The Healthy Skeptic

In Part I and Part II of this series, we examined drug-free alternatives to treating depression including exercise, psychotherapy, light therapy, St. John’s Wort and acupuncture. We have learned that all of these treatments are at least as effective as antidepressants in the short term, and some (exercise and psychotherapy) are more effective in the long-term. All of these treatments have far fewer side effects, risks and complications than antidepressants. In fact, the only “side effects” of exercise and psychotherapy are positive ones: improved physiological and mental health!

Today we will look at other lifestyle-based approaches to treating depression without drugs. As I mentioned in the previous article, because 70% of research is funded by drug companies, many of these non-drug approaches have not been studied as extensively as antidepressant medication.

Nevertheless, there is enough data from clinical and epidemiological studies to support the following strategies - especially since they are superior to antidepressants from a “cost/risk - benefit” analysis. In other words, though some of the approaches I will propose in this article have not been exhaustively proven according to the standards of Western science, there are several lines of evidence supporting their effectiveness and without exception they have beneficial side effects and improve the quality of patient’s lives.

What’s more, all of these approaches can be combined together along with the treatments mentioned in the two previous articles to obtain the maximum effect. Based on the available evidence which we have extensively reviewed, these non-drug treatments should without a doubt be the first line of defense (as well as the second, third, fourth, etc.) in treating depression.

Nutrition

At some point in the future, I hope to dedicate an entire post (or perhaps more) to the subject of nutrition and depression. I personally believe that inadequate nutrition is a significant contributing factor to the continuously rising rates of depression in this country. Consequently, I also believe that proper nutrition can be one of the most effective treatments for depression.

For now, I will go over what I feel are the most important aspects of nutritional causes and treatment of depression, and hopefully address the subject in more detail later.

SUGAR

Diabetes is correlated with higher rates of depression. In 2005, researchers discovered a positive connection between higher levels of insulin resistance and severity of depressive symptoms in patients with impaired glucose tolerance, before the occurrence of diabetes. Based on these findings, it was suggested that insulin resistance could be the result of an increased release of counter-regulatory hormones linked to depression; however, this has not been confirmed.

Sugar can increase fasting levels of glucose and can cause reactive hypoglycemia. Sugar can also cause a decrease in your insulin sensitivity thereby causing an abnormally high insulin levels and eventually diabetes. Based on the study results above, this is one mechanism by which sugar could contribute to depression.

There is no doubt that increased sugar intake leads to hormonal changes that can lead to emotional instability. Therefore, people who are depressed (and all people, in fact) should significantly decrease their sugar consumption.

OMEGA-6 / OMEGA-3 RATIO

Anthropological evidence suggests that the intake of omega-6 (n-6) and omega-3 (n-3) polyunsaturated fatty acids (PUFA) during the Paleolithic era was roughly equal, whereas the present n-6 to n-3 PUFA in western countries has ben estimated to be between 10 and 25 to 1. The n-6 to n-3 PUFA imbalance has been due mainly to the increase in vegetable and seed oil use and the rise in consumption of processed foods (which contain these oils).

Two major studies have provided direct evidence for the role of the n-6 to n-3 PUFA ratio in depression. The studies found that depression is associated with significantly decreased total n-3 PUFA and increased n-6 to n-3 PUFA ratio (Maes et al. 1996; Maes et al. 1999) . A supporting study carried out in 1998 also found a significant depletion in total n-3 PUFA, and in particular DHA, in the erythrocyte membranes of depressed patients.

Epidemiological data show the trend in decreasing dietary n-3 PUFA consumption and the increasing evidence of depression, both over time and between nations (Hibbeln et al. 1995). Further investigation suggests that the significance lies in the increase in n-6 to n-3 ratio, rather than simply low n-3 intake alone, as these two fatty acids compete in binding to enzyme systems that produce chain elongation and further desaturation. A diet high in n-6 fatty acids prevents the incorporation of n-3 PUFA into cell membranes and phospholipids (Spector et al. 1985).

All polyunsaturated fatty acids - including n-3 PUFA - have been shown to make lipoproteins more vulnerable to oxidative damage (Reaven et al. 1991), and oxidative damage is a significant risk factor for heart disease, cancer and many other conditions. As mentioned above, n-6 consumption actually prevents the incorporation of n-3 into our cells. Therefore, rather than increasing our consumption of n-3 PUFA to treat depression, as is often suggested, it makes more sense to dramatically decrease our consumption of n-6 PUFA. This will help our bodies to incorporate the small, but adequate amount of n-3 PUFA we get in a whole-foods based diet. Avoiding n-6 PUFA (primarily found in vegetable and seed oils, and in animals fed vegetables high in n-6 like pigs and chickens) will not only alleviate depression, but also benefit our health in many other ways.

VITAMIN D

In a 1998 controlled experiment, Australian researchers found that vitamin D (400 and 800 IU), significantly enhanced positive affect when given to healthy individuals. Forty-four subjects were given 400 IU cholecalciferol, 800 IU cholecalciferol, or placebo for 5 days during late winter in a random double-blind study. Results on a self-report measure showed that vitamin D3 enhanced positive affect a full standard deviation and there was some evidence of a reduction in negative affect. The authors concluded: “vitamin D3 deficiency provides a compelling and parsimonious explanation for seasonal variations in mood” (Landsdowne & Provost, 1998).

In another study in 1999, the vitamin D scientist, Bruce Hollis, teamed up with Michael Gloth and Wasif Alam to find that 100,000 IU of vitamin D given as a one time oral dose improved depression scales better than light therapy in a small group of patients with seasonal affective disorder. All subjects in the vitamin D group improved in all measures and, more importantly, improvement in 25(OH)D levels levels was significantly associated with the degree of improvement (Gloth et al. 1999).

According to the Vitamin D Council:

If you suffer from depression, get your 25(OH)D level checked and, if it is lower than 35 ng/mL (87 nM/L), you are vitamin D deficient and should begin treatment. If you are not depressed, get your 25(OH)D level checked anyway. If it is lower than 35 ng/mL (87 nM/L), you are vitamin D deficient and should begin treatment.

Recommended intake is up to 5,000 IU per day of vitamin D through exposure to sunshine and/or supplementation. See this article on vitamin D to learn to calculate how much vitamin D is produced given a certain amount of exposure to sunlight, and to learn more about vitamin D supplementation. It is important to remember that D works synergistically with A & K2, so if you increase your intake of D you must also increase your intake of A & K2 to avoid D toxicity.

Finally, I’d like to share with you a comment I received from a reader about how he/she has cured depression with nutritional intervention. Note that I endorse just about every suggested step, with the exception of the significant increase in n-3 intake. Based on the evidence above, I suspect that his/her improvement was a result of the decrease in n-6 PUFA more than it was the increase in n-3 PUFA.

Following the reader’s advice will not only relieve depression, it will dramatically improve all aspects of your physical, emotional and mental health.

Adequate sleep and rest

Recent studies have definitively linked insomnia with depression and increased suicidal behavior. A research abstract that was presented on June 12 at SLEEP 2008, the annual meeting of the Associated Professional Sleep Societies, found a link between poor sleep and suicidal behavior among children and adolescents with depressive episodes. 83.8% of the depressed patients in the study had sleep disturbances, and there was a significant association between suicidal behavior and the presence of sleep complaints.

Another recent study confirmed the persistent nature of insomnia and the increased risk of subsequent depression among individuals with insomnia. According to the study, 17% - 50% of subjects with insomnia lasting just two weeks or longer developed a major depressive episode reported in a later interview.

Other research has indicated that insomnia can cause depressed mood and adversely affect endocrine function (Banks 2007).

Most Americans are chronically sleep deprived. The foundation’s 2001 national “Sleep in America” poll reported that almost seven out of 10 Americans experienced frequent sleep problems, and that most were undiagnosed. The same poll in 2003 found that 67 percent of older adults had frequent sleep problems and only one in eight had been diagnosed.

This alone could explain the epidemic increase in depression over the last several decades. But when sleep deprivation is added to other factors such as increased intake of n-6 PUFA, increased stress, the use of antidepressant drugs, the breakdown of family, community and other social support structures, it isn’t difficult at all to understand why so many of us are depressed.

The American Academy of Sleep Medicine (AASM) offers the following tips on how to get a good night’s sleep:

• Follow a consistent bedtime routine.
• Establish a relaxing setting at bedtime.
• Get a full night’s sleep every night.
• Avoid foods or drinks that contain caffeine, as well as any medicine that has a stimulant, prior to bedtime.
• Keep computers and TVs out of the bedroom.
• Do not go to bed hungry, but don’t eat a big meal before bedtime either.
• Avoid any rigorous exercise within six hours of your bedtime.
• Make your bedroom quiet, dark and a little bit cool.
• Get up at the same time every morning.

