you want will.

Even if you don’t succeed in earning what you want, the act of trying alone will make you feel better about yourself.

4. Interrupting.

Interrupting isn’t just rude. When you interrupt someone, what you’re really saying is, “I’m not listening to you so I can understand what you’re saying; I’m listening to you so I can decide what I want to say.”

Want people to like you? Listen to what they say. Focus on what they say. Ask questions to make sure you understand what they say.

They’ll love you for it–and you’ll love how that makes you feel.

5. Whining.

Your words have power, especially over you. Whining about your problems makes you feel worse, not better.

If something is wrong, don’t waste time complaining. Put that effort into making the situation better. Unless you want to whine about it forever, eventually you’ll have to do that. So why waste time? Fix it now.

Don’t talk about what’s wrong. Talk about how you’ll make things better, even if that conversation is only with yourself.

And do the same with your friends or colleagues. Don’t just be the shoulder they cry on.

Friends don’t let friends whine–friends help friends make their lives better.

6. Controlling.

Yeah, you’re the boss. Yeah, you’re the titan of industry. Yeah, you’re the small tail that wags a huge dog.

Still, the only thing you really control is you. If you find yourself trying hard to control other people, you’ve decided that you, your goals, your dreams, or even just your opinions are more important than theirs.

Plus, control is short term at best, because it often requires force, or fear, or authority, or some form of pressure–none of those let you feel good about yourself.

Find people who want to go where you’re going. They’ll work harder, have more fun, and create better business and personal relationships.

And all of you will be happier.

7. Criticizing.

Yeah, you’re more educated. Yeah, you’re more experienced. Yeah, you’ve been around more blocks and climbed more mountains and slayed more dragons.

That doesn’t make you smarter, or better, or more insightful.

That just makes you you: unique, matchless, one of a kind, but in the end, just you.

Just like everyone else–including your employees.

Everyone is different: not better, not worse, just different. Appreciate the differences instead of the shortcomings and you’ll see people–and yourself–in a better light.

8. Preaching.

Criticizing has a brother. His name is Preaching. They share the same father: Judging.

The higher you rise and the more you accomplish, the more likely you are to think you know everything–and to tell people everything you think you know.

When you speak with more finality than foundation, people may hear you but they don’t listen. Few things are sadder and leave you feeling less happy.

9. Dwelling.

The past is valuable. Learn from your mistakes. Learn from the mistakes of others.

Then let it go.

Easier said than done? It depends on your focus. When something bad happens to you, see that as a chance to learn something you didn’t know. When another person makes a mistake, see that as an opportunity to be kind, forgiving, and understanding.

The past is just training; it doesn’t define you. Think about what went wrong, but only in terms of how you will make sure that, next time, you and the people around you will know how to make sure it goes right.

10. Fearing.

We’re all afraid: of what might or might not happen, of what we can’t change, or what we won’t be able to do, or how other people might perceive us.

So it’s easier to hesitate, to wait for the right moment, to decide we need to think a little longer or do some more research or explore a few more alternatives.

Meanwhile days, weeks, months, and even years pass us by.

And so do our dreams.

Don’t let your fears hold you back. Whatever you’ve been planning, whatever you’ve imagined, whatever you’ve dreamed of, get started on it today.

If you want to start a business, take the first step. If you want to change careers, take the first step. If you want to expand or enter a new market or offer new products or services, take the first step.

Put your fears aside and get started. Do something. Do anything.

Otherwise, today is gone. Once tomorrow comes, today is lost forever.

Today is the most precious asset you own–and is the one thing you should truly fear wasting.

Retrieved from: http://www.inc.com/jeff-haden/how-to-be-happier-work-10-things-stop-doing.html

Cannabis and the Adolescent Brain

In Brain studies, Fitness/Health, Neuropsychology, Neuroscience on Sunday, 14 October 2012 at 11:23

Cannabis and the Adolescent Brain

By India Bohanna, PhD

For some time, people have known that using cannabis during adolescence increases the risk of developing cognitive impairment and mental illness (e.g. depression, anxiety or schizophrenia) later in life. Importantly however, the mechanisms responsible for this vulnerability are not well understood. A new study, published in Brain, shows that long-term cannabis use that starts during adolescence damages the neural pathways connecting brain regions, and that this may cause the later development of cognitive and emotional problems.

The authors used diffusion tensor imaging (DTI), a MRI technique that measures water diffusion, to examine the microstructure of white matter in 59 heavy cannabis users, who used cannabis at least twice a month for three years or longer, as well as 33 non-users. In the human brain, white matter pathways are formed by bundles of axons, which carry the neural signals, and myelin, which coat the axons and speeds up signal transfer. These white matter pathways are crucial for normal brain function as they enable disparate regions of the brain to communicate, and act together.

When the authors investigated white matter microstructure in the cannabis users, they found damage in the white matter pathways of the hippocampus, crucial for memory, and the corpus callosum, which connects the brain’s two hemispheres. Both pathways are critical for normal brain function. The authors suggest that impaired connectivity due to damage in these pathways may be the cause of the cognitive impairment and vulnerability to schizophrenia, depression and anxiety seen in long-term users.

The authors also show an inverse relationship between the amount of white matter damage and the age of first use. That is, participants who started using cannabis younger had more white matter damage and showed poorer brain connectivity. Adolescence is a critical period in the development of white matter in the brain, when the neural connections we rely on in adulthood are being finally formed. The authors point out that white matter cells have cannabinoid receptors (those susceptible to cannabis) during adolescence, which disappear as the brain matures. This new study demonstrates a mechanism that may help explain how cannabis use in adolescence causes long-term changes in brain function. The cannabis users in the study had significantly higher levels of depression and anxiety compared to the non-users.

This important new study suggests that young people’s brains are at risk of white matter injury due to cannabis, and that cannabis exposure during adolescence may permanently damage white matter development. Future research must address the question; can white matter pathways and connectivity recover when a person quits using cannabis?

References

Zalesky A, Solowij N, Yücel M, Lubman DI, Takagi M, Harding IH, Lorenzetti V, Wang R, Searle K, Pantelis C, & Seal M (2012). Effect of long-term cannabis use on axonal fibre connectivity. Brain : a journal of neurology, 135 (Pt 7), 2245-55 PMID: 22669080

Retrieved from: http://brainblogger.com/2012/08/18/cannabis-and-the-adolescent-brain/

Smoking and the Adolescent Brain

In Fitness/Health, Neuropsychology, Neuroscience on Sunday, 14 October 2012 at 11:18

Smoking and Adolescent Brain Development

By Shefali Sabharanjak, PhD

When it comes to substance abuse like smoking or abuse of intoxicating drugs, it is very difficult to determine what a “safe” limit of exposure is.  Quite often, the initial exposure to mood altering substances like nicotine occurs during the teenage years. The period ofadolescence is marked by a tendency towards risk-taking behavior which often results in ‘experimental’ exposure to psychedelic substances. Adolescents who tend to flirt with danger in this fashion are often convinced that a small trial will not actually have lasting damaging effects. However, research on the development of prefrontal cortex in similarly age-matched animals says otherwise.

The prefrontal cortex in teenagers is in a state of growth and development. Contrary to established notions, brain development continues well into the teenage years and changes in synapses (connections between brain cells that facilitate the transmission of chemical messengers between cells) occur well into adolescence.  Research on adolescent mice and rats shows that exposure to nicotine during this period has long-lasting effects. For starters, nicotine is known to be able to excite neurons bearing nicotinic acetylcholine receptors. In the prefrontal cortex, nicotine has been shown to induce greater expression of a specific subset of nicotinic acetylcholine receptors, by 34%.  In the normal course of development, the number of acetylcholine receptors declines in these cells. This phenomenon is specific to the period of adolescence since a similar increase in the number of receptors is not seen when the initial exposure to nicotine occurs in adulthood, in these animals. Research has also shown that exposure to nicotine in early adolescence enhances the nicotinic ‘reward’ feeling during adulthood. It is therefore surmised that early exposure to smoking is likely to set the stage for long-term addiction and perhaps it also explains why addiction to nicotine is so prevalent, worldwide.

One might argue that since the teenage years are a short period in the life-span of a person, occasional exposure to nicotine is not likely to leave lasting damage. Here’s the catch. Exposure to nicotine also changes the pattern of synaptic connectivity between neurons in the prefrontal cortex.  The ability of neurons to establish new synaptic connections and develop new firing patterns in response to different stimuli is also known as “synaptic plasticity”. Neuroscientists have shown that all “learning” as well as  information analysis and assimilation in the brain is a net result of the pattern of exchange of neurotransmitter molecules (also referred to as pattern of ‘firing’) between neurons which respond to training stimuli. So, the more you learn, the better you get at learning by stimulating your neurons to make new synaptic connections. However, exposure to nicotine in early adolescence, changes the pattern of firing of neurons in the prefrontal cortex. Now this change reduces the capability of neurons in the prefrontal cortex to make new synaptic connections. Therefore exposure to psychedelic and addictive substances like nicotine results in reduced synaptic plasticity and has a negative impact on cognitive processes in adult life.

All these significant changes take place in early adolescence and perhaps parental guidance may play a huge role in preventing nicotine addiction and associated cognitive deficits.

References

Adriani W, Macrì S, Pacifici R, & Laviola G (2002). Peculiar vulnerability to nicotine oral self-administration in mice during early adolescence. Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 27 (2), 212-24 PMID: 12093595

Counotte DS, Goriounova NA, Moretti M, Smoluch MT, Irth H, Clementi F, Schoffelmeer AN, Mansvelder HD, Smit AB, Gotti C, & Spijker S (2012). Adolescent nicotine exposure transiently increases high-affinity nicotinic receptors and modulates inhibitory synaptic transmission in rat medial prefrontal cortex. FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 26 (5), 1810-20 PMID: 22308197

Goriounova NA, & Mansvelder HD (2012). Nicotine exposure during adolescence alters the rules for prefrontal cortical synaptic plasticity during adulthood. Frontiers in synaptic neuroscience, 4 PMID: 22876231

Goriounova NA, & Mansvelder HD (2012). Nicotine exposure during adolescence leads to short- and long-term changes in spike timing-dependent plasticity in rat prefrontal cortex. The Journal of neuroscience : the official journal of the Society for Neuroscience, 32 (31), 10484-93 PMID: 22855798

Kawai HD, Kang HA, & Metherate R (2011). Heightened nicotinic regulation of auditory cortex during adolescence. The Journal of neuroscience : the official journal of the Society for Neuroscience, 31 (40), 14367-77 PMID: 21976522

Kota D, Robinson SE, & Imad Damaj M (2009). Enhanced nicotine reward in adulthood after exposure to nicotine during early adolescence in mice. Biochemical pharmacology, 78 (7), 873-9 PMID: 19576867

Retrieved from: http://brainblogger.com/2012/10/14/smoking-and-adolescent-brain-development/?utm_source=feedburner&utm_medium=email&utm_campaign=Feed%3A+GNIFBrainBlogger+%28Brain+Blogger%29

 

autism and asanas…new information

In Autism Spectrum Disorders, Fitness/Health, Meditation, Mindfulness on Saturday, 13 October 2012 at 09:50

Yoga Helps Children With Autism Remain Calm, Improves Social Bonding

BY AMBER MOORE

New York University researchers say that daily yoga can boost social bonding and focus in children who have been diagnosed with autism.

The intervention program, “Get Ready to Learn,” (GRTL) uses yoga and breathing techniques to calm children who have Autism Spectrum Disorder. The program has five steps that are done for 17 minutes each day. According to NYU researcher Kristie Koenig, this program can lower the levels of aggression, social withdrawal and anxiety in children with ASD.

“We found that teachers’ ratings of students who participated in the daily yoga routine showed improved behavior compared with teachers’ ratings of students who did not. Our aim in this research was to examine the effectiveness of an occupational therapy yoga intervention,” said Koenig, assistant professor of occupational therapy at NYU.

Currently, there is no cure for autism. However, studies suggest that certain intervention programs may help improve a child’s development. Interventions are most efficient when started early, before age 3.

Another study published last year in the Journal of Alternative and Complementary Medicine had also said that movement-based therapy including yoga and dance can help treat some behavioral problems associated with autism.

“Children with Autism often exhibit characteristics of ‘fight-or-flight’ response. They are in a constant state of stress and struggle with staying calm, trying to concentrate, communicating clearly, or even controlling their movements,” said Anne Buckley-Reen occupational therapist and yoga instructor.

The present study was published in The American Journal of Occupational Therapy.
Retrieved from:  http://www.medicaldaily.com/articles/12640/20121011/yoga-helps-children-autism-remain-calm-improves.htm#5Uri5TY1f6SU5fUp.99

get up! get moving!

In Fitness/Health, Uncategorized on Wednesday, 3 October 2012 at 16:24

http://www.huffingtonpost.com/2012/10/03/sitting-chronic-kidney-disease-risk-_n_1929684.html#slide=1586572

Can Parents’ Divorce Boost Son’s Risk for Stroke?

In Fitness/Health on Sunday, 30 September 2012 at 12:20

Can Parents’ Divorce Boost Son’s Risk for Stroke?

Researchers suspect stress hormone may play a role

 WEDNESDAY, Sept. 26 (HealthDay News)

New research suggests a strong association between parental divorce and boys’ risk for stroke later in life.

Researchers from the University of Toronto found that boys whose parents divorce before they turn 18 years old are three times more likely to suffer a stroke as adults than men who grow up in intact families. They noted this greater risk of stroke was not the result of other contributing factors such as family violence or parental addiction.

“The strong association we found for males between parental divorce and stroke is extremely concerning,” study lead author Esme Fuller-Thomson, chair of the university’s Factor-Inwentash Faculty of Social Work, said in a university news release.

Even after adjusting for factors such as race, income and education, and adult health behaviors such as smoking, parental divorce was still associated with a threefold risk of stroke among males, said Fuller-Thomson.

Although the reason why these men seem at greater risk for stroke remains unclear, the study authors suggested it may have something to do with their levels of the stress hormone cortisol.

“It is possible that exposure to the stress of parental divorce may have biological implications that change the way these boys react to stress for the rest of their lives,” noted Fuller-Thomson.

Women from divorced families do not face the same increased risk, the researchers found.

Although an association was noted between sons of divorced parents and later stroke risk, the research did not establish a cause-and-effect relationship. More research is needed to confirm their findings, the researchers said.

“If these findings are replicated in other studies, then perhaps health professionals will include information on a patient’s parental divorce status to improve targeting of stroke prevention education,” said Fuller-Thomson.

The findings are published in the September issue of the International Journal of Stroke.

More information

The U.S. National Library of Medicine has more about stress and health.

SOURCE: University of Toronto, news release, September 2012

Last Updated: Sept. 26, 2012

Copyright © 2012 HealthDay. All rights reserved.

Retrieved from: http://consumer.healthday.com/Article.asp?AID=668686

 

be happy, do nothing…

In Fitness/Health, Inspiration, Mindfulness on Thursday, 27 September 2012 at 11:42

To be Mentally Sound, DO NOTHING! Says Psychologist!

Practically the whole planet is on the move to find ways to maintain a sound psychological health. This can prove to be counter-productive according to a psychologist. In a recent report, Jamie Gruman says the key to a great mental well-being is to actually do nothing at all.

“Health: Social Psychologist Proposes Science of Positive Thinking”

Canadian social psychologist Jamie Gruman is proposing a new way of achieving nirvana: Do nothing.

Instead, live in the moment and embrace the “serene and contented acceptance of life as it is, with no ambitions of acquisition, accomplishment or progress toward goals,” said Gruman, co-founder of the newly created Canadian Positive Psychology Association, a network of scholars and academics studying human well-being and happiness.

Psychology has long focused on our inner torment: understanding why people get depressed or anxious, and how to alleviate it. The emphasis has been on “disorders,” “deficits,” “neuroses” and the need for “therapy.”

Positive psychology emphasizes strengths more than illness. It focuses on happiness, well-being, resilience, empathy, gratitude and forgiveness — how to “flourish” as a human. One idea, said Frank Farley, an Edmonton native and a past president of the American Psychological Association who studies heroism and personality, is that maybe it can inoculate people against mental distress.

