One of the most hotly debated subjects over the past few years has been the cause of the obesity epidemic, and along with that, the best strategy for weight loss.

Some folks (Atkins, Taubes, Eades, etc.) believe that carbohydrates are to blame. Others (Ornish, Campbell, Esselstyn, Fuhrman, etc.) believe that fat is the problem. More recently, researchers like Seth Roberts and Stephan Guyenet and clinicians like Dr. Sharma have raised awareness of another hypothesis, called the food reward theory, which holds that the consumption of highly palatable foods leads to overeating and weight gain. And Paul Jaminet and others have argued that micronutrient deficiencies, toxins and infections may play a significant role in the obesity epidemic.

Here’s what I think: the most accurate answer to “why do people get fat?” and “what’s the most effective weight loss strategy?” is: “it depends.”

Separating cause from mechanism and effect

One of the biggest mistakes often made in this debate is the confounding of cause, mechanism and effect. A classic example is the assumption that if reducing carbohydrate or fat intake leads to weight loss, then the original weight gain must have been caused by excess carbohydrate or fat consumption.

While it’s tempting to make such an assumption, the logic is faulty. It’s kind of like saying “Advil cures headaches. Therefore, headaches must be caused by Advil deficiency.”

Let’s look at some definitions.

Cause: something that brings about an effect or a result

Mechanism: the fundamental processes involved in or responsible for an action, reaction, or other natural phenomenon

Effect: an outward sign

Obesity is an effect. Insulin resistance, leptin resistance, lipotoxicity, disruption of the mesolimbic dopamine reward pathway and inflammation of the hypothalamus are presumed mechanisms. Excess consumption of carbohydrates, fat, highly palatable food and food toxins (wheat, seed oils, liquid fructose, etc.), exposure to environmental toxins (chemicals), stress, infections, etc. are presumed causes.

Say we do a study on obese people and we observe that they eat a lot of carbohydrates and are insulin and leptin resistance. It’s easy to assume that the chain of causality worked like this: normal weight person eats high-carbohydrate diet, becomes insulin and leptin resistant, and then becomes obese.

But again, this is faulty logic. There’s no proof that A (high carbohydrate intake) was what led to B (insulin and leptin resistance) was what led to C (obesity).

In fact, we could disprove that theory simply by observing another individual or group that eats a very high carbohydrate diet, but does not develop insulin or leptin resistance and obesity. Guess what? Such individuals and groups most certainly exist. There goes that theory.

Likewise, we could also disprove this theory by observing people that are insulin and leptin resistant, but don’t become obese. Such people do exist, and I’ve written about them in my series on diabesity here.

A more rigorous approach

How have we developed our theories on obesity and weight regulation? It seems to me they come from a blend of personal experience, belief and facts. And I think it’s time to become more rigorous about keeping them separate. Here’s an example of what I mean:

Personal experience: I lose weight on an low-carb diet, therefore low-carb diets must be best for weight loss.

Belief: carbohydrates are responsible for the obesity epidemic, via their effects on insulin.

Fact: many cultures around the world eat high-carbohydrate diets and are exceptionally lean.

Those who’ve lost a lot of weight on a low-carb diet have a tendency to become convinced that their wife, friends, family, plumber and everyone else will also lose weight following the same diet.

From this personal experience, a belief is formed. And once we believe in something, we have a remarkable ability to filter out any evidence that might contradict that belief.

This is especially true if our reputation or financial livelihood is tied to said belief. As Upton Sinclair famously said:

It’s difficult to get a man to understand something when his salary is dependent upon him not understanding it.

When a belief like “carbs cause obesity” is shared between enough individuals, it becomes a meme. Once that happens, it is accepted by most as fact – regardless of whether it has any scientific basis. Hence we had the idea for decades that eating fat makes you fat, and now the more recent idea that eating carbs makes you fat.

There’s no single cause (or treatment) of obesity

Perhaps one of the reasons it’s so easy to confuse cause, mechanism and effect and personal experience, belief and fact is that obesity is an incredibly complex disease. Just how complex is it?

Click on the Obesity Systems Influence Diagram below to find out.

Click image for larger version

Wow. That should give you a rough idea of how many variables are potentially involved in weight regulation. Now you know why it has been such a challenge to come up with a single, unified theory of obesity.

That said, of all of the hypotheses advanced to explain the mechanisms behind obesity, I think the food reward theory is the most inclusive.

However, as even its proponents would agree, it doesn’t tell the whole story because there are people and groups that eat large amounts of highly palatable foods that do not become obese.

My opinion is that the modern lifestyle (i.e. food and environmental toxins, stress, poor gut health, infections, micronutrient deficiencies, sleep deprivation, etc.) interfere with hypothalamic hormonal regulation, dopamine signaling, leptin and insulin sensitivity at the cellular level, glucose metabolism and a range of other mechanisms that lead to obesity.

This is consistent with the observation that obesity is extremely rare or nonexistent in traditional cultures that do not consume modern foods and do not live a “modern” lifestyle.

But even this theory is incomplete, because there are people fully exposed to the modern lifestyle that do not become overweight or obese. This suggests that genetics, and perhaps other undiscovered factors, also play a role.

We’re not robots

Humans are not robots. We’re living, breathing, dynamic organisms influenced by varying genetics and environmental conditions.

Anthropological evidence combined with modern research has helped us to reveal the basic template of a species-appropriate diet. However, it has also shown us that humans can thrive on a wide variety of macronutrient ratios and foods within that basic template.

This is not a belief. It’s a fact, supported by the evidence as a whole. Ignoring the evidence doesn’t make it go away. Believing passionately in something doesn’t make it true. Experiencing something personally doesn’t make it fact for everybody else.

19th century philosopher Charles Peirce said:

The state of belief is a calm and satisfactory state which we do not wish to avoid, or to change to a belief in anything else.

And Tolstoy said:

I know that most men, including those at ease with problems of the greatest complexity, can seldom accept even the simplest and most obvious truth if it be such as would oblige them to admit the falsity of conclusions which they have delighted in explaining to colleagues, which they have proudly taught to others, and which they have woven, thread by thread, into the fabric of their lives.

Recognizing this basic human trait, philosopher of science Karl Popper advised every researcher to earnestly try to discredit their own hypotheses.

That is no easy task, and it asks a lot of us. Yet intellectual rigor, emotional maturity and personal integrity are characterized by the capacity to question our own beliefs, no matter how deeply cherished they are or how much is at stake.

I sometimes wonder why we’re all so sure of ourselves. It helps me to remember that at every point in history scientists (and the general public) were convinced they had the right answers. At one time the world was flat, the earth was the center of the solar system and disease was caused by foul humors and could be cured by bloodletting.

Nowadays we look back on those fallacies with a smirk. But are we so arrogant to assume that our great-grandchildren won’t do the same?

The truth is, there’s far more we don’t know than we do know.

