Archive for the ‘Mood Disorders’ Category

Phillip Seymour Hoffman did not have choice or free will and neither do you.

In ADHD, Anxiety, Brain imaging, Brain studies, Child/Adolescent Psychology, General Psychology, Medicine, Mood Disorders, Neuropsychology, Neuroscience, Psychiatry on Tuesday, 11 March 2014 at 12:37

one of the best things about this subject that i’ve read in a long time.  give it a read. it makes you think.

Phillip Seymour Hoffman did not have choice or free will and neither do you..


what causes depression? a possible answer.

In Genes, Genomic Medicine, Mood Disorders, Neuropsychology, Neuroscience, Psychiatry, Psychopharmacology on Thursday, 21 February 2013 at 06:54

Potential Cause of Depression Identified

By: Meagan Brooks

A protein involved in synaptic structure has been identified as a potential cause of depression, a finding that according to researchers has “enormous therapeutic potential for the development of biomarkers and novel therapeutic agents.”

Investigators at the Mount Sinai School of Medicine in New York City found decreased expression of Rac1 in the postmortem brains of people with major depressive disorder (MDD) and in mice subjected to chronic stress. They were able to control the depressive response in mice by manipulating the expression of Rac1.

“Our study is among only a few in depression research in which 2 independent human cohorts and animal models validate each other. Rac1 has enormous therapeutic potential, and I look forward to investigating it further,” study investigator Scott

Looking for Drug Targets

Rac1 is a small Rho GTPase protein involved in modulating synaptic structure.

“There is a hypothesis that depression and stress disorders are caused by a restructuring of brain circuitry,” Dr. Russo explained in an interview with Medscape Medical News.

The scientists subjected mice to repeated bouts of social stress and then evaluated the animals for changes in gene expression in the nucleus accumbens (NAc), the brain’s reward center.

The researchers found that expression of Rac1 was significantly downregulated in the brains of mice for at least 35 days following the end of the chronic social stressor. Rac1 was not affected by only a single episode of stress, indicating that only prolonged stressors that induce depression are capable of downregulating Rac1.

The scientists note that chronic stress in the mice caused epigenetic changes in chromatin that led to Rac1 downregulation.

They were able to control the depressive response to chronic stress to some extent by chronic antidepressant treatment. Histone deacetylase (HDAC) inhibitors were “extremely effective in both normalizing the reduction in Rac1 and also promoting antidepressant responses,” Dr. Russo told Medscape Medical News.

“What we think is happening is that chronic stress leads to a lasting change in the ability of our genes to transcribe this RAC1 gene, and if you target the epigenome, you can reverse that loss of Rac1 and promote synapses and more normal healthy responses,” he said.

As in the mice, Rac1 expression was also strongly downregulated in the NAc in postmortem brains of patients with MDD, who displayed similar epigenetic changes. In most of the individuals with MDD who were taking antidepressants at the time of death, Rac1 expression was not restored to the levels seen in control participants, “suggesting a need for more direct RAC1-targeting strategies to achieve therapeutic effects,” the authors write.

“Currently, there aren’t any approved drugs or even experimental drugs that target Rac1 that are safe and effective,” Dr. Russo said. “It would be nice if we could team up with some chemists or pharma and figure out if there are some safe and effective Rac activators.”

However, there are caveats to that, he said.

“It might be difficult to target Rac specifically, because it is involved in cell proliferation and restructuring so it may be difficult to get a compound that doesn’t cause cancer. It might be better to screen for targets that more generally regulate synaptic plasticity. Ketamine is a drug that does this, and there is huge interest in ketamine” in depression, Dr. Russo said.

Experts Weigh In

Commenting on the findings for Medscape Medical News, David Dietz, PhD, assistant professor of pharmacology and toxicology, State University of New York at Buffalo, who was not involved in the research, said the study “is exquisitely well done. The researchers did an excellent job of translating their findings in the rodent model to the human condition.”