More than a decade after its founding, the field is undergoing something of a revival. The neuroscience behind it is advancing. Researchers are finding links between positive emotions and a longer, healthier life span.

At the same time, the notion of a healthy national psyche is being embraced more openly by economists, politicians and political scientists around the globe, including in Canada, where, for example, Green Party leader Elizabeth May recently introduced a private member’s bill in the House of Commons meant to develop a set of indicators to measure “the real health and well-being of people.” A United Nations expert panel earlier this year called for nations around the globe to track the happiness of their people, arguing that economic wealth doesn’t equal psychological health.

Except for those living below the poverty line, “the correlation between money and happiness is almost non-existent,” said Gruman, an associate professor of organizational behaviour at the University of Guelph.

“We’re trying to find out what makes people happy,” Gruman said, “because we’ve learned it isn’t money.”

Science is searching for prescriptions for happiness at a time when North American adults increasingly are being medicated with anti-depressants.

According to new figures released exclusively to Postmedia News by market research firm IMS Brogan, Canadian pharmacists dispensed 40.2 million prescriptions worth $1.7 billion for anti-depressants in 2011 — a 7.5 per cent increase over 2010.

Over the last five years, the use of anti-depressants has increased on a per-person basis in every province except Prince Edward Island. Of the 40.2 million prescriptions dispensed across the nation last year, Quebec had the largest share (14.2 million) followed by Ontario (13.8 million) and B.C. (4.1 million).

In all, Canadians made 7.9 million visits to a doctor for symptoms of depression in 2011, according to IMS Brogan.

Gruman said positive-psych isn’t the Pollyannaish, “lollipops-and-rainbows” approach to living that some critics dismiss it as.

“It’s about living the best possible life. I don’t think that only understanding pathology and misery leads us to knowing how to live the best possible life we can.”

Humans have an innate tendency to focus on the negative, he said, and there’s an evolutionary reason for that.

“When you’re feeling good, that’s the body’s signal that everything is hunky-dory. When you’re feeling upset or anxious or scared, that’s your body’s way of telling you something is wrong. So it’s evolutionarily adaptive for us to be drawn to the negative — it helps us survive.

“When there’s a sabre-toothed tiger running after you, it’s healthy to be scared. You’re going to run away and you’re going to live.”

A healthy dose of pessimism is appropriate at times, he said, adding that life “necessarily requires admitting the negative and recognizing the negative and respecting the negative.”

“But it also involves trying to understand, when you’re not dying of cancer, when you’re not suffering your heart attack, when you’re not suffering depression, when you have a positive moment, how do you make the most of those moments?”

Dr. Adam Anderson is Canada Research Chair in Affective Neuroscience at the University of Toronto. Anderson said a part of the brain called the medial prefrontal cortex is activated in response to positive emotions. “You find it in jazz musicians improvising,” he said.

If that is the brain’s “positivity muscle,” can we cultivate it? In randomized, controlled trials, his team has found that mindfulness meditation alters the brain; it changes the activity in the prefrontal cortex.

“Some people are lucky and have the right genes, we think, to be able to live the good life. And, if you don’t, you have to exercise in some way to try to boost that,” Anderson said.

Some equate the good life with constantly seeking the next pleasure, which Anderson said is like an addiction. “That’s like saying a cocaine addict has a really good model for living the good life because they’re trying to maximize the number of pleasures they have.”

Thinking positive is easy when you know how. Gordon McInnis shares useful advice on how to have a positive mindset.

Anderson said it’s not about seeking out or wanting things, “but to explore. To be creative, to play.”

The function of happiness isn’t to be happy, said Anderson, who isn’t a positive psychologist but who will be a featured speaker at the Canadian Positive Psychology Association’s inaugural conference this month in Toronto. “It’s evolution’s way of saying, go out and discover new things. Go play, go explore.”

Not everyone is enthused by the rush to “positivity.” All of us struggle with a tension “between our own dark feelings and the grating call of the bright, shiny, happy world,” said Eric Wilson, author of Against Happiness. Self-help books can further guilt us into thinking, “I’m not happy enough.”

But Anderson said the word “happy” seems “so loaded and confused.”

Our economy is built on selling happiness through consumption, he argued — and that increasing depression could, paradoxically, be a fallout of seeking happiness.

“If you go out seeking happiness and you don’t find it — you desire something, you assume that’s going to make you happy, you get it and you’re not happier, or you’re happier for a little bit of time, ultimately, that will make you depressed,” he said.”

This news came from Vancouversun.com.

When you think about it, people indeed have the tendency to be very busy on things to the point that it becomes unhealthy. Slowing down to smell the roses, although a cliché, should be put to practice especially in a world that moves so fast that it leaves everyone behind scrambling and stressed out to keep up.

Please make sure everybody you know in Twitter and Facebook knows this information by sharing this article with them. Also, to make sure you get updates about psychology, remember to leave some comments and subscribe. Thanks and stay positive!

Retrieved from: http://psychologyonlinecourses.net/to-be-mentally-sound-do-nothing-says-psychologist/

 

Aspartame and Neurotoxicity

In Fitness/Health on Thursday, 27 September 2012 at 10:02

New Study Shows Aspartame is neurotoxic, damages, the brain & still approved for use in over 90 countries.

Submitted by Michelle on 26 September 2012 – 9:48am

 

A new study on aspartame has the potential to reignite the decades-old controversy behind this artificial sweetener’s safety, or lack thereof. As far back as 1996, folks were writing about the potential link between aspartame and increasing brain tumor rates.

Indeed, its intrinsic neurotoxicity and carcinogenicity has been confirmed in the biomedical literature. And yet, aspartame has been approved for use in thousands of consumer products in over 90 countries, and is still being consumed by millions worldwide on a daily basis – despite the fact that over 40 adverse health effects of aspartame have been documented.

The new study, published in the September edition of the Journal of Bioscience and titled, “Effect of chronic exposure to aspartame on oxidative stress in the brain of albino rats,” aimed to test the hypothesis that chronic consumption of aspartame may be causing neurological damage in exposed populations. They found that chronic (90 day) administration of aspartame to rats, at ranges only 50% above what the FDA considers safe for human consumption, resulted in blood and brain tissue changes consistent with brain damage.

Aspartame is metabolized into three distinct components: aspartic acid, methanol andphenylalanine. While aspartic acid is a well-known excitotoxin, phenylalanine only presents a serious health concern to those with a genetic disorder known as phenyletonuria. Methanol, on the other hand, is far more problematic, as it is not naturally found in significant quantities in the human diet.

According to a recent review until 200 years ago, methanol was an extremely rare component of the human diet and is still rarely consumed in contemporary hunter and gatherer cultures. With the invention of canning in the 1800s, canned and bottled fruits and vegetables, whose methanol content greatly exceeds that of their fresh counterparts, became far more prevalent. The recent dietary introduction of aspartame, an artificial sweetener 11% methanol by weight, has also greatly increased methanol consumption.

Moreover, the aspartame metabolite methanol (also known as wood alcohol) is highly toxic and is metabolized into the known human carcinogen formaldehyde and formic acid, which is known to be highly toxic to the central nervous system. Considering the fact that the normal human body temperature is approximately 98.6 degrees Farenheit, and that aspartame will convert to its toxic metabolites at temperatures as low as 86 degrees Farenheit, the finding that aspartame is neurotoxic to animals is not a surprise. T

The authors of the new study surmised that the observed adverse brain changes were due to the generation of oxidative stress in brain regions.

Aspartame, of course, is a proprietary synthetic chemical not found in nature, and exists primarily because plants like stevia, which have significant, clinically-substantiated healing properties, can be grown in your back yard for free and are therefore not profitable commodities that can be produced and controlled only by a few.

But, aspartame is not the only toxic sweetener on the market. A growing body of research now shows that sucralose, known by the brand-name Splenda, is also capable of suppressing the immune system, causing inflammatory bowel conditions such as Crohn’s and ulcerative colitis, migraine headaches, and DNA damage.

The trick is to stick with naturally occurring compounds, whose sweetness is not associated with adverse health effects. Compounds whose sweetness is not associated with adverse health effects include: Honey, Xylitol,Erythritol, Stevia

Article by Ji Sayer of GreenMedInfo

Retrieved from: http://theallergymenu.com/blog/new-study-shows-aspartame-neurotoxic-damages-brain-still-approved-use-over-90-countries

Poor Sleep and Hypertension

In Fitness/Health, Insomnia on Wednesday, 26 September 2012 at 07:36

Poor Sleep Relted to Resistant Hypertension

Sue Hughes

September 24, 2012 (Washington, DC) — Poor sleep quality is associated with a doubling in the risk of resistant hypertension in women, with the mechanism possibly mediated by depression, a new study shows [1].

The study was presented here at last week’s American Heart Association High Blood Pressure Research 2012 Scientific Sessions by Dr Rosa Maria Bruno (University of Pisa, Italy).

“I would say that treating insomnia may improve resistant hypertension, although we need further data before we make firm clinical recommendations on this,” Bruno told heartwire .

She commented: “There is lots of evidence that sleep disorders are related to cardiovascular events, but most relate to sleep-disordered breathing such as sleep apnea. Also, there have been many studies showing an association between short sleep duration and the incidence of cardiovascular events or hypertension. But we looked at whether insomnia was linked to the severity of hypertension, and we found poor sleep quality was significantly more prevalent in patients with resistant hypertension.”

Quality Rather Than Quantity

The researchers reported that it was the quality of sleep rather than the duration of sleep that seemed to be the important factor in the relationship with resistant hypertension. They also found a large difference between men and women.

Bruno noted: “In women, poor sleep quality was strongly related to anxiety and depression and resistant hypertension, but this was not the case for men. This difference remained after accounting for other confounding factors. In women, we found that poor sleep quality was associated with a fivefold increase in the probability of having resistant hypertension, even after adjustment.”

She cautioned that as this was only a cross-sectional study, they can conclude there is an independent association between poor sleep quality and resistant hypertension, but they cannot deduce that this is a causal effect. “This needs to be confirmed in a prospective study. It could also be that the hypertension is causing the insomnia, but we believe that the insomnia is making the hypertension worse.”

Experimental evidence supports this view. It is known that interrupted sleep stimulates the sympathetic nervous system and increases cortisol levels, both of which cause an increase in blood pressure.

For the study, data on sleep quality, anxiety/depression, and cardiovascular risk factors were collected for 270 patients from a hypertension outpatient unit. Sleep quality was measured by the Pittsburgh Sleep Quality Index (PSQI), and anxiety and depression with the Beck Depression Inventory (BDI). Poor sleep quality was defined as PSQI >5, mild to severe depressive symptoms as BDI score >10. Patients with obstructive sleep apnea were excluded. Resistant hypertension was defined as a failure to control hypertension with three or more drugs.

Complete data were available for 234 patients, half of whom were women. Mean sleep duration was 6.4 hours, and 49% of participants had short sleep duration (less than six hours), which was similar in both sexes.

However, women had higher PSQI scores and a higher prevalence of poor sleep quality. Women showed also higher depression scores and prevalence of depressive symptoms than men.

Sleep and Depression Scores in Women vs Men

Score Women Men p
PSQI score 5.2 3.6 0.03
Poor sleep quality (%) 46 30 0.01
Depression score 4.5 1.8 0.006
Prevalence of depressive symptoms (%) 20 7 0.003

Resistant hypertension was present in 15% of patients, and these individuals had higher PSQI scores than those without resistant hypertension, a difference shown in women but not in men. The association between depression score and resistant hypertension showed a similar trend.

Sleep Scores (PSQI) Related to Resistant Hypertension

Group Resistant hypertension No resistant hypertension p
Entire population 5.8 4.1 0.03
Women 6.8 4.8 0.04
Men 4.7 3.5 0.37

Depression Scores (BDI) Related to Resistant Hypertension

Group Resistant hypertension No resistant hypertension p
Entire population 3.6 2.8 0.02
Women 5.1 3.7 0.03
Men 2.0 1.9 0.53

In a multiple logistic regression analysis (including age, sex, obesity, diabetes, previous CV events, sleep duration, use of hypnotic drugs) poor sleep quality was independently associated with resistant hypertension (OR 2.2). But this relationship lost significance when depressive symptoms were included in the model.

References

  1. Bruno RM, Palagini L, Di Giulio A, et al. Relation between poor sleep quality and resistant hypertension. American Heart Association High Blood Pressure Research Scientific Sessions; September 21, 2012; Washington, DC. Abstract 63.

Retrieved from: http://www.medscape.com/viewarticle/771457?src=nl_topic

The root of chocolate cravings…

In Fitness/Health on Wednesday, 26 September 2012 at 06:56

Brain Study Reveals the Roots of Chocolate Temptations

ScienceDaily (Sep. 20, 2012) — Researchers have new evidence in rats to explain how it is that chocolate candies can be so completely irresistible. The urge to overeat such deliciously sweet and fatty treats traces to an unexpected part of the brain and its production of a natural, opium-like chemical, according to a report published online on September 20th in Current Biology, a Cell Press publication.

“This means that the brain has more extensive systems to make individuals want to overconsume rewards than previously thought,” said Alexandra DiFeliceantonio of the University of Michigan, Ann Arbor. “It may be one reason why overconsumption is a problem today.”

DiFeliceantonio’s team made the discovery by giving rats an artificial boost with a drug delivered straight to a brain region called the neostriatum. Those animals gorged themselves on more than twice the number of M&M chocolates than they would otherwise have eaten. The researchers also found that enkephalin, the natural drug-like chemical produced in that same brain region, surged when rats began to eat the candy-coated morsels, too.

It’s not that enkephalins or similar drugs make the rats like the chocolates more, the researchers say, but rather that the brain chemicals increase their desire and impulse to eat them.

The findings reveal a surprising extension of the neostriatum’s role, as DiFeliceantonio notes that the brain region had primarily been linked to movement. And there is reason to expect that the findings in rats can tell us a lot about our own binge-eating tendencies.

“The same brain area we tested here is active when obese people see foods and when drug addicts see drug scenes,” she says. “It seems likely that our enkephalin findings in rats mean that this neurotransmitter may drive some forms of overconsumption and addiction in people.”

The researchers now hope to unravel a related phenomenon that some of us might wish we could do more to control: what happens in our brains when we pass by our favorite fast food restaurant and feel that sudden desire to stop.

Journal Reference:

  1. Alexandra G. DiFeliceantonio, Omar S. Mabrouk, Robert T. Kennedy, Kent C. Berridge. Enkephalin Surges in Dorsal Neostriatum as a Signal to Eat. Current Biology, 2012; DOI: 10.1016/j.cub.2012.08.014

Cell Press (2012, September 20). Brain study reveals the roots of chocolate temptations. ScienceDaily. Retrieved September 23, 2012, from http://www.sciencedaily.com­ /releases/2012/09/120920135605.htm?goback=%2Egde_2514160_member_166874293

Retrieved from: http://www.sciencedaily.com/releases/2012/09/120920135605.htm?goback=%2Egde_2514160_member_166874293

Get moving!

In Fitness/Health, Psychiatry, Well-being on Tuesday, 18 September 2012 at 16:29

The exercise effect

Evidence is mounting for the benefits of exercise, yet psychologists don’t often use exercise as part of their treatment arsenal. Here’s more research on why they should.

By Kirsten Weir

December 2011, Vol 42, No. 11

When Jennifer Carter, PhD, counsels patients, she often suggests they walk as they talk. “I work on a beautiful wooded campus,” says the counseling and sport psychologist at the Center for Balanced Living in Ohio.

Strolling through a therapy session often helps patients relax and open up, she finds. But that’s not the only benefit. As immediate past president of APA’s Div. 47 (Exercise and Sport Psychology), she’s well aware of the mental health benefits of moving your muscles. “I often recommend exercise for my psychotherapy clients, particularly for those who are anxious or depressed,” she says.

Unfortunately, graduate training programs rarely teach students how to help patients modify their exercise behavior, Carter says, and many psychologists aren’t taking the reins on their own. “I think clinical and counseling psychologists could do a better job of incorporating exercise into treatment,” she says.

“Exercise is something that psychologists have been very slow to attend to,” agrees Michael Otto, PhD, a professor of psychology at Boston University. “People know that exercise helps physical outcomes. There is much less awareness of mental health outcomes — and much, much less ability to translate this awareness into exercise action.”