In this series we’re going to explore natural childbirth (home birth) as an alternative to industrialized childbirth. Industrialized childbirth could also be called “disturbed birth”, which Australian family physician Sarah J. Buckley, MD defines as follows:

Anything that disturbs a laboring woman’s sense of safety and privacy will disrupt the birth process. This definition covers most of modern obstetrics, which has created an entire industry around the observation and monitoring of pregnant and birthing women. Some of the techniques used are painful or uncomfortable, most involve some some transgression of bodily or social boundaries, and almost all techniques are performed by people who are essentially strangers to the woman herself. All of these factors are as disruptive to pregnant and birthing women as they would be to any other laboring mammal – with whom we share the majority of our hormonal orchestration in labor and birth.¹

Buckley embraces an evolutionary perspective on pregnancy and childbirth. Such a perspective affirms the natural process of gestation and birth and recognizes a woman’s genetically inherited capacity to give birth without medical intervention.

In the same way that we evolved to eat a species-appropriate diet (i.e. paleo), we evolved to give birth in an undisturbed environment.

This innate system of birth has been refined over 100,000 generations. It involves a complex, finely tuned orchestration of hormones that prepare both the mother and baby for a successful birth and catalyze profound neurological changes that promote the bond between a mother and her new baby.

And just as we experience health problems when we stray from the evolutionary dietary template, women are more likely to experience complications and difficulty in labor when they stray from the evolutionary template of “undisturbed birth”.

Natural childbirth is in our genes

Throughout the vast majority of human history, women have always given birth in a familiar place, with family members or other trusted companions.

Even now, babies are still born at home in most places around the world. And although the move from birth at home to the hospital began in the 18th century, home birth was the norm even in westernized countries until the 1950s.

Think of it this way: humans have been giving birth at home for 999,998 generations, and it’s only in the last 2 generations that hospital birth has become common.

This means that women have given birth at home for 99.998% of human history.

Yet in the U.S. today, fewer than 1 percent of births happen in the home. This abrupt and almost complete transition from natural childbirth toward industrialized childbirth has had profound repercussions on mothers, babies and the culture at large.

My wife Elanne and I have chosen to have a home birth with our first child (who is, as of this writing, due in about 2 weeks!) It has been fascinating to watch people’s reactions – outside of our close friends, who have almost all had home births – when we tell them this.

Some come right out and say “that’s brave!” Others are more suspect, using words like “interesting” or maybe even wondering out loud if it wouldn’t be a better idea to use a hospital midwife. Still others are more direct in their opposition to our choice.

This is evidence that the medical establishment has done a fantastic job convincing people that hospital birth is “normal”, in spite of the fact that home birth has been the default choice for 99.998% of human history.

Doctors and the medial have also managed to convince most people that hospital birth is safer than home birth. But is that really true?

Another myth bites the dust: hospital birth is not safer than home birth

In the Netherlands, where 1/3 of babies born at home under care of midwife, outcomes for first babies are equivalent to those of babies born to low-risk women in the hospital, and outcomes of second or subsequent babies are even better.

A UK analysis found that birth at home or in small family practice units is safer than birth in an obstetric hospital for mothers and babies in all categories of risk.

Other studies have shown that modern obstetric interventions have made birth more dangerous, not safer.

In fact, in terms of outcomes for mothers & babies, studies show that planned home birth has perinatal mortality levels (the numbers of babies dying around the time of birth) at least as good as – and often better than – hospital figures, with lower rates of complications and interventions.

A landmark study by Johnson and Daviss in 2005 examined over 5,000 U.S. and Canadian women intending to deliver at home under midwife. They found equivalent perinatal mortality to hospital birth, but with rates of intervention that were up to ten times lower, compared with low-risk women birthing in a hospital. The rates of induction, IV drip, episiotomy, and forceps were each less than 10% at home, and only 3.7% of women required a cesarean (c-section).

Other studies have shown that women who plan home birth have around a 70-80% chance of giving birth without intervention. And because of low use of drugs, home-born babies are more alert and in better condition than those born in the hospital.

Contrast this with the 2002 and 2006 Listening to Mothers surveys which examined 3,000 births in conventional settings. They found “virtually no natural childbirth” in either survey.

In the 2006 survey, around 50% of women were artificially induced; almost 75% had an epidural; and 33% gave birth by c-section.

Finally, in a review of the safety of home birth by the esteemed Cochrane collaboration, the study author states:

There is no strong evidence to favour either home or hospital birth for selected low-risk pregnant women. In countries where it is possible to establish a home birth service backed up by a modern hospital system, all low-risk women should be offered the possibility of considering a planned home birth…

I agree with the author’s conclusion that hospital birth is no safer than home birth. But if you consider the statistics above which suggest that having a natural, undisturbed birth in a hospital setting is exceedingly difficult, I would argue that there is strong evidence to favor a home birth.

Birth complications are more likely to occur in a hospital environment

A common defense of hospital birth by medical professionals and laypeople is the assertion that it’s necessary to be in a hospital during birth in case something goes wrong.

While it is certainly true that complications may arise during labor that require medical intervention, what is often ignored by proponents of hospital birth is the fact that such complications are more likely to occur in the hospital environment.

In other words, the distortion of the process of birth – what Buckley calls “disturbed birth” – has come to be what women expect when they have a baby and in a way has become a self-fulfilling prophecy.

As Buckley states:

Under this model women are almost certain to need the interventions that the medical model provides, and to come away grateful to be saved no matter how difficult or traumatic their experience.²

TV shows almost always depict birth as some kind of medical emergency, with the woman being rushed down the hallway on a gurney or connected to machines and wires in the delivery room surrounded by medical personnel. Since most people have never witnessed a home birth (or any other birth) before giving having a child themselves, their impression of what labor is like comes almost entirely from television.

It’s easy, then, to understand why people are afraid of birth and feel the need to be in a hospital setting in case something goes wrong. But that doesn’t mean giving birth in a hospital is safer. The studies I’ve presented in this article demonstrate that it’s not.

I want to be clear: no matter where birth takes place, complications may arise that require medical intervention and I am 100% in support of it in these cases.

When the mother or baby’s life is at risk, we are fortunate to have access to surgical techniques that can save lives or prevent serious complications.

The point I am making in this article, and will make in more detail in the articles to follow, is that the scale of medical intervention in birth today is not only far beyond what is necessary, but is contributing to the very of the problems it attempts to solve.

If you’re interested in learning more about natural childbirth, I highly recommend Buckley’s book Gentle Birth, Gentle Mothering. I’d also suggest checking out her free eBook called Ecstatic Birth and her eBook/audio package Giving Birth At Home.

Note: this series will very likely be interrupted by the home birth of my own child. Elanne is due on the 17th of July, so the baby could be coming anytime. When that happens, I’ll be taking some time off to spend time with my new family. I’ll pick this up again when I return from paternity leave.

Articles in this series:

• Natural childbirth I: is homebirth more dangerous than hospital birth?
• Natural childbirth IIa: is ultrasound necessary and effective during pregnancy?
• Natural childbirth IIb: ultrasound not as safe as commonly thought
• Natural childbirth III: why undisturbed birth?
• Natural childbirth IV: the hormones of birth
• Natural childbirth V: epidural side effects and risks
• Natural childbirth VI: Pitocin side effects and risks
• Natural childbirth VII: Cesarean risks and complications

I was happy to see a new blog post by Kurt Harris over at PaleoNu yesterday. He’s one of my favorite bloggers, and he hasn’t written much over the last several months. Turns out he’s been boning up on evolutionary biology and paleoanthropology to determine what is currently knowable – and unknowable – about how our paleolithic ancestors lived and ate.