Maria V. Tejada-Simon, PhD, who also was not involved in this research but who has studied Rac1, noted that her group has been “highlighting the importance of Rac1 in the brain in general, and in psychiatric diseases in particular, for a while now. Therefore, I am not surprised that Rac1 has been found to be also associated to stress disorders and depression.”

“Mood disorders have been linked to changes in synaptic structure, and it is certain that small GTPases such as Rac1 have a tremendous role as modulators of these processes. However, we need to understand that alterations in Rac1 signaling are not likely to be the primary defect in mood disorders.

“Thus, targeting Rac1 to moderate clinical symptoms (while there is potential for a translational approach there) has to be done very carefully, given the broad role of Rac1 in many cellular functions involving the actin cytoskeleton,” said Dr. Tejada-Simon, assistant professor of pharmacology and adjunct assistant professor of biology and psychology at University of Houston College of Pharmacy in Texas.

“The highlight of this research is in identifying a possible mechanism by which we can study pathways that are involved in remodeling of the brain; we might be able to find something a little bit more specific down the line,” Dr. Dietz said.

He noted that Rac1 has also been linked to addiction.

“It’s well known that there is comorbidity between depression and addiction, that one may lead to the other, so there seems to be something fundamentally related between Rac1 and these 2 psychiatric disease states.”

The research was supported by the National Institute of Mental Health and the Johnson and Johnson International Mental Health Research Organization Rising Star Award (presented to Dr. Russo). The other authors, Dr. Tejada-Simon, and Dr. Dietz have disclosed no relevant financial relationships.

Nat Med. Published online February 17, 2013. Abstract

Retrieved from: http://www.medscape.com/viewarticle/779544?src=nl_topic

Epigenetic regulation of RAC1 induces synaptic remodeling in stress disorders and depression

Sam A Golden, Daniel J Christoffel, Mitra Heshmati, Georgia E Hodes, Jane Magida,Keithara Davis, Michael E Cahill, Caroline Dias, Efrain Ribeiro, Jessica L Ables, Pamela J Kennedy, Alfred J Robison, Javier Gonzalez-Maeso, Rachael L Neve, Gustavo Turecki, Subroto Ghose, Carol A TammingaScott J Russo

Nature Medicine(2013) doi:10.1038/nm.3090; Received 11 October 2012.  Accepted 14 January 2013.  Published online 17 February 2013.


Depression induces structural and functional synaptic plasticity in brain reward circuits, although the mechanisms promoting these changes and their relevance to behavioral outcomes are unknown. Transcriptional profiling of the nucleus accumbens (NAc) for Rho GTPase–related genes, which are known regulators of synaptic structure, revealed a sustained reduction in RAS-related C3 botulinum toxin substrate 1 (Rac1) expression after chronic social defeat stress. This was associated with a repressive chromatin state surrounding the proximal promoter of Rac1. Inhibition of class 1 histone deacetylases (HDACs) with MS-275 rescued both the decrease in Rac1 transcription after social defeat stress and depression-related behavior, such as social avoidance. We found a similar repressive chromatin state surrounding the RAC1 promoter in the NAc of subjects with depression, which corresponded with reduced RAC1 transcription. Viral-mediated reduction of Rac1 expression or inhibition of Rac1 activity in the NAc increases social defeat–induced social avoidance and anhedonia in mice. Chronic social defeat stress induces the formation of stubby excitatory spines through a Rac1-dependent mechanism involving the redistribution of synaptic cofilin, an actin-severing protein downstream of Rac1. Overexpression of constitutively active Rac1 in the NAc of mice after chronic social defeat stress reverses depression-related behaviors and prunes stubby spines. Taken together, our data identify epigenetic regulation of RAC1 in the NAc as a disease mechanism in depression and reveal a functional role for Rac1 in rodents in regulating stress-related behaviors.

