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bicyclistThe 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”:

“Some investigators have argued that the relatively high relapse rate after drug treatment indicates that depression should be treated like a chronic medical disease requiring ongoing, long-term medical treatment indefinitely. This logic appears tautological: Drug treatment results in a higher relapse rate than cognitive-behavioral therapy; therefore, the patients should be maintained on drugs to prevent relapse.” (Antonuccio 1995)

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:

“This was an unexpected finding because it was assumed that combining exercise with medication would have, if anything, an additive effect.

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

“One of the positive psychological benefits of systematic exercise is the development of a sense of personal mastery and positive self-regard, which we believe is likely to play some role in the depression-reducing effects of exercise. It is conceivable that the concurrent use of medication may undermine this benefit by prioritizing an alternative, less self-confirming attribution for one’s improved condition. Instead of incorporating the belief “I was dedicated and worked hard with the exercise program; it wasn’t easy, but I beat this depression,” patients might incorporate the belief that “I took an antidepressant and got better”.

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.

vegetable oilEasy! 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.

According to Steinberg, progress has been made in the treatment of coronary heart disease in adults with cholesterol lowering drugs like statins. However, while studies show a 30% decrease in death and disability from heart disease in patients treated with statins, 70% of patients have cardiac events while on statin therapy.

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.

In fact, they propose that lowering low-density lipoproteins (the so-called “bad cholesterol”) to less than 50 mg./dl. even in children and young adults is a safe and potentially life-saving standard, through lifestyle (diet and exercise) changes if possible. Drug treatment may also be necessary in those at very high risk.

“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:

“If saturated fats caused even a portion of the damage for which they are frequently blamed, their negative effects should be readily and repeatedly demonstrable in controlled clinical trials. However, after excluding the results of the poorly designed and sloppily conducted northern European studies, it quickly becomes apparent that there does not exist a single tightly controlled trial which shows that saturated fat restriction can save even a single life.”

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

“lowering low-density lipoproteins to less than 50mg/dL even in children and young adults is a safe and potentially life-saving standard.”

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”?

“Drug treatment may also be necessary in those [children] at very high risk.

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:

“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.

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.”

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.

man on bench

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!

Please remember to always seek the guidance of a qualified psychiatrist when attempting to withdraw from psychoactive drugs. It is very dangerous to stop taking the drugs abruptly or to begin the withdrawal process without supervision. Psychiatrist Peter Breggin is considered to be one of the foremost experts in psychiatric drug withdrawal, and he has written a book (linked to below) for helping patients wean off of drugs. If you are considering stopping your medication, I recommend you read this book and discuss it with your doctor.

Recommended books

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

veggie basket In today’s article we’ll discuss how to prevent heart disease without drugs. If you haven’t already read Part 1 of this series, which examined the problems with statin drugs, and Part 2, which debunks the myth that cholesterol causes heart disease, you might want to do that before reading this article.

Last week I mentioned the INTERHEART study, which looked at the relationship between heart disease and lifestyle in 52 countries around the world. What this study revealed is that approximately 90% of heart disease could be prevented by simple changes to diet and lifestyle.

Let’s just make this crystal clear: 9 out of 10 cases of heart disease are completely preventable without drugs. With sales of statin drugs reaching close to $30 billion this year with Lipitor alone bringing in close to $14 billion, this might come as some surprise. But the pharmaceutical companies are, quite literally, invested in people taking their cholesterol-lowering drugs in spite of the complete lack of evidence that lowering cholesterol prevents heart disease.

In order to understand the changes we need to make to prevent heart disease, we have to briefly examine what causes it. By now you know that the answer is not “cholesterol”. In fact, as I mentioned briefly in last week’s article, the two primary contributing mechanisms to heart disease are inflammation and oxidative damage.

Inflammation is the body’s response to noxious substances. Those substances can be foreign, like bacteria, or found within our body, as in autoimmune diseases like rheumatoid arthritis. In the case of heart disease, inflammatory reactions within atherosclerotic plaques can induce clot formation.

When the lining of the artery is damaged, white blood cells flock to the site, resulting in inflammation. Inflammation not only further damages the artery walls, leaving them stiffer and more prone to plaque buildup, but it also makes any plaque that’s already there more fragile and more likely to burst.