He has also been cultivating a relationship with a PaleoNu reader who happens to be a tutor in Zoology at an “institute of prominence” in the UK, with over 20 years of research and teaching in this field behind him. Preferring to remain anonymous, this fellow will be writing occasional guest articles under the pen name “Professor Gumby” (love it).

Paleo ambiguity

So what did Professor Gumby and Dr. Harris have to say in this first collaboration? In short:

• It’s very difficult for us to know with any certainty what paleo people ate or how they lived.
• The vast majority of studies of modern hunter-gatherers (HGs) have been ethnographic in nature, and as such are heavily influenced by the researchers own assumptions and objectives. This is a problem in all research, but it’s particularly notable in the anthropological literature.
• Modern HGs are not analogous to paleolithic HGs. Even limited amounts of contact with modern people can have a profound impact on the diet and lifestyle of HG populations. This means we can’t simply study modern HG groups and assume that their habits reflect our distant ancestors.
• Observer bias and influence are also issues with studies of modern HG populations. Professor Gumby (and others) have noted that the people they study will often change their dietary habits while being studied, perhaps to impress the researchers. In my family there’s a funny story about me when I was 8 years old eating a whole plate of spinach when a special guest came to visit for dinner one night. I hated spinach and wouldn’t touch it any other time. Turns out this phenomenon is common in anthropological field studies.
• Along the same lines, modern HGs aren’t living in their traditional habitats. They’ve been displaced from their more optimal habitats by agriculturists and pastoralists. This means the diet they’re currently eating is probably atypical – “more akin to a ‘fall-back’ or ‘subsistence’ diet than an optimal one”, as Professor Gumby put it.

This last point is particularly salient. We can’t determine the optimal diet of a particular group of people simply by observing what they currently eat. As Dr. Harris points out:

It should be instructive to ask apparently healthy HGs what they prefer to eat in addition to what they have to eat. In a population that is healthy and not conditioned to a lifetime of non-foods as in the diet of a westerner with metabolic syndrome, it may have meaning to know what they prefer to eat. Not accounting for costs, how would they apportion their caloric intake from their extant food sources? I see no reason that relative food preferences could not be genetically or epigenetically influenced in addition to culturally influenced. Absent the interference of modern medicine, could a preference for the foods that make one live a healthier, more robust life be selected for and rapidly move through a population in a few generations? Do the Kitavans actually prefer yams/sweet potatoes/cassava over coconut and fish in the same ratio as the proportions they eat them in? Would Inuit happily prefer half their calories as sweet potatoes if they grew in the arctic? Or does each dietary pattern just reflect the preference to avoid starvation?

What we don’t know about paleo

The takeaway is simply this: it’s impossible to know for certain what our paleolithic ancestors ate by studying modern HG people. It’s difficult even to know what modern HG people eat when a bunch of researchers aren’t hanging around watching them.

There’s been a lot of discussion in the “paleo-sphere” about this lately. It comes up every time a fossil study is reported on, such as the most recent one that found starch on the teeth of Neaderthals, suggesting that they may have – gasp! – eaten grains on occasion. Of course these stories are pounced on by the anti-paleo set as evidence that grains have been a regular part of our diet for a long time and that proponents of the paleo diet don’t know what they’re talking about.

So on the one hand you’ve got paleo fundamentalists claiming to know exactly what paleolithic people ate, and stating with apparent certainty that grains and legumes were absolutely not included in their diets. Then you’ve got folks on the other end of the spectrum who claim that paleo is a just another “fad diet”, like the Zone or Atkins, with absolutely no basis in clinical or anthropological evidence.

They’re both wrong, of course.

It should be abundantly clear that we can’t know for certain what paleo people ate. They lived a long time ago, and we don’t have a time machine. Even if we did, and went back to study them, they’d probably pull the equivalent of me eating spinach when that special guest visited.

But this doesn’t mean we simply disregard what we do know about our paleolithic ancestors and modern HGs, nor does it mean that we can’t extrapolate that knowledge into helpful guidelines for what a species-appropriate diet might be for us humans.

What we do know about paleo

We still know, for example, that modern diseases like diabetes, obesity, cancer, autoimmunity and heart disease were rare (or even nonexistent) in paleo people and are still rare in the few HG groups around the world that have been lucky enough to preserve their traditional diet and lifestyle.

We also know that when modern foods like wheat flour, industrial seed oils and sugar are introduced in these populations, the incidence of modern diseases goes up commensurately. And, even more telling, when these groups return to their traditional ways, the modern diseases disappear again. This suggests that it wasn’t some genetic vulnerability that caused them to develop modern diseases with the introduction of modern foods.

So yes, paleo may not actually be paleo. We will probably never know exactly what our paleo relatives ate.

My response to that? I couldn’t care less.

Why? Because we know enough about ancestral diets in a general sense to suggest that they are superior to modern diets for human health. And we know enough – thanks to current clinical research – about modern foods like flour, seed oils and sugar to know that we shouldn’t be eating them.

That’s enough for me.

I really wish there was a word (other than paleo) I could use to describe a nutrient-dense, toxin-free, whole-foods based diet. Because that’s kind of a mouthful, and it leaves a lot open to interpretation. A raw-food vegan could hear me say that and think I’m talking about their diet. I’m not.

So I go on using the term “paleo” to loosely refer to a diet that emphasizes animal protein and fats, starchy & non-starchy vegetables, fermented foods, raw dairy (when tolerated) and fruit, nuts & seeds (in moderation).

I wish there was another term I could use that didn’t evoke a quasi-religious debate. But I don’t know of one, so for now, I guess I’ll just have to deal with all of the baggage that comes with “paleo”.

I know this was all over the blogosphere yesterday but I think it’s important enough for a repost.

One thing I can count on every time I write an article extolling the health benefits of animal products is someone sending me an email or posting a comment like this:

I think you’re absolutely wrong. You should read: The China Study, by Dr. T. Collin Campbell.

Sorry to be contrary, but T. Colin Campbell’s “The China Study” should put this issue to rest. Please consider the information presented there. The methodology is impressive.

Campbell recommends a vegan diet–no animal based food at all. He claims that population studies demonstrate that vegan populations do not suffer from the high incidence of cardiovascular disease and cancer that we in the West do with our diets heavy on animal protein.

In fact, those are direct quotes from comments that have been left on my blog over the past year. I can’t even show you some of the emails people have sent because the language might offend you.

Usually I direct those folks to Chris Masterjohn’s excellent critique of the China Study. Now, however, I’ll be sending them over to read Denise Minger’s freshly published China Study smackdown.

Here’s the introduction:

When I first started analyzing the original China Study data, I had no intention of writing up an actual critique of Campbell’s much-lauded book. I’m a data junkie. Numbers, along with strawberries and Audrey Hepburn films, make me a very happy girl. I mainly wanted to see for myself how closely Campbell’s claims aligned with the data he drew from—if only to satisfy my own curiosity.

But after spending a solid month and a half reading, graphing, sticky-noting, and passing out at 3 AM from studious exhaustion upon my copy of the raw China Study data, I’ve decided it’s time to voice all my criticisms. And there are many.