Stress Management

An increasing amount of evidence (along with common sense) indicates that chronic stress directly contributes to depression. Please see my recent article for more information about this.

I am not aware of any well-designed clinical trials examining the effects of stress reduction on depression. However, logic dictates that since stress is a cause of and contributing factor to depression, managing stress is an important aspect of treating depression.

One study published in 1995 showed that meditation can improve mood. Another small study demonstrated that mindfulness-based cognitive therapy (MBCT) significantly improved depression and reduced relapse. A series of studies and case studies have shown that biofeedback can also be effective for depression and mood disorders.

The reality is that there are many ways to manage and reduce stress, from yoga to meditation to mindfulness-based stress reduction to progressive relaxation techniques. The important thing is not which method you choose, but that you commit to something and do it on a regular basis.

Prayer & Spiritual Practice

You’re not going to see much scientific research into the role of prayer and spiritual practice in treating depression. Nevertheless, for as long as people have been “depressed” they have used their relationship with God, nature, a “higher power” or whatever guiding principles they embrace to get through difficult times.

People who are depressed often feel isolated, alienated or alone. A strong faith in God or in the interconnectedness of all life can re-establish a sense of belonging and support. Prayer and spirituality can also re-frame the depression one is experiencing in a larger and less “personal” context.

In my previous article called The Heart of Depression, we examined how cultural, religious and spiritual beliefs in these traditional societies provide a context in which symptoms of depression and other mental illness can be understood outside of the label of medical disease or pathology. Possession and rites of passage are two examples of such contexts.

The words and labels we use to “frame” our experience have tremendous power. In the U.S. today, depression is viewed as a sickness that must be cured, as a pathology, as a “biological disease”. There is little doubt that the people who seek treatment for depression are suffering. But should psychological and emotional suffering always be viewed as “something to get rid of”?

Great religious and spiritual traditions from around the world view suffering as an avenue to greater understanding of oneself, life and God. Suffering can be viewed as a signal drawing our attention to issues in our life that need to be addressed.

Spirituality and prayer can help people who are suffering to understand their experience in a more empowering and self-validating context than what is offered by mainstream medicine. When one views their suffering as an opportunity for growth and evolution, rather than as a disease requiring treatment with drugs, it is far more likely that lasting, positive change will occur.

In the next and final article (for a while, at least) in my series on depression and antidepressants, I will summarize everything we’ve covered so far and offer my recommendations for treating depression holistically.

Popularity: 2%

People taking prescription antidepressants appear to drive worse than people who aren’t taking such drugs, and depressed people on antidepressants have even more trouble concentrating and reacting behind the wheel.

These were the conclusions of a study recently released at the Annual Convention of the American Psychological Association.

The group taking antidepressants who reported a high number of symptoms of depression performed significantly worse than the control group on several of the driving performance tasks.

Participants in the study had to make a series of common driving decisions, such as reacting to brake lights, stop signs or traffic signals while being distracted by speed limit signs, pylons, animals, other cars, helicopters or bicyclists. The simulation tested steering, concentration and scanning.

This is, of course, further evidence that antidepressants create rather than cure abnormal brain states.

And one more reason, of many, not to take them.

Popularity: 2%

In the first article in this three-part series on treating depression without drugs, we established that several non-drug treatments are at least as effective in treating depression than antidepressants - with few, if any of their side effects. Specifically, we learned that both psychotherapy and exercise compare favorably with antidepressants for treating even serious depression in the short-term, and are both more effective than antidepressants in the long-term.

Today we will examine three other drug-free treatments for depression: light therapy, St. John’s Wort and acupuncture. In the final article, we will look at lifestyle-based treatments such as nutrition, adequate sleep and rest, stress management, pleasure and bibliotherapy (prayer or spiritual practice).

Light Therapy

Researchers at the National Institute for Mental Health are credited for the idea that perhaps more people are apt to become depressed during dark, dreary winter days than on bright, crisp spring days because they are not getting enough light. Since then, people around the world have begun to use “light therapy” to overcome Seasonal Affective Disorder. However, light therapy is also being used to successfully treat major depression at any time of the year.

Beginning the day sitting in front of a fluorescent light box that typically emits about 10,000 lux units of light has helped many people who might otherwise struggle with depression throughout the day. Bright light has been shown by numerous studies to act as a specific antidepressant in depressed patients. In a recent meta-analysis of published studies on light therapy and depression which appeared in the April 2005 issue of the American Journal of Psychiatry, the authors found that bright light treatment for nonseasonal depression is efficacious, with effect sizes equivalent to those in most antidepressant studies.

Once again, as was the case with both exercise and psychotherapy, the combining light therapy with antidepressants was no more effective than light therapy alone.

In contrast to exercise and psychotherapy, bright light therapy does occasionally have some side effects, including headache, eye strain, nausea and agitation. But these are very mild when compared against the side effect profile of antidepressants.

It is very important to note that some psychotropic medication (and psychotropic herbs such as St. John’s Wort) may increase sensitivity to light, so light therapy should probably not be combined with St. John’s Wort or antidepressants.

Some critics of light therapy have pointed out that it could be a placebo and there is no way to prove otherwise. It is not possible to keep someone from knowing whether they are being exposed to very bright light or the placebo (dim light). Therefore the “blind” is broken and patients will know whether they are receiving the active or “inert” treatment. Could it be that the positive effects of bright light are simply due to the assumption or expectation of the patients that they will improve, rather than a result of the bright light itself?

Sure it is. But perhaps a more important question is, “does it matter?” If we use Antonuccio’s criteria for evaluating a potential treatment (i.e. 1) first do no harm, 2) cost-benefit analysis) then it becomes clear that light therapy compares very favorably with antidepressants even if it is “merely a placebo”. As you will know if you’ve been following my blog, antidepressants could also be referred to as placebos because they have been shown to be no more effective than placebo in treating depression. The criteria for whether a drug gets approved or not by the FDA is that it must outperform placebo; otherwise, it is simply considered a placebo itself.

Although light therapy may have some side effects, they pale in comparison to those of antidepressants and, unlike antidepressants, light therapy poses no significant risks or long-term complications. A typical light therapy device costs between $200-$300, so over the long-term it is much more cost-effective than medication. Finally, light therapy is just as effective as pharmacotherapy for treating depression.

When all of this is taken together, light therapy is superior to antidepressants - even if it is a placebo.

St. John’s Wort

St. John’s Wort (Hypericum) is an herb that can be used to make tea, or the “active ingredients” with the herb that can be extracted and put into capsules. In Europe SJW is widely prescribed as an antidepressant, but in the U.S., it is available over-the-counter.

St. John’s Wort has repeatedly been shown to work as well as or better than antidepressants in double-blind, placebo-controlled studies. For example, compared to Paxil, depression scores fell more (56.6% vs. 44.8%) and side effects were less (Szegedi et al. 2005). Similar results were found for Prozac (Schulz 2002). A comparison with both Zoloft and Celexa found St. John’s Wort again performed as well as the antidepressant drug without as many side effects (Gastpar 2005; Gastpar 2006).

While St. John’s Wort is clearly as effective as antidepressants, the number of adverse effects is ten times less - being essentially equivalent to taking a placebo. The most common adverse events (1 per 300,000 treated cases) concern reactions of the skin exposed to light (due to potential increased photosensitivity caused by SJW and other psychotropic substances).

Please do note that St. John’s Wort is contraindicated for concurrent use with certain medications, including antidepressant drugs, coumarin-type anticoagulants, the immunosuppressants cyclosporine and tacrolimus, protease and reverse transcriptase inhibitors used in anti-HIV treatment and with certain antineoplastic (cancer) agents.

However, these potential interactions can be easily avoided with proper supervision from a health-care professional who is experienced with the use of St. John’s Wort.

Once again, to be accurate we must point out the possibility that St. John’s Wort is merely a placebo. If it is roughly as effective as antidepressants, and antidepressants are themselves placebo, then it follows that St. John’s Wort may also be a placebo. However, the same analyses that we used for light therapy applies here. The question is, how does St. John’s Wort compare against the primary treatment for depression - antidepressants? As we have seen, SJW is just as effective as antidepressants with only a fraction of the side effects, so there is absolutely no reason not to choose it over a synthetic antidepressant.

Before we move on to acupuncture, nutrition, rest and other lifestyle-based treatments for depression, I want to briefly discuss the criteria we’ve used so far for evaluating the effectiveness of a treatment. As I’m sure you’ve noticed, I am primarily basing the determination of the effectiveness (or lack thereof) of a treatment on well-designed, placebo-controlled, double-blind scientific studies.