Oxidative damage is a natural process of energy production and storage in the body. Oxidation produces free radicals, which are molecules missing an electron in their outer shell. Highly unstable and reactive, these molecules “attack” other molecules attempting to “steal” electrons from their outer shells in order to gain stability. Free radicals damage other cells and DNA, creating more free radicals in the process and a chain reaction of oxidative damage.

Normally oxidation is kept in check, but when oxidative stress is high or the body’s level of antioxidants is low, oxidative damage occurs. Oxidative damage is strongly correlated to heart disease. Studies have shown that oxidated LDL cholesterol is 8x greater stronger a risk factor for heart disease than normal LDL.

Since there may be some confusion on this point, I want to make it clear: normal LDL cholesterol is not a risk factor for heart disease in most populations, but oxidated LDL cholesterol is. This points to oxidation as the primary risk factor, not cholesterol. Why? Because when an LDL particle oxidizes, it is the polyunsaturated fat that oxidizes first. The saturated fat and the cholesterol, hidden deep within the core of the lipoprotein, are the least likely to oxidize.

It follows, then, that if we want to prevent heart disease we need to do everything we can to minimize inflammation and oxidative damage.

Top four causes of oxidative damage & inflammation

  1. Stress
  2. Smoking
  3. Poor nutrition
  4. Physical inactivity

By focusing on reducing or completely eliminating, when possible, the factors in our life that contribute to oxidative stress and inflammation, we can drastically lower our risk for heart disease. Let’s take a brief look at each risk factor.

Stress

In the INTERHEART study, stress tripled the risk of heart disease. This was true across all countries and cultured that were studies. The primary mechanism by which stress causes heart disease is by dysregulating the hypothalamic-pituitary-adrenal (HPA) axis. The HPA axis is directly intertwined with the autonomic nervous system, and it governs the “fight-or-flight” response we experience in reaction to a stressor.

Continued activation of this “fight-or-flight” response leads to hyper-arousal of the sympathetic nervous system, which in turn leads to chronically elevated levels of cortisol. And elevated levels of cortisol can cause both inflammation and oxidative damage.

Stress management, then, should be a vital part of any heart disease prevention program. In fact, some researchers today believe that stress may be the single most significant factor in the cause and prevention of heart disease. There are several proven methods of stress reduction, including mindfulness-based stress reduction (MBSR), acupuncture and biofeedback. It doesn’t matter which method you choose. It just matters that you do it, and do it regularly.

Smoking

I assume that you are already well aware of the dangers of smoking, so I won’t spend much time on this one. For the purposes of this discussion, I will point out that smoking as few as 1-4 cigarettes a day has been shown to increase the risk of heart disease by 40%. But smoking 40 cigarettes a day increases that risk by 900%.

So if you smoke and you’re concerned about heart disease – quit.

Nutrition

Over the past century we’ve seen a consistent decline in the consumption of traditional, nutrient-dense foods in favor of highly processed, nutrient-depleted products. The flawed hypothesis that cholesterol causes heart disease has wrongly identified health-promoting foods like meat, organ meats, eggs and dairy products as harmful, and replaced them with toxic, processed alternatives such as chips, white breads, pastries, crackers, cookies, frozen foods, candy and soda.

There are two ways that nutrition contributes to heart disease: too much of the wrong foods, and not enough of the right ones.

The average American gets 57% of his/her calories from highly refined cereal grains and polyunsaturated (PUFA) oils. The #3 source of calories, behind grains and PUFA, is sugar and high-fructose corn syrup. Refined grains, polyunsaturated oils and sugar are all major contributors to both inflammation and oxidative damage.

Not only do refined carbohydrates, vegetable oils and sugar contribute to inflammation and oxidative damage, they are also completely devoid of micronutrients that would protect us from these processes. Meats, fruits and vegetables are all high in antioxidants that prevent oxidative damage, and rich in other micronutrients that play important roles in preventing heart disease.