Denise got hold of the raw study data and took it apart with a fine-toothed comb. And what she found is that the claims Campbell made in his China Study book are not supported by the data. She also found important data points Campbell never bothered to mention in the book because they didn’t support his vegan agenda.

For example, Campbell conveniently fails to mention the county of Tuoli in China. The folks in Tuoli ate 45% of their diet as fat, 134 grams of animal protein each day (twice as much as the average American), and rarely ate vegetables or other plant foods. Yet, according to the China Study data, they were extremely healthy with low rates of cancer and heart disease; healthier, in fact, than many of the counties that were nearly vegan.

This is just one of many cases of the selective citation and data cherry picking Campbell employs in the China Study. Denise’s critique masterfully reveals the danger of drawing conclusions from epidemiological studies, which can only show correlations between variables – not causal relationships. Campbell should be well aware of this. After all, in his book he rails against the nutritional bias rampant in the scientific community. Yet nowhere is such bias more evident than in Campbell’s own interpretation of the China Study data.

Denise concludes:

Ultimately, I believe Campbell was influenced by his own expectations about animal protein and disease, leading him to seek out specific correlations in the China Study data (and elsewhere) to confirm his predictions.

Campbell’s response to previous critics of the China Study has been something to the effect of: “I’m a trained scientist. Therefore you should believe me and not my critics.” That is a weak argument – to put it mildly. You don’t need six years of graduate school to learn to think critically. Nor does having a lot of letters after your name make you immune to biased thinking or intellectual blindness. A lot of smart, educated people believed the cholesterol hypothesis for decades. But that never made it true.

You can read more – and I mean a lot more – over at Denise’s blog. I recommend starting with her article China Study: Fact or Fallacy? For many of you, it will be more than enough. But if you’re interested in this stuff, she has written several other articles worth reading.

There are also reviews of Denise’s article at Free the Animal, Whole Health Source, Robb Wolf and PaNu. If you don’t have time to read Denise’s article, read Dr. Harris’s review at PaNu. It’s the next best thing.

Rest in peace, China Study.

P.S. You might also want to check out this debate between T. Colin Campbell and Loren Cordain on human protein requirements. Notice that Cordain’s articles contain 164 citations of research studies. How many references do Campbell’s articles contain? Zero. And Campbell’s typical “I’m more educated than the other guy” won’t fly here. Dr. Cordain has some serious chops.

An estimated 20 million Americans have some form of thyroid disease. Up to 60 percent of these people are unaware of their condition. One in eight women will develop a thyroid disorder during her lifetime. Levothyroxine, a synthetic form of thyroid hormone, is the 4th highest selling drug in the U.S. 13 of the top 50 selling drugs are either directly or indirectly related to hypothyroidism. The number of people suffering from thyroid disorders continues to rise each year.

Hypothyroidism is one of the most common thyroid disorders. One recent analysis suggested up to 10% of women over 60 have clinical or subclinical hypothyroidism. It is characterized by mental slowing, depression, dementia, weight gain, constipation, dry skin, hair loss, cold intolerance, hoarse voice, irregular menstruation, infertility, muscle stiffness and pain, and a wide range of other not-so-fun symptoms.

Every cell in the body has receptors for thyroid hormone. These hormones are responsible for the most basic aspects of body function, impacting all major systems of the body.

Thyroid hormone directly acts on the brain, the G.I. tract, the cardiovascular system, bone metabolism, red blood cell metabolism, gall bladder and liver function, steroid hormone production, glucose metabolism, lipid and cholesterol metabolism, protein metabolism and body temperature regulation. For starters.

You can think of the thyroid as the central gear in a sophisticated engine. If that gear breaks, the entire engine goes down with it.

That’s why people with hypothyroidism experience everything from weight gain and depression to infertility, bone fractures and hair loss.

One of the biggest challenges facing those with hypothyroidism is that the standard of care for thyroid disorders in both conventional and alternative medicine is hopelessly inadequate.

The dream of patients with thyroid disorders and the practitioners who treat them is to find that single substance that will magically reverse the course of the disease. For doctors, this is either synthetic or bio-identical thyroid hormone. For the alternative types, this is iodine.

Unfortunately, in the vast majority of cases neither approach is effective. Patients may get relief for a short period of time, but inevitably symptoms return or the disease progresses.

So what’s the problem? Why have replacement hormones and supplemental iodine been such dismal failures?

Because hypothyroidism is caused by an autoimmune disease.

Studies show that 90% of people with hypothyroidism are producing antibodies to thyroid tissue. This causes the immune system to attack and destroy the thyroid, which over time causes a decline in thyroid hormone levels.

This autoimmune form of hypothyroidism is called Hashimoto’s disease. Hashimoto’s is the most common autoimmune disorder in the U.S., affecting between 7-8% of the population. While not all people with Hashimoto’s have hypothyroid symptoms, thyroid antibodies have been found to be a marker for future thyroid disease.

Most doctors know hypothyroidism is an autoimmune disease. But most patients don’t. The reason doctors don’t tell their patients is simple: it doesn’t affect their treatment plan.

Conventional medicine doesn’t have effective treatments for autoimmune disease. They use steroids and other medications to suppress the immune system in certain conditions with more potentially damaging effects, such as multiple sclerosis, rheumatoid arthritis and Crohn’s disease.

But in the case of Hashimoto’s, the consequences – i.e. side effects and complications – of using immunosuppressive drugs are believed to outweigh the potential benefits. (Thanks to conventional medicine for a relative moment of sanity here.)

So the standard of care for a Hashimoto’s patient is to simply wait until the immune system has destroyed enough thyroid tissue to classify them as hypothyroid, and then give them thyroid hormone replacement. If they start to exhibit other symptoms commonly associated with their condition, like depression or insulin resistance, they’ll get additional drugs for those problems.

The obvious shortcoming of this approach is that it doesn’t address the underlying cause of the problem, which is the immune system attacking the thyroid gland. And if the underlying cause isn’t addressed, the treatment isn’t going to work very well – or for very long.

If you’re in a leaky rowboat, bailing water will only get you so far. If you want to stop the boat from sinking, you’ve got to plug the leaks.

Extending this metaphor to Hashimoto’s disease, thyroid hormones are like bailing water. They may be a necessary part of the treatment. But unless the immune dysregulation is addressed (plugging the leaks), whoever is in that boat will be fighting a losing battle to keep it from sinking.

What the vast majority of hypothyroidism patients need to understand is that they don’t have a problem with their thyroid, they have a problem with their immune system attacking the thyroid. This is crucial to understand, because when the immune system is out of control, it’s not only the thyroid that will be affected.

Hashimoto’s often manifests as a “polyendocrine autoimmune pattern”. This means that in addition to having antibodies to thyroid tissue, it’s not uncommon for Hashimoto’s patients to have antibodies to other tissues or enzymes as well. The most common are transglutaminase (Celiac disease), the cerebellum (neurological disorders), intrinsic factor (pernicious anemia), glutamic acid decarboxylase (anxiety/panic attacks and late onset type 1 diabetes).