I obviously have great respect for this method of inquiry and it has led (and continues to lead) to many important advances in medicine. However, it must be pointed out that this standard of proof has limitations. For example, 2/3 of medical research is funded by pharmaceutical companies. This means that the lines of investigations most often pursued in scientific research are those that are likely to lead to new therapies that can be monetized by the drug companies. There is little incentive for a drug company to dedicate research dollars to a study on how nutrition affects depression, unless there’s a product they can imagine marketing based on the study results. The result is that there are relatively few studies evaluating the effect of nutritional intake on depression.

Another limitation of double-blind, placebo-controlled research is that it is difficult (if not impossible) to maintain that standard with treatment modalities that depend on the unique interaction that happens between a practitioner and a patient. Western science is often skeptical, of course, that this interaction that occurs influences the treatment in any way. They do not understand how the interaction could influence the treatment, and what Western science does not understand, is often dismissed as “new-age fluff”.

What is remarkable about this is not just the arrogance of such a position, but also the ignorance it demonstrates. Over the last two decades, research into the placebo effect and growing understanding of how the nervous, endocrine and immune systems are inter-related have proven beyond a shadow of a doubt - according to the most rigorous Western scientific standards - that the interaction between a doctor or clinician and their patient absolutely influences the outcome of the treatment. In fact, many studies have shown that this interaction may be more important than the treatment itself; or, perhaps more accurately, the interaction is the treatment.

With this in mind, it becomes clear that the efficacy of acupuncture as a treatment for depression - or anything else - can never be accurately measured in a double-blind, placebo-controlled study. As much as Western science hates to admit this, we are not machines that respond in entirely an predictable manner given the same circumstances. There is no way to “standardize” the interaction that happens between an acupuncturist (or any healing professional) and a patient, because each person and, therefore, each relationship is unique.

Acupuncture

Considering all of the caveats above, can acupuncture help with depression? According to the Cochrane Database Systematic Review (the gold standard for medical research reviews today), “there is no evidence that medication was better than acupuncture in reducing the severity of depression.” In many of the studies they reviewed, acupuncture and electro-acupuncture either cured or remarkably improved depression scores, performing just as well as synthetic antidepressants.

However, it must also be noted that the studies were few in number, often poorly designed and did not have enough subjects to draw definitive conclusions. The authors of the review concluded that there was “insufficient evidence to determine the efficacy of acupuncture compared to medication”.

And of course, we always have the issue of placebo. It is possible that the benefit the patients are receiving comes from the interaction with the practitioner and their expectation that they will improve - rather than as a result of the needles themselves.

Once again, though, if we evaluate acupuncture based on a “cost-benefit” analysis, it compares very well against antidepressants. It has been shown to be at least as effective as medication in many studies as noted above, and the side effects are minimal when compared with antidepressants. Acupuncture has also been shown to be effective in treating other conditions that may occur alongside of depression, such as pain and stress.

Stay tuned for the third-part of this series which will consider lifestyle-based treatments such as nutrition, adequate sleep and rest, stress management, pleasure and prayer.

Popularity: 3%

The most widely prescribed drugs in the U.S. are not for pain management, cholesterol lowering, heartburn or hypertension.

They’re for depression.

Last year doctors wrote $232.7 million prescriptions for antidepressants. That’s an increase of 25 million prescriptions since 2003 and translates into an estimated 30 million patients in the United States who spent $12 billion on antidepressants in 2007.

With numbers like these, a person might make these assumptions:

• Antidepressants are effective treatments for depression
• There are few, if any, effective alternatives to antidepressants

As reasonable as these assumptions would be based on the popularity of antidepressants, they are both wrong.

In my preceding articles in this ongoing series on depression and antidepressants, I’ve presented clear evidence that antidepressants are not effective for treating depression.

In this article and the following two, I will present evidence that several non-drug treatments for depression are at least as effective as antidepressants, with few (if any) of their side effects, risks and costs.

As you may recall from the previous articles in this series, recent meta-analyses have shown that antidepressants have no clinically meaningful advantage over placebos. What I have not yet pointed out is that the effectiveness of antidepressant drugs has probably been overstated due to methodological factors in the studies.

In the studies performed on antidepressant drugs, the people taking the drugs also received supportive weekly visits with doctors or researchers along with the medication. The resulting “therapeutic alliance” may have enhanced the efficacy of these drugs and given an inaccurate picture of their effectiveness in a managed care environment where antidepressants are often delivered in conjunction with infrequent visits to a physician or mental health professional.

We know from placebo research that the contact which occurs between the patient and practitioner can be a powerful treatment in itself. Therefore, the supportive visits that patients received during the drug trials could have easily amplified the effect of the drug and made it seem far more effective than it would be in a “normal” clinical situation where visits to a physician or psychiatrist are not regular or frequent.

With this in mind, it is very likely that antidepressants are less effective than placebos in normal clinical practice. Indeed, researcher Joanne Moncrieff has repeatedly pointed out that the term “antidepressant” is a misnomer. The drugs collectively referred to as “antidepressants” do not specifically treat depression (any more than placebo), and therefore should not be called “antidepressants” at all.

What are the alternatives, then, to treating depression? Imagine having a choice between five treatments. Treatment A produces a therapeutic response but also a large number of adverse effects including diarrhea, nausea, anorexia, sweating, forgetfulness, bleeding, seizures, anxiety, mania, sleep disruption and sexual dysfunction. Treatments B, C, D & E produce therapeutic responses similar to Treatment A, but with far fewer adverse effects and costs. Treatments B & C, in fact, have no adverse effects at all and have been shown to be significantly more effective than Treatment A in the long-term.

This is not, of course, simply a hypothetical question. Treatment A corresponds to the selective serotonin reuptake inhibitors (SSRIs) that have become so overwhelmingly popular. Treatment B is psychotherapy, which is as effective as antidepressants in the short term (even for serious depression), and is more effective in the long term. Treatment C is exercise, which has been reported to have lasting therapeutic benefits in the treatment of major depression with no “side effects” except for improved physiological and mental health. Treatment D is light therapy, which has been recently assessed in several clinical studies and is just as effective as antidepressant medication. Treatment E is St. John’s Wort, an herb that has been extensively studied and shown to be similar in efficacy to antidepressants with 10 times fewer adverse effects.

As depression researcher David Antonuccio points out, “whether one subscribes to the Hippocratic dictum ‘first do no harm’ or takes a cost-benefit approach to treatment, it is impossible to ignore the fact that antidepressants are not medically benign treatments. Antidepressants have serious side effects (listed above) as well as medical risks (including increased risk of dying) when combined with other medications - as is often the case in clinical settings. Antidepressants have been shown to cause potentially permanent changes to the brain that can predispose a patient to depression in the future, and the withdrawal symptoms of SSRIs are substantial for many, if not most, patients.

A frequent argument made by supporters of antidepressants is that patients with serious depression need antidepressants to stave off suicide. However, there is no evidence whatsoever that antidepressants reduce the risk of suicide or suicide attempts in comparison with placebo in clinical trials. On the contrary, in a recent analysis of the data that compensated for erroneous methodologies, Dr. Grace Jackson found that antidepressants increased the risk of suicide by two to four times in adults, and by three times in children (Jackson 2005, p.122)

It has also been demonstrated that recent sharp increases in antidepressant use have been accompanied by increased prevalence and duration of depressive episodes and rising levels of sickness absence (Patten 2004). Naturalistic studies have also shown that depressive episodes are more frequent and last longer among antidepressant users than among nonusers, and that sickness absence is more prolonged (Moncrieff 2006). Finally, long-term follow-up studies show very poor outcomes for people treated for depression with drugs, and the overall prevalence of depression is rising despite increased use of antidepressants (Fombonne 1994).

Please allow me to summarize the research and simplify the preceding paragraphs:

Antidepressants don’t work. If anything, they make things worse.

Now that we have firmly established the ineffectiveness and dangers of antidepressants, let’s look more closely at the alternatives. We will evaluate each treatment based on Antonuccio’s criteria above:

• Does the treatment do any harm?
• How do the “costs” compare with the “benefits”?

and we will also compare their efficacy with that of antidepressants.

Psychotherapy

Several studies show that psychotherapy (particularly cognitive therapy, behavioral activation, and interpersonal therapy) compares favorably with medication in the short-term, even when the depression is severe, and appears superior to medications over the long term (Antonuccio 2002). When medical cost offset, relapse and side effects are considered in a cost-benefit analysis, psychotherapy can be very cost-effective - particularly in a psychoeducational (e.g. therapist-assisted bibliotherapy) or group format (Antonuccio et al. 1997). Finally, studies show that most patients prefer psychotherapeutic intervention to drugs when given the choice. (Unfortunately, they are rarely given the choice; today, fewer than 10% of psychiatrists offer psychotherapy to their patients.)