More than 85% of Americans are not getting the federally recommended five servings of fresh fruit and vegetables each day. The intake of dark leafy green or yellow/orange veggies for the average American is equivalent to 18g – one-half of one small carrot. Iceberg lettuce, tomatoes, french fries, orange juice and bananas constitute 30% of fruit and vegetable intake for most Americans.

Many people know that the “Standard American Diet” is extremely unhealthy. But what most do not know is that the so-called “heart-healthy” diet that has been vigorously promoted for decades actually contributes to heart disease! The “heart-healthy” diet is high in refined carbohydrates and polyunsaturated oils, which, as we have seen, cause inflammation and oxidative damage.

On the other hand, saturated fats (which have been demonized by the medical mainstream) such as butter, coconut oil, lard, tallow and ghee are protected against oxidation and possess many other important health benefits. These fats are the ones we need to be eating to protect ourselves from heart disease.

It is extremely important to buy organic meat, eggs and dairy products that come from animals that have been raised on fresh pasture rather than in commercial, factory feedlots. See this article and this one for more information on why this is so essential.

Finally, it must be pointed out that not all “organic” products are healthy. Most packaged food (including organic cereals, crackers, chips and so-called “nutrition bars”) are full of highly refined carbohydrates, sugar, and vegetable oils. And by now, I don’t need to tell you what that means!

So what would a truly heart healthy diet look like, then? Download my Guidelines for Natural Prevention of Heart Disease to find out.

Physical Inactivity

Physical inactivity is likely a major causative factor in the explosive rise of coronary heart disease in the 20th century. During the vast majority of evolutionary history, humans have had to exert themselves to obtain food and water. Even at the turn of the 20th century in the U.S., a majority of people had jobs that required physical activity (farmers, laborers, etc.) Now the majority of the workforce has sedentary occupations with little to no physical activity at all.

Currently more than 60% of American adults are not regularly active, and 25% of the adult population is completely sedentary. People that are physically inactive have between 1.5x and 2.4x the risk of developing heart disease.

On the other hand, regular exercise reduces both inflammation and oxidative damage. Even relatively low levels of activity are protective – as long as they are consistent. A public review at Harvard University showed that 30-minutes of moderate physical activity on most days of the week decreases deaths from heart disease by 20-30%.

The best strategy for people struggling to find time to exercise is to make it part of their daily life (i.e. riding a bike or walking to work, choosing the stairs over the escalator or elevator, etc.)

When combined, the four strategies listed above will significantly reduce your chances of getting heart disease – without taking a single pill of any kind.

If you already have heart disease, or you are at high risk for heart disease (overweight, high blood pressure, diabetic, etc.), then you may need additional support. See my

Recommended articles

 

In last week’s article about the ineffectiveness of statin drugs in reducing mortality in most populations I promised I would follow-up with an article on drug-free prevention of heart disease. I will do that this week, but it occurred to me that the first article in this series should have been one that dispels the myth that cholesterol causes heart disease. Understanding that is the key to the prevention strategies that will follow in the next article. So without further ado…

butterYou are all no doubt acquainted with the popular hypothesis on cholesterol and heart disease. It has two parts: first, that eating cholesterol in the diet raises cholesterol levels in the blood; and two, that high cholesterol levels in the blood cause heart disease.

You might be surprised to learn that neither of these statements is true. The first one is relatively easy to dispatch. In the Framingham Heart Study, which is the longest-running and perhaps most significant study on heart disease done to date, it was demonstrated that intake of cholesterol in the diet had absolutely no correlation with heart disease. If you look at the graph below, you’ll see that both men and women with above average intake of cholesterol had nearly identical rates of heart disease as men and women with below average intake of cholesterol.

framingham

In fact, the “diet-heart hypothesis”, which is the scientific name for the idea that eating cholesterol causes heart disease, has even been discounted by the researchers who were responsible for its genesis. Ancel Keys, who in many ways can be considered the “father” of the cholesterol-heart disease hypothesis, had this to say in 1997:

“There’s no connection whatsoever between the cholesterol in food and cholesterol in the blood. And we’ve known that all along. Cholesterol in the diet doesn’t matter at all unless you happen to be a chicken or a rabbit.”