Researchers are still working out the details of that action: how much exercise is needed, what mechanisms are behind the boost exercise brings, and why — despite all the benefits of physical activity — it’s so hard to go for that morning jog. But as evidence piles up, the exercise-mental health connection is becoming impossible to ignore.

Mood enhancement

If you’ve ever gone for a run after a stressful day, chances are you felt better afterward. “The link between exercise and mood is pretty strong,” Otto says. “Usually within five minutes after moderate exercise you get a mood-enhancement effect.”

But the effects of physical activity extend beyond the short-term. Research shows that exercise can also help alleviate long-term depression.

Some of the evidence for that comes from broad, population-based correlation studies. “There’s good epidemiological data to suggest that active people are less depressed than inactive people. And people who were active and stopped tend to be more depressed than those who maintain or initiate an exercise program,” says James Blumenthal, PhD, a clinical psychologist at Duke University.

The evidence comes from experimental studies as well. Blumenthal has explored the mood-exercise connection through a series of randomized controlled trials. In one such study, he and his colleagues assigned sedentary adults with major depressive disorder to one of four groups: supervised exercise, home-based exercise, antidepressant therapy or a placebo pill. After four months of treatment, Blumenthal found, patients in the exercise and antidepressant groups had higher rates of remission than did the patients on the placebo. Exercise, he concluded, was generally comparable to antidepressants for patients with major depressive disorder (Psychosomatic Medicine, 2007).

Blumenthal followed up with the patients one year later. The type of treatment they received during the four-month trial didn’t predict remission a year later, he found. However, subjects who reported regular exercise at the one-year follow-up had lower depression scores than did their less active counterparts (Psychosomatic Medicine, 2010). “Exercise seems not only important for treating depression, but also in preventing relapse,” he says.

Certainly, there are methodological challenges to researching the effects of exercise, from the identification of appropriate comparison groups to the limitations of self-reporting. Despite these challenges, a compelling body of evidence has emerged. In 2006, Otto and colleagues reviewed 11 studies investigating the effects of exercise on mental health. They determined that exercise could be a powerful intervention for clinical depression (Clinical Psychology: Science and Practice, 2006). Based on those findings, they concluded, clinicians should consider adding exercise to the treatment plans for their depressed patients.

Mary de Groot, PhD, a psychologist in the department of medicine at Indiana University, is taking the research one step further, investigating the role exercise can play in a particular subset of depressed patients: those with diabetes. It’s a significant problem, she says. “Rates of clinically significant depressive symptoms and diagnoses of major depressive disorder are higher among adults with diabetes than in the general population,” she says. And among diabetics, she adds, depression is often harder to treat and more likely to recur. The association runs both ways. People with diabetes are more likely to develop depression, and people with depression are also more likely to develop diabetes. “A number of studies show people with both disorders are at greater risk for mortality than are people with either disorder alone,” she says.

Since diabetes and obesity go hand-in-hand, it seemed logical to de Groot that exercise could effectively treat both conditions. When she reviewed the literature, she was surprised to find the topic hadn’t been researched. So, she launched a pilot project in which adults with diabetes and depression undertook a 12-week exercise and cognitive-behavioral therapy (CBT) intervention program (Diabetes, 2009). Immediately following the program, the participants who exercised showed improvements both in depression and in levels of A1C, a blood marker that reflects blood-sugar control, compared with those in a control group. She’s now undertaking a larger study to further explore exercise and CBT, both alone and in combination, for treating diabetes-related depression.

Fight-or-flight

Researchers have also explored exercise as a tool for treating — and perhaps preventing — anxiety. When we’re spooked or threatened, our nervous systems jump into action, setting off a cascade of reactions such as sweating, dizziness, and a racing heart. People with heightened sensitivity to anxiety respond to those sensations with fear. They’re also more likely to develop panic disorder down the road, says Jasper Smits, PhD, Co-Director of the Anxiety Research and Treatment Program at Southern Methodist University in Dallas and co-author, with Otto, of the 2011 book “Exercise for Mood and Anxiety: Proven Strategies for Overcoming Depression and Enhancing Well-being.”

Smits and Otto reasoned that regular workouts might help people prone to anxiety become less likely to panic when they experience those fight-or-flight sensations. After all, the body produces many of the same physical reactions — heavy perspiration, increased heart rate — in response to exercise. They tested their theory among 60 volunteers with heightened sensitivity to anxiety. Subjects who participated in a two-week exercise program showed significant improvements in anxiety sensitivity compared with a control group (Depression and Anxiety, 2008). “Exercise in many ways is like exposure treatment,” says Smits. “People learn to associate the symptoms with safety instead of danger.”

In another study, Smits and his colleagues asked volunteers with varying levels of anxiety sensitivity to undergo a carbon-dioxide challenge test, in which they breathed CO2-enriched air. The test often triggers the same symptoms one might experience during a panic attack: increased heart and respiratory rates, dry mouth and dizziness. Unsurprisingly, people with high anxiety sensitivity were more likely to panic in response to the test. But Smits discovered that people with high anxiety sensitivity who also reported high activity levels were less likely to panic than subjects who exercised infrequently (Psychosomatic Medicine, 2011). The findings suggest that physical exercise could help to ward off panic attacks. “Activity may be especially important for people at risk of developing anxiety disorder,” he says.

Smits is now investigating exercise for smoking cessation. The work builds on previous research by Bess Marcus, PhD, a psychology researcher now at the University of California San Diego, who found that vigorous exercise helped women quit smoking when it was combined with cognitive-behavioral therapy (Archives of Internal Medicine, 1999). However, a more recent study by Marcus found that the effect on smoking cessation was more limited when women engaged in only moderate exercise (Nicotine & Tobacco Research, 2005).

Therein lies the problem with prescribing exercise for mental health. Researchers don’t yet have a handle on which types of exercise are most effective, how much is necessary, or even whether exercise works best in conjunction with other therapies.

“Mental health professionals might think exercise may be a good complement [to other therapies], and that may be true,” says Blumenthal. “But there’s very limited data that suggests combining exercise with another treatment is better than the treatment or the exercise alone.”

Researchers are starting to address this question, however. Recently, Madhukar Trivedi, MD, a psychiatrist at the University of Texas Southwestern Medical College, and colleagues studied exercise as a secondary treatment for patients with major depressive disorder who hadn’t achieved remission through drugs alone. They evaluated two exercise doses: One group of patients burned four kilocalories per kilogram each week, while another burned 16 kilocalories per kilogram weekly. They found both exercise protocols led to significant improvements, though the higher-dose exercise program was more effective for most patients (Journal of Clinical Psychiatry, 2011).

The study also raised some intriguing questions, however. In men and women without family history of mental illness, as well as men with family history of mental illness, the higher-dose exercise treatment proved more effective. But among women with a family history of mental illness, the lower exercise dose actually appeared more beneficial. Family history and gender are moderating factors that need to be further explored, the researchers concluded.

Questions also remain about which type of exercise is most helpful. Most studies have focused on aerobic exercise, though some research suggests weight training might also be effective, Smits says. Then there’s the realm of mind-body exercises like yoga, which have been practiced for centuries but have yet to be thoroughly studied. “There’s potential there, but it’s too early to get excited,” he says.

Buffering the brain

It’s also unclear exactly how moving your muscles can have such a significant effect on mental health. “Biochemically, there are many things that can impact mood. There are so many good, open questions about which mechanisms contribute the most to changes in depression,” says de Groot.

Some researchers suspect exercise alleviates chronic depression by increasing serotonin (the neurotransmitter targeted by antidepressants) or brain-derived neurotrophic factor (which supports the growth of neurons). Another theory suggests exercise helps by normalizing sleep, which is known to have protective effects on the brain.

There are psychological explanations, too. Exercise may boost a depressed person’s outlook by helping him return to meaningful activity and providing a sense of accomplishment. Then there’s the fact that a person’s responsiveness to stress is moderated by activity. “Exercise may be a way of biologically toughening up the brain so stress has less of a central impact,” Otto says.

It’s likely that multiple factors are at play. “Exercise has such broad effects that my guess is that there are going to be multiple mechanisms at multiple levels,” Smits says.

So far, little work has been done to unravel those mechanisms. Michael Lehmann, PhD, a research fellow at the National Institute of Mental Health, is taking a stab at the problem by studying mice — animals that, like humans, are vulnerable to social stress.

Lehmann and his colleagues subjected some of their animals to “social defeat” by pairing small, submissive mice with larger, more aggressive mice. The alpha mice regularly tried to intimidate the submissive rodents through the clear partition that separated them. And when the partition was removed for a few minutes each day, the bully mice had to be restrained from harming the submissive mice. After two weeks of regular social defeat, the smaller mice explored less, hid in the shadows, and otherwise exhibited symptoms of depression and anxiety.

One group of mice, however, proved resilient to the stress. For three weeks before the social defeat treatment, all of the mice were subjected to two dramatically different living conditions. Some were confined to spartan cages, while others were treated to enriched environments with running wheels and tubes to explore. Unlike the mice in the bare-bones cages, bullied mice that had been housed in enriched environments showed no signs of rodent depression or anxiety after social defeat (Journal of Neuroscience, 2011). “Exercise and mental enrichment are buffering how the brain is going to respond to future stressors,” Lehmann says.

Lehmann can’t say how much of the effect was due to exercise and how much stemmed from other aspects of the stimulating environment. But the mice ran a lot — close to 10 kilometers a night. And other experiments hint that running may be the most integral part of the enriched environment, he says.

Looking deeper, Lehmann and his colleagues examined the mice’s brains. In the stimulated mice, they found evidence of increased activity in a region called the infralimbic cortex, part of the brain’s emotional processing circuit. Bullied mice that had been housed in spartan conditions had much less activity in that region. The infralimbic cortex appears to be a crucial component of the exercise effect. When Lehmann surgically cut off the region from the rest of the brain, the protective effects of exercise disappeared. Without a functioning infralimbic cortex, the environmentally enriched mice showed brain patterns and behavior similar to those of the mice who had been living in barebones cages.

Humans don’t have an infralimbic cortex, but we do have a homologous region, known as cingulate area 25 or Brodmann area 25. And in fact, this region has been previously implicated in depression. Helen Mayberg, MD, a neurologist at Emory University, and colleagues successfully alleviated depression in several treatment-resistant patients by using deep-brain stimulation to send steady, low-voltage current into their area 25 regions (Neuron, 2005). Lehmann’s studies hint that exercise may ease depression by acting on this same bit of brain.

Getting the payoff

Of all the questions that remain to be answered, perhaps the most perplexing is this: If exercise makes us feel so good, why is it so hard to do it? According to the Centers for Disease Control and Prevention, in 2008 (the most recent year for which data are available), some 25 percent of the U.S. population reported zero leisure-time physical activity.

Starting out too hard in a new exercise program may be one of the reasons people disdain physical activity. When people exercise above their respiratory threshold — that is, above the point when it gets hard to talk — they postpone exercise’s immediate mood boost by about 30 minutes, Otto says. For novices, that delay could turn them off of the treadmill for good. Given that, he recommends that workout neophytes start slowly, with a moderate exercise plan.

Otto also blames an emphasis on the physical effects of exercise for our national apathy to activity. Physicians frequently tell patients to work out to lose weight, lower cholesterol or prevent diabetes. Unfortunately, it takes months before any physical results of your hard work in the gym are apparent. “Attending to the outcomes of fitness is a recipe for failure,” he says.

The exercise mood boost, on the other hand, offers near-instant gratification. Therapists would do well to encourage their patients to tune into their mental state after exercise, Otto says — especially when they’re feeling down.

“Many people skip the workout at the very time it has the greatest payoff. That prevents you from noticing just how much better you feel when you exercise,” he says. “Failing to exercise when you feel bad is like explicitly not taking an aspirin when your head hurts. That’s the time you get the payoff.”

It may take a longer course of exercise to alleviate mood disorders such as anxiety or depression, Smits adds. But the immediate effects are tangible — and psychologists are in a unique position to help people get moving. “We’re experts in behavior change,” he says. “We can help people become motivated to exercise.”


Kirsten Weir is a writer in Minneapolis.

Retrieved from http://www.apa.org/monitor/2011/12/exercise.aspx

 

The state of sleep in the U.S.

In ADHD, ADHD Adult, ADHD child/adolescent, ADHD stimulant treatment, Anxiety, Fitness/Health, Medication, Well-being on Tuesday, 18 September 2012 at 05:04

stress, anxiety, and depression are but three related etiologies for insomnia.  people with ADHD also suffer from insomnia, either as a side-effect of psychostimulants or because of the ADHD itself.  insomnia can have significant effects on quality of life, work/school life, and health.  statistics show that insomnia is a growing problem in the U.S. today and sleep aids are being prescribed at an increasing rate.  the following are some statistics related to insomnia as well as a case-study/research article on insomnia. 

to be followed by an article about hypnotic use and associated risk-factors.

***

General Insomnia Statistics

  • People today sleep 20% less than they did 100 years ago.
  • More than 30% of the population suffers from insomnia.
  • One in three people suffer from some form of insomnia during their lifetime.
  • More than half of Americans lose sleep due to stress and/or anxiety.
  • Between 40% and 60% of people over the age of 60 suffer from insomnia.
  • Women are up to twice as likely to suffer from insomnia than men.
  • Approximately 35% of insomniacs have a family history of insomnia.
  • 90% of people who suffer from depression also experience insomnia.
  • Approximately 10 million people in the U.S. use prescription sleep aids.
  • People who suffer from sleep deprivation are 27% more likely to become overweight or obese. There is also a link between weight gain and sleep apnea.
  • A National Sleep Foundation Poll shows that 60% of people have driven while feeling sleepy (and 37% admit to having fallen asleep at the wheel) in the past year.
  • A recent Consumer Reports survey showed the top reason couples gave for avoiding sex was “too tired or need sleep.”

Financial Implications of Insomnia

Insomnia statistics aren’t confined to the relationship between insomnia and health. This sleep disorder costs government and industry billions of dollars a year.

  • The Institute of Medicine estimates that hundreds of billions of dollars are spent annually on medical costs that are directly related to sleep disorders.
  • The National Highway Traffic Safety Administration statistics show that 100,000 vehicle accidents occur annually drowsy driving. An estimated 1,500 die each year in these collisions.
  • Employers spend approximately $3,200 more in health care costs on employees with sleep problems than for those who sleep well.
  • According to the US Surgeon General, insomnia costs the U.S. Government more than $15 billion per year in health care costs.
  • Statistics also show that US industry loses about $150 billion each year because of sleep deprived workers. This takes into account absenteeism and lost productivity.

These sobering insomnia statistics underscore the importance of enhancing sleep disorder awareness and why individuals need to seek immediate treatment for the health and the well-being of others.

Sources: National Sleep Foundation, Better Sleep Council, Gallup Polls, Institute of Medicine, National Highway Traffic Safety Administration, US Surgeon General’s Office

http://www.better-sleep-better-life.com/insomnia-statistics.html

Manifestations and Management of Chronic Insomnia: NIH State-of-the-Science Conference Findings and Implications

Authors: William T. Riley, PhD; Carl E. Hunt, MD

http://www.medscape.org/viewarticle/517618

Introduction

The Problem of the Inadequate Identification and Treatment of Chronic Insomnia

Despite considerable advances in the understanding of and treatments for chronic insomnia, this condition remains inadequately identified and treated. Approximately one third of US adults report difficulty sleeping, and 10% to 15% have the clinical disorder of insomnia.[1] Among primary care patients, approximately half have sleep difficulties, but these difficulties often are undetected by health professionals.[2,3] Even if detected and appropriately diagnosed, these patients are more likely to receive treatments of questionable safety and efficacy rather than treatments with substantial, evidence-based support for safety and efficacy.