It is important to note that several studies have shown that combined treatment (psychotherapy + medication, exercise + medication) produces inferior results when compared to the non-drug modality alone (Hollon et al. 1992). The failure of this combined approach is not surprising when one considers the counter-productive effects of invasive chemical interventions (e.g. suppression of REM sleep, elevation of cortisol, induction of mania).

Unfortunately, the mental health profession remains largely ignorant to this “tragedy of its own making”:

Exercise

Several studies have shown that aerobic exercise is at least as effective as antidepressants in treating depression. For example, one recent study published in the American Journal of Preventative Medicine in 2005 indicated that the “public health dose” (5x/week frequency burning 17.5 kcal/kg/week) of exercise led to remission rates of 42%. For the sake of comparison, the Collaborative Depression Study, conducted by the National Institute for Mental Health, indicated remission rates of 36% for cognitive behavioral therapy and 42% for antidepressant medication.

A frequent criticism of exercise as a treatment for depression is the supposed lack of compliance in patients. The argument is that people who are depressed are too depressed to exercise. While this may be true in some cases, adherence rates in exercise studies were comparable to many medication trials, where rates vary from 60%-80%. Thus, evidence does not support the notion that exercise is not a feasible treatment for depressed patients.

Another benefit of exercise as a treatment for depression is that the only “side effects” are improved physiological and mental health. In contrast to antidepressants, exercise has no adverse effects whatsoever. Instead, it has a moderate reducing effect on anxiety, can improve physical self-perceptions and in some cases global self-esteem, and can enhance mood states and - in older adults - improve cognitive function.

In a study published in Psychosomatic Medicine in 2000, another important advantage of exercise over antidepressants was revealed. Participants in the exercise group were less likely to relapse than participants in the two groups receiving medication. Other studies have confirmed this effect, demonstrating that aerobic exercise is especially helpful in the prevention of relapse and recurrence of depression.

Once again, as was the case with psychotherapy, there was no benefit when combining antidepressant drugs with exercise. In fact, the opposite was the case, at least with respect to relapse for patients who initially responded well to treatment. According to the authors of the study:

The authors go on to speculate on why antidepressant drugs would decrease the exercise’s beneficial effects on depression:

It is also possible that the metabolic and physiological effects of antidepressants described above (suppression of REM sleep, elevated cortisol levels, etc.) could counteract the positive benefits of exercise to a certain degree.

In part II of this article I will discuss light therapy, St. John’s Wort and acupuncture as treatments for depression. In Part III I will examine other lifestyle modifications that can both prevent and treat depression, such as proper nutrition, stress management, getting adequate sleep, the experience of pleasure and prayer or spiritual practice.

Popularity: 4%

In the last few articles in my series on antidepressants and depression, I have presented evidence demonstrating that - despite popular belief - depression is not caused by a deficiency of serotonin in the brain.

However, this of course does not suggest that depression is completely divorced from biochemical processes in the body. The brain is a “living orchestra” of complex, interconnected systems that are in continuous relationship with one another. Everything from the food that we eat to the chemicals we’re exposed to in our environment to the hormones we produce effects the functioning of the brain.

This will likely come as no surprise to you. It’s simply common sense. But as you may have noticed, in the world of scientific research common sense must first be proven according to the established standards of scientific proof before it is accepted.

Such has been the case with the link between stress and depression. I’ll wager that if I asked ten people on the street whether chronic stress caused depression, probably all ten of them would say “yes”. However, scientific proof of the causal link between chronic stress and depression has only begun to emerge over the past few years. It has been known for much longer that depressed people have elevated levels of cortisol (an indicator of chronic stress), but it was not known whether those elevated levels were the result or cause of depression.

In 2006 Ardyfio & Kim published a study indicating that chronic hypercortisolemia (elevated cortisol levels in the blood) causes anxiety-related behavior in mice. These results suggest that elevated cortisol levels may contribute to the symptom profile of depression rather than simply being a consequence of it.

Ardyfio & Kim’s study also confirmed the results of other studies which suggest that while acute stress is adaptive (helps us adjust to our changing circumstances), chronic stress has detrimental effects on the brain and behavior. Indeed, chronic stress has been linked to a wide variety of modern diseases, including (but not limited to) heart disease, cancer, diabetes, autoimmune disease, irritable bowel syndrome and fibromyalgia.

In a more recent study published in 2007, work stress was demonstrated to precipitate diagnosable depression and anxiety-related disorders in previously healthy, young individuals. The authors point out that stressful work conditions predict poor mental health, and that currently as many as 40% of people are exposed to work stress. (That’s funny, I would have thought the number to be closer to 100%).

The relationship between psychological job demands and the risk of depression and anxiety was graded; in study members exposed to high psychological job demands the risk was two times higher than in those with low demands. The combination of multiple work stressors conferred an even higher risk, especially in men.

Once again, this probably does not come as a surprise to you. It makes sense that high stress at work may cause depression and anxiety. But, believe it or not, this is relatively recent news to the mainstream scientific establishment.

Finally, in a study published today, researchers have shown how cortisol (one of the stress hormones) regulates brain neurotransmission in both the short and long term and enables neuronal connections to adapt.

In the short term, cortisol increases the mobility of receptors found on the surface of neurons, thus allowing synaptic connections to adapt more effectively to the demands of brain activity. The stress hormone might be considered as an “alarm” that mobilizes the receptors for action. This behavior is adaptive, as it helps the organism (us) prepare and mobilize for action when faced with stress (a threat).

However, in the case of prolonged stress (which is the type of stress most prevalent in modern life) cortisol actually reduces synaptic plasticity. Lack of receptor mobility contributes to a lack of adaptation, which of course, is bad news for us.

The relevance to all of these studies to our recent discussion about depression and its treatment is this: stress is likely a significant contributing factor to depression for most people, and stress-management should play an important role in the treatment of depression.

Stress-management strategies are drug-free, non-invasive, cost-effective and have a wide range of beneficial “side effects” such as happiness, relaxation, improved sleep, more energy, improved libido, increased productivity, and protection from the legion of diseases that have been linked to stress.

In short, there is absolutely no reason not to include stress management in your treatment regimen for depression, or in your daily life even if you are currently healthy and free of disease.

There are many ways to reduce stress, including meditation, prayer, gentle movement (yoga, tai chi, Feldenkrais), exercise, deep relaxation techniques, spending time in nature, listening to music. What’s most important is that you find something that works for you and stick with it.

Mindfullness-Based Stress Reduction (MBSR), created by Dr. Jon Kabat-Zinn, is a very successful approach that has been clinically proven in well-designed studies to reduce pain and stress and improve health. I recommend his book Full Catastrophe Living, as well as the CD recordings of the techniques.

I also recommend a system of gentle movement and breathing exercises called “mini-moves”. Although they are marketed as a treatment for insomnia, the creator (Michael Krugman) of the system believes (quite correctly) that the best way to cure insomnia is to manage daytime stress successfully. You can download the “Secrets of Sounder Sleep” audio here. They are very simple and can be performed in as little as 5-15 minutes at a time.

I’ve used both of these systems myself with great success.

Next week will be the final article in the depression series (for now): drug-free alternatives to treating depression. Until then…

Popularity: 6%

Easy! Just follow Dr. Steinberg’s recent recommendations.

Dr. Daniel Steinberg, author of “The Cholesterol Wars”, has just issued new recommendations proposing that “proposing that aggressive intervention to lower cholesterol levels as early as childhood is the best approach available today to reducing the incidence of coronary heart disease.”

In a review article published in the August 5, 2008 issue of the American Heart Association journal Circulation, Steinberg and his colleagues stat that “with a large body of evidence proving that low cholesterol levels equate with low rates of heart disease, “…our long-term goal should be to alter our lifestyle accordingly, beginning in infancy or early childhood” and that “…instituting a low-saturated fat, low-cholesterol diet in infancy (7 months) is perfectly safe, without adverse effects…”

I don’t know whether to scream or cry when I read this stuff. Or both. Why? Because Dr. Steinberg’s dietary recommendations - if embraced by parents - are sure to increase the risk of heart disease and cause developmental problems in the children unfortunate enough to adopt them.

Let’s take a closer look at each part of the article on ScienceDaily.com describing the new recommendations and see if Steinberg’s claims make any sense.

Progress in treating heart disease? What progress? Heart disease is the #1 cause of death in the U.S. today. In the early part of the 20th Century, heart disease was relatively unknown. I would hardly call that progress.

As for statins, please refer to my previous article “The Truth About Statin Drugs” for a more accurate appraisal of the effectiveness (or lack thereof) of statins. In short, statins don’t reduce the risk of death in 95% of the population, including healthy men with no pre-existing heart disease, women of any age and the elderly. While statin drugs do reduce mortality for young and middle-aged males with pre-existing heart disease, the benefit is small and not without significant adverse effects, risks and costs.