Retrieved from: http://www.nature.com/nm/journal/vaop/ncurrent/abs/nm.3090.html

bye bye, bipolar disorder!

In Education, General Psychology, Mood Disorders, School Psychology on Tuesday, 19 February 2013 at 06:57

i love this website and the information.  i find it useful in general and in my work in the schools.  if you work with children with behavioral issues or are interested in learning more, i recommend you join dr. mac’s b-list email list.  i always find interesting and useful articles like the one below.  thanks, dr, mac!

Bye-Bye Bi-Polar Disorder

Hello again, fellow B-Lister!  Where are you located right now on the mood spectrum?  Forlorn?  So-So?  Ecstatic?  How’s the energy level right now? Are you sinking into the sofa for the 3rd day in a row, taking a short-lived seat to read this communication, or jumping up and down on it?

We all have ups and downs in mood, energy, or ability to function well in our daily tasks.  Some folks, though,  re-cycle through these ups and downs, reaching the extreme ends of the continuum.

Back-in-the-day, I typically heard the term “Manic Depression” used for the condition under discussion in our newsletter today.  When I first heard the term “Bi-Polar”, I thought it had something to do with the melting of the polar ice caps or penguins moving up to Santa’s domain!

Bipolar disorder: A mental illness that is evidenced by extreme shifts in mood, energy and functioning.

Yes, now Bipolar Disorder is the clinically correct terminology for the dramatic, recycled changes experienced by individuals with this mental health disorder.  However, I must admit that manic-depressive held more meaning for me. It identified the two opposites of the continuum rather than using vague terminology as a label.

There are different variations of Bipolar Disorder listed in the two mental health diagnostic manuals, the DSM-IVtr (soon to become DSM-5) and the International Classification of Diseases (ICD-10).  Once thought to be a rare condition in children and youth, the 1990’s era saw a massive increase in Bipolar diagnoses for kids with severe sadness, irritability, anger, and grumpiness. a rise of 4000% in just 12 years!  As might be expected, the dramatic increase sparked discussion and disagreement about whether children were being misdiagnosed and then prescribed powerful psychotropic mediations with significant negative side effects. (A future topic for a B-List members)

Bipolar disorder is a life-long mental disability, but most research has shown that  kids diagnosed with childhood bipolar disorder (the expansive version) are no more likely to develop classic Bipolar Disorder than their non-diagnosed peers.  Additionally, the prescribed medications didn’t work as well in children as in adults.  Certainly, these youngsters possessed a legitimate mood disorder, one that may very well extend into adulthood. but for most of them, it wasn’t Bipolar Disorder.

One of the graduate students in my teacher preparation program in behavior disorders created a wonderful video regarding authentic Bi-Polar Disorder in children.  Using a case study of a 6 year old boy, Michelle then compares the youngster’s symptoms with the criteria for the condition, before offering strategies and approaches for intervention. (Thanks, Michelle!)

*Health note: Omega 3 oil, lecithin, and vitamins B6 & B12 have been implicated in the condition, with Bi-Polar individuals being deficient in these nutrients.  If you are seeking a natural alternative or supplement to Lithium and/or the other common medications you can find them in their purest form here: http://www.shop.com/healthnutrition-a.xhtml (Your purchases result in discounts & cash-back while supporting a kid’s pre-teen swim team.  My nutrition consultant, Cindy, is also available to assist you at this site)

A rose by any other name.

In response to the great controversy & disagreement as to whether this mental health disability should be diagnosed in kids, DSM-5 (due for distribution in May 2013) makes an effort to reduce the numbers of Bipolar diagnoses… by creating a new diagnosis!…: Distemper.  Oh Wait!!!  That’s my dog.  For our kids, the mental health diagnostic manual it will soon contain a new condition titled “Temper Dysregulation Disorder with Dysphoria” (TDD).

Dysphoria: An emotional state of feeling unwell or unhappy.