The inadequate identification and treatment of chronic insomnia has serious medical and public health implications. Chronic insomnia results in impaired occupational performance and diminished quality of life.[4,5] Insomnia is associated with higher healthcare usage and costs, including a 2-fold increase in hospitalizations and physician visits.[6] Insomnia is also a risk factor for a number of other disorders, particularly psychiatric disorders, such as depression, and an important sign or symptom for a range of medical and other psychiatric disorders.[7]

In a recent review, Benca[8] identified the following 5 barriers to the recognition, diagnosis, and treatment of insomnia in primary care settings:

  • Inadequate knowledge base: In the 1990s, about one third of medical schools had no formal sleep medicine training. A majority of practitioners rate their knowledge of sleep medicine as only “fair.”
  • Office visit time constraints: Unless sleep difficulties are the presenting complaint, visit time may be inadequate for sleep difficulties to be addressed.
  • Lack of discussion about sleep: Less than half of patients with insomnia have discussed this problem with their physicians, and most of these discussions were patient-initiated.
  • Misperceptions regarding treatment: Health professionals may have greater concerns than warranted about the safety and efficacy of pharmacologic treatments, and they may not be aware of or have access to effective nonpharmacologic approaches.
  • Lack of evidence for functional outcomes: Although treatments for insomnia reduce symptoms in the short term, there is inadequate evidence for long-term efficacy, improvements in daytime functioning, or the impact on comorbid disorders.

Addressing these barriers could lead to improved recognition and treatment of chronic insomnia and may substantially reduce the personal and public health burden of this disorder.

The Importance of Appropriate Recognition and Treatment of Chronic Insomnia: NIH State-of-the-Science Conference Statement

The purpose of this Clinical Update is to emphasize the importance of appropriate recognition of and treatment for chronic insomnia based on the recently published statement from the National Institutes of Health (NIH) State-of-the-Science Conference on the Manifestations and Management of Chronic Insomnia in Adults.[9] An independent panel of health professionals convened in June 2005 to evaluate the evidence from (1) systematic literature reviews prepared by the Agency for Health Research and Quality, (2) presentations by insomnia researchers over a 2-day public session, (3) questions and comments by conference attendees during the public sessions, and (4) closed deliberations by the panel. This process resulted in a State-of-the-Science (SOS) Conference Statement on chronic insomnia, including implications for clinical and research efforts.

The SOS Conference proceedings and statement were organized around the following 5 questions, which serve as the outline for this Clinical Update:

  • How is chronic insomnia defined, diagnosed, and classified, and what is known about its etiology?
  • What are the prevalence, natural history, incidence, and risk factors for chronic insomnia?
  • What are the consequences, morbidities, comorbidities, and public health burden associated with chronic insomnia?
  • What treatments are used for the management of chronic insomnia, and what is the evidence regarding their safety, efficacy, and effectiveness?
  • What are important future directions for insomnia-related research?

The SOS Conference focused on adults with chronic insomnia, not acute or episodic manifestations, which typically resolve in a few weeks, often without intervention. Although secondary or comorbid insomnia (insomnia associated with other conditions) was considered with respect to diagnosis and classification, the conference focused on the treatment of primary insomnia, not on any existing comorbid conditions. This Clinical Update, therefore, follows the scope of the SOS Conference and focuses on chronic primary insomnia in adults. Information in the SOS Conference Statement is augmented by the research literature, including a number of excellent, recent reviews on the clinical management of insomnia.[8,10-14]

How Is Chronic Insomnia Defined, Diagnosed, and Classified, and What Is Known About Its Etiology?

Case Study: Part 1

A 56-year-old woman presents for routine monitoring of postmenopausal symptoms and bone density, following a 2-year course of hormone replacement therapy that was initiated 5 years ago when she began experiencing hot flashes and depressive symptoms. During the visit, she is asked about her sleep and reveals that she has difficulty falling asleep most nights and sometimes awakens in the middle of the night, and is unable to go back to sleep. She notes frustration at her inability to get a good night’s sleep, particularly because she often feels tired and has difficulty concentrating at work. She reports that her insomnia began about the time of her menopausal symptoms, but has continued even though her other menopausal symptoms have resolved.

What steps should be taken to diagnose her condition?

Detecting Sleep Difficulties

The patient in the case above has a distinct advantage over many patients who suffer with insomnia because her healthcare professional specifically asked about her sleep. As early as Hippocrates, sleep has been an important indicator of patient health. “Disease exists, if either sleep or watchfulness be excessive”: Hippocrates, Aphorism LXXI.[12] In a recent study of adult primary care patients with insomnia, only about half reported discussing insomnia with their physicians.[15] Other studies have found that only 10% to 30% of those with insomnia discussed this problem with their physicians,[16] and most healthcare providers fail to ask about sleep.[2] Asking a simple question, such as “How have you been sleeping?” can lead to the detection of insomnia and a range of other sleep-related conditions.[17]

Definitions and Diagnostic Criteria for Chronic Insomnia. Insomnia is a sleep disturbance that most often manifests as difficulty initiating sleep, but also manifests as difficulty maintaining sleep or experiencing early-morning awakenings.

How much sleep disruption is sufficient for the diagnosis of insomnia? Normal sleep needs vary greatly from individual to individual. Moreover, the degree of sleep disturbance in those with insomnia can be quite variable from night to night, including nights without any sleep disturbance. Although quantitative indices for sleep-onset latency (≥ 30 minutes) and for sleep efficiency (percentage of total time asleep over total time in bed ≤ 85%) have been used for research purposes,[18] these indices do not correlate well with the patient’s experience of insomnia.[19] Therefore, the subjective experience of inadequate sleep is frequently more important than quantitative sleep indices in diagnosing insomnia.

The Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) defines primary insomnia as a difficulty initiating or maintaining sleep or experiencing nonrestorative sleep that results in clinically significant distress or impairment in functioning.[20] Based on these criteria, someone who does not appear to have objective manifestations of sleep disturbance but whose sleep is sufficiently inadequate or nonrestorative to produce distress or dysfunction would meet the criteria for insomnia. In contrast, someone who gets only a few hours of sleep each night but feels rested and without associated distress or dysfunction does not meet the criteria for insomnia. Therefore, subjective impressions of nonrestorative sleep with associated distress or dysfunction are important symptoms of insomnia.

These complaints of disturbed sleep also must occur in the context of adequate opportunity and circumstances for sleep. Although disruption of sleep from environmental perturbations may place someone at risk for insomnia, sleep disruption is not classified as insomnia unless there is adequate opportunity to sleep. Resident physicians on call or mothers of newborns commonly experience sleep disturbances, nonrestorative sleep, and daytime distress or impairment from inadequate sleep, but these problems are not diagnosed as insomnia because they are the result of having an inadequate opportunity to sleep.

Many people experience insomnia on occasion, but most of these “acute” or “episodic” forms of insomnia are transient and typically resolve without treatment. The duration required for insomnia to be “chronic” has varied from as little as 1 month to as long as 6 months. Based primarily on recent Research and Diagnostic Criteria (RDC) for insomnia,[21] the SOS Conference Statement concluded that insomnia lasting 1 month or more is clinically important and indicates the need for professional attention.

The SOS Conference Statement concluded that insomnia lasting 1 month or more is clinically important and indicates the need for professional attention.

RDC for insomnia. The Academy of Sleep Medicine recently developed RDC for insomnia[21] in an effort to merge different nosologies and improve the diagnostic reliability of insomnia. The RDC criteria also provide 3 subclassifications of primary insomnia: Psychophysiologic Insomnia, Paradoxical Insomnia (Sleep State Misperception), and Idiopathic Insomnia, which may facilitate research on potential etiologies of this disorder. These diagnostic criteria will be included in the second edition of the International Classification of Sleep Disorders (ICSD-2) and will likely be adopted in the next International Classification of Diseases (ICD) version. The RDC diagnostic scheme first delineates the criteria for an insomnia disorder and then specifies the exclusion criteria for primary insomnia. Compared with the DSM-IV criteria, the RDC insomnia criteria specify the requirement for adequate opportunity or circumstances for sleep and provide greater detail of the distress or functional impairment criteria. The RDC criteria for primary insomnia also clarify that the presence of a comorbid disorder does not exclude the diagnosis of primary insomnia unless the insomnia can be attributed exclusively to the comorbid disorder.

Comorbid insomnia. Primary insomnia is a diagnosis of exclusion. Numerous other conditions can contribute to the onset or maintenance of insomnia, including psychiatric disorders, substance abuse, other sleep disorders, or medical conditions/treatments. In the past, insomnia was considered “secondary” if it appeared due to another condition, but this was often difficult to determine clinically.[22] In addition, the relationship between insomnia and various comorbid disorders is complex and multidirectional. For example, insomnia may be a symptom of comorbid depression, but it may also be a separate and predisposing condition for depression.[23]

Given these complexities, the SOS Conference Panel recommended that “comorbid insomnia” replace the term “secondary insomnia.” The practical implication of this terminology for clinicians is that insomnia should not be relegated to secondary status whenever a comorbid disorder exists. The presence of comorbid disorders needs to be evaluated, and temporal relationships between the course of the comorbid disorder and the insomnia may shed light on possible etiologic relationships between them,[7] but it cannot be assumed that treating only the comorbid disorder will result in resolution of the insomnia as well.

The SOS Conference Panel recommended that “comorbid insomnia” replace the term “secondary insomnia.”

Clinical assessment of insomnia. The diagnosis of insomnia is based primarily on the patient’s history. Reports by family members, particularly the bed partner, can augment the assessment of sleep behavior and daytime functioning. Medical history and physical examination are also useful for determining the presence of possible comorbid syndromes.[7]

Sleep diaries are frequently used to document sleep-and-wake behaviors. In addition to providing data to support a diagnosis, these data are often used to devise treatment plans and to monitor treatment outcomes. Patients are typically instructed to complete the diary each morning after awaking and provide their best estimates of variables, such as time in bed, time of sleep onset, awakenings, and wake time. These data are only estimates by patients and tend to underestimate actual sleep time, but they are useful for assessing individual sleep patterns, possible factors associated with poor sleep, and changes in sleep over time. There are also a number of self-report instruments, a few of which have been adequately standardized and validated for monitoring outcomes.[24]

To provide more objective measures of sleep behavior, actigraphs or accelerometers have been used in research trials to infer sleep-and-wake behaviors from changes in the amount of movement. Although useful, actigraphs have not been fully validated and may underestimate sleep time if sleep is restless or fitful (eg, with comorbid restless legs syndrome). Actigraphs and other automated measures of sleep behavior have not typically been used in routine practice, but can provide more objective measures of sleep patterns, especially when the patient’s report is in question (eg, sleep-state misperception).[25]

Polysomnography remains the gold standard for measuring sleep-wake states; however, the American Academy of Sleep Medicine does not recommend polysomnography for the assessment of insomnia except when needed to rule out a comorbid disorder, such as sleep apnea.[26] In addition to expense, polysomnography is unlikely to provide an accurate representation of an insomnia patient’s sleep difficulties given the night-to-night variability of sleep behavior and influence of the sleep environment on insomnia symptoms.

The American Academy of Sleep Medicine does not recommend polysomnography for the assessment of insomnia except when needed to rule out a comorbid disorder, such as sleep apnea.

Etiology of insomnia. Although there is growing consensus about the appropriate diagnostic criteria and procedures for insomnia, the possible etiologic factors for insomnia remain poorly understood. Spielman’s 3 Ps — predisposing, precipitating, and perpetuating factors — is a useful model for organizing various etiologic factors.[27]

Very little is known about possible predisposing factors for insomnia. Other than some limited research suggesting familial aggregation,[28,29] there are no data on genetic predisposition for insomnia. There is considerable research on the neurobiology of sleep-wake states, including the inhibitory feedback loop involving the GABA and galanin neurons in the ventrolateral preoptic nucleus of the hypothalamus and the orexin or hypocretin neurons in the posterior hypothalamus, which serve as a “flip-flop” switch of major cortical arousal systems.[30,31] It remains unclear, however, how these systems are dysfunctional in insomnia. Deficiencies in endogenous melatonin or benzodiazepine receptors and hyperactivity of corticotropin-releasing factor neurons are possible etiologic factors, but further research is needed to better understand these potential etiologies for insomnia.[32]

The possible etiologic factors for insomnia remain poorly understood, and little is known about possible predisposing factors for insomnia.

Hyperarousal appears to be an important mechanism for insomnia. Research has shown increased brain glucose metabolism when awake or asleep, increased beta and decreased theta and delta during sleep, and increased adrenocorticotropic hormone activity.[33,34] Results from recent functional imaging studies provide additional support for the central nervous system hyperarousal hypothesis.[35]

Potential precipitating factors for insomnia are numerous and include many of the possible disorders that are comorbid with insomnia, such as psychiatric disturbance, sleep-wake schedule changes, medical conditions and their treatments, other sleep disorders, and substance use. Substances, including caffeine, theophylline and other stimulants, steroids, antihypertensives, and antidepressants, can also precipitate insomnia.[12] A recent study found that family, health, and work-school-related events were the most common precipitating factors for insomnia, and that even positive events can precipitate insomnia.[36]

There is general agreement that insomnia, regardless of how it is precipitated, is perpetuated by cognitive and behavioral mechanisms. Cognitive factors involved in perpetuating insomnia include misconceptions about normal sleep needs and stability, misattributions about the causes of sleep disturbance, and catastrophic worry about the daytime effects of inadequate sleep.[18,37] These dysfunctional beliefs often promote behaviors that are intended to improve sleep but are disruptive to sleep homeostasis and a consistent sleep-wake cycle (eg, taking naps and sleeping in late to “catch up” on sleep). These sleep-disruptive behaviors are further perpetuated by behavioral conditioning, which produces conditioned arousal to stimuli that would normally be associated with sleep.[38] It is important to recognize that these cognitive and behavioral perpetuating factors may be present in both comorbid and primary

What Are the Prevalence, Course, Incidence, and Risk Factors for Chronic Insomnia?

Prevalence of Chronic Insomnia

Estimates of the prevalence of insomnia vary depending on the definition used. Approximately one third of the general population complains of sleep disruption, and 9% to 15% of the population report associated daytime impairment consistent with the diagnosis of insomnia.[1] However, the proportion of those reporting sleep disturbance with daytime impairment who would meet the diagnostic criteria for insomnia is unclear. Among patients in primary care, the prevalence rates for insomnia are much higher, as high as 50%.[4] In a large survey of managed care participants, over one third experienced symptoms of insomnia, although less than 1% presented with an insomnia complaint.[39]

Incidence, Natural Course, and Duration of Chronic Insomnia

The SOS Conference Statement noted that there is very little known about the incidence, natural course, and duration of insomnia. Limited evidence suggests that insomnia is a chronic and persisting condition with low rates of spontaneous remission and possible recurrence after a period of remission, but these processes are poorly understood.

There is very little known about the incidence, natural course, and duration of insomnia.

Risk Factors for Chronic Insomnia

Given that most research on risk factors for insomnia is cross-sectional, not longitudinal, it is difficult to know whether potential risk factors are causal or correlational. The prevalence of insomnia is higher in divorced, separated, or widowed adults, and in those with lower education and income levels.[1] Insomnia is also more likely to occur in women, especially postmenopausal women.[1] There is an increased prevalence of insomnia in older adults, but it remains unclear to what extent this is independent of declining health and comorbid influences. Sleep patterns, however, do change with age. Older people experience more awakenings during the night, lower sleep efficiency, less sleep, more variable sleep, and lighter sleep than younger adults.[40]

Several psychiatric and medical disorders are associated with insomnia. As noted earlier, however, these relationships are complex and multidirectional. For example, research on the relationship between insomnia and depression indicates that it is more likely that insomnia is a risk factor for depression than that depression is a risk factor for insomnia. Insomnia appears to be predictive of a number of disorders, including depression, anxiety, alcohol abuse/dependence, drug abuse/dependence, and suicide.[41] Medical and sleep disorders that potentially disrupt sleep (eg, chronic pain conditions, such as arthritis, or sleep apnea) may be precipitants of or risk factors for insomnia. Substance abuse and the use of prescribed medications that can disturb sleep also can be risk factors for insomnia.

It is difficult to know whether potential risk factors are causal or correlational. Several psychiatric and medical disorders are associated with insomnia, but these associations are complex and multidirectional.

What Are the Consequences, Morbidities, Comorbidities, and Public Health Burden Associated With Chronic Insomnia?