For example, in the six largest studies done on statins and mortality to date, the absolute risk reduction ranged from -0.3% to 3.3%. In two of those studies, statins actually increased the risk of death. In an analysis of this data, the UK Medical Research Council determined that even if you were in the 5% of the population that statins benefit, you’d have to take a statin for 30 years at a cost of $42,000 just to add nine months (best case) to your life.

Even that scenario is entirely hypothetical, because statins cause cancer in lab animals. Although this hasn’t been shown in humans to date, the window between exposure to a carcinogen and development of cancer can be as long as 25 years for humans. Since no one has been on statins for that long, there is still reason to believe that they might have the same effect in humans that they do on animals.

Progress? I don’t think so.

“Bad cholesterol”? That’s so 1975. It is well accepted even within the mainstream scientific community today that normal LDL cholesterol (so-called “bad cholesterol”) is not a risk factor for heart disease. Instead, it is the oxidation of the polyunsaturated fatty acid in the membrane of the LDL particle (when the level of antioxidants in the diet is insufficient to protect them) that contributes to heart disease.

Therefore, the only LDL cholesterol that could be called “bad” is oxidized LDL.
And what promotes oxidation of the LDL particle? Eating polyunsaturated fat (found in vegetable oils, nuts and seeds and in almost all processed food). Of course, these are exactly the fats the American Heart Association has promoted as “heart-healthy” for decades.

In addition to promoting oxidation of LDL particles, polyunsaturated fats contribute directly to atherosclerosis and heart attacks. 75% of arterial plaque is made up of unsaturated fat, of which 50% is polyunsaturated (only 25% is saturated). The greater the concentration of polyunsaturated fat in the plaque, the more likely it is to rupture. Such ruptures, and the ensuing blood clots that form, are a primary cause of heart attacks.

Another well-established cause of heart disease is inflammation. Omega-6 polyunsaturated fats, which constitute a large percentage of caloric intake for most Americans, are known to promote inflammation. Indeed, excess linoleic acid (LA) in the diet from vegetable oil has been shown to contribute directly to heart disease.

So, the notion that saturated fat “clogs arteries” and causes heart attacks is totally false. It is actually polyunsaturated fat - the so-called “heart-healthy fat - which has those effects.

If people’s lives weren’t at stake the irony of such a situation might be almost funny. As it stands it’s one of the great public health tragedies of modern times.

And what about the notion that eating cholesterol raises cholesterol levels in the blood? It turns out to be false - and Steinberg even admits as much in his own book. There are two parts of the hypothesis that cholesterol causes heart disease. The first part, called the “diet-heart hypothesis”, is that eating cholesterol in the diet raises cholesterol levels in the blood. The second part, called the “lipid hypothesis”, holds that high cholesterol levels in the blood cause heart disease.

We’ve already addressed the “lipid hypothesis” above. As for the “diet-heart hypothesis”, Steinberg clearly states in his book that there is little evidence to support it. Tightly controlled egg-feeding studies have shown that eating cholesterol only raises cholesterol levels in about 30% of the population (”hyper-responders”).

However, these same studies showed that egg consumption led to an increase in “light, fluffy LDL” that was actually protective against heart disease. Why? Because these large, buoyant LDL particles are protected against oxidation.

Finally, what about saturated fat? Does it cause heart disease as Steinberg suggests? Once again, the evidence squarely contradicts Dr. Steinberg’s claim. In 22 of 26 published studies there was no significant relationship between saturated fat intake and either coronary or all-cause mortality. Among the studies that Dr. Steinberg failed to mention in his book or in his recent recommendation:

• Rose, et al. (1965): Replacing animal fat with corn oil for two years lowered serum cholesterol by 23 mg/dL but quadrupled cardiac and total mortality.
• Sydney Diet-Heart Study (1978): Replacing animal fat with vegetable fat for five years lowered cholesterol by five percent but increased total mortality by 50 percent.

What’s more, in the few studies where saturated fat restriction did reduce deaths from heart disease, deaths from cancer, brain hemorrhage, suicide & violent death went up! In his book The Great Cholesterol Con, Anthony Colpo concludes:

There are two more claims made by Dr. Steinberg that I need to address.

As stated above, there is absolutely no evidence that lowering LDL protects against heart disease. More than 40 trials have been performed to see if cholesterol lowering can prevent heat attacks. When all the results were pooled together, just as many died in the treatment groups as the control groups.

But what is most disturbing to me about Steinberg’s statement is the idea that lowering LDL to such unnatural levels is a “safe and potentially life-saving standard”. Cholesterol is a vital substance in our bodies. 50% of all cell membranes are made up of cholesterol; it is a precursor to sex hormones which govern fertility, reproduction and sexual development; it is an antioxidant that helps prevent free radical damage; and it is needed particularly by infants and children to ensure proper development of the brain and nervous system.

In fact, evidence in adults shows that low cholesterol levels can be dangerous and even life-threatening:

• Low cholesterol is associated with increased total mortality in elderly people.
• Framingham (1987): “There is a direct association between falling cholesterol levels over the first 14 years and mortality over the following 18 years.” In other words, as cholesterol fell death rates went up.
• Honolulu Heart Program (2001): “long-term persistence of low cholesterol concentration actually increases the risk of death. Thus, the earlier the patients start to have lower cholesterol concentrations, the greater the risk of death.”
• J-LIT (2002): The highest death rate was observed among those with lowest cholesterol (under 160mg/dl); the lowest death rate was observed with those whose cholesterol was between 200-259mg/dl.

Low cholesterol has also been associated with increased rates of cancer, depression, violent and aggressive behavior, and suicide.

With that in mind, how could anyone possibly claim that reducing cholesterol to extremely low levels in children is “safe”?

I’m not even sure where to start with this one, except to recommend that people like Dr. Steinberg be prosecuted for making such unfounded, irresponsible and dangerous recommendations.

According to the American Academy of Pediatrics:

Which is to say there is no evidence suggesting that cholesterol levels in kids are a risk factor for adult heart disease.

Furthermore, as we have already discussed, cholesterol is absolutely essential for brain development. Lowering brain levels of cholesterol in children, whose brains are still developing at a rapid rate, could have dire consequences.

Surely Dr. Steinberg must be aware of this? There is nothing controversial about the role of cholesterol in brain development. You can find this information in any physiology or biochemistry textbook. So why - especially in light of the lack of evidence linking cholesterol to heart disease in kids - is he suggesting that we give statins to children?

I really have no idea. In all likelihood Dr. Steinberg means well and believes he’s acting in the interest of our children. But I cannot understand how a respected medical doctor and researcher could overlook such an elementary and important fact and ignore the weight of scientific evidence.

We’ve all heard the saying “when all you’ve got is a hammer, everything looks like a nail.” When someone like Dr. Steinberg has invested so much of their life and energy into the theory that cholesterol causes heart disease, I guess it’s hard to let it go.

Popularity: 7%

A study recently published in Human Reproduction demonstrated that intake of soy foods significantly reduces sperm counts in men.

The study is especially significant because it is the largest study in humans to examine the relationship between semen quality and phytoestrogens (plant compounds that can mimic the physiological effects of the endogenous hormone, estrogen).

Dr. Jorge Chavarro of the Harvard School of Public Health and his colleagues found that men who ate the most soy food had 41 million sperm per milliliter less than men who did not consume soy products. The normal sperm concentrations for men ranges between 80 and 120 million/ml.

The association between soy food intake and sperm concentrations was even stronger in men who were overweight or obese, and 72% of study participants were. They also found the relationship between soy foods and sperm concentration was strongest in men with “normal or high” sperm counts.

Animal studies have linked the high consumption of isoflavones with infertility, but until now there has been little evidence of this effect in humans. Isoflavones are plant compounds with estrogen like effects and are found mainly in soybeans and soy-derived products.

What is particularly revealing is that the men in the highest intake group (who had the largest sperm count reduction) had a mean soy food intake of only half a serving per day. This is equivalent to having one cup of soy milk or one serving of tofu, tempeh or soy burgers every other day!

I don’t know about you, but I happen to know quite a few people who consume a lot more soy than than that on a regular basis. Sadly, many of them are children whose parents innocently believe that soy products are “healthy”. This is not their fault, of course; this erroneous and dangerous message has been aggressively promoted in the mainstream media for decades.

If the effect of such moderate servings of soy on adult males is so significant, what effect might soy foods have on developing boys who have not yet reached sexual maturity?

“Early puberty (caused by consuming soy products) may increase a boy’s chances of developing testicular cancer later in life, because it means longer exposure to sex hormones,” said University of North Carolina researcher Marcia Herman-Giddens. Congenital abnormalities of male genital tracts are also increasing. Recent studies found a higher incidence of birth defects in male offspring of vegetarian, soy-consuming mothers.