In the next post we’ll look more closely at why Hashimoto’s can’t be treated successfully without addressing the autoimmune component, and why both the conventional and alternative approaches to treating hypothyroidism are destined to fail from the start.

Over the next eight weeks I’m going to be studying like a madman for the California State Board Acupuncture licensing exam. I won’t have time to write any special reports or long, “researchy” articles. But I hope to be able to share some of my thoughts here and there. Like this.

I was talking with a colleague the other day (let’s call her M). M related a story one of her patients told her. This patient is a nurse at Kaiser. The nurse was telling M about a meeting she recently attended with the rest of the clinical staff at Kaiser. The purpose of the meeting was to inform all of the doctors and nurses about new clinical guidelines for preventing heart disease.

And what were these clinicians told? To encourage their patients to eat fewer refined carbs, less vegetable oil and less sugar? To engage in a stress management program? To get a moderate amount of physical activity?

Hardly. They were told, in a nutshell, to give everyone statins. The idea communicated to them was that statins are “like vitamins” (a direct quote), and should be distributed in a similar manner.

This got me thinking about the concept of “evidence-based medicine”. I’m all for it, by the way. Evidence-based medicine, that is. The problem is that it doesn’t really exist in the conventional medical model.

Actually, I take that back. It does exist. But to be more accurate we’d have to call it “20-or-30-year-old-evidence-based medicine”. That’s a more representative term for the kind of medicine being practiced today.

The story above is a perfect case in point. The evidence is clear that statins don’t work. (If you don’t believe that, watch this presentation.) Furthermore, the evidence is also clear that the low-fat, high carbohydrate, vegetable oil-fueled diet promoted for decades by the American Heart Association (AHA) has not only failed to prevent heart disease, it has promoted it.

Anyone who actually reads the scientific literature with an open mind and a critical eye could reach these conclusions. The studies aren’t top secret. They’re not kept in an underground fortress. They’re readily available online or at your local medical library.

Yet in spite of the overwhelming evidence against statins and the low-fat AHA diet, this is still the standard of care for heart disease in the medical profession.

I wish I could say this is an isolated case. But you see the same thing in just about every disease or health condition. The standard of care for hypothyroidism is a complete joke. (More on this after I pass my licensing exam, I promise!) Type II diabetes can, for the vast majority of people, be managed and prevented by a low-carb diet. GERD is treated with PPIs and acid stopping drugs, in spite of the evidence that it is actually caused by low stomach acid in most cases.

Maybe the best example, though, is the 2010 dietary guidelines recently published by the USDA. Tom Naughton over at Fat Head published a post on this recently, so I’ll just crib from that:

I started reading the USDA’s 2010 Dietary Guidelines this week. For those of you who hoped the federal government would finally wise up and dump the high-carb/low-fat nonsense … come on, you didn’t really expect that, did you?

Did you honestly believe the government would put together a panel of so-called experts who would announce that the government has been wrong for the past 40 years? That the food pyramid was a disaster? That billions of taxpayer dollars are subsidizing the same foods that are making us fat and diabetic?

Of course not. The new guidelines are, if anything, a perfect example of something I’ve said in previous posts (which I believe I may have borrowed from Milton Friedman): when a government program produces disastrous results, those results are offered as proof that we need to do the same thing again … only bigger!

That’s mostly what the new guidelines are: the same old $#@%, only bigger. Bigger reductions in saturated fat, bigger reductions in salt, bigger reductions in cholesterol, and of course (this is a government committee, after all) lots of “calls to action” … otherwise known as BIG federal programs to convince us poor fools in the public to finally start heeding their advice.

Everywhere you look, you see medicine that isn’t evidence-based – or medicine that’s based on evidence that’s ten, twenty and even fifty years old.

The truth is we don’t have evidence-based medicine. We have profit-based medicine. And as long as the insurance and pharmaceutical companies are running the show, that’s what we’ll continue to have.

Did you know Big Pharma is the second-most profitable industry in the world, behind only the oil industry? Did you know that these companies fund 2/3 of all medical research? Do you really think honest-to-goodness evidence-based medicine is even a possibility in this environment?

Luckily we’ve got the Internet, and some conscientious and intelligent researchers and medical professionals that are willing to look beneath the veil and share what they find with the rest of us.

These days that’s really our only hope as people trying to live healthy lives: to be our own advocates, to seek out information that comes from people without a vested financial interest in selling you something, to maintain a “healthy skepticism” (if I may use the term) about any claims made, whether they come from the conventional or alternative world.

Because let’s face it, evidence-based medicine is a myth.

Still think saturated fat is bad for you? Still think eating eggs raises cholesterol? Still think high cholesterol causes heart disease?

If you answered yes to any of those questions, you really need to watch these videos. (But hey, you might learn something even if you answered “no”.)

In this presentation I:

• debunk the myth that eating saturated fat and cholesterol causes heart disease.
• explain why LDL and total cholesterol are not useful markers for heart disease.
• present three markers that are useful markers for heart disease.
• demonstrate that low-fat, high carb diets promote – rather than protect against – heart disease.
• show you how eating saturated fat and cholesterol can prevent heart attacks
• tell you how to order a test that more accurately predicts your risk of heart disease

At the end of these two videos, you’ll be heading to the fridge for some extra butter or cheese on those veggies or a little extra cream in your coffee!

In this second podcast episode I cover the basics of essential fatty acids, discuss the importance of reducing intake of omega-6 and increasing intake of omega-3, and compare the relative benefits of fish vs. fish oil as sources of omega-3.

I go through most of the material I’ve written about in my special report on essential fatty acids, fish and fish oil, but there is some additional material in the podcast that isn’t in the written series.

I’ve also answered a few of the most common questions that came up in the comments section, or were emailed to me by readers.

Topics include:

• Why flax oil isn’t an adequate source of omega-3 fats
• The importance of reducing omega-6 consumption
• How much omega-3 is enough to prevent disease and promote health
• The advantages and disadvantages of fish vs. fish oil as sources of omega-3
• Criteria for choosing a fish oil
• Is vitamin A safe in cod liver oil?
• Is EPA or DHA more important in human health?

Click here to subscribe to and download the podcast in iTunes. (For those of you already subscribed to the podcast in iTunes, keep in mind that it sometimes takes up to a day for the feed to update.)

Click here to listen to an MP3 of the podcast, or right-click to download the MP3 to your computer.

So far in this series we’ve looked at why fish is superior to plant-based sources of omega-3. We’ve examined the importance of reducing consumption of omega-6 fats. We’ve considered how much omega-3 is needed to support health and treat disease. And we’ve revealed that concerns about the safety of fish consumption have been overblown, and that eating fish regularly is not only safe, but incredibly beneficial.

In this article we’re going to compare fish with fish oil as a means of meeting our omega-3 needs, and for overall health and wellness. The comparison will be based on the following criteria: nutrient content, potency, absorption, cost and environmental impact.

Fish oil has become wildly popular in the last few years, as people increasingly understand the importance of omega-3 in the diet. However, part of the reason for fish oil’s popularity is related to concerns about the safety of eating whole fish – concerns that we now know are unfounded.

With this in mind, let’s see whether whole fish or fish oil are the best choice for most people.