TDD displays itself in severe outbursts of anger/temper interchanging with negative mood states.  Unlike Bipolar Disorder, it does not include phases of mania (but neither did the criteria used to diagnose kids as having Bipolar Disorder… Odd, eh?… Labeling kids as being Bipolar when they didn’t have a second pole).  TDD is also not considered to be a life-long disorder.

The American Psychiatric Association states that it hopes that the majority of kids (perhaps 60-70%) who have or might have been diagnosed with Bipolar Disorder will now receive the TDD label.  This re-diagnosis would probably also include many youngsters with Conduct Disorder who were labeled as being Bipolar in order to obtain health insurance coverage for treatment

The symptoms of TDD in the upcoming DSM-5 manual are similar in many ways to the broad type of childhood bipolar disorder (as it was diagnosed). The proposed diagnostic criteria for TDD include:

severe recurrent temper outbursts that are grossly out of

proportion to the intensity of the situation

frequency of at least three temper outbursts per week

temper outbursts ongoing for at least one year

temper outbursts present in at least two settings (for

example, at home and at school)

onset before age 10

There is an excellent 10 minute video on the new disorder in the archives of National Public Radio: http://www.npr.org/player/v2/mediaPlayer.html?action=1&t=1&islist=false&id=123544191&m=123564957


For those of you working with youngsters who have the symptoms mentioned above:

1. Rob Plevin’s 3-part FREE video series on working effectively with disruptive kids is still availabe.  Click here to view effective strategies for quieting noisy classes and kids.

2. Modify the character of the youngster using the Circle of Courage model of intervention.  This comprehensive, intensive and positive program changes lives.

3.  The Behavior Intervention Guide allows you to determine a disruptive youngster’s present level of readiness to change behaviour.  Based on the outcome of the assessment, strategies are provided that move the youngster toward greater levels of willingness to change his/her behavior for the better.

4.  Use “The Behavior Survival Guide for Kids: How to make good choices and stay out of trouble” in your social skills/anger management programs, or place it in the class library.  Stellar reviews by websites, magazines, parents, teachers, and the kids themselves let you know the effectiveness of this self-help book for kids.  It’s written on a 4th grade reading level… just like these weekly newletters!

5. Implement the FREE 100+ lesson plans that accompany The Behavior Survival Guide (or use them in isolation)

For Parents of Defiant & Angry Youngsters

1. Develop a home-school behavior change program based on the monetary system.  When money and priviledges are involved, kids listen!

2. Learn the principles of changing behaviour for the better, and effective strategies for helping your child make better behavior choices.

3.  Leave “The Behavior Survival Guide for Kids: How to make good choices and stay out of trouble” out on the coffee table for your child to pick up.

4. Seek out family counseling.

5. Acquire the comprehensive program designed specifically to help parents of children with Conduct Disorder/highly disobedient behavior change their child’s behavior for the better. (Click on the Total Transformation box below)

NEXT WEEK: Disruptive Behavior (Not otherwise specified)

(When the actions are disruptive, defiant, and/or aggressive,but don’t meet the criteria for ODD or Conduct Disorder)

Dr. Mac

Room 914west,

Department of Special Education, Hunter College,

695 Park Avenue,

New York,

NY 10021


Retrieved from: http://www.behavioradvisor.com

Depression, Other Psychosocial Disorders Linked to Stroke

In Anxiety, Mood Disorders, Well-being on Friday, 14 December 2012 at 08:35

Depression, Other Psychosocial Disorders Linked to Stroke

Pauline Anderson

Older adults who are depressed, stressed, or dissatisfied with their life are at increased risk of suffering a stroke and of dying from a stroke, a new study has found.

The study showed that those who faced the highest level of psychosocial distress had a significantly increased risk of having a stroke and up to 3 times the risk of stroke mortality compared with those with the least amount of distress.

“Our findings clearly document important adverse effects of psychosocial distress on cerebrovascular disease risk in the elderly,” write the authors, including senior author Susan Everson-Rose, PhD, associate professor of medicine and associate director of the Program in Health Disparities Research, University of Minnesota, Minneapolis.