This is a reference to early studies performed on chickens and rabbits where they force-fed these animals high-levels of cholesterol. Since rabbits and chickens are mostly vegetarian, their physiology is not adapted for processing such large amounts of dietary cholesterol, so it’s no surprise they developed atherosclerosis. The mistake was assuming that the results of this experiment could be extrapolated to humans, who are omnivores with significant differences in physiology.

The second tenet of the cholesterol-heart disease hypothesis, the notion that high cholesterol levels in the blood cause heart disease, is referred to as the “lipid hypothesis” in the scientific community. Though it still accepted as gospel truth by the general public and many medical professionals, most researchers now believe the primary causes of heart disease are inflammation and oxidative stress. Unfortunately, the rest of us haven’t gotten the memo, so to speak, that cholesterol isn’t the cause of heart disease.

It would take several articles to explain this in complete detail, but I’d like to give at least a brief summary here.

If cholesterol caused heart disease, it should be a risk factor in 1) all ages, 2) both sexes and 3) all populations around the world (barring any protective factor, of course). Also, if cholesterol caused heart disease we would expect that lowering cholesterol would reduce heart disease. But none of these assumptions turn out to be true.

The rate of heart disease in 65-year old men is ten times that of 45-year old men. Yet a recent study in the Journal of American Medical Association indicated that high LDL cholesterol is not a risk factor for from coronary heart disease (CHD) mortality or total mortality (death from any cause). It is extremely unlikely that a risk factor for a disease would stop being a risk factor at a time when that disease kills the greatest number of people. That is akin to suggesting that smoking causes lung cancer in young men, but somehow stops doing so in older men!

Another consistent thorn in the side of supporters of the “lipid hypothesis” is that women suffer 300% less heart disease than men, in spite of having higher average cholesterol levels. At the recent Conference on Low Blood Cholesterol, which reviewed 11 major studies including 125,000 women, it was determined that there was absolutely no relationship between total cholesterol levels and mortality from cardiovascular or any other causes.

Nor is cholesterol a risk factor in all populations around the world. In fact, some of the populations with the highest levels of blood cholesterol have among the lowest rates of heart disease, and vice versa. Dr. Malcom Kendrick, a well-known skeptic of the lipid-hypothesis, explains this very well in the video below:

Finally, more than 40 trials have been performed to determine whether lowering cholesterol levels can prevent heart disease. In some trials heart disease rates went down, in others they went up. But when the results of all of the trials were taken together, just as many people died in the treatment groups (who had their cholesterol levels lowered by drugs) as in the control groups (who had no treatment).

If you’re still skeptical after reading all of this, perhaps William Castelli, the director of the famed Framingham Heart Study mentioned above can convince you:

“Serum cholesterol is not a strong risk factor for CHD, in the sense that blood pressure is a strong risk factor for stroke or cigarette smoking is a risk factor for lung cancer.”

Or how about Frederick Stare, a long-time American Heart Association member and (former) proponent of the lipid hypothesis:

“The cholesterol factor is of minor importance as a risk factor in CVD. Of far more importance are smoking, hypertension, obesity, diabetes, insufficient physical activity, and stress.”

So there you have it. Contrary to popular belief, cholesterol is not a dangerous poison that causes heart disease. Rather, it is an essential nutrient present in the cell membranes of all tissues of all mammals, and has some very important functions in the body. In fact, in many studies low cholesterol has been associated with an increase in total mortality!

Again, the Framingham Study which followed 15,000 participants over three generations:

“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.

The Honolulu Heart Program study, with 8,000 participants, published in 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.”

And finally, the huge Japanese Lipid Intervention Trial with over 47,000 participants:

“The highest death rate observed was among those with lowest cholesterol (under 160mg/dl); lowest death rate observed was with those whose cholesterol was between 200-259mg/dl”

In other words, those with the lowest cholesterol had the highest death rate, and those with cholesterol levels that would today be called “dangerous” had the lowest death rate.

As you can see, not only does high cholesterol not cause heart disease, low cholesterol can actually be dangerous to your health. So toss out your vegetable oil and start eating butter and eggs again! But more on that next week…

Recommended links

kids shoes
The Healthy Skeptic reader Jessica wrote in with this topic suggestion:

“I like the “what to feed children” idea. But it has to be food they will actually EAT.”