Economic Costs of Insomnia

Insomnia is associated with high healthcare utilization. Walsh and Ustun[42] estimated annual direct total costs for insomnia at about $12 billion for healthcare services and $2 billion for sleep-promoting agents. People with insomnia have more medical problems and use more medications than those without insomnia, and they have double the number of office visits and hospitalizations as those without insomnia.[6,43]

The relative contribution of insomnia and comorbid conditions to these costs remains unclear. Indirect costs of insomnia are even less clear. In 1994, the economic costs of insomnia were estimated at $80 billion annually.[44,45] These indirect cost estimates are higher than those for other chronic conditions, such as rheumatoid arthritis,[46] but there are limited data available to reliably estimate the indirect costs of insomnia.

Effects of Insomnia on Functioning and Quality of Life

Sleep loss does result in impaired psychomotor and cognitive functioning, but these impairments are less pronounced for insomnia.[47] Despite the equivocal impact of insomnia on memory and cognitive functioning, insomnia is related to occupational role dysfunction, including increased absenteeism and decreased work performance.[4,43] These daytime impairments, however, may be more related to the chronic hyperarousal state[48] or to perceptions of sleep deprivation[49] than to actual sleep loss from insomnia.

In considering the consequences of insomnia, it is important to differentiate being sleepy from being tired or fatigued. Sleepiness involves recurrent episodes of being drowsy and involuntarily falling asleep in nonstimulating environments (ie, dozing off). Sleepiness is more often associated with other primary sleep disorders, such as narcolepsy, sleep apnea, and periodic limb movement disorder. In contrast, those with insomnia are often tired or fatigued but not sleepy.[48,50]

Insomnia is associated with substantial impairments in quality of life. Although insomnia is often considered more benign than most other chronic medical and psychiatric disorders, the impairments in quality of life in insomnia are comparable to those observed in diabetes, arthritis, and heart disease.[5] Quality of life also improves with treatment for insomnia, although not to the level of the normal population.[51]

Insomnia is associated with substantial impairments in quality of life that are comparable to the impairments observed in other chronic medical disorders.

Comorbidities and Morbidities

Approximately 40% of adults with insomnia also have a diagnosable psychiatric disorder.[16] In addition, approximately three quarters of people presenting to sleep clinics or general medical practices with insomnia have a comorbid psychiatric disorder.[52] Although there are a number of psychiatric disorders that are comorbid with insomnia (eg, generalized anxiety disorder, attention-deficit/hyperactivity disorder, and schizophrenia), depression has received the most attention. Insomnia was once considered only a symptom of depression or secondary to depression. Recent research, however, has consistently shown that insomnia is a predisposing factor for depression. Insomnia often occurs prior to the onset of depression,[53] and often precedes depression relapses.[54,55] Those with persistent insomnia are also much more likely to develop depression at a later time.[16,56] In addition to depression, insomnia is associated with an increased risk for suicide[57] and is a precipitant of manic episodes in those with bipolar disorder.[58]

Insomnia is common in other primary sleep disorders, such as sleep apnea (sleep-disordered breathing [SDB]), restless legs syndrome, and periodic limb movement disorder. In these cases, insomnia may be secondary or fully attributable to the underlying sleep disorder, but often is a comorbid disorder precipitated by the other primary sleep disorder but perpetuated by cognitive and conditioning factors.[59] SDB typically presents clinically with nonrestorative sleep complaints and disturbed sleep maintenance with normal sleep onset. Snoring and/or apnea episodes are often reported by the bed partners, but patients are typically unaware of their sleep-related symptoms. If positive indications of SDB are found during a clinical interview, then overnight sleep recording is typically performed to establish the diagnosis and determine its severity.[7,59] SDB may be exacerbated by benzodiazepines, so it is important to rule out this condition before proceeding with insomnia treatment.

A number of chronic medical conditions are associated with insomnia, including chronic pain syndromes, coronary heart disease, asthma, gastrointestinal disorders, vascular disorders, chronic fatigue, and endocrine and metabolic disorders.[7] In addition, substances, including caffeine, theophylline and other stimulants, steroids, antihypertensives, and antidepressants, can precipitate insomnia.[12]

Although many of the disorders comorbid with insomnia are associated with increased mortality rates, insomnia itself does not appear to be associated with higher mortality. In a recent longitudinal study, neither insomnia nor the use of hypnotics for insomnia increased the risk for mortality over a 6-year period.[60] Higher mortality has been associated with either too much or too little sleep, but not with insomnia disorder per se.[61,62]

Insomnia is frequently comorbid with psychiatric disorders, other primary sleep disorders, and chronic medical conditions.

What Treatments Are Used for the Management of Chronic Insomnia, and What Is the Evidence Regarding Their Safety, Efficacy, and Effectiveness?

Case Study: Part 2

The patient’s medical history reveals menopausal symptoms that were controlled on hormone replacement therapy and did not recur following discontinuation 3 years ago. Her insomnia symptoms, however, have continued and worsened in the past 5 years. The patient is otherwise healthy. She does not report pain at night, snoring or gasping for air during sleep, or restless legs. She does report awakening at least once a night to urinate, but indicates that she is sometimes unable to return to sleep after awakening.

The clinical interview reveals no other psychiatric disorder. She has no history of substance abuse or dependence, but does indicate that she has begun drinking a glass or 2 of wine at night to help her fall asleep. She describes primarily being unable to fall asleep, and says it takes her an hour or 2 to fall asleep most nights. She also describes awakening during the night, sometimes being unable to go back to sleep, and that these sleep-maintenance symptoms have worsened in the past 6 months. She reports hearing that older people can get by on less sleep, but that she feels tired and irritable after nights of inadequate sleep. She is beginning to believe that she is not functioning as well at work because of her sleep difficulties. She reports feeling particularly distressed in the evening as her bedtime approaches and worries whether she will get enough sleep to perform well the next day.

The patient is provided with general information about sleep and insomnia and reassured that her sleep difficulties can be managed. She is provided with a sleep diary and asked to record her sleep-wake patterns for 2 weeks and then to return with her husband to complete the evaluation.

At the second visit, her husband confirms that she does not snore loudly or excessively and does not appear to experience short bouts of not breathing while asleep. He reports that she does have difficulty going to sleep and will toss and turn for an hour or so before falling asleep. On 2-3 mornings each week, he wakes up and finds that she is not in bed but that she got up during the night and later fell asleep while watching television downstairs. On weekends, he usually lets her sleep in late. He reports that she is sometimes so tired after a bad night that she will come home from work and take a nap before dinner. Her sleep diary reveals an average sleep-onset latency of about 45 minutes each night, that she is awake for over an hour during the night on about half the nights, a mean total sleep time of 6 hours and 30 minutes per night, and a mean sleep efficiency of 82%.

Based on this assessment, what treatment approaches should be considered?

Cognitive Behavioral Therapy

Cognitive behavioral therapy for insomnia (CBTI) addresses the hyperarousal, cognitive, and conditioning factors that appear to perpetuate the disorder. CBTI typically consists of 5 major components:[38]

  • Sleep-hygiene strategies to promote a sleep environment and routine that promote sleep.
  • Relaxation therapy (progressive muscle relaxation, visual imagery, etc) to reduce physiologic arousal.
  • Cognitive restructuring to change dysfunctional attitudes about sleep (eg, attempting to will oneself to sleep or excessive worrying about the effects of not sleeping).
  • Stimulus control to reassociate the bed and bedroom with going to sleep instead of staying awake. These instructions include (1) going to bed only when sleepy, (2) establishing a standard wake-up time, (3) getting out of bed whenever awake in bed for 15 minutes or more, (4) avoiding doing sleep-incompatible behaviors (reading or watching television) while in bed, and (5) refraining from daytime napping.
  • Sleep restriction to condense time in bed to the average time typically asleep. For this component, the time to bed is set based on the average time asleep but not less than 5 hours, and then it is gradually increased as sleep efficiencies improve.

The American Academy of Sleep Medicine Task Force on nondrug alternatives for primary chronic insomnia[63] found that CBTI produced reliable and durable improvement in chronic insomnia. Nearly 80% of those treated with CBTI show measurable benefit, but the magnitude of the benefit varies. CBTI produces objective improvements as well as subjective improvements in sleep and appears to improve homeostatic sleep regulation.[64] Although most of the research on CBTI is with primary insomnia, CBTI has been shown to produce benefits for the comorbid condition as well as for the insomnia.[65]

Sleep hygiene is the component of CBTI that is most often provided by healthcare providers,[66] and patients tend to like and adhere to sleep-hygiene strategies.[67] Unfortunately, sleep hygiene appears to be the least effective CBTI component. Stimulus control and sleep restriction are the most effective CBTI components,[68] but patients have the most difficulty adhering to these components.[67]

When CBTI is compared with medications, sedative hypnotics appear to produce more rapid improvements, but the long-term safety and efficacy of sedative hypnotics are less well established than CBTI.[69,70] The efficacy of CBTI, particularly long-term, and the minimal apparent adverse effects of this treatment have resulted in it being considered a first-line treatment for primary insomnia.[70]

Challenges with CBTI. Although CBTI is clearly efficacious, accessibility to this treatment has been severely limited by a general lack of knowledge regarding efficacy, inadequate coverage of this treatment by insurance carriers, and a lack of professionals trained in CBTI, even at certified sleep disorder centers.[38] The treatment is generally well accepted by patients when they are provided this option,[71] and the treatment is relatively short. Although session dosage remains unclear, Edinger and Means[38] have suggested that 4 sessions at 2-week intervals may be optimal based on their review of this treatment approach.

To increase availability, researchers have experimented with alternative methods of CBTI treatment delivery. Treatment delivery in individual, group, or phone-based sessions appears to be equally helpful.[72] Although self-help interventions appear less effective than professional assistance, self-help versions of CBTI still provide modest benefit over controls.[73] Delivery of CBTI via the Internet and other technologies is a promising new approach area for potentially improving the accessibility of this efficacious treatment for insomnia.[74]

Although CBTI is not typically provided by primary care health professionals, recent efforts show this to be another potential strategy for providing this treatment to those with insomnia. Indeed, allied healthcare providers have been trained to deliver CBTI with some success.[75] Recently, Edinger and Sampson[76] devised a “primary care friendly” form of CBTI. This abbreviated form of CBTI involves two 25-minute sessions 2 weeks apart. Session 1 consists of reviewing sleep logs and providing sleep education, stimulus control, and sleep-restriction instructions, such as eliminating activities that are incompatible with sleep, avoiding daytime naps, and setting up a consistent sleep-wake schedule (including sleep restriction). Session 2 consists of reviewing progress, addressing adherence difficulties, and modifying sleep strategies accordingly. This abbreviated treatment was significantly better than sleep-hygiene instructions alone for most insomnia measures and resulted in reductions of insomnia symptoms to normal levels in over half of patients.[76]

Although CBTI is efficacious, accessibility to this treatment has been severely limited by a general lack of knowledge regarding efficacy, inadequate coverage of this treatment by insurance carriers, and a lack of professionals trained in CBTI, even at certified sleep disorder centers.

US Food and Drug Administration-Approved Medications

Benzodiazepine and nonbenzodiazepine hypnotics. Both benzodiazepine and nonbenzodiazepine hypnotics have been approved for the treatment of insomnia.

Benzodiazepine hypnotics. The benzodiazepine hypnotics approved by the US Food and Drug Administration (FDA) for the treatment of insomnia are estazolam, flurazepam, quazepam, temazepam, and triazolam. These medications have been found effective in a number of double-blind, placebo-controlled trials, but these trials have typically been short-term (4-6 weeks).[77] Even with longer term use, there is a reduced effect after 4-8 weeks.[78] Except for triazolam, these benzodiazepine hypnotics have long half-lives, which contribute to their efficacy for maintaining sleep, but also result in higher rates of next-day impairments, such as morning sedation, cognitive impairment, and motor incoordination.[79] Temazepam is the most commonly prescribed benzodiazepine hypnotic,[80] but, despite its long half-life, it appears to have minimal impact on number of awakenings, and produces tolerance, morning sedation, and cognitive impairment.[8] Triazolam, the only short half-life agent in this group, has more of an impact on sleep onset than maintenance, but possible amnestic effects have been a concern.[81,82]

Except in those with a history of substance abuse, abuse liability from these benzodiazepine hypnotics appears to be minimal.[83] However, due to concerns about abuse liability, the FDA has indicated that these medications should be limited to 7-10 days of use with reevaluation if used for more than 2-3 weeks. Some have argued that these limitations were based on now obsolete guidelines,[84] and that longer term use may not increase the risk for abuse liability,[85] but the long-term effects of these medications on tolerance and abuse liability require further study.

Nonbenzodiazepine hypnotics. Nonbenzodiazepine hypnotics are a new class of hypnotics that act on specific benzodiazepine receptor subtypes, but have a nonbenzodiazepine structure. Three nonbenzodiazepine hypnotics — zaleplon, zolpidem, and eszopiclone — have been approved by the FDA for the treatment of insomnia. As a class, these medications generally have shorter half-lives than their benzodiazepine predecessors, which results in greater effects on sleep onset than sleep maintenance and minimal morning sedation and other daytime impairments. Nonbenzodiazepine hypnotics also may have less abuse liability potential than benzodiazepine hypnotics, although further research is needed.[86]

Zolpidem is the most commonly prescribed agent for insomnia,[80] and due to its rapid onset and short half-life (1.5-4 hours), it has more of an effect on sleep onset than sleep maintenance.[87] Modified-release formulations may provide better sleep-maintenance effects, but data on these formulations are still needed.[88] Efficacy data do not extend beyond 1-2 months, so the effects of longer term use are unknown.[89]

Zaleplon has a very short half-life of only about 1 hour and, therefore, affects primarily sleep onset.[90] Higher doses may affect sleep maintenance and may increase the risk for side effects.[91] Although studies of zaleplon have been of longer duration than zolpidem, long-term safety and efficacy beyond 1-3 months have not been established.[92,93]

Eszopiclone is the newest medication in this group, and it has the longest half-life (5-6 hours). Studies show that this half-life appears adequate to produce effects on sleep maintenance as well as sleep onset while also resulting in minimal morning sedation.[94,95] Eszopiclone does not have a limitation on duration of use, and recent findings have shown efficacy and safety with minimal tolerance or abuse liability over 12 months of use.[96]

As a group, these medications appear to produce minimal sedation effects or psychomotor impairment.[97,98] These reduced side effects relative to benzodiazepine hypnotics appear to be due to their short half-lives more so than their selective receptor agonist effects.[99] Nonbenzodiazepine hypnotics also may produce potentially fewer or less severe drug interactions than many of the benzodiazepine hypnotics because they rely less exclusively on CYP3A4 metabolism.[100] Substantial proportions of these medications, however, are still metabolized through CYP3A4; so these medications, as is the case with the most traditional benzodiazepine hypnotics, should be carefully monitored if CYP inducers (rifampicin) or CYP3A4 inhibitors (ketoconazole, erythromycin, and cimetidine) are also being prescribed.[100] Alcohol also potentiates the effects of all hypnotics, so patients should be instructed not to drink, and if they do, to understand that they will feel more sedated the next morning, potentially affecting their ability to drive.

Medications for insomnia are typically taken every night on a prophylactic basis to manage insomnia. Due to the rapid onset and minimal abuse liability of nonbenzodiazepine hypnotics, nonnightly or as-needed use has been considered and appears safe and efficacious in preliminary trials.[101] Further trials, however, are needed to substantiate the safety and efficacy of long-term, nonnightly administration.

Nonbenzodiazepine hypnotics have shorter half-lives, which result in greater effects on sleep onset than sleep maintenance and minimal morning sedation and other daytime impairments. They may also be associated with fewer or less severe drug interactions, and may have less abuse liability than benzodiazepine hypnotics.