Nutrient content

Fish: contain not only EPA and DHA, but also vitamin D, selenium, protein, co-factors and a more complete fatty acid profile than fish oil. Selenium, in particular, is important because it protects against mercury toxicity. Vitamin D protects against nearly every modern disease plaguing us today. A 6 oz. portion of wild salmon contains 1,700 IU of D, which is difficult to obtain in that amount from other dietary sources.

Fish oil: most oils contain only EPA and DHA, although salmon and cod liver oil also contain moderate amounts of vitamin D. Fish oil has a more limited fatty acid profile than whole fish, and doesn’t contain selenium.

Potency (levels of EPA & DHA)

Fish: a 6 oz. portion of wild salmon contains 883 mg of EPA and 1,111 mg of DHA. 2-3 servings a week of salmon, combined with a low intake on omega-6, would be adequate for most people.

Fish oil: this is where fish oil may have an advantage over fish. Because it is molecularly distilled and purified, fish oil can have high concentrations of DHA and EPA. 6 capsules of Jarrow Max DHA would provide 1.5g/day of DHA, a level that would be difficult to obtain from eating fish. You’d have to eat approximately 8.5 ounces of wild salmon every day to obtain that much DHA.

Absorption

Here’s where things get a bit tricky. I talked about potency above, and mentioned the levels of EPA and DHA in both fish and fish oil. However, those levels mean very little unless we consider how well they’re absorbed.

Several studies indicate that fish oil supplementation is not as effective as epidemiological evidence on the benefits of fish consumption suggest it would be. It appears that the presence of other fats in the fish activates processes required to absorb the EPA and DHA properly. This explains why the EPA and DHA are better absorbed from eating whole fish than from taking fish oil.

In one study comparing the effects of fish and fish oil, researchers found that levels of DHA after 6 weeks of salmon consumption were nine times higher than after fish oil administration.

The authors hypothesized that the configuration of fatty acids in whole fish is familiar to our body and thus easier to absorb. Conversely, the fish oil alone doesn’t adequately activate the process of fat absorption required to assimilate the fatty acids.

Another study confirmed this by demonstrating that fish oil is absorbed much better in the presence of a high-fat meal. They found that the content of n-3 fatty acids in the body tissues rose dramatically when the fish oil was taken along with 12g of olive oil.

We can draw two conclusions from these studies:

1. EPA, and especially DHA, is much better absorbed from fish than fish oil. The effect may be as great as nine-fold. This means that we would need nine times less DHA from fish to obtain the same amount of DHA from fish oil. Put another way, we’d need nine times more DHA from fish oil to obtain the same amount of DHA from fish. So, using the 6 oz. portion of salmon as an example, with 1.1g of DHA, we would need to take 9.9g of DHA from fish oil – roughly 36 capsules/day of the Jarrow Max DHA – to obtain the same amount of DHA we’d get from the salmon. That’s a lot of fish oil!
2. On the other hand, taking fish oil capsules with a high-fat meal can greatly improve their absorption, to the point where they may be on par with whole fish. (I say “may be” because the scientific literature is mixed on this.) This is likely due to the effect described above, where the presence of other fats activates the body’s fat absorption mechanisms.

Cost

This is also tricky to compare, since prices and availability of fish vary regionally. A straight comparison of the cost of DHA obtained from fish and fish oil also ignores other important factors, which we’ve already discussed above, such as the presence of other nutrients and the differences in absorption.

Let’s assume for the sake of comparison that fish oil is taken with a high-fat meal to improve absorption and that absorption rates of EPA and DHA are roughly similar between the two. Let’s assume that wild salmon is available for $13/lb. (I know it is much less in some areas, and much more in others).

Let’s assume also that we’re shooting for a daily intake of 500 mg of DHA.

To obtain this amount of DHA from salmon, you’d have to eat just over one pound per week (19 ounces). That would cost you $15.45.

To obtain this amount of DHA from Jarrow Max DHA, you’d have to take 2 capsules per day. Assuming you bought a bottle of 180 capsules from Vitacost for $14.70, you’d pay just $1.14 for the same amount of DHA.

However, you’d have to consider the following caveats:

1. It’s uncertain whether, even with a high fat meal, you’d be absorbing the same amount of DHA from the fish oil as you would from the salmon
2. The salmon has large amounts of protein, selenium, vitamin D and other fatty-acids and co-factors that the Jarrow fish oil doesn’t have
3. Other oily fish that are significantly cheaper than salmon, such as sardines and mackerel, are also very high in EPA and DHA.

Environmental impact

Overfishing and fish farming have already seriously damaged the health of marine ecosystems, and threaten to do even more damage if fish and fish oil consumption increases.

Much has been written about this elsewhere. Charles Clover’s The End of the Line: How Overfishing is Changing the World and What We Eat provides a particularly astute (and scary) analysis of the impacts of current methods of fishing on global ecosystems.

In short, I believe the most responsible choice we can make is to limit the fish we eat to those certified by groups like the Marine Stewardship Council (MSC).

However, even those groups are not infallible. Recently concerns have been raised over MSC’s decision to certify a salmon fishery in British Columbia where the salmon population is declining rapidly. Environmentalists and scientists have protested the decision, but the MSC seems to have moved ahead regardless.

Unfortunately it’s not a cut and dry issue, and those who are interested in eating fish harvested in a sustainable matter will have to do their own research and stay abreast of changing policies and practices.

In general, though, most environmentalists and scientists support the MSC certification. MSC has a list of fish they consider safe to eat on their website, which you can refer to.

MSC also has a certification label (pictured below) they provide to vendors of MSC-certified fish that you can look for when you’re shopping.

The sustainability of fish oil production is even more difficult to gauge. Some oils are produced as a byproduct of fish harvesting, and manufacturers claim that they are simply making use of something that would normally be discarded. While this is certainly better than harvesting fish solely for their oil, it still supports harmful fishing practices.

The safest bet is to only use fish oil that is made from fish that are certified by MSF or a similar organization, such as the Environmental Defense Fund. Vital Choice Wild Salmon Oil is one example, as is Jarrow Max DHA (which is made from anchovies and sardines, both of which are generally regarded as safe to eat from an environmental standpoint).

The verdict

The question of whether fish or fish oil is a better choice is complex and depends upon several different factors. These include whether DHA is needed for maintenance or therapeutic effect, access to sustainability caught wild fish, financial considerations, and the presence of other nutrients in fish.

For those who are generally healthy and want to stay that way, I think reducing omega-6 consumption and eating a moderate amount of oily fish (2-3 6 oz. portions per week) is the best choice. This will get you plenty of EPA & DHA along with high quality protein, selenium and vitamin D. If wild salmon is out of your price range, mackerel and sardines are both high in EPA and DHA and certified by the MSC as safe to eat.

For those who have a chronic, inflammatory condition such as cardiovascular disease or an autoimmune disorder, I would recommend a combination of whole fish (perhaps the same 2-3 6 oz. portions per week) along with a high quality fish oil. This ensures that you are getting the benefits of whole fish along with the added therapeutic effect of higher doses of DHA and EPA. Somewhere around 1.5g per day of DHA would be a good therapeutic dose, which would mean taking 1g/day of DHA in fish oil capsules in addition to the three 6 oz. portions of oily fish.

In the next and final article of this series, I’ll discuss the criteria for choosing a fish oil and make recommendations based on those criteria and clinical experience.

This is going to be a long article and I know not everyone will have time to read it. So I’m going to summarize the key points right up front because I think this information is so important:

Overview

• Selenium protects against mercury toxicity, and 16 of the 25 highest dietary sources of selenium are ocean fish
• If a fish contains higher levels of selenium than mercury, it is safe to eat
• Most species of commonly eaten fish in the U.S. have more selenium than mercury
• Fish are not significant sources of PCBs and dioxins when compared to meat, dairy or vegetables
• The benefits of eating fish regularly far outweigh the potential risks, which are neglible
• Pregnant mothers and young children should eat 2-3 servings of oily ocean fish each week

These days a lot of people are scared to eat fish. They’ve been told that fish are full of contaminants like mercury, PCBs and dioxins that cause neurological problems and may increase the risk of cancer. Pregnant women have been especially warned due to the supposed risk of these toxins to the developing fetus.

In the last few articles I’ve established the importance of the long-chain omega-3 fatty acids EPA and DHA in human health. I’ve argued that the conversion of plant-based omega-3 fats like ALA into the longer chain EPA and DHA is extremely poor in most people.

The conclusion is obvious: fish should be a part of our diet. But is it safe to eat fish?

You might be surprised to learn that the answer is a resounding yes. In this article I’ll demonstrate that concerns about toxins in fish have been overblown, and that there is almost no risk associated with eating fish when a few simple precautions are taken.

The selenium story

Although people are increasingly concerned about the effects of mercury levels in fish, recent evidence suggests that the trace amounts of mercury in the fish Americans eat aren’t high enough to pose a health risk.

But measuring only mercury significantly exaggerates this risk, because it ignores the important role of selenium.

Selenium is plentiful in many ocean fish species, but the public is unaware of its protective role against mercury. Selenium has high binding affinity for mercury. This means that when the two elements are found together, they connect, forming a new substance.

This new substance makes it hard for the body to absorb the mercury separately. Simply put, when selenium binds to mercury, mercury is not longer free to bind to anything else – like brain tissue.

Studies have shown that relevant amounts of selenium (Se) can prevent oxidative brain damage and other adverse effects associated with mercury toxicity. (PDF)

University of North Dakota researcher Richard Ralston has published several papers on the protective effects of selenium. He describes the relationship between selenium and mercury as follows:

Think of dietary selenium as if it were your income and dietary mercury as if it were a bill that you need to pay. Just as we all need a certain amount of money to cover living expenses such as food and rent, we all need a certain amount of selenium.

And guess what foods are highest in selenium? You’re right! 16 of the 25 best sources of dietary selenium are ocean fish.

He goes on:

Only one major study has shown negative effects from exposure to mercury from seafood, and that seafood was pilot whale meat. Pilot whale meat is unusual in that it contains more mercury than selenium. When you eat pilot whale meat it’s like getting a bill for $400 and a check for less than $100. If that happens too much, you go bankrupt. On the other hand, if you eat ocean fish, it’s like getting a check in the mail for $500 and getting a bill for $25. The more that happens, the happier you are.

What Ralston is telling us is that as long as the fish we’re eating has more selenium than mercury, there’s nothing to worry about.

Fortunately, studies by several independent organizations have consistently shown that most of the fish we eat contain significantly more selenium than mercury. Fish that contain more mercury than selenium include pilot whale, tarpon, marlin, swordfish and some shark.

The following chart illustrates the relative levels of selenium and mercury in commonly eaten ocean fish:

The selenium health benefit value (SeHBV)

Researchers have proposed a new measure of seafood safety called the Selenium Health Benefit Value (SeHBV) that takes the protective role of selenium into account.

Fish with a positive (above zero) SeHBV ratio would be safe to eat, whereas fish with a negative ratio would be unsafe. Using these criteria, most varieties of ocean fish have positive SeHBV ratios and are thus safe to eat.

A study conducted by the Energy & Environmental Research Center (EERC) and the Environmental Protection Agency (EPA) also found that an estimated 97% of the freshwater fish from lakes and rivers in the western U.S. are safe to eat. It is the only study I’m aware of that has measured both mercury and selenium levels in the tissues of freshwater fish. ¹

So how much fish is safe to eat?

The joint recommendation for fish consumption of the EPA and FDA as of 2004 is as follows:

• Eat up to 12 ounces (2 average meals) a week of a variety of commonly eaten fish and shellfish found consistently low in mercury, including shrimp, canned light tuna, salmon, pollock, and catfish
• Limit albacore tuna to 6 oz. per week
• Do not eat shark, swordfish, king mackerel, or tilefish because they contain high levels of mercury

Notice that these recommendations are already quite liberal compared to the fish-phobes who suggest we avoid fish entirely.

But even these recommendations are too strict, because they don’t take the protective effects of selenium into account. As long as the fish is higher in selenium than it is in mercury, there’s no reason to limit consumption to 12 ounces per week.

What about dioxins and PCBs?

PCBs are synthetic organochlorine compounds previously used in industrial and commercial processes. Dioxins are organochlorine by-products of waste incineration, paper bleaching, pesticide production, and production of certain plastics. Yummy!

While it makes perfect sense to try to avoid these toxins to the greatest extent possible, abstaining from fish isn’t a particularly good strategy.

The highest dietary sources of PCBs and dioxins are not fish, but beef, chicken and pork (34%), dairy products (30%) and vegetables (22%). Fish constitute only 9% of our dietary intake of these chemicals.

The primary concern with PCBs and dioxins is cancer. Animal studies and some evidence in humans suggest that both are carcinogenic.

However, an analysis has shown that, per 100,000 individuals, consumption of farmed vs. wild salmon would result in 24 vs. 8 excess cancer deaths, respectively, while consumption of either farmed or wild salmon would result in 7,125 fewer coronary heart disease (CHD) deaths.

Another analysis of the same data suggested that, for all ages evaluated (25-35 to 85 years), CHD benefits outweighed cancer risks by 100- to 370-fold for farmed salmon and by 300- to more than 1000-fold for wild salmon.

It’s important to note that the benefits of fish consumption are based on prospective studies and randomized trials in humans, whereas estimated cancer risks include a 10-fold safety factor and are based on experimental data in animals and limited studies in humans at extremely high doses.

Cancer estimates also assumed lifetime salmon consumption of 1,000 mg/d of EPA & DHA (four 6-oz servings of wild salmon every week for 70 years). Of course virtually nobody in the U.S. currently eats this much salmon.

On the other hand, CHD mortality reduction may be achieved with lower intake (i.e. 250 mg/d – one 6-oz. wild salmon serving per week). At this intake, CHD benefits would be the same (7,125 fewer deaths) while lifetime cancer risk would decrease by 75% (6 and 2 estimated deaths per 100,000 for farmed and wild salmon respectively). The CHD benefits would outweigh cancer risks by more than 3500-fold in the case of wild salmon.

Once again, with few exceptions (the species of fish with more mercury than selenium), it’s not only safe but incredibly beneficial to eat fish regularly.

How beneficial? Let’s find out.