The question of how to nourish our children so they develop into healthy adults is one of the most important questions we can ask. Tragically, the answers that the medical mainstream has come up with have contributed to unprecedented epidemics of childhood disease and endangered the health and well-being of our children.

The numbers of overweight and obese children worldwide are expected to climb dramatically by 2010, according to a study by Youfa Wang, PhD, MD at the Johns Hopkins Bloomberg School of Public Health. By the end of the decade, 46 percent of children in North and South America are projected to be overweight and 15 percent will be obese. It’s been assumed that U.S. life expectancy would rise indefinitely, but a new data analysis which was published as a special report in the March 17, 2005 issue of New England Journal of Medicine suggests that this trend is about to reverse itself – due to the rapid rise in obesity, especially among children.

Increasing numbers of children are being treated for depression, according to a 2004 study in the British Journal of Medicine. A 1999 report in California from the state’s Department of Developmental Services found that autism had increased by 273 percent from 1987 to 1998. Current estimates for the incidence of autism are as high as 1 in 120. A national review by The Advocacy Institute in 2002 revealed that learning disabilities in children increased by 30 percent from 1990 to 2000.

These studies show that our children are more obese, more depressed, and have more learning disabilities and behavioral problems than ever before. What could be the cause of such a dramatic change?

Although each of these diseases is complex and multifactorial, it is safe to say that diet and nutrition play a significant role in all of them. For example, consider the key nutrients for brain development in children:

Key nutrients for brain development

  • Vitamin A
  • Vitamin D
  • Choline
  • DHA
  • Zinc
  • Tryptophan
  • Cholesterol

Many parents probably know that these nutrients aren’t found in the refined carbohydrates, vegetable oils and sugars which form the bedrock of the standard American diet. Yet many parents may be unaware that even foods widely assumed to be nutritional – including packaged foods commonly described as “organic”, “natural” or “fortified” – are themselves highly processed and stripped of nutritional value, and little better than their “non-organic” alternatives.

So what should we be feeding our children to ensure healthy growth and development? The following “First Steps” recommended by children’s health advocacy group Nourishing Our Children will get you started:

First steps to healthier children

  1. Replace sugar with natural sweeteners like honey and rapadura.
  2. Replace fruit juices with whole, raw milk.
  3. Replace breakfast cereals with non-nitrate bacon, eggs from hens on pasture, whole milk yogurt, homemade kefir, soaked oatmeal or soaked, wholegrain pancakes.
  4. Replace pasteurized dairy products with raw and cultured dairy.
  5. Eliminate all processed soy foods from your household (this includes soy milk, “protein bars” with soy, baked tofu products and all “soy fast food”).
  6. Replace polyunsaturated vegetable oils and trans fats with traditional fats such as butter, olive oil, coconut oil, palm oil, lard, and tallow.
  7. Replace processed, convenience foods (boxed, packaged, prepared and canned food items) with fresh, organic, whole foods
  8. Provide a daily dose of high vitamin cod liver oil (with no synthetic vitamins added)

In contrast to the bland, unsatisfying (and dangerous) low-fat diet recommended by medical authorities, kids naturally love the foods in a nutrient-dense, whole foods diet. However, it is true that if they’ve been on a diet high in sugar and refined carbohydrates for a long time, there will be an adjustment period as they transition away from those highly processed foods.

My suggestion is to take one item on the list above at a time, and be gentle with yourself. It may take a while longer that way to get to where you want to be, but it’s worth the effort! Some of the changes will be more difficult than others. For example, most children (and adults) prefer the taste of saturated fats like butter, cream and whole-fat dairy to low-fat alternatives such as vegetable oil and skim milk – but may not yet have acquired a taste for cod liver oil!

I’ve provided links to some articles below with some helpful ideas on how to encourage even the most finicky eaters to enjoy nutrient-dense foods and some ideas for quick and healthy brown-bag lunch suggestions for parents.