Discontinuation of hypnotics. Little research has been conducted on the persistence or reappearance of symptoms after prescription therapy is discontinued. Discontinuation of hypnotics, whether benzodiazepine or nonbenzodiazepine, generally results in relapse of symptoms. Many of the benzodiazepines also produce rebound insomnia, insomnia that is worse than pretreatment levels, for a few days. Rebound insomnia also may be reduced with the newer nonbenzodiazepine hypnotics, although further research is needed.[78] CBTI has been used to reduce relapse rates after benzodiazepine discontinuation.[102]

Melatonin receptor agonists. The FDA recently approved ramelteon for the treatment of chronic insomnia. Ramelteon is a selective melatonin receptor agonist (MT1, MT2) that is rapidly absorbed (< 1 hour) and has a relatively short half-life (2-5 hours). Initial studies of ramelteon have shown reduced sleep-onset latency compared with placebo, with a low rate of side effects and adverse events.[103] Abuse liability also appears to be minimal. Ramelteon should not be prescribed concomitantly with strong CYP1A2 inhibitors, such as fluvoxamine. Although ramelteon is a promising alternative to sedative-hypnotics, further research on its safety and efficacy, particularly long-term, is needed.

Prescription Drugs Without FDA Approval for Insomnia

Trazodone is one of the most commonly prescribed medications for the treatment of insomnia, comparable to zolpidem.[80] The low cost of antidepressant medications along with unrestricted long-term use and minimal abuse liability may be factors leading to the increased use of these medications for insomnia.

Trazodone is sedating, but there is a paucity of data on its effects on insomnia. Research has usually been performed with small, comorbid, depressed samples with short and equivocal effects on sleep.[104,105] Trazodone can have significant side effects, including orthostatic hypotension, blurred vision, nausea, dry mouth, constipation, drowsiness, headache, and (rarely) priapism. These side effects also increase the risk for falls and accidents, which can have serious consequences in the elderly. Although these risks are less pronounced at the lower doses typically used for insomnia, the risk-benefit ratio may be too great in some situations to use trazodone for insomnia.[106] There are also limited data on the short-term effects of doxepin[107] for insomnia. The potential adverse effects from trazadone, doxepin, and other antidepressants overshadow the limited efficacy data on these medications. Dose-response relationships of antidepressants for insomnia also are poorly understood.[108,109]

The SOS Conference Statement notes that various other medications have been used in the treatment of insomnia, including barbiturates (phenobarbital) and antipsychotics (quetiapine and olanzapine). These medications, however, have serious side effects and adverse risks with little to no data supporting their efficacy. Therefore, these medications are not recommended for the treatment of insomnia.

According to the SOS Conference Statement, the risk-benefit ratio may be too great in some situations to use trazodone or other antidepressants for the treatment of insomnia. In addition, barbiturates (phenobarbital) and antipsychotics are not recommended for the treatment of insomnia.

Over-the-Counter Medications

Over-the-counter (OTC) medications are frequently used for insomnia. About one fourth of US adults with sleep difficulties use OTC sleep aids.[110]

Antihistamines (H1 receptor agonists, such as diphenhydramine) are the most commonly used OTC medications for insomnia. There is, however, no systematic evidence of efficacy for insomnia, and there are significant side effects, including dry mouth, blurred vision, urinary retention, constipation, and a risk for increased intraocular pressure in patients with narrow angle glaucoma.[111]

Alcohol is often used to reduce sleep-onset latency. Although alcohol does reduce sleep latency, it also results in poorer quality sleep and nighttime awakening. Alcohol also is clearly not appropriate for someone with a risk for substance use. Therefore, alcohol cannot be recommended as a sleep aid.[112]

Melatonin is a natural hormone that is produced by the pineal gland that has a role in circadian rhythm control. Melatonin may be helpful for reducing symptoms of jet lag, but there is minimal evidence of efficacy for insomnia. Melatonin appears to be safe for short-term use, but long-term safety is unknown. Except for the recently FDA-approved ramelteon, melatonin compounds are unregulated, and preparations may vary.[113]

L-tryptophan is an endogenous amino acid sometimes used as a hypnotic. Evidence of efficacy for insomnia, however, is extremely limited and there are possible toxic interaction effects with some psychiatric medications.[114]

Valerian is derived from the valeriana plant root and thought to promote sleep, but there is no proven benefit for insomnia. Valerian is unregulated and possibly associated with hepatotoxicity. Other herbal products are sometimes used for insomnia, but there are no data supporting their efficacy and there are similar concerns about safety and drug interactions.[115]

Other alternative treatments, such as tai chi, yoga, acupuncture, and light therapy, have been used to treat insomnia, but they have not been adequately evaluated.[114,116]

OTC products, alternative treatments, and complementary therapies are often used to treat insomnia. These therapies, however, have not been systematically evaluated; efficacy data are lacking; and there are concerns about side effects.

Case Study: Part 3

Following the clinical assessment, the patient is advised regarding treatment approaches. Although menopausal symptoms appear to have been a precipitant of the insomnia, these symptoms have resolved and no longer appear to be related to the insomnia. The patient is counseled about cognitive behavioral and sedative-hypnotic approaches for insomnia. Given the minimal risks, she would prefer to try CBTI first, but the nearest specialist with expertise in CBTI is 2 hours away. Therefore, she agrees to try one of the newer sedative-hypnotics and to obtain an abbreviated form of CBTI from the nurse practitioner who has some limited training in this approach.

Because she presents with both sleep-onset and sleep-maintenance difficulties, and may require long-term medication use to control her insomnia, she is started on an agent appropriate for long-term administration immediately before bed each night, and advised that it may be necessary to increase her prescription if her sleep difficulties, particularly sleep maintenance difficulties, persist.

The patient meets with the nurse practitioner who provides information about sleep hygiene and instructs her to refrain from using alcohol to fall asleep, particularly in combination with her medication. A consistent wake time of 7:00 am is agreed to and a time to bed of 12:30 am is determined based on her average time asleep from her sleep diaries. The patient is concerned that she may be more tired than usual if she goes to bed this late, but is reassured that she will be getting the same amount of sleep as she usually does, just more consolidated. She is also instructed to get out of bed if she does not fall asleep within 15 minutes, to do something restful, and then return to bed when she feels sleepy again. She is assured that she can function adequately the next day if she does not get much sleep, which she has been doing for years, and that she can only control getting in and out of bed, not if and when she falls asleep while in bed. She is encouraged not to take naps and to maintain her regular wake time even if she did not sleep well the night before or can sleep later that morning.

After 2 weeks, the patient’s sleep diary shows that she has generally adhered to her new sleep schedule and that her sleep efficiencies are above 90% as a result of her bedtime restrictions. She is instructed to adjust her bedtime 15 minutes earlier and to readjust her bedtime earlier each week if her sleep efficiencies average above 90%. She is encouraged to continue the strategies that appear to be working, particularly maintaining a consistent bedtime, not taking naps, and getting out of bed if she is unable to fall asleep.

At a follow-up visit 1 month later, the patient reports sleeping well and feeling rested although her total sleep time is only 7.5 hours, less than she thought was adequate. She is reassured that sleep needs change over time and that her sense of feeling rested and restored is more important than how much sleep she gets. She is encouraged to continue the CBTI strategies that she has found helpful thus far. She wonders whether the medication is still needed to control her sleep. She is instructed to shift from taking it every night to taking it as needed after getting out bed if she is unable to fall asleep within 15 minutes.

At a follow-up visit 3 months later, the patient reports that she no longer takes the medication for sleep, that she continues to get about 7.5 hours of sleep per night with little to no difficulty initiating or maintaining sleep, and that she feels rested and refreshed most mornings.

What Are Important Directions for Insomnia-Related Research?

Based on what is known about the manifestations and management of insomnia, the SOS Conference Panel made a number of recommendations for future research needs:[9]

  1. Developing and validating instruments to assess chronic insomnia, particularly measures of outcome and diurnal consequences;
  2. Conducting more research on possible genetic and neural mechanisms of insomnia;
  3. Conducting longitudinal observational studies to better understand the incidence, course, and correlates of insomnia, including the adoption of sleep-disturbance items in national health survey research;
  4. Obtaining more information on the impact of insomnia on quality of life and the indirect and direct impact on individuals, caregivers, and society as a whole;
  5. Providing better estimates of the cost of illness to determine cost-effectiveness of treatments;
  6. Obtaining more long-term outcome data, particularly following discontinuation of treatment;
  7. Performing large-scale, multisite comparative treatment trials, including studies of the efficacy of combined or sequenced administration of medications and CBTI;
  8. Conducting more research on OTC and alternative remedies for insomnia;
  9. Conducting efficacy trials in subpopulations, such as children, nursing home residents, and postmenopausal women, and in those with comorbid as well as primary chronic insomnia; and
  10. Assessing clinician decision making with insomnia patients; although much is known that can inform clinical decision making, much more research is needed in this area.

Conclusions

Insomnia is a major public health problem affecting millions of individuals, their families, and their communities. Little is known about etiologic mechanisms, but hyperarousal, cognitive processes, and behavioral conditioning have some support as possible factors. Current evidence supports the efficacy of CBTI and sedative-hypnotics for the treatment of insomnia. Despite widespread use, there is very little evidence supporting the use of other treatments, such as antidepressants and OTC agents, for the treatment of insomnia.

Although there are a number of efficacious medications for insomnia, the SOS Conference Panel noted concern about the mismatch between the chronic, long-term nature of the disorder and the short duration of most clinical trials. Only eszopiclone has been evaluated in trials lasting 6-12 months. Newer medications not yet approved, such as indiplon (a short-acting nonbenzodiazepine hypnotic), provide additional options for the treatment of chronic insomnia, but there remains a clear need for new and more targeted drug therapies that can be used safely and effectively long-term. CBTI shows promising long-term effects with minimal safety concerns, and accessibility to this treatment option should be expanded.