What about babies? Preliminary studies indicate that children given soy formula go through puberty much earlier than children who were not fed soy products. A 1994 study done in New Zealand revealed that, depending on age, potency of the product, and feeding methods, infants on soy formula might be consuming the equivalent of up to 10 contraceptive pills a day. By exposing your baby to such large amounts of hormonal-like substance, you are risking permanent endocrine system damage (pituitary gland, pineal gland, hypothalamus, thyroid, thymus gland, pancreas, ovary, testis, adrenal glands).

Dr Chavarro speculates that the increased estrogenic activity caused by consumption of soy foods may have an adverse effect on the production of sperm by interfering with other hormonal signals. This effect could be strengthened further in overweight and obese men because men with high levels of body fat produce more oestrogen than slimmer men, leading to high overall levels of oestrogen in the body and reproductive organs.

If you’re wondering how soy continues to be so widely accepted and aggressively promoted as a “health food” in spite of the overwhelming evidence to the contrary, I recommend reading The Whole Soy Story by Kaayla Daniel, PhD, CCN. You can read introduction to this eye-opening book here.

The history of soy products and their designation as a “health food” is particularly revealing, as Daniel points out:

Soy is one of the “Big Four” cash crops in the U.S. and the funds for its marketing are enormous:

And of course, these advertising dollars are largely responsible for creating the erroneous notion that highly processed soy foods are “healthy”:

However, in spite of advertising and popular belief, processed soy products are not health foods. Because of their estrogenic effects, they act more like drugs in the body than foods. And as we all know, drugs can be extremely dangerous when taken irresponsibly and without indication. Millions of men, women and children around the world are “drugging” themselves daily with soy products, and the tragic irony is that this is done in the name of “health”.

Keep in mind that tofu, tempeh and soy milk are not the only sources of soy. In fact, almost all processed food has soy in it, in the form of soy oil, soy lecithin, soy flour or soy protein. Everything from your favorite corn chips to hamburger buns to mayonnaise is likely to contain a substantial amount of soy.

The most sensible approach, then, is to eliminate processed soy products from your diet and dramatically reduce or eliminate your consumption of processed food (of course there are many other reasons to do this - soy is just one).

A small amount of miso or natto or other fermented soy product as a condiment every now and then is probably not harmful. But those are not the soy products Americans tend to eat.

For more information about the dangers of soy products, please see my recent article called The Soy Ploy.

Popularity: 9%

Today’s article is the sixth in an ongoing series on antidepressants and depression. It’s long, so you might want to print it out or go grab a cup of tea. If you are visiting the blog for the first time, or you haven’t had a chance to read the previous articles, you might find it helpful to do so before diving into this one.

The treatment of depression with drugs is based on the enormous collective delusion that psychiatric drugs act by correcting a chemical imbalance in the brain. As a result, a large percentage of the population has been convinced to take drugs in order to deal with the problems of daily life. Everything from break-ups to job difficulties to worries about the future have been transformed into “chemical problems”.

The myth that depression is caused by a chemical imbalance has permeated public consciousness, changing the way we view our lives and ourselves. We have become, in the words of sociologist Nicholas Rose, a society of “neurochemical selves”, recoding our moods and ills in terms of the supposed functioning of our brain chemicals and acting on ourselves in light of this belief.

This is reflected in the growing market for non-prescription products claiming to “enhance serotonin levels” in health food shops and on the Internet, and the cascade of claims that everything from chocolate to exercise makes you feel good because it “balances brain chemicals”. It also largely explains the 1300% growth between 1990 and 2000 in prescriptions of selective serotonin reuptake inhibitors (SSRIs), the most popular class of antidepressant drugs.

Yet, as I have explained in a previous article, there is no evidence to support the notion that depression is associated with an abnormality or imbalance of serotonin (or any other brain chemical), or that antidepressants work by reversing such a problem. Moreover, recent meta-analyses (Kirsh et al. 2008; Kirsh et al. 2004) suggest that antidepressants have only a small advantage over placebo, and that this advantage is most likely clinically meaningless. It has never been demonstrated that antidepressants act in a specific, disease-centered manner, nor have antidepressants ben shown to be superior to other drugs with psychoactive properties (Moncrieff & Cohen, 2006).

In spite of the complete lack of evidence supporting their use, one still often hears the familiar refrain “yes, but drugs are necessary in some cases!” This statement may in fact be true, but not because drugs have been demonstrated to be effective for certain types of depression or with certain patients. Instead, drugs may be necessary in a society where traditional social support structures which play a therapeutic role have completely broken down.

Studies have shown that most individuals with a healthy social support network are able to easily handle major stressors in life. When that network is underdeveloped or non-existent, it is far more likely that depression will occur (Wade & Kendler, 2000).

It has been observed, for example, that schizophrenia and other mental disorders occur less frequently and have a much more favorable prognosis in so-called “Third World” countries than in the West (Sartorious et al 1986). The influence of culture has been mentioned as an important determinant of differences in both the course and outcome of mental illness.

In developing countries strong connections between family members, kin groups and the local community are more likely to be intact. In addition, cultural, religious and spiritual beliefs in these societies provide a context in which symptoms of depression and other mental illness can be understood outside of the label of medical disease or pathology. Possession and rites of passage are two examples of such contexts.

In the West, however, these traditional support structures have been replaced by new cultural norms that do not offer support or therapeutic value to people experiencing mental distress. Among the socio-cultural factors identified by researchers as having a negative influence in Western societies are: extreme nuclearization of the family and therefore lack of support for mentally ill members of the kin group; covert rejection and social isolation of the mentally ill in spite of public assertions to the contrary; immediate sick role typing and general expectation of a chronic mental illness if a person shows an acute psychotic reaction; and the assumption that a person is insane if beliefs or behavior appear somewhat strange or “irrational”.

Therefore, in the West depression is far more likely to occur because of the breakdown of strong family and community support structures, the stigmatization of mental illness, the belief (perpetuated by drug companies) that all mental illness is “chronic”, and the lack of any cultural, religious or spiritual support for people who do not share the consensus view of reality. Statistics measuring the prevalence of depression around the world bear this out. According to the World Health Organization, if current trends continue, by the year 2020 depression will be the leading cause of disability in the West.

In contrast, in developing countries that have not yet fully adopted Western culture transient (i.e. temporary) psychotic reactions and brief depressive episodes are more common than chronic mental illness. When an individual begins to experience distress, the surrounding family and community respond with sympathy, support and traditional therapeutic resources. Surrounded by a rich support structure, the individual is able to return relatively quickly to healthy mental functioning - without drugs.

The cultural differences in the incidence of and response to mental illness suggests something that may be entirely obvious to you but has been largely forgotten in contemporary discussions about depression: that it cannot be properly defined or understood without considering the social context in which it occurs.

In other words, depression is both an individual and a social disease.

Unsurprisingly, epidemiological evidence has tied depression to poor housing, poverty, unemployment and precarious or stressful working conditions. Imagine, for example, a single parent working two low-paying jobs trying to support her child with no family or close friends nearby to help and little time to spend with them even if they were present. Or consider a child that spends most of his days in a school that doesn’t value his style of learning, eats a steady diet of sugar and processed food and lives with an alcoholic parent who is verbally and perhaps physically abusive. It makes perfect sense that both of these individuals could frequently feel sad, hopeless and even desperate. But are these individuals “depressed”?

Even if we agree that the intense feelings they are experiencing could be labeled as “depression”, perhaps a more relevant question might be this: is depression always a pathology? Or is it possible that much of what we call depression is simply a natural and entirely human response to certain circumstances in life?

This is exactly what Allan Horwitz and Jerome Wakefield argue in their book “The Loss of Sadness: How Psychiatry Transformed Normal Sorrow into Depressive Disorder“. The authors point out that the current epidemic of depression has been made possible by a change in the psychiatric definition of depression that allows the classification of normal sadness as a disease, even when it is not.

Horwitz and Wakefield define normal sadness as having three components: it is context-specific; it is of roughly proportionate intensity to the provoking loss/stimulus; and it tends to end roughly when the loss or situation ends, or else it gradually ceases as coping mechanisms adjust individuals to new circumstances.

The hypothetical examples I gave above of the single parent and the child living in an abusive home environment undoubtedly meet Horwitz & Wakefield’s criteria for “normal sadness”. The feelings occur in a specific context and are roughly proportionate to the circumstances. And though we can’t know this for sure since our example is hypothetical, one might assume that if the conditions of their lives were more favorable they may not feel so sad, hopeless and desperate. Nevertheless, in the West today both of these individuals would almost certainly be labeled as depressed and treated with psychoactive drugs.

While I appreciate the importance of Horwitz and Wakefield’s distinction between normal sadness and depression, I believe it is incomplete. In their framework, there must be some stimulus such as the death of a loved one, the loss of a job or the end of a relationship in order for someone to “escape” the depression label. Yet such events are not the only causes of discontent.

