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Excerpted from Sciencedaily.com, 9/4/08

In an effort to better understand how chronic stress affects the human body, researchers at the Yerkes National Primate Research Center and the Department of Psychiatry and Behavioral Sciences, Emory University, have created an animal model that shows how chronic stress affects behavior, physiology and reproduction.

According to lead researcher Mark Wilson, PhD, chief of the Division of Psychobiology at Yerkes, “Chronic stress can lead to a number of behavioral changes and physical health problems, including anxiety, depression and infertility.”

Via the animal model, the researchers found corticotropin releasing factor (CRF) is a key neurohormone involved in stress response. Wilson explains, “CRF is located in several different brain regions, serving different functions. Its release is important for our ability to adapt to every day stressors and to maintain our physical and emotional health.”

In response to stress, CRF levels rise; CRF levels decrease when the stressor no longer is present. Chronic stress, however, increases the length and volume of expression of CRF in areas of the brain associated with fear and emotion, including the amygdala. Such chronic stress changes the body’s response, and the resulting increased expression of CRF is thought to be the cause of such health-related stress problems including anxiety, depression and infertility.

Intuitively most people know that chronic stress wreaks havoc on their health. But until quite recently, most physicians and researchers denied such a connection between stress and disease existed at all. Thankfully, that time has passed. The new scientific discipline of “psychoneuroimmunology”, or PNI, is illuminating the mechanisms behind the stress-disease connection and revealing just how damaging chronic stress is to our health.

Stress has been shown to be a risk factor in almost every serious disease that plagues human beings, including heart disease, cancer, diabetes and depression. Stress management techniques should be a consistent, regular aspect of your preventative medicine program.

Stay tuned for some of the techniques and practices I’ve found to be most helpful.

magnifying glassI’d like to thank everyone for their comments, both online and “offline” about my recent “Placebos as Effective as Antidepressants” article. Some very good questions were raised in a comment from Stephan, author of the highly recommended Whole Health Blog that I would like to address in today’s article.

The tricky thing about doing scientific research, as I explained in last week’s article, is that conflicts of interest between doctors, researchers and pharmaceutical companies have become so prevalent that the results of even studies published in prominent, peer-reviewed journals cannot be taken at face value.

One must ask: was the study designed properly? Do the author’s conclusions match their own data? Have the authors reported all of the relevant results? Who funded the study, and what role did they have in choosing the subjects, overseeing the methodology and publishing the results?

When looking at a body of research, one must also consider whether there are unpublished studies on the topic and what the effect of those studies might be. This is particularly true in the case of antidepressants, where it has been estimated that approximately 23% of studies have not been published. Why? Because those studies had even less favorable results than those studies that have been published, and the drug companies who paid for them are under no legal obligation (currently – hopefully this might change in the future) to publish study results.

With that in mind, let’s consider Stephan’s comment and each of the points he brings up in turn:

“I fully agree with you about the “chemical imbalance” thing; it’s incredibly dense. They try to spin it like you were born with depression and there’s nothing you can do about it but take a drug. I have a friend who’s into mood disorder research and I’ve talked to him about that meta-analysis showing no significant effect of ADs.

First of all, he has no dog in the fight because his interest in mood disorders is purely academic. I can vouch for his lack of bias toward antidepressants. Here’s what he told me. Basically, what we call “depression” is actually a collection of related disorders. Antidepressants only work on a subset of them.

There are “responders” and “non-responders” in any group of people who receive antidepressants. For responders, antidepressants can be very effective. When you do a meta-analysis where you’re averaging everyone with “depression” together, the effect of an antidepressant will be small or nonexistent because of the heterogeneity. So this is a problem with saying that antidepressants aren’t effective based on that analysis.

I don’t have a problem believing that antidepressants work for some people. They certainly work in animal models of depression, where there is no placebo effect. I don’t think we should banish them from planet Earth. But I do think the fact that we use them so much points to a bigger problem that we should be addressing by other means.”

I want to thank Stephan again for his comment and for raising these important issues.

Let’s start with the parts that I agree with. Certainly, depression has become so broad a term that some have argued that it is an essentially meaningless clinical designation. Unlike other conditions that have measurable physiological markers, people that are diagnosed as depressed do not usually have any features that categorically distinguish them from other people. The sorts of problems that are diagnosed as depression can very considerably depending upon which diagnostic criteria are used, the interpretation of those criteria, and cultural and professional attitudes.

In their book The Loss of Sadness, Horwitz and Wakefield point out that the diagnosis of depression has now come to include transient and completely appropriate responses to life such as sadness after the passing of a loved one, disappointment after the loss of a job or anxiety about financial troubles. They argue, very convincingly, that the DSM IV criteria for depression do not adequately distinguish between what they call “normal sadness” and depression, and the result has been the almost complete medicalization of our emotional response to life. I will be writing an article on this very soon, as I believe it’s a critical perspective to understand in our exploration of depression and antidepressants.

Secondly, I certainly cannot argue with the statement that “antidepressants work for some people”. However, the important questions to ask in relation to that statement are:

  • Why do antidepressants work