References

  1. Ohayon MM. Epidemiology of insomnia: what we know and what we still need to learn. Sleep Med Rev. 2002;6:97-111.
  2. Haponik EF, Frye AW, Richards B, et al. Sleep history is neglected diagnostic information. Challenges for primary care physicians. J Gen Intern Med. 1996;11:759-761.
  3. Allaert FA, Urbinelli R. Sociodemographic profile of insomniac patients across national surveys. CNS Drugs. 2004;18(suppl1):3-7.
  4. Simon GE, VonKorff M. Prevalence, burden, and treatment of insomnia in primary care. Am J Psychiatry. 1997;154:1417-1423.
  5. Chevalier H, Los F, Boichut D, et al. Evaluation of severe insomnia in the general population: results of a European multinational survey. J Psychopharmacol. 1999;13(suppl1):S21-24.
  6. Leger D, Guilleminault C, Bader G, Levy E, Paillard M. Medical and socio-professional impact of insomnia. Sleep. 2002;25:625-629.
  7. Thase ME. Correlates and consequences of chronic insomnia. Gen Hosp Psychiatry. 2005;27:100-112.
  8. Benca RM. Diagnosis and treatment of chronic insomnia: a review. Psychiatr Serv. 2005;56:332-343.
  9. The National Institutes of Health Consensus Development Program. NIH State-of-the-Science Conference Statement on Manifestations and Management of Chronic Insomnia in Adults. Available at: http://consensus.nih.gov/2005/2005InsomniaSOS026html.htm Accessed November 17, 2005.
  10. Wilson S, Nutt D. Assessment and management of insomnia. Clin Med. 2005;5:101-104.
  11. Silber MH. Chronic insomnia. N Engl J Med. 2005;343:803-810.
  12. Sateia MJ, Nowell PD. Insomnia. Lancet. 2004;364:1959-1973.
  13. Yang CM, Spielman AJ, Huang YS. Insomnia. Curr Treat Options Neurol. 2005;7:373-386.
  14. Neubauer DN. Insomnia. Prim Care. 2005;32:375-388.
  15. Aikens JE, Rouse ME. Help-seeking for insomnia among adult patients in primary care. J Am Board Fam Pract. 2005;18:257-261.
  16. Ford DE, Kamerow DB. Epidemiologic study of sleep disturbances and psychiatric disorders. An opportunity for prevention? JAMA. 1989;262:1479-1484.
  17. Doghramji PP. Recognizing sleep disorders in a primary care setting. J Clin Psychiatry. 2004;65(suppl16):23-26.
  18. Epsie CA. Insomnia: conceptual issues in the development, persistence, and treatment of sleep disorder in adults. Annu Rev Psychol. 2002;53:215-243.
  19. Erman MK. Sleep architecture and its relationship to insomnia. J Clin Psychiatry. 2001;62(suppl10):9-17.
  20. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders — Text Revision. 4th ed. Washington, DC: American Psychiatric Publishing; 2000.
  21. Edinger JD, Bonnet MH, Bootzin RR, et al. Derivation of Research Diagnostic Criteria for Insomnia: Report of an American Academy of Sleep Medicine Workgroup. Sleep. 2004;27:1567-1596.
  22. Edinger JD. Classifying insomnia in a clinically useful way. J Clin Psychiatry. 2004;65(suppl8):36-43.
  23. Billiard M, Bentley A. Is insomnia best categorized as a symptom or a disease? Sleep Med. 2004;5(suppl1):S35-S40.
  24. Devine EB, Hakim Z, Green J. A systematic review of patient-reported outcome instruments measuring sleep dysfunction in adults. Pharmacoeconomics. 2005;23:889-912.
  25. Ancoli-Israel S, Cole R, Alessi C, Chambers M, Moorcroft W, Pollak CP. The role of actigraphy in the study of sleep and circadian rhythms. Sleep. 2003;26:342-392.
  26. Chesson A, Hartse K, Anderson WM, et al. Practice parameters for the evaluation of chronic insomnia. An American Academy of Sleep Medicine report. Standards of Practice Committee of the American Academy of Sleep Medicine. Sleep. 2000;23:237-241.
  27. Spielman AJ, Caruso LS, Glovinsky PB. A behavioral perspective on insomnia treatment. Psychiatr Clin North Am. 1987;10:541-553.
  28. Yves E, Morin C, Cervena K, Carlander R, Beset A, Billard M. Family studies in insomnia. Sleep. 2003;26:A304.
  29. Dauvilliers Y, Morin C, Cervena K, et al. Family studies in insomnia. J Psychosom Res. 2005;58:271-278.
  30. Roth T. Characteristics and determinants of normal sleep. J Clin Psychiatry. 2004;65(suppl16):8-11.
  31. Siegel JM. The neurotransmitters of sleep. J Clin Psychiatry. 2004;65(suppl16):4-7.
  32. Richardson GS, Roth T. Future directions in the management of insomnia. J Clin Psychiatry. 2001;62(suppl10):39-45.
  33. Perlis ML, Smith MT, Pigeon WR. Etiology and pathophysiology of insomnia. In: Kryger MH, Roth T, Dement WC, eds. Principles and Practice of Sleep Medicine. 4th ed. Philadelphia, Pa: Elsevier; 2005:714-725.
  34. Bonnet MH, Arand DL. Hyperarousal and insomnia. Sleep Med Rev. 1997;1:97-108.
  35. Drummond SPA, Smith MT, Orff HJ, Chengazi V, Perlis ML. Functional imaging of the sleeping brain: review of findings and implications for the study of insomnia. Sleep Med Rev. 2004;8:227-242.
  36. Bastien CH, Vallieres A, Morin CM. Precipitating factors of insomnia. Behav Sleep Med. 2004;2:50-62.
  37. Harvey AG, Tang NKY, Browning L. Cognitive approaches to insomnia. Clin Psychol Rev. 2005;25:593-611.
  38. Edinger JD, Means MK. Cognitive-behavioral therapy for primary insomnia. Clin Psychol Rev. 2005;25:539-558.
  39. Hatoum HT, Kania CM, Kong SX, et al. A survey of enrollees at five managed care organizations. Am J Manag Care. 1998;4:79-86.
  40. Nau SD, McCrae CS, Cook KG, Lichstein KL. Treatment of insomnia in older adults. Clin Psychol Rev. 2005;25:645-672.
  41. Taylor DJ, Lichstein KL, Durrence HH. Insomnia as a health risk factor. Behav Sleep Med. 2003;1:227-247.
  42. Walsh J, Ustun B. Prevalence and health consequences of insomnia. Sleep. 1999;22:S427-S436.
  43. Leger D, Guilleminault C, Bader G, Levy E, Paillard M. Medical and socio-professional impact of insomnia. Sleep. 2002;25:625-629.
  44. Stoller MK. Economic effects of insomnia. Clin Ther. 1994;16:873-897.
  45. Martin SA, Aikens JE, Chervin RD. Toward cost-effectiveness analysis in the diagnosis and treatment of insomnia. Sleep Med Rev. 2004;8:63-72.
  46. Yelin E, Callahan LF. The economic cost and social and psychological impact of musculoskeletal conditions. National Arthritis Data Work Groups. Arthritis Rheumatol. 1995;38:1351-1362.
  47. Sateia MJ, Doghramji K, Hauri PJ, Morin CM. Evaluation of chronic insomnia: an American Academy of Sleep Medicine review. Sleep. 2000;23:243-308.
  48. Bonnet MH, Arand DL. The consequences of a week of insomnia. Sleep. 1996;19:452-461.
  49. Semler CN, Harvey AG. Misperception of sleep can adversely affect daytime functioning in insomnia. Behav Res Ther. 2005;43:843-856.
  50. Reidel BW, Lichstein KL. Insomnia and daytime functioning. Sleep Med Rev. 2000;4:277-298.
  51. Reimer MA, Flemons WW. Quality of life in sleep disorders. Sleep Med Rev. 2003:7:335-349.
  52. Katz DA, McHorney CA. The relationship between insomnia and health related quality of life in patients with chronic illness. J Fam Pract. 2002;51:229-235.
  53. Breslau N, Roth T, Rosenthal L, et al. Sleep disturbance and psychiatric disorders: a longitudinal epidemiologic study of young adults. Biol Psychiatry. 1996;39:411-418.
  54. Ohayon MM, Roth T. Place of chronic insomnia in the course of depressive and anxiety disorders. J Psychiatr Res. 2003;37:9-15.
  55. Lustberg L, Reynolds CF. Depression and insomnia: questions of cause and effect. Sleep Med Rev. 2000;4:253-262.
  56. Riemann D, Voderholzer U. Primary insomnia: a risk factor to develop depression. J Affect Disord. 2003;76:255-259.
  57. Agargun MY, Kara H, Solmaz M. Sleep disturbances and suicidal behavior in patients with major depression. J Clin Psychiatry. 1997;58:249-251.
  58. Wehr TA. Sleep loss: a preventable cause of mania and other excited states. J Clin Psychiatry. 1989;50(suppl):8-16.
  59. Chung KF. Insomnia subtypes and their relationship to daytime sleepiness in patients with obstructive sleep apnea. Respiration. 2005;72:460-465.
  60. Phillips B, Mannino DM. Does insomnia kill? Sleep. 2005;28:965-971.
  61. Kripke DF, Garfinkel L, Wingard DL, Klauber MR, Marler MR. Mortality associated with sleep duration and insomnia. Arch Gen Psychiatry. 2002;59:131-136.
  62. Youngstedt SD, Kripke DF. Long sleep and mortality: rationale for sleep restriction. Sleep Med Rev. 2004;8:159-174.
  63. Morin CM, Hauri PJ, Espie CA, et al. Nonpharmacologic treatment of chronic insomnia: an American Academy of Sleep Medicine Review. Sleep. 1999;22:1134-1156.
  64. Cervena K, Dauvilliers Y, Espa F, et al. Effect of cognitive behavioural therapy for insomnia on sleep architecture and sleep EEG power spectra in psychophysiological insomnia. J Sleep Res. 2004;13:385-393.
  65. Smith MT, Huang MI, Manber R. Cognitive behavior therapy for chronic insomnia occurring within the context of medical and psychiatric disorders. Clin Psychol Rev. 2005;25:559-592.
  66. Allaert FA, Urbinelli R. Sociodemographic profile of insomniac patients across national surveys. CNS Drugs. 2004;18(suppl1):3-7.
  67. Vincent N, Lionberg C. Treatment preference and patient satisfaction in chronic insomnia. Behav Sleep Med. 2003;1:125-139.
  68. Morin CM, Culbert JP, Schwartz SM. Nonpharmacological interventions for insomnia: a meta-analysis of treatment efficacy. Am J Psychiatry. 1994;151:1172-1180.
  69. McClusky HY, Milby JB, Switzer PK, et al. Efficacy of behavioral vs. triazolam treatment in persistent sleep onset insomnia. Am J Psychiatry. 1991;148:121-126.
  70. Jacobs GD, Pace-Schott EF, Stickgold R, et al. Cognitive-behavior therapy and pharmacotherapy for insomnia. Arch Intern Med. 2004;164:1888-1896.
  71. Morin CM, Gaulier B, Barry T, Kowatch RA. Patients’ acceptance of psychological and pharmacological therapies for insomnia. Sleep. 1992;15:302-305.
  72. Bastien CH, Morin CM, Ouellet MC, et al. Cognitive-behavioral therapy for insomnia: comparison of individual therapy, group therapy, and telephone consultations. J Cons Clin Psychol. 2004;72:653-659.
  73. Mimeault V, Morin CM. Self-help treatment for insomnia: bibliotherapy with and without professional guidance. J Cons Clin Psychol. 1999;67:511-519.
  74. Strom Pettersson R, Andersson G. Internet-based treatment for insomnia: a controlled evaluation. J Cons Clin Psychol. 2004;72:113-120.
  75. Espie CA, Inglis SJ, Tessier S, Harvey L. The clinical effectiveness of cognitive behaviour therapy for chronic insomnia: implementation and evaluation of a sleep clinic in general medical practice. Behav Res Ther. 2001;39:45-60.
  76. Edinger JD, Sampson WS. A primary care “friendly” cognitive behavioral insomnia therapy. Sleep. 2003;26:177-182.
  77. Walsh JK. Pharmacologic management of insomnia. J Clin Psychiatry. 2004;65(suppl16):41-45.
  78. Mendelson WB, Roth T, Cassella J, et al. The treatment of chronic insomnia: drug indications, chronic use and abuse liability. Summary of a 2001 New Clinical Drug Evaluation Unit meeting symposium. Sleep Med Rev. 2004;8:7-17.
  79. Kripke DF, Hauri P, Ancoli-Israel S, et al. Sleep evaluation in chronic insomniacs during 14-day use of flurazepam and midazolam. J Clin Psychopharm. 1990;10:32S-43S.
  80. IMS Health. National Prescription Audit Plus. Fairfield, Conn: IMS Health; 2003.
  81. Kales A, Manfredi RL, Vgontzas AN, et al. Rebound insomnia after only brief and intermittent use of rapidly eliminated benzodiazepines. Clin Pharmacol Ther. 1991;49:468-476.
  82. Bunney WE, Azarnoff DL, Brown BW, et al. Report of the Institute of Medicine Committee on the efficacy and safety of Halcion. Arch Gen Psychiatry. 1999;56:349-352.
  83. Busto U, Sellers EM, Naranjo CA, et al. Patterns of benzodiazepine abuse and dependence. Br J Addict. 1986;81:87-94.
  84. National Institutes of Health Consensus Conference. Drugs and insomnia: the use of medications to promote sleep. JAMA. 1984;251:2410-2414.
  85. Krystal AD. The changing perspective on chronic insomnia management. J Clin Psychiatry. 2004;65(suppl8):20-25.
  86. Jaffe JH, Bloor R, Crome I, et al. A postmarketing study of relative abuse liability of hypnotic sedative drugs. Addiction. 2004;99:165-173.
  87. Saletu-Zyhlarz G, Anderer P, Brandstatter N, et al. Placebo-controlled sleep laboratory studies on the acute effects of zolpidem on objective and subjective sleep and awakening quality in nonorganic insomnia related to neurotic and stress-related disorder. Neuropsychobiology. 2000;41:139-148.
  88. Erman MK, Young T, Patel SR, Neubauer DN. The role of modified-release formulations in hypnotic therapy for insomnia. CNS Spectr. 2005;10(suppl9):1-13.
  89. Swainston HT, Keating GM. Zolpidem: a review of its use and management of insomnia. CNS Drugs. 2005;19:65-89.
  90. Elie R, Ruther E, Farr I, et al. Sleep latency is shortened during 4 weeks of treatment with zaleplon, a novel nonbenzodiazepine hypnotic. J Clin Psychiatry. 1999;60:536-544.
  91. Barbera J, Shapiro C. Benefit-risk assessment of zaleplon in the treatment of insomnia. Drug Saf. 2005;28:301-318.
  92. Ancoli-Israel S, Richardson GS, Mangano RM, et al. Long term exposure to zaleplon is safe and effective for younger-elderly and older-elderly patients with primary insomnia. Sleep. 2003;26:A77.
  93. Fry J, Scharf M, Mangano R, et al. Zaleplon improves sleep without producing rebound effects in outpatients with insomnia. Int Clin Psychopharmacol. 2000;15:141-152.
  94. Krystal AD, Walsh JK, Laska E, et al. Sustained efficacy of eszopiclone over six months of nightly treatment: results of a randomized, double-blind, placebo controlled trial in adults with chronic insomnia. Sleep. 2003;26:793-799.
  95. Melton ST, Wood JM, Kirkwood CK. Eszopiclone for Insomnia. Ann Pharmacother. 2005;39:1659-1666.
  96. Roth T, Walsh HK, Krystal A, Wessel T, Roehrs TA. An evaluation of the efficacy and safety of eszopiclone over 12 months in patients with chronic primary insomnia. Sleep Med. In press.
  97. Verster JC, Volkerts ER, Schreuder AH, et al. Residual effects of middle-of-the-night administration of zaleplon and zolpidem on driving ability, memory functions, and psychomotor performance. J Clin Psychopharm. 2002;22:576-583.
  98. Terzano MG, Rossi M, Palomba V, Smerieri A, Parrino L. New drugs for insomnia: comparative tolerability of zopiclone, zolpidem, and zaleplon. Drug Saf. 2003;26:261-282.
  99. Staner L, Ertle S, Boeijinga P, et al. Next-day residual effects of hypnotics on DSM-IV primary insomnia: a driving simulator study with simultaneous electroencephalogram monitoring. Psychopharmacology. 2005;181:790-798.
  100. Hesse LM, vonMoltke LL, Greeblatt DJ. Clinically important drug interactions with zopiclone, zolpidem, and zaleplon. CNS Drugs. 2003;17:513-532.
  101. Perlis ML, McCall WV, Krystal AD, Walsh JK. Long-term, non-nightly administration of zolpidem in the treatment of patients with primary insomnia. J Clin Psychiatry. 2004;65:1128-1137.
  102. Morin CM, Belanger L, Bastien C, Vallieres A. Long-term outcome after discontinuation of benzodiazepines for insomnia: a survival analysis of relapse. Behav Res Ther. 2005;43:1-14.
  103. Roth T, Stubbs C, Walsh JK. Ramelteon (TAK-375), a selective MT1/MT2-receptor agonist, reduces latency to persistent sleep in a model of transient insomnia related to a novel sleep environment. Sleep. 2005;28:303-307.
  104. Parrino L, Spaggiari MC, Boselli M, et al. Clinical and polysomnographic effects of trazodone CR in chronic insomnia associated with dysthymia. Psychopharmacology. 1994;116:389-395.
  105. Montgomery I, Oswald I, Morgan K, et al. Trazadone enhances sleep in subjective quality but not in objective duration. Br J Clin Pharmacol. 1983;16:139-144.
  106. Mendelson WB. A review of the evidence for the efficacy and safety of trazodone in insomnia. J Clin Psychiatry. 2005;66:469-476.
  107. Hajak G, Rodenbeck A, Voderholzer U, et al. Doxepin in the treatment of primary insomnia: a placebo-controlled, double-blind, polysomnographic study. J Clin Psychiatry. 2001;62:453-463.
  108. Mayer AG, Baldwin DS. Antidepressants and their effect on sleep. Hum Psychopharmacol Clin Exp. In press.
  109. Wilson S, Argyropoulos S. Antidepressants and sleep: a qualitative review of the literature. Drugs. 2005;65:927-947.
  110. 2002 Sleep in America Poll. Washington, DC: National Sleep Foundation; 2002.
  111. Rickels K, Morris RJ, Newman H, et al. Diphenhydramine in insomniac family practice patients: a double-blind study. J Clin Pharmacol. 1990;23:234-242.
  112. Brower KJ. Insomnia, alcoholism, and relapse. Sleep Med Rev. 2003;7:523-539.
  113. Brzezinski A, Vangel MG, Wurtman RJ, et al. Effects of exogenous melatonin on sleep: a meta-analysis. Sleep Med Rev. 2005;9:41-50.
  114. Larzelere MM, Wiseman P. Anxiety, depression, and insomnia. Prim Care. 2002;29:339-360.
  115. Wheatley D. Medicinal plants for insomnia: a review of their pharmacology, efficacy, and tolerability. J Psychopharmacol. 2005;19:414-421.
  116. Lack L, Wright H, Kemp K, Gibbon S. The treatment of early morning awakening insomnia with 2 evenings of bright light. Sleep. 2005;28:616-623.

 

some days you’re the pigeon…

In Fitness/Health, Humor, Inspiration, Mindfulness, Well-being on Sunday, 16 September 2012 at 10:23

i can’t recall where i found this but i really like it!

***

A lecturer, when explaining stress management to an audience, raised a glass of water and asked, “How heavy is this glass of water?”

Answers called out ranged from 20g to 500g.

The lecturer replied, “The absolute weight doesn’t matter. It depends on how long you try to hold it. If I hold it for a minute, that’s not a problem. If I hold it for an hour, I’ll have an ache in my right arm. If I hold it for a day, you’ll have to call an ambulance. In each case, it’s the same weight, but the longer I hold it, the heavier it becomes. And that’s the way it is with stress management. If we carry our burdens all the time, sooner or later, as the burden becomes increasingly heavy, we won’t be able to carry on. As with the glass of water, you have to put it down for a while and rest before holding it again. When we’re refreshed, we can carry on with the burden.

So, before you return home tonight, put the burden of work down. Don’t carry it home. You can pick it up tomorrow. Whatever burdens you’re carrying now, let them down for a moment if you can. Relax; pick them up later after you’ve rested. Life is short. Enjoy it!”

And then he shared some ways of dealing with the burdens of life:

  • Accept that some days you’re the pigeon, and some days you’re the statue.
  • Always keep your words soft and sweet, just in case you have to eat them.
  • Always read stuff that will make you look good if you die in the middle of it.
  • Drive carefully. It’s not only cars that can be recalled by their maker.
  • If you can’t be kind, at least have the decency to be vague.
  • If you lend someone $20 and never see that person again, it was probably worth it.
  • It may be that your sole purpose in life is simply to serve as a warning to others.
  • Never put both feet in your mouth at the same time, because then you won’t have a leg to stand on.
  • Nobody cares if you can’t dance well. Just get up and dance. Melody:
  • Since it’s the early worm that gets eaten by the bird…sleep late.
  • The second mouse gets the cheese. (so, don’t always be in such a hurry)
  • You may be only one person in the world, but you may also be the world to one person.
  • We could learn a lot from crayons. Some are sharp, some are pretty and some are dull. Some have weird names, and all are different colors, but they all have to live in the same box.
  • A truly happy person is one who can enjoy the scenery on a detour.

Multi-Vitamin Supplements and Brain Function

In Alternative Health, Brain studies, Fitness/Health on Saturday, 15 September 2012 at 08:24

Multivitamin supplements boost brain function, say UK researchers

Taking a multivitamin supplement daily can improve cognitive performance in both children and adults, say UK researchers.

Diet and ADHD

In ADHD, Fitness/Health, School Psychology on Wednesday, 12 September 2012 at 07:24

Healthy vs Western Diet Linked to Better Outcomes in ADHD

Megan Brooks & Penny Murata, MD

http://www.medscape.org/viewarticle/757166

Clinical Context

In children with attention-deficit/hyperactivity disorder (ADHD), the effectiveness of diet and dietary supplements is not clear. Dietary measures that have been proposed include sugar restriction; the additive- and salicylate-free Feingold diet; the oligoantigenic or elimination diet; and ketogenic, megavitamin, and polyunsaturated fatty acid (PUFA) supplements. In the July 2011 issue of the Journal of Attention Disorders, Howard and colleagues reported a link between ADHD and a “Western” diet high in fat, refined sugars, and sodium.

This review of the literature assesses the evidence for dietary treatment in children with ADHD.

Study Synopsis and Perspective

When drug therapy fails to control ADHD or is unacceptable, adopting a “healthy” diet, eliminating items known to predispose to ADHD, and adding omega-3 fatty acid supplementation may be worth trying, new research suggests.