The study is published online December 13 in Stroke.

Distress Score

The study used data from the Chicago Health and Aging Project (CHAP), an ongoing, longitudinal study investigating chronic illnesses in elderly residents of 3 adjacent neighborhoods in Chicago, who represent a broad range of socioeconomic backgrounds. Researchers conducted baseline interviews to gather information on medical history, cognitive health, socioeconomic status, behavioral patterns, and psychosocial characteristics, repeating the interviews in 3-year cycles.

The second cycle of interviews (1997 to 1999) assessed the broadest range of psychosocial characteristics and served as the baseline for the current analysis, which included 4120 mostly black and female participants whose average age was 77 years. Most had a high school education and an average of 1 chronic condition; 13.1% reported a history of stroke.

For information on stroke hospitalizations, researchers accessed the Centers for Medicare and Medicaid Services Medicare Claims data (because some participants were involved in a health maintenance organization, only 2649 participants were analyzed for rates of incident stroke). To verify deaths, the authors used linkages with the National Death Index.

To assess psychosocial distress, investigators created a distress score that factored in 4 psychosocial measures: depressive symptoms, perceived stress, neuroticism (a personality domain characterized by anxious, angry, and vulnerable traits), and life satisfaction. The higher the score is, the higher the distress.

The study showed a dose-response pattern of risk for incident stroke. Relative to the least distressed quartile, the hazard ratios (HRs) for the second, third, and fourth quartiles were 1.27 (95% confidence interval [CI], 0.98 – 1.65; P = .067), 1.44 (95% CI, 1.10 – 1.87; P = .0068), and 1.54 (95% CI, 1.16 – 2.04;P = .0025), respectively, in a model adjusted for age, race, and sex. Associations were reduced after adjustment for stroke risk factors.

With distress modeled categorically and adjusting for age, race, and sex, participants in the highest quartile had nearly a 3 times (HR, 2.97; 95% CI, 1.81 – 4.88; P < .0001) greater risk of dying from stroke relative to those with the lowest distress scores. Those in the third quartile had nearly 2 times the risk (HR, 1.98; 95% CI, 1.19 – 3.30; P = .0091).

Analyses of stroke subtypes revealed that distress was significantly related to incident hemorrhagic strokes, but not to ischemic strokes after adjustment for covariates.

Behavioral Factors

Psychological and behavioral factors may play a role in raising stroke risk. Very distressed people may be less likely or less able to comply with treatment recommendations or to maintain a healthy lifestyle.

“Our most distressed participants were less physically active, and had a higher prevalence of cardiovascular disease and diabetes mellitus, suggesting potentially greater disease burden in this group, which could make lifestyle management more challenging,” the authors write. However, in this study, controlling for these factors had little effect on the relationship between distress and either stroke mortality or hemorrhagic strokes.

The pathways by which distress increases stroke risk are not fully understood, said the authors. Possible mechanisms may involve hypothalamic-pituitary-adrenal dysregulation related to stress that may increase circulating catecholamines, endothelial dysfunction, and platelet activation, culminating in a hypercoaguable state.

Neuroendocrine and inflammatory effects of chronic stress and negative emotional states may also contribute to the increased risk. However, the authors pointed out that these pathways are probably more important for ischemic than hemorrhagic stroke and that the current study found much stronger findings for hemorrhagic stroke.

The study lacked data on inflammatory and neuroendocrine biomarkers that might have shed more light on pathways that may link psychosocial distress to stroke risk. Another limitation was that CHAP doesn’t include imaging data that might provide important information about the types of strokes experienced by study participants. Also, the study assessed psychosocial distress at just one point in time, so it couldn’t determine whether distress levels changed or whether such changes influenced stroke risk.

Dr. Everson-Rose is supported in part by a grant from the National Institute on Minority Health and Health Disparities (NIMHD).

Stroke. Published online December 13, 2012.

Retrieved from: http://www.medscape.com/viewarticle/776137?src=smo_neuro

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.


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

Managing Holiday Anxieties | Anxiety and Depression Association of America, ADAA

In Anxiety, Mood Disorders on Friday, 23 November 2012 at 11:03

Managing Holiday Anxieties | Anxiety and Depression Association of America, ADAA.

The Serotonin Hypothesis, Informed Consent and SSRI Antidepressants

In Medication, Mood Disorders, Neuropsychology, Neuroscience, Psychiatry on Wednesday, 31 October 2012 at 15:36

The Serotonin Hypothesis, Informed Consent and SSRI Antidepressants.

Depression 101…

In Mood Disorders, Psychiatry, School Psychology on Tuesday, 16 October 2012 at 07:15

Depression 101: Treatment & Tips To Ward Off Depression

Depression is a common mental health illness in the US and around the world. In fact, the Center for Disease Control and Prevention states that 1 in 10 adults in the US report experiencing depression. What is most troubling to me is that only about 51% of those people suffering from depression seek out treatment according to the National Institute of Mental Health. Depression may begin at any age and may be caused by any number of triggers such as bullying, parental or marital conflict, sense of isolation, loss, seasonal causes, etc.

As a result, I wanted to write a blog post specifically on depression, its treatment, and offer wellness tips to ward off depression. Please note that depression is one of several mood disorders and is different than bipolar, dysthymia, and other mood disorders. This blog post will focus on depression technically known as Major Depressive Disorder. I also want to make it very clear that depression is a treatable illness but, like many illnesses, it can require ongoing “maintenance.”

First let me review the symptoms of depression, followed by the treatment, and then offer some tips to ward off depression.

Symptoms of Depression: To meet criteria, five or more symptoms must be present for at least a 2 week period according to the Diagnostic and Statistical Manual of Mental Disorders. It is also very important to rule out physiological effects of a substance/drug, other psychiatric disorders such as bereavement, and medical conditions such as thyroid problems that may cause depressive symptoms.

  Sad or depressed mood most of the day, almost every day.

  Anhedonia, which is loss of interest in previously enjoyed activities.

  Sleep problems, usually hypersomnia but can also be insomnia.

  Weight gain or loss not due to diet or exercise.

  Low of energy or fatigue even with sufficient rest.

  Psychomotor agitation or retardation, which is usually moving or talking slower.

  Poor concentration or ability to think.

  Feeling of worthlessness or excessive guilt.

  Thoughts of death or suicide, which could be the most serious of all the symptoms and must be taken seriously even in children.

Here are some other symptoms to look for that are frequently present in depression:

  Thoughts of helplessness

  Thoughts of hopelessness

  Isolation

  Changes in appetite

  Irritability

  Crying

  Decrease in sex drive

Treatment for Depression

Treatment for depression begins with an evaluation by a licensed mental health professional to determine severity of depression, to rule out other possible issues, and to refer for appropriate services. Treatment usually entails either counseling or psychotropic medication or a combo of both, depending on severity. Severe depression usually requires a psychiatric evaluation by a psychiatrist for psychotropic medication to help improve symptoms enough for counseling to be effective, while mild to moderate depression can usually be treated with counseling alone. It is important to know there are a countless approaches to counseling such as cognitive behavior, psychodynamic, humanistic, and many more. Many approaches explore the person’s feelings, thoughts, and behaviors. The trust developed between the client-therapist relationship is what many approaches have in common and what research has found to be an essential ingredient to effective treatment. That is why it is imperative that one choose a therapist that is a good fit.

In addition, there are other interventions or activities such as exercise and meditation that have been found to be effective treatment for mild to moderate depression. Family therapy can also be helpful at alleviating tensions at home that may be impacting one’s depression and hindering treatment progress.