Regardless of economic status people in the West live in increasing isolation and alienation from each other, their communities and the natural world. Phone and email have replaced face-to-face interaction. The impersonality of big-box chain stores and strip mall outlets have replaced the intimacy and familiarity of the local corner store. The pace of life has become so fast that most people feel they are struggling just to get by. And even though we are far richer as a nation now, studies show that people today are not as happy as they were in the 1950s.

Sociologist Alain Ehrenberg has recently suggested that depression is a direct result of the new conceptions of individuality that have emerged in modern societies (Ehrenberg 2000). In societies that celebrate individual responsibility and personal initiative, the reciprocal of that norm of active self-fulfillment is depression - now largely defined as a pathology involving a lack of energy or an inability to perform the tasks required for work or relations with others. The continual incitements to action, to choice, to self-realisation and self-improvement act as a norm in relation to which individuals govern themselves, and against which differences are judged as pathologies.

Another way to speak of this change is as an increase in psychological stress. It is difficult to accurately compare stress levels today to those of the past, but sociologists like Juliet B. Schorr at Harvard University have observed that Americans (and likely people in all Western societies) are working longer hours, often with less pay, and have far less time for leisure. Since recent studies have identified a causal link between work stress and depression, one can safely make the assumption that the increase in work hours together with the decrease in leisure time could very well be contributing to the epidemic of depression.

Consider a middle-class individual living in an “exurban” housing tract 100 miles from their workplace. Each day they commute for two hours in each direction, fighting traffic all the way. Their job lacks any relevance or meaning to them and is simply done to make money and survive, without any joy or satisfaction. They have little control or agency at work and spend there day performing trivial tasks that do not challenge or engage them. They do not know their neighbors, they are disconnected from nature, and perhaps they have recently gone through a painful divorce.

If this person is experiencing apathy, sadness and a lack of enthusiasm for life, does that mean they are depressed? And even if we do label their condition as “depression”, can we truly understand or treat them successfully without addressing the circumstances (or root causes) of this person’s so-called depression?

There is little doubt that the people who seek treatment for depression are suffering. But should psychological and emotional suffering always be viewed as “something to get rid of”? Despite claims made by the companies who market antidepressant drugs, suffering cannot be pulled out of the brain like a splinter from the foot. Great religious and spiritual traditions from around the world view suffering as an avenue to greater understanding of oneself, life and God. Suffering can be viewed as a signal drawing our attention to issues in our life that need to be addressed.

If we simply use chemicals to diminish these signals and numb ourselves from their effects, we lose the opportunity to grow, evolve and heal. According to world-renowned psychiatrist David Healy, when strong feelings are suppressed by rejecting them or with drugs, people become “binded” to their own psychological or spiritual state. Psychiatric drugs blunt and confuse essential emotional signals and make it very difficult for people to know what they are really feeling. And because the pharmacological effects of drugs impair mental functioning, they can reinforce the patient’s sense of helplessness and dependence upon chemicals - even when those chemicals are preventing them from full recovery.

People who are depressed have lost touch with their hopes and dreams. Yet they wouldn’t be depressed if they did not still have a vision for a better life. If drugs are used to obliterate the feelings of discontent or suffering, the connection to that vision for a better life may be lost.

One might legitimately wonder, then, whether it is wise to attempt to treat such complex human and social problems with chemicals. Such a treatment strategy can only be useful if the goal is to perpetuate the status quo, to continue with “business as usual” at all costs, rather than addressing the psychosocial problems that are at the root of the discontent.

The message that drugs can cure our problems has profound consequences. Individual human beings with their unique life histories and personal characteristics have been reduced to biochemical entities and in this way the reality of human experience and suffering is denied (Moncrief 2008). People have come to view themselves as “victims of their own biology”, rather than as autonomous individuals with the power to make positive changes in their lives.

At another level such an exclusive focus on drug treatment allows governments and institutions to ignore the social and political reasons why so many people feel discontented with their lives. This is not surprising, of course. Both governments and corporations stand to benefit from maintaining the status quo and are often threatened by social change.

The “disease-centered” model of depression is presented as objective, unassailable fact, but it is instead an ideology (Moncrieff 2008). All forms of ideology convey a partial view of human experience and activities that is motivated by a particular interest; in this case, the interest of multinational pharmaceutical companies. The best selling drugs today are those that are taken indefinitely. This has fueled the drug companies’ efforts to label depression as a chronic, lifelong disease in spite of epidemiological studies which indicate that, even when untreated, depressive episodes tend to last no longer than nine months.

In her article called “Disease Mongering in Drug Promotion“, Barbara Mintzes describes the effort of pharmaceutical companies to “widen the boundaries of treatable illness in order to expand markets for those who sell and deliver treatments”. This phenomenon is known as “disease mongering”, and involves several tactics including the introduction of new, questionable diagnoses; the promotion of drugs as the first line of defense for problems not previously considered medical; the expansion of current definitions of mental illness; and the inflation of disease prevalence rates.

In a blatant example of the last strategy, pharmaceutical companies have estimated in their promotional literature that up to one-third of people worldwide have a mental illness. This ridiculous (and in my opinion, transparent) claim is not supported anywhere in the scientific literature. Peer-reviewed studies put the figure at significantly less than 5%.

It should be obvious that drug companies would be the first to benefit from such grossly overstated estimates of the prevalence of depression. In fact, executives in the pharmaceutical industry have even admitted as much. Thirty years ago Henry Madsen, the CEO of Merck, made some very candid comments as he approached his retirement. Suggesting he’d rather Merck to be more like chewing gum maker Wrigley’s, Gadsen said that it had “long been his dream to make drugs for healthy people.”

Sadly, Madsen’s dream has been realized with the advent of not only antidepressants, but also statins, antacids and other drugs sold to essentially healthy people. These medications are now the top-selling drugs around the world. (Madsen’s sense of morality may have been skewed, but he certainly was a visionary businessman.)

The field of psychiatry has largely collaborated with the pharmaceutical industry in defining intense and painful emotions as “disorders”. Diagnoses like “panic disorder” and “clinical depression” give a medical aura to powerful emotions and make them seem dangerous, pathological, unnatural or out of control. In an astute observation of this state of affairs, psychiatrist Steven Sharfstein remarked in the March, 2006 issue of Psychiatric News that the biopsychosocial model of depression has been replaced by the “bio-bio-bio” model.

It has now become common practice for psychiatrists to prescribe drugs on their very first visit with a patient, and to tell that patient that they will likely need to take drugs for the rest of their lives. Such a prognosis is offered in spite of the fact that no attempt has been made whatsoever to try proven, non-drug treatment alternatives such as psychotherapy and exercise!

The increasing rates of depression and poor long-term treatment outcomes clearly indicate that the current drug-centered strategy is not effective. For real progress to be made the psychological, social, economic and political roots of depression must be addressed. This will require a coordinated effort on the part of patients, physicians, communities and politicians. It will not be easy, because we are fighting deeply entrenched beliefs about the “biochemical” nature of depression as well as a $500 billion dollar pharmaceutical industry that is not likely to willingly give up the $20 billion in sales represented by antidepressants.

There is no doubt that the systemic changes I am describing are far more difficult to implement than administering a drug. Nevertheless, we must begin if we hope to heal ourselves, our culture and our world.

In the final article of the series, I will present proven non-drug alternatives for treating depression. Stay tuned!

Recommended books

• Your Drug May Be Your Problem: How and Why to Stop Taking Psychiatric Medications, by Peter Breggin

Popularity: 10%

Statins for pregnant women?

Statin manufacturers, the sycophantic researchers they pay, and the shameless hucksters who sell them are always up to no good, but their recent attempts to market them to pregnant women are simply horrifying.

According to a recent news article published in Mail online, researchers from liverpool believe that taking statins during pregnancy might help women avoid caesarean sections by promoting more robust uterine contraction. They hope to begin human trials in three to five years.

Somehow, the author of this article failed to react with the shock and horror appropriate to the situation — which should be the same shock and horror with which we would react to the suggestion that pregnant women should take thalidomide to avoid morning sickness.

Back in 2004, a report in the New England Journal of Medicine showed that the use of statins in the first trimester of pregnancy was associated with birth defects, especially severe central nervous system defects and limb deformities. In fact, 20 out of 52 women exposed to statins gave birth to offspring with such defects, which represents a birth defect rate of 38 percent, nearly 20 times the background rate of birth defects!

Even before this report was published, researchers already knew that statins caused birth defects in animal experiments, and the FDA already required the drugs to carry a label warning pregnant women to stay away from them. The article linked to above stated the following:

“FDA took this action because it was recognized that fetal cholesterol synthesis was essential for development, and because animals given statins during pregnancy had offspring with a variety of birth defects,” [one of the study's authors] said.

Less than a year later, Merck and Johnson & Johnson jointly asked the FDA for permission to market an over-the-counter statin. One of the concerns about the proposal was the risk to pregnant women. USA Today reported:

The FDA classifies Mevacor and other statins as pregnancy category X, which means they are not supposed to be taken by pregnant women. Not only have category X drugs been linked to fetal abnormalities in animal or human studies, but the FDA also has declared that the benefits of taking them do not outweigh potential risks.

According to the same article, Merck made a disturbing admission:

“Of course, there will be women who take it off-label,” acknowledges Merck executive Edwin Hemwall, referring to the use of non-prescription Mevacor by women under 55.

And what could prompt women to use statins during pregnancy against recommendations? Certainly a news article declaring that statins might prevent the need for caesarean sections and their associated complications could prompt some women to do so.

So what ground-breaking research made these Liverpool researchers so confident that taking drugs associated with twenty times the normal rate of major birth defects during pregnancy might be a good idea that they put out a press release declaring this confidence to the public before any trials were even under way?

Well, according to the article:

Tests have already shown that raising levels of cholesterol interferes with womb tissue’s ability to contract.
Really. Raising levels of cholesterol. You might wonder how they accomplished that. Did they use cholesterol-raising drugs? I don’t know of any drugs that do that. Did they use egg yolks, or the dreaded dietary villain — gasp — saturated fats?

No, the story is quite different.

The apparent basis for this ridiculous statin cheerleading is a 2004 study published by researchers from the University of Liverpool in the American Journal of Physiology — Cell Physiology entitled “Increased cholesterol decreases uterine activity: functional effects of cholesterol alteration in pregnant rat myometrium.”

Rather than feeding anything to pregnant women or pregnant rats, the researchers took pregnant rats and killed them. So the first thing we can say is that statins might help you deliver a baby if your doctor kills you first.

Then they extracted the uterine tissue and either extracted cholesterol from it with a chemical solvent called methyl beta-cyclodextrin, or enriched it either with cholesterol mixed with this solvent or with LDL (which they didn’t measure for oxidation prior to use). Then they added drugs to induce contraction under either cholesterol-depleted or cholesterol-enriched conditions, and found that contraction was greater under cholesterol-depleted conditions.

So now we know that — wait, what is it we know?

Well, quite clearly, we don’t know anything that we can have any confidence has any physiological relevance at all. That is, except the fact that statins cause birth defects in animals, and they increase the rate of birth defects in humans by nearly twenty times, primarily by causing severe defects of the central nervous system and limb deformities.

To add to that, we also know that the vast majority of humans conceived with Smith-Lemli-Opitz Syndrome (SLOS), a genetic inability to synthesize enough cholesterol, die of spontaneous abortion in the first 16 weeks of gestation. Those who live long enough to be born suffer from mental retardation, autism, facial and skeletal malformations, visual dysfunctions and failure to thrive.

Statins for pregnant women? I don’t think so.

Article written by Chris Masterjohn

Statins for 8-year old children?

The American Academy of Pediatrics recently announced new recommendations for giving cholesterol-lowering drugs to children as young as eight years old. They also recommend giving low-fat milk to infants as young as one year old.

The New York Times published several articles on this, first announcing the recommendation the day the academy made it, then describing the backlash of saner doctors and other members of the public against it, and finally editorializing that while they were first “appalled” at the recommendation, after reading the report they were more dismayed at the state of our children’s health.

Concerning this frightful state of children’s health, the Times reported the following:

“We are in an epidemic,” said Dr. Jatinder Bhatia, a member of the academy’s nutrition committee who is a professor and chief of neonatology at the Medical College of Georgia in Augusta. “The risk of giving statins at a lower age is less than the benefit you’re going to get out of it.”

Dr. Bhatia said that although there was not “a whole lot” of data on pediatric use of cholesterol-lowering drugs, recent research showed that the drugs were generally safe for children.

An epidemic of what? High cholesterol? Not according to the academy’s report, which states that cholesterol levels in children declined between 1966 and 1994 and stayed the same between 1994 and 2000.

No, we are in an epidemic of obesity. As the Times reported:

But proponents say there is growing evidence that the first signs of heart disease show up in childhood, and with 30 percent of the nation’s children overweight or obese, many doctors fear that a rash of early heart attacks and diabetes is on the horizon as these children grow up.

Is there any evidence that statins lead to weight loss? If there is, I am not aware of it.

The point is immaterial, because the academy doesn’t claim to have any evidence for its position in the first place. For example, its report states the following:

Also, data supporting a particular level of childhood cholesterol that predicts risk of adult CVD do not exist, which makes the prospect of a firm evidence-based recommendation for cholesterol screening for children elusive.
And further down:

It is difficult to develop an evidence-based approach for the specific age at which pharmacologic treatment should be implemented. . . . It is not known whether there is an age at which development of the atherosclerotic process is accelerated.

In other words, they don’t know what level of cholesterol is risky and at what age it starts posing a risk, but they will nevertheless assume that there is some level that does start to pose a risk at some age and they will thus have to make a guess just what that level and what that age is.

The report discusses evidence that the “metabolic syndrome” and the “recent epidemic of childhood obesity” are tied to the risk of diabetes and heart disease and evidence that even modest weight loss at a level of five to seven percent is sufficient to prevent diabetes. Yet somehow instead of making a recommendation about how to more effectively lose weight the authors derive from this data a much less logical but much more profitable conclusion that 8-year-olds should be put on statins.

As to the recommendation to feed infants low-fat milk, the Times reported the following:

The academy also now recommends giving children low-fat milk after 12 months if a doctor is concerned about future weight problems. Although children need fat for brain development, the group says that because children often consume so much fat, low-fat milk is now appropriate.

This is rather remarkable, because the academy attributed the drop in childhood cholesterol levels to the successes of the anti-fat, anti-cholesterol campaign that began in the 1950s. But now children no longer need milkfat because they are getting plenty of fat. Well which is it? Are they getting more fat now or less fat?

Of course milkfat is also a source of choline, along with liver and egg yolks, which is essential to brain development.

But even this misses the point. Cholesterol is essential to brain development!

One of the first articles I added to my section on the functions of cholesterol was an article entitled “Learning, Your Memory, and Cholesterol.” It discusses the evidence uncovered eight years ago that cholesterol is the limiting factor for the formation of synapses, which are the connections between neurons that allow learning and memory to take place.

Lowering brain levels of cholesterol can be detrimental at any age beacause of this, but the consequences for children — whose brains are still developing at a much more rapid rate — could be much more dire.

No doubt, most researchers and medical doctors mean well and are honestly trying to help our children. But surely someone in these drug companies must know that cholesterol is necessary for brain development, and that cholesterol-lowering drugs reduce mental performance in adults. Surely they must know that if we raise our next generation of children on statins during the critical periods of brain development, we may raise a whole generation with compromised intelligence.

And if that’s the case, are they trying to dumb us down? Sometimes it seems like that’s the case.

Article written by Chris Masterjohn

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A study was just published in the New England Journal of Medicine on July 17th comparing the effectiveness and safety of three different weight loss diets. 322 moderately obese subjects were assigned to one of three diets: low-fat, restricted-calorie; Mediterranean, restricted-calorie; or low-carbohydrate, non-restricted calorie.

The rate of adherence to the study diet was 95% at year one and 85% at year two. Among the 272 participants who completed the intervention, the mean weight losses were 3.3 kg for the low-fat group, 4.6 kg for the Mediterranean-diet group, and 5.5 kg for the low-carbohydrate group.

Perhaps more significantly, the relative reduction in the ratio of total cholesterol to HDL was 20% in the low carbohydrate group while only 12% in the low-fat group. Among the 35 subjects with diabetes, changes in fasting plasma glucose and insulin levels were more favorable among those assigned to the Mediterranean diet than among those assigned to the low-fat diet.

Unfortunately, the bias against saturated fat and animal products that is still so prevalent in the mainstream (in spite of the lack of evidence to support it) prevailed in this study. The research team advised those following the low-carb diet to “choose vegetarian sources of fat and protein” and moderate their consumption of saturated fats and meat.

This suggests that the low-fat dieters may have consumed a substantial portion of their calories as fat in the form of omega-6 polyunsaturated fatty acids. Excess intake of omega-6 fatty acids contributes to a host of problems including heart disease, diabetes, and cancer; but even more relevant to this study and its results is the fact that omega-6 fatty acids can cause increased water retention. And as everyone knows, increased water retention equals increased weight.

This certainly causes me to wonder how much more dramatic the results of this study might have been if the low-carb subjects were encouraged to significantly restrict their consumption of omega-6 fats (w