“The recent increase of interest in this form of therapy for ADHD, and especially in the use of omega supplements, significance of iron deficiency, and the avoidance of the ‘Western pattern’ diet, make the discussion timely,” the authors write.

Many parents and physicians continue to be interested in how diet and dietary changes, particularly parents wanting to find an alternative to stimulant medication or a complementary therapy. Nevertheless, it remains a “controversial” topic, the authors note.

For their review, J. Gordon Millichap, MD, and Michelle M. Yee, CPNP, from Children’s Memorial Hospital in Chicago, Illinois, searched PubMed for relevant studies on the role of diet and dietary supplements for the treatment of children with ADHD.

They note that their recommendations on diet and dietary supplements are based on a critical review of the data and their own experience in a neurology clinic for children and adolescents with ADHD.

The study was published online on January 9 in Pediatrics.

Elimination Diets Not Advisable

Perhaps the “most promising and practical” complementary or alternative treatment, write Dr. Millichap and Ms. Yee, is adopting a “healthy” dietary pattern, omitting items shown to predispose to ADHD or to make the condition worse. These items include fast foods, red meat, processed meat, potato chips, high-fat dairy foods, and soft drinks.

They point to a “provocative” study published last year, which found a link between ADHD in adolescents and a “Western-style” dietary pattern that was high in fat, refined sugars, and sodium and low in fiber, folate, and omega-3 fatty acids (Howard et al, J Atten Disord. 2011;15:403-411). ADHD was not associated with a “healthy” dietary pattern rich in fish, vegetables, fruit, legumes, and whole-grain foods.

Adopting a healthy dietary pattern “may offer an alternative method of treatment of ADHD and less reliance on medications,” the authors of the current study write.

They also note that although many parents report worsening of hyperactivity symptoms after consumption of foods and drinks containing sugar or aspartame — and isolated reports support the parents’ observations — most controlled studies have failed to find a significant harmful effect of sugar or aspartame, the authors note.

Additionally, they say that the elimination of sugar and aspartame and adapting additive-free diets are complicated, disruptive, and often impractical; such measures are indicated only in select cases.

Fatty Acid Supplements May Be Helpful

Low levels of long-chain PUFAs have been reported in the plasma and red cells of children with ADHD in comparison with their ADHD-free peers, Dr. Millichap and Ms. Yee note. Some studies have demonstrated a reduction in ADHD symptoms with PUFA supplementation, although no definitive conclusions can be drawn.

However, the authors note that “on the basis of reports of efficacy and safety, we use doses of 300 to 600 mg/day of omega-3, and 30 to 60 mg/day of omega-6 fatty acids, continued for 2 or 3 months, or longer if indicated.”

“As initial or add-on therapy, we have occasional reports of improved school grades and lessening of symptoms of ADHD, without occurrence of adverse effects. Most parents are enthusiastic about trying the diet supplements, despite our explanation of only possible benefit and lack of proof of efficacy,” they note.

They also note that iron and zinc supplementation is advisable when there is a known deficiency in these minerals, and this may “enhance the effectiveness” of stimulant therapy.

Pediatrics. Published online January 9, 2012.

Related Link
The National Institute of Mental Health’s Attention Deficit Hyperactivity Disorder (ADHD) site offers a wide range of information helpful for parent education including a downloadable booklet discussing the condition and its management.

Study Highlights

  • This review study provides an overview of the role diet has in children with ADHD. The following supplements, foods, and diets affect the children’s health outcomes in various ways, according to several studies.
  • Omega-3 and omega-6 fatty acid supplements
    • Low long-chain PUFA levels were reported in children with ADHD vs control patients.
    • Some studies showed that PUFA reduced ADHD symptoms, but other studies did not.
    • Doses of omega-3, 300 to 600 mg/day, and omega-6, 30 to 60 mg/day, for 2 to 3 months or longer have been used.
    • Concurrent ADHD medication is almost always needed.
  • Additive and salicylate-free (Feingold) diet
    • Adherence to the diet is complicated and may be disruptive or impractical.
    • Foods to be avoided are apples, grapes, luncheon meats, sausage, hot dogs, and cold drinks with artificial flavors and coloring agents.
    • Permitted foods are grapefruit, pears, pineapple, bananas, beef, lamb, plain bread, certain cereals, milk, eggs, and color-free vitamins.
    • Controlled trials found a small subgroup of preschool children had an adverse response to challenges of additives and preservatives.
    • Children with ADHD and atopy vs no atopy have a higher response to elimination of foods, artificial colorings, and preservatives.
  • Oligoantigenic (hypoallergenic/elimination) diet
    • Adherence to the diet is complicated and may be disruptive or impractical.
    • The oligoantigenic diet eliminates sensitizing food antigens or allergens, including cow’s milk, cheese, wheat cereals, egg, chocolate, nuts, and citrus fruits.
    • Elimination of some foods appeared to decrease some ADHD symptoms, but plays an uncertain role in ADHD treatment.
    • A 2- to 3-week period of elimination diet is followed by the reintroduction of single items each week until the food sensitivity is identified.
    • Behavior improvements might not occur for up to 2 weeks.
    • Enzyme-potentiated desensitization might enable children to become tolerant of provoking foods.
  • Sugar and aspartame
    • Sugar does not affect behavior or cognitive performance, but might affect a subset.
    • In preschool boys, daily sucrose and total sugar intake correlated with duration of aggression.
    • Reactive hypoglycemia after sugar load might reduce cognitive function.
    • Hypoglycemia is linked with impaired electrical activity of the cerebral cortex and slow rhythms on electroencephalogram.
  • Ketogenic diet
    • A ketogenic diet high in fats and low in carbohydrates for children with intractable seizures helped to control seizures and improve behavior, attention, and social functioning.
  • Iron deficiency
    • Iron deficiency is not consistently linked with ADHD severity or frequency.
    • 1 study showed that low serum ferritin correlated with baseline inattention, hyperactivity, impulsivity, and effective amphetamine dose needed.
  • Zinc deficiency
    • Low zinc levels were found in the serum, red cells, hair, urine, and nails of children with ADHD, but mostly in countries with endemic zinc deficiency.
    • In the United States, low serum zinc was linked with inattention, but not with hyperactivity or impulsivity.
    • Zinc supplements might enhance the effect of d-amphetamine, but are not routinely recommended.
  • Other alternative dietary therapies
    • Orthomolecular medicine and megavitamin therapy refer to combination of minerals and nutrients.
    • A study of megavitamin therapy in children with ADHD showed no improvement in behavior, but 42% had elevated serum transaminase levels.
  • “Healthy” vs “Western” diet pattern
    • A cohort study of children from birth to age 14 years found a “Western” dietary pattern associated with ADHD diagnosis and a “Healthy” diet pattern not associated with ADHD diagnosis.
    • The Western dietary pattern includes fast foods, red and processed meats, potato chips, high-fat dairy products, and soft drinks.
    • The Healthy dietary pattern includes fish, vegetables, tomatoes, fresh fruit, whole grains, and low-fat dairy products.

Clinical Implications

  • Indications for dietary therapy in children with ADHD include medication failure or adverse reactions, patient or parental preference, mineral deficiency, and need for change from an ADHD-linked Western diet to an ADHD-free Healthy diet.
  • In children with ADHD, additive-free and elimination diets are time-consuming and disruptive, but might be indicated in selected patients; iron and zinc are indicated for deficiencies; omega-3 supplements have inconsistent effects; and a Healthy diet rich in fish, vegetables, fruit, legumes, and whole grains might be beneficial vs a Western diet of fast foods, red or processed meats, high-fat dairy products, soft drinks, and potato chips.

Crave, much?

In Fitness/Health on Saturday, 8 September 2012 at 13:36

The New Way to Conquer Cravings

The latest research says you can actually rewire your brain to keep temptation at bay. Here’s how to do it.

You’re sitting at your desk going about your workday when suddenly, out of nowhere, you’re overcome with the desire—no, need is more like it—to devour a giant sticky bun. Your mouth is watering just thinking about the gooey-sweet glaze, the ribbons of butter and cinnamon. Is it your imagination, or is your heart beating faster

Willpower, shmillpower
That’s when the bargaining begins: I’ll have just a bite and freeze the rest. Or maybe I’ll eat half of it—I’ve been good today—no, all of it, but I’ll skip dinner tonight…

Cravings. Research is only just beginning to shed light on why so many of us succumb to them. Although scientists are still piecing together the puzzle of what exactly happens when you’re in the throes of a craving, this much they know for sure: Every craving begins with a cue. The cue for a sticky bun may be something as simple as getting a whiff of its buttery aroma as you walk past your favorite bakery, or catching a glimpse of a TV commercial featuring one.

“Any cue that’s repeatedly associated with high-fat and/or sugary foods can trigger a craving,” explains Ashley Gearhardt, PhD, a psychologist and food addiction expert at the Rudd Center for Food Policy and Obesity at Yale University.

In other words, if you like to celebrate the end of a workweek with margaritas and Tex-Mex, eventually a craving for those things will automatically kick in every Friday afternoon. If you grew up equating, even subconsciously, your mother’s homemade chocolate layer cake with comfort, you’ll likely crave some version of that whenever you have a bad day.

The cue activates your brain’s pleasure center, causing it to release dopamine, a neurotransmitter that pushes you to seek out the very thing you’re lusting after, explains Gearhardt. Over time, this feel-good experience rewires the brain so that you’re more likely to crave the food again in the future.

What’s more, when you’re in full-on craving mode, your brain convinces you that you are famished, making the food more difficult to resist. “Your brain starts pumping out the hunger hormone ghrelin, and your insulin levels drop, making you even hungrier than usual,” Gearhardt says. As a result, it’s very difficult to satisfy the craving with just a taste.

It almost seems unfair that cravings can increase feelings of hunger. You assume you’ll satisfy a longing for sticky buns by eating one, but research suggests just the opposite will happen: Instead of paying attention to the physical cues of hunger and fullness, you’re driven by the rush of dopamine that’s telling you to find and scarf down a sticky bun (now!). And then another.

This also helps explain why you may be powerless in the presence of a dessert tray—even if you polished off a steak, two sides, and a roll only moments before. “The dessert tray, as well as the spoons and forks that are put in front of you, are all cues that you should eat,” says Mark Gold, MD, chairman of the department of psychiatry at the University of Florida and a specialist in addiction medicine research.

It doesn’t help that the dopamine signal occurs immediately when you come up against a cue, while the satiety signals—those telling you to stop eating—are much slower, taking 12 or more minutes after you eat to kick in. “Your brain can always find more room for food, and for a while after eating, so can your stomach,” adds Dr. Gold.

Your brain on brownies
Believe it or not, cravings originally served a useful purpose, namely to keep our loincloth-clad ancestors alive. “They had powerful urges for energy-dense foods and were driven to get their hands on them in order to survive and reproduce,” says Eric Stice, PhD, a senior scientist at the Oregon Research Institute.

Of course, our predecessors didn’t face high-cal temptations at every turn. Today, we’re bombarded by food cues (we view, on average, 7,000-plus food and beverage ads on TV per year). And we don’t need to put our lives on the line every time a craving strikes. We just open our pantry, hit up the office vending machine, or take a lap around our favorite drive-thru.

It’s not just that these high-fat, sugar-filled, sodium-laden foods are convenient—it’s that they’re actually engineered to make us crave them. “These foods have an effect on the brain that’s much stronger than those produced by foods that you could hunt or grow,” Dr. Gold says. “Eating fast food french fries, for instance, yields a greater dopamine release than if you were to eat a tomato picked fresh from your garden.”

The complexity of tastes, flavors, and textures in processed foods is simply more stimulating for the brain than something that comes from the earth, he explains. Plus, you get a hit of dopamine each time you try a different flavor—making you crave not just one, but a variety of treats so you’ll get that feel-good experience again.

“The fact that you could have a burger one day, a burrito the next, and orange sesame chicken the day after that means we live in a sea of dopamine-releasing triggers,” says Dr. Gold.

Born to love chips
That explains part of the puzzle, but not all of it. New research suggests that your food preferences—and thus your cravings—may be formed not just in childhood, but in utero. “One theory is that pregnant women begin teaching their children what’s safe and good to eat while they’re still in the womb,” says Annie Murphy Paul, author of Origins: How the Nine Months Before Birth Shape the Rest of Our Lives. So if your mom ate lots of potato chips and cheesy fries, you may be programmed to crave the same kinds of fatty, salty foods.

What’s more, if you equate certain foods with feel-good moments from your childhood, you’re likely to turn to them for an emotional pick-me-up. That’s because often it’s not the foods that we crave as much as the emotions we associate with them. In other words, it isn’t just your mom’s chocolate cake you’re wanting, but the warm feeling you had whenever she gave you a slice.

“Pairing foods with particular feelings or situations can imprint an association between an experience and a food,” explains Michelle May, MD, author of Eat What You Love, Love What You Eat. “What you might really want is to feel safe or to remember a time in your life when things were simpler.”

Emotional cravings tend to sneak up on us since we’re often not aware of the correlation between what we’re eating and what we’re feeling. For instance, if you experience a longing for a glass of wine and a bowl of pasta in the middle of a hectic workday, you may not realize or even care that what you really want is to feel relaxed and carefree—the way you do on a girls’ night out at your favorite Italian bistro.

Manage your munchies
If you can identify the emotions behind the craving, you can try to find ways to fulfill those needs that are more productive than sinking your teeth into a 500-calorie sugar bomb. For instance, you might send an email to schedule a meeting with your boss to discuss your workload and the unrealistic deadlines you’ve been given.

“If that seems impossible, then maybe what you really need is a vacation to look forward to in order to make the work more bearable,” Dr. May says. “In some small way, take steps toward meeting that need, such as making a list of the top 10 places you’d like to visit, putting in a request for time off, or taking 15 minutes to browse websites of locations you want to travel to. Even closing your eyes and taking a mini beach vacation in your mind while you breathe deeply can help short-circuit the emotions—and the craving.”

A smart strategy
No matter the source of your craving (whether it began with an environmental cue or an emotional need) there’s another tactic that helps derail the chemical cascade: Focus on your short- and long-term health goals.

In a recent study published in the journal Proceedings of the National Academy of Sciences, researchers examined participants’ brains in an MRI scan during a craving and found that paying attention to a goal, such as getting in shape, activates the prefrontal cortex—a part of the brain that can inhibit the reward region.

The technique provides a one-two punch. In addition to dulling the craving, it also increases your ability to resist temptation. It may even keep you from rationalizing or bargaining with yourself.

Here’s how to make it work for you: Write down a detailed list of health goals you’d like to achieve. If you’re trying to slim down, list your current weight and how much you want to lose. “Being specific is crucial because it offers you more details that help you to say ‘no,’ ” Dr. Gold says.

For instance, when you know you need to cut 500 calories a day in order to lose a pound a week, and that eating an ice cream sundae will prevent that from happening, you’re already engaging the prefrontal cortex and dampening the dopamine release. As soon as a craving strikes, think back to those numbers in order to fight off the urge to give in to that sundae.

Also important: Jot down everything you eat throughout the day in a food journal—especially if you’re trying to lose weight. Often when we’re motivated to eat by cravings, we tend to inhale the food and quickly forget about it, adds Dr. Gold.

Knowing that you’ll have to come back to that food journal may reduce your desire to eat it in the first place. “With practice, your ability to resist temptation becomes stronger over time—like a muscle,” Gearhardt says. Your prefrontal cortex will kick in more quickly to disrupt the dopamine release and, of course, your craving. Sweet.

Retrieved from: http://www.health.com/health/article/0,,20587784,00.html

Bad bosses, poor health?

In Fitness/Health on Friday, 7 September 2012 at 09:56

http://www.usatoday.com/money/workplace/story/2012-08-05/apa-mean-bosses/56813062/1?goback=.gde_85886_member_153125998

 

What To Do About The 4 Excuses For Why You’re Staying In Your Toxic Job?

In Fitness/Health on Thursday, 6 September 2012 at 11:20

What To Do About The 4 Excuses For Why You’re Staying In Your Toxic Job?.

%d bloggers like this: