Ending a Midlife Affair with Meds

By Paulina Porizkova


I felt guilty. I felt unnatural. I felt ashamed. Finally, I broke down and confessed my dirty little secret to a girlfriend and found that she not only knew what I was talking about, but she was doing it, too. And the more I opened up about it, the more I found that I was not alone. Women in their late 30s and 40s were all having the same affair.

With an antidepressant.

I started taking Lexapro after my anxiety attacks came back and, for all intents and purposes, practically crippled me. I’ve always had anxiety attacks, or panic attacks as some know them, but after years of learning how to deal with them, I thought I had them under control. While my kids were little, the anxiety attacks even subsided to the point where they hardly bothered me. But at the stroke of 40, they came back worse than ever.

Full story at Huffington Post

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Tai Chi Aids Seniors in Fighting Depression

By DAVID MCCRACKEN, MA, LP


With more than 2 million people age 65 and older suffering from depression in the U.S., including half of those living in nursing homes, effectively treating the elderly is a growing problem – especially as the numbers of seniors rise.

Researchers at UCLA found that an ancient martial art can help significantly.

When a gentle, Westernized version of tai chi chih was combined with a standard drug treatment for a group of depressed elderly adults, researchers found greater improvement in the level of depression — along with improved quality of life, better memory and cognition, and more overall energy — than among a different group in which the standard treatment was paired with a weekly health education class.

“This is the first study to demonstrate the benefits of tai chi in the management of late-life depression, and we were encouraged by the results,” said first author Dr. Helen Lavretsky, a UCLA professor-in-residence of psychiatry.

“We know that nearly two-thirds of elderly patients who seek treatment for their depression fail to achieve relief with a prescribed medication.”

In the study, 112 adults age 60 or older with major depression were treated with the drug escitalopram (brand name Lexapro), a standard antidepressant, for approximately four weeks. From among those participants, 73 who showed only partial improvement continued to receive the medication daily but were also randomly assigned to 10 weeks of either a tai chi class for two hours per week or a health education class for two hours per week.

All the participants were evaluated for their levels of depression, anxiety, resilience, health-related quality of life, cognition and immune system inflammation at the beginning of the study and again four months later.

The level of depression among each participant was assessed using a common diagnostic tool known as the Hamilton Rating Scale for Depression, which involves interviewing the individual. The questions are designed to gauge the severity of depression. A cut-off score of 10/11 is generally regarded as appropriate for the diagnosis of depression.

The researchers found that among the tai chi participants, 94 percent achieved a score of less than 10, with 65 percent achieving remission (a score of 6 or less). By comparison, among participants who received health education, 77 percent achieved scores of 10 or less, with 51 percent achieving remission.

While both groups showed improvement in the severity of depression, greater reductions were seen among those taking escitalopram and participating in tai chi.

“Depression can lead to serious consequences, including greater morbidity, disability, mortality and increased cost of care,” Lavretsky said. “This study shows that adding a mind-body exercise like tai chi that is widely available in the community can improve the outcomes of treating depression in older adults, who may also have other, co-existing medical conditions, or cognitive impairment.

“With tai chi,” she said, “we may be able to treat these conditions without exposing them to additional medications.”

The results of the study appear in the current online edition of the American Journal of Geriatric Psychiatry.

Source Psych Central

New Studies Examine the Many Facets of Depression

By KATHLEEN DOHENY Psych Central News
Reviewed by John M. Grohol, Psy.D. on November 18, 201


Treatments for depression have improved greatly over the years, yet there are still many patients not helped by traditional offerings of medications and talk therapy.

”Roughly 20 to 40 percent of people with depression aren’t helped by existing therapies,” said Robert Greene, M.D., Ph.D., of the University of Texas Southwestern Medical School in Dallas.  On Monday, he moderated a news conference at the annual meeting of the Society of Neuroscience in San Diego to update research on new options under study.

Among the promising research is new data on:

  • How being stressed out may play a role in depression;
  • How the immune system may play a role in depression;
  • The role of a specific molecule, Cdk5, in nerve cell signaling and how the information might be used for an antidepressant effect;
  • The role of a small protein known as p11 and how it affects antidepressant-like  responses.

To the first of these, Herwig Baier, Ph.D., a researcher at the University of California San Francisco, said, ”An inability to cope with stress may play a role in depression.” He found in a study that zebra fish who have a mutation in a receptor important for stress management displayed abnormal behavior similar to depression. Normally social fish, the zebra fish stopped swimming and hid in the corner of their tanks when isolated from others.

But when these fish were given fluoxetine (Prozac), the behavior disappeared, he found. Studying the fish makes sense, Baier says, as the ”stress axis” in this fish and humans is identical.

The zebra fish’s mutation is in the gene known as the glucocorticoid receptor (GR) gene, and one of its jobs is to ”dial down” the secretion of stress hormones from the brain. Either too much or too little GR activity has been linked with depression.

If the fish story holds true for people, Baier said, new strategies for depression could be developed that don’t block GR activity but activate it to just the right amount so mood is not depressed.

The immune system could also play a role in depression, said Simon Sydserff, PHD, a senior research scientist at BrainCells, Inc., a drug development company in San Diego involved in stem cell technology to develop CNS treatments.

Here’s how:  When you get sick, the immune system hormone IL6 or interleukin 6, carries ”sickness” signals to the brain. When Sydserff activated the immune system of mice to mimic sickness, they displayed behavior representing depression.

“Patients who are depressed who are medically healthy and also those who are medically ill, have high levels of immune system signaling cytokines such as IL6,” he said.

“Interferon alpha, a cancer treatment, increases IL-6 and has also been linked to major depression,” he said. If the research bears out, he said, ”blocking IL-6 may prevent or reverse depression,” offering another option.

He conducted the research, supported by AstraZeneca Pharmaceuticals, while on staff there.

In  another study, James Bibb, Ph.D., of the University of Texas Southwestern Medical Center, Dallas, found that mice lacking a molecule known as Cdk5 like mice given an antidepressant: They were more active, one marker of effective antidepressant action. Without the molecule, the wave of a signaling molecule known as cyclic AMP doesn’t stop as it typically does, and this was linked with antidepressant-like responses. Learning how to block this molecule in the future could provide more options, he said.

Meanwhile, figuring out why an antidepressant can take a while to ”kick in” is the focus of another study. Jennifer Warner-Schmidt, Ph.D., a researcher at The Rockefeller University in New York, zeroed in on a regulator of antidepressant responses known as p11.  It’s a small protein expressed in depression-related brain regions.

She found in animal studies that over-expression of p11 results in an antidepressant effect and that another key regulator, brain-derived neurotrophic factor (BDNF) is required for the serotonin-induced increase in the p11.

”Understanding better the role of p11 in antidepressant response could lead to faster acting antidepressants with fewer side effects,” she said.

SOURCE: Society for Neuroscience.