Tips to Ward Off Depression

  Exercise Regularly as it has been found to be fantastic not only for managing stress and preventing physical problems but also at reducing depression and anxiety.

  Be Present is where people often report being happy while being in the future can create anxiety and being in the past can lead to feelings of regret, guilt, and depression. Focus on being more mindful about how you are feeling right now rather than how you felt weeks or years ago.

  Seek Support from licensed mental health professionals, friends, family and even animals, whom can be helpful. Surround yourself with people that are positive and validating.

  Know the Signs of depression so that you know when you or someone you in your life needs help.

  Know your Depression and be proactive. If you know that you happen to be extra susceptible to depression during the winter months, prepare for it by scheduling regular activities or seeking extra support during this time.

  Get Outside because sunlight can be helpful and so can nature. Experiencing the grandeur nature can help put one’s problems into perspective and when our problems seem small they don’t bother us as much.

  Find Meaning or a reason for living as it can be a powerful motivation to keep living. One’s meaning can be their partner, children, or even a cause.

  Sleep is vital to good health and mental functioning. Avoid sleep problems by having a regular bedtime even on weekends, keeping distractions from the bedroom (e.g., TV), and creating a bedtime that is conducive for relaxation.

  Visit Your Primary Care Doctor regularly to prevent, catch, or treat medical illnesses early that can create depressive symptoms.

  Eat Healthy meals to improve physical, mental, and emotional functioning. Eating unhealthy foods erodes your physical health, impairs cognitive functioning, and also impacts how you feel about yourself.

  Respect your Emotions rather than stuffing them. Bottling your feelings can be toxic to your body while expressing how you feel can be very relieving especially when your feelings are validated.

Author: Yoendry Torres, Psy.D., Clinical Psychologist

Retrieved from: http://www.intuitionwellness.com/blog/2012/10/12/depression-101-treatment-tips-to-ward-off-depression/

ketamine isn’t just for kitties anymore…

In Medication, Mood Disorders, Neuroscience, Psychiatry, Psychopharmacology on Thursday, 11 October 2012 at 14:43

Ketamine a Viable Option for Severe Depression?

Megan Brooks

October 11, 2012 — The discovery that ketamine produces rapid antidepressant effects in patients with severe treatment-resistant depression is fueling basic neuroscience research, leading to a greater understanding of the neurobiology of depression and maybe more effective treatments, a new review suggests.

Ketamine, an N-methyl-D-aspartate (NMDA) glutamate receptor antagonist, is best known in medicine as an anesthetic but also has some notoriety as a street drug, sometimes dubbed “Special K,” and is taken illicitly for its psychedelic effects.

However, recently ketamine has gained interest among researchers for its potential as a unique, rapid-acting antidepressant.

Typical antidepressants such as the serotonin selective reuptake inhibitors (SSRIs) take weeks to months to have an effect and are only moderately effective, leaving more than one third of depressed patients resistant to drug therapy.

“The rapid therapeutic response of ketamine in treatment-resistant patients is the biggest breakthrough in depression research in half a century,” review author Ronald Duman, PhD, professor of psychiatry and neurobiology at Yale University in New Haven, Connecticut, said in a statement.

However, Dr. Dunham told Medscape Medical News, although clearly promising for depression, ketamine does have some roadblocks.

“It produces transient side effects [for about 1 hour], including mild hallucinations and dissociative effects in some patients, subsequent to the antidepressant response. Ketamine is also a drug of abuse, so caution is needed when considering widespread use of this agent.”

“Nevertheless, there are millions of depressed patients who do not respond to conventional antidepressants and are in dire need of a drug like ketamine,” Dr. Duman added.

With Dr. Duman and coauthor George Aghajanian, MD, professor emeritus of psychiatry at Yale University, the review was published October 5 in Science.