Recommended links

  • Articles on children’s health – Weston A. Price Foundation
  • Feeding Our Children, by Thomas Cowan, M.D.
  • Taking the Icky out of Picky Eaters
  • Foods to Tantalize Toddlers and Preschoolers
  • Packing the Perfect Lunch Box
  • Nourishing Our Children – children’s health advocacy group

Most health-conscious folks have heard of essential fatty acids (EFAs) by now. It isn’t unusual for a health food store to sell several different brands of fish oils, flax oil and other blends of “essential fatty acids”. We’ve been told that consuming these oils will keep us healthy and protect us from disease.

Today’s nutrition textbooks refer to omega-6 (linoleic) acid and omega-3 (alpha-linolenic) acid as essential components of the human diet, and cite the requirement as something between one and four percent of total caloric intake. When scientists say a nutrient is “essential”, they mean it cannot be synthesized within our bodies from other components by any known mechanism – and therefore must be obtained from the diet.

But are “essential fatty acids” truly essential?

Chris Masterjohn, a PhD candidate in Nutritional Science at the University of Connecticut, has just published a paper which directly challenges the belief that omega-6 linoleic acid and omega-3 alpha-linolenic acid are essential.

His review of the scientific research suggests that omega-6 arachidonic acid (AA) and the omega-3 docosahexaenoic acid (DHA) are the only fatty acids that are truly essential – and thus necessary in the diet – for humans. Further, the true requirement for EFA during growth and development (during childhood, pregnancy or recovery from injury and illness) is less than one-half of one percent of calories when supplied by most animal fats, and even less (0.12 percent) when supplied by liver. In healthy adults, the requirement is “infinitesimal if it exists at all.”

So why is this a concern? Excess consumption of linoleate (omega-6 fatty acid) from vegetable oil will interfere with the production of DHA , while an excess of EPA from fish oil will interfere with the production and utilization of AA. So, by consuming an abundance of the oils which are today heavily promoted as “essential” – vegetable oil and fish oil – we are actually reducing the amount of the fatty acids that are truly essential – DHA & AA.

Finally, it must be pointed out that EFAs of all types, even the health promoting DHA & AA, are polyunsaturated fatty acids (PUFAs). PUFAs are widely known to contribute to oxidative stress, and oxidative stress directly contributes to many diseases including cancer and heart disease. This is why it is important to restrict our intake of EFAs to as close to the minimum requirement as possible.
Most people are far above this requirement, since vegetable oil is pervasive in the American diet. It’s in just about all processed foods (even the “healthy” ones), fried foods and everything cooked in a restaurant. And many people cook with it at home, without knowing what the dangers are.

The best sources of EFA in the diet are liver, egg yolk and butter from grass-fed animals. Obtaining these foods from pasture-raised animals is important, as they contain significantly higher concentrations of DHA and AA (the truly essential EFAs) and fat-soluble vitamins than their commercial feedlot counterparts.

THS recommendations:

  • Gradually replace all vegetable oils in your diet with healthy traditional fats (which are protected from oxidative stress) such as butter, virgin (unrefined) coconut oil, palm oil, lard and beef tallow.
  • Eliminate (or at least dramatically reduce) consumption of processed and fried foods.
  • Do not take flax oil or fish oil supplements on a regular basis. Cod liver oil is recommended during pregnancy, lactation and childhood to provide extra DHA and to obtain fat-soluble vitamins.

Following these recommendations, along with a nutrient-dense, whole foods based diet low in sugar and rich in essential minerals, should reduce your intake of PUFA to closer to the recommended 0.5 (one-half of one) percent of calories, and ensure adequate intake of the truly essential DHA & AA.

Women who are pregnant or lactating, and perhaps attempting to become pregnant, children, and adults recovering from injury and suffering from chronic, degenerative disease can safely consume up to one percent of calories as PUFA. Studies have suggested that a subset of patients with pre-existing cardiovascular disease also benefit from a moderate dose of fish oil (up to one gram per day); however, in those same studies people with stable angina and with no heart disease at all, fish oil actually increased their risk of heart attack.

Check back here for a future post on what the research has to say about using omega-3 fatty acids (fish oil) in the treatment of heart disease.

Make sure to visit Chris Masterjohn’s website, where you can purchase the excellent full report for $15. It’s a worthwhile investment, in my opinion, if you want to get the straight scoop about EFAs and their role in our diet.

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