Timely, Authoritative

Commenting for Medscape Medical News, James W. Murrough, MD, from Mount Sinai School of Medicine’s Mood and Anxiety Disorders Program in New York City, described the article as a “timely, well written, and authoritative review by 2 neuroscience researchers who have really done the bulk of the work looking at the biological basis for how ketamine might bring about a rapid antidepressant effect.”

The original link between ketamine and relief of depression was made by John Krystal, MD, chair of the Department of Psychiatry at Yale, and Dennis Charney, MD, formerly of Yale, now professor of psychiatry, neuroscience, and pharmacology and dean at Mount Sinai School of Medicine.

In 2000, they published results of a small, double-blinded, placebo-controlled study showing that intravenous infusions of ketamine produced significant and rapid antidepressant effects (Berman et al; Biol Psychiatry, 2000;47:351-354).

“That was the first controlled study that showed that ketamine had sort of an unexpected rapid antidepressant effect in patients,” said Dr. Murrough. “We knew it was a glutamate antagonist, but at this time (in 2000), the role of glutamate in depression was not at all on the radar.”

That study was followed by an article published in 2006 that also showed rapid (within 2 hours) and significant antidepressant effects after a single infusion of ketamine in 18 patients with treatment-resistant depression (Zarate Jr et al; Arch Gen Psychiatry, 2006;63:856-864).

Since then, a number of studies replicated and extended the findings — including a study by Carlos Zarate Jr, MD, and colleagues published in 2010 in Archives of General Psychiatry and reported by Medscape Medical News at the time.

These studies sent neuroscientists on a quest to figure out at a cellular level, using animal models, how ketamine worked and what it could reveal about depression.

Jury Still Out

The literature suggests that depression is caused by disruption of homeostatic mechanisms that control synaptic plasticity, resulting in destabilization and loss of synaptic connections in mood and emotion circuitry, the authors note. Ketamine appears to target synaptic dysfunction in depression.

The findings highlight the “central importance of homeostatic control of mood circuit connections and form the basis of a synaptogenic hypothesis of depression and treatment response,” the review authors write.

Is ketamine currently used to treat refractory depression?

“A year ago, I would have said no, it’s not being used clinically. But in the last year, I’ve run into patients who’ve said they had been treated with low-dose ketamine by their psychiatrist, and doctors at national meetings who’ve said they’ve used it in their practice, but it’s very sparse, it’s far from widespread,” said Dr. Murrough.

It is important to note, he added, that to date, most of the research has been limited to the effects of a single dose.

At a medical conference in June, as reported by Medscape Medical News, Dr. Murrough and colleagues demonstrated that administration of 6 low-dose infusions of ketamine over 2 weeks improved symptoms in a small study of patients with treatment-resistant depression.

It helped “at least while they were getting the ketamine, then there was a relapse that came in as few as a couple days to several months or longer in a few cases,” he said.

Dr. Murrough said he and his colleagues are now “closing out” another study of ketamine that should be published in a couple of months. Other trials are ongoing.

“The jury is still out on whether ketamine itself could be developed into a bona fide treatment. We happen to believe that it can be. We advocate a cautious approach, but we are cautiously optimistic that ketamine could be a treatment option for severe refractory depression,” he said.

“The benchmark treatment right now for severe refractory depression is electroconvulsive therapy [ECT],” Dr. Murrough pointed out, “so you’d have to believe that ketamine has a worse risk-benefit profile than ECT, and so far, we don’t see that; it appears to be very well tolerated.”

Dr. Duman and Dr. Aghajanian have disclosed no relevant financial relationships. In the past 2 years, Dr. Murrough has received research support from Evotec Neurosciences and Janssen Research & Development. Dr. Charney has been named as an inventor on a use patent of ketamine for the treatment of depression. If ketamine were shown to be effective in the treatment of depression and received approval from the US Food and Drug Administration for this indication, Dr. Charney and Mount Sinai School of Medicine could benefit financially.

Science. 2012;338:68-72. Abstract

Retrieved from: http://www.medscape.com/viewarticle/772467?src=nl_topic

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