Fish consumption, cardiovascular disease and total mortality

In 2006 Mozaffarian & Rimm published a paper in JAMA called “Fish Intake, Contaminants and Human Health: Evaluating the Risks and Benefits“. They analyzed several studies that examined the impact of fish consumption on both coronary and total mortality. They found that modest fish consumption (e.g. 1-2 servings/wk) – especially of oily fish higher in EPA and DHA – reduced the risk of coronary death by 36% and total mortality by 17%, and may favorably affect other clinical outcomes.

The authors summarized their findings this way:

For major health outcomes among adults, based on the strength of the evidence and the potential magnitudes of effect, the benefits of fish exceed the potential risks.

And:

For women of childbearing age, benefits of modest fish intake, excepting a few selected species, also outweigh risks.

They also pointed out that the Japanese eat 900 mg/d of EPA & DHA on average, and have death rates from coronary heart disease 87% lower than those in Western populations (like the U.S.).

If you’re interested in learning more about this study, I recommend listening to the JAMA Audio in the Room interview with its lead author, Mozaffarian.

Fish consumption, pregnant mothers, and children

DHA is essential for proper development of the brain. It is preferentially incorporated into the rapidly developing brain during gestation and the first two years of infancy, concentrating in the gray matter and retinal membranes.

In a meta-analysis of 14 trials, DHA supplementation improved visual acuity in a dose dependent manner. In another trial of 341 pregnant women, treatment with cod liver oil from week 18 until 3 months postpartum raised mental processing scores at age 4 years.

This is consistent with observational studies showing positive associations between maternal DHA levels or fish intake during pregnancy and behavioral attention scores, visual recognition, memory, and language comprehension in infancy.

An FDA report issued in 2008 noted that the nutrients in fish – especially n-3 LCFAs, selenium, and vitamin D – could boost a child’s IQ by an estimated ten points. ²

The FDA report summarizes evidence suggesting that the greatest benefits to children would result if pregnant women of childbearing age, nursing mothers and young children ate more than the 12 ounces of fish per week currently recommended by the EPA.

According to the National Fisheries Institute, Americans currently consume only five ounces a week of fish high in n-3 LCFA, which is less than half the recommended amount. The NFI also estimates that up to 14 percent of women of childbearing age eat no fish at all, despite the fact that n-3 LCFA are essential to proper fetal brain and eye development.

Based on the new understanding of selenium’s protective role, and the importance of DHA for fetal and early childhood development, pregnant mothers should be advised to eat oily ocean fish regularly.

Fish consumption and autoimmune and inflammatory disease

The first evidence of the significant role of dietary intake of n-3 LCFA in reducing inflammation came from epidemiological observations of the low incidence of autoimmune and inflammatory disorders in a population of Greenland Eskimos compared with gender- and age-matched groups living in Denmark. The Eskimos in this study had dramatically lower rates of psoriasis, asthma and type 1 diabetes, as well as a complete absence of multiple sclerosis.

Animal and human studies suggest that n-3 LCFA suppresses cell mediated immune responses. Increasing the amount of n-3 LCFA while decreasing omega-6 fatty acids leads to improvements and a decrease of steroid use in patients with rheumatoid arthritis and asthma.

This is because omega-3s have been shown to suppress the capacity of monocytes to synthesize interleukin-1 (IL-1) and tumor necrosis factor (TNF). IL-1 and TNF are the principal mediators of mediation in several different inflammatory and autoimmune conditions.

Summary

This is simply a re-cap of the overview presented at the beginning of the article. But it’s worth repeating.

• Selenium protects against mercury toxicity, and 16 of the 25 highest dietary sources of selenium are ocean fish
• If a fish contains higher levels of selenium than mercury, it is safe to eat
• Most species of commonly eaten fish in the U.S. have more selenium than mercury
• Fish are not significant sources of PCBs and dioxins when compared to meat, dairy or vegetables
• The benefits of eating fish regularly far outweigh the potential risks, which are neglible
• Pregnant mothers and young children should eat 2-3 servings of oily ocean fish each week

Welcome to the first episode of The Healthy Skeptic Podcast! To listen to this podcast and subscribe to future episodes in iTunes, click here or click the new iTunes podcast button in the sidebar to the right.

If you don’t use iTunes, you can listen to the file by clicking this link. If you’d like to download it, just right-click the link and download it to your computer. If you’re an Android user or prefer subscribing to an RSS feed of the podcast and blog together, click here.

We’re kicking things off with an interview with Dr. Stephan Guyenet, Ph.D. on obesity, body fat regulation, and weight loss. Stephan is a researcher at the University of Washington studying the neurobiology of fat regulation. He also writes one of my favorite blogs on nutrition and health, Whole Health Source.

Topics covered include:

• The little known causes of the obesity epidemic
• Why the common weight loss advice to “eat less and exercise more” isn’t effective
• The long-term results of various weight loss diets (low-carb, low-fat, etc.)
• The body-fat setpoint and its relevance to weight regulation
• The importance of gut flora in weight regulation
• The role of industrial seed oils in the obesity epidemic
• Obesity as immunological and inflammatory disease
• Strategies for preventing weight gain and promoting weight loss

It’s a bit long at 1:20, but I think you’ll enjoy it if you’re interested in this topic.

Please let me know what you think!

In the last article we discussed the problems humans have converting omega-3 (n-3) fats from plant sources, such as flax seeds and walnuts, to the longer chain derivatives EPA and DHA. Since EPA and DHA (especially DHA) are responsible for the benefits omega-3 fats provide, and since EPA and DHA are only available in significant amounts in seafood, it follows that we should be consuming seafood on a regular basis.

But how much is enough? What does the research literature tell us about the levels of EPA and DHA needed to prevent disease and ensure proper physiological function?

I’m going to answer this question in detail in the next article. But before I do that, I need to make a crucial point: the question of how much omega-3 to eat depends in large part on how much omega-6 we eat.

Over the course of human evolution there has been a dramatic change in the ratio of omega-6 and omega-3 fats consumed in the diet. This change, perhaps more than any other dietary factor, has contributed to the epidemic of modern disease.

The historical ratio of omega-6 to omega-3

Throughout 4-5 million years of hominid evolution, diets were abundant in seafood and other sources of omega-3 long chain fatty acids (EPA & DHA), but relatively low in omega-6 seed oils.

Anthropological research suggests that our hunter-gatherer ancestors consumed omega-6 and omega-3 fats in a ratio of roughly 1:1. It also indicates that both ancient and modern hunter-gatherers were free of the modern inflammatory diseases, like heart disease, cancer, and diabetes, that are the primary causes of death and morbidity today.

At the onset of the industrial revolution (about 140 years ago), there was a marked shift in the ratio of n-6 to n-3 fatty acids in the diet. Consumption of n-6 fats increased at the expense of n-3 fats. This change was due to both the advent of the modern vegetable oil industry and the increased use of cereal grains as feed for domestic livestock (which in turn altered the fatty acid profile of meat that humans consumed).

The following chart lists the omega-6 and omega-3 content of various vegetable oils and foods:

Vegetable oil consumption rose dramatically between the beginning and end of the 20th century, and this had an entirely predictable effect on the ratio of omega-6 to omega-3 fats in the American diet. Between 1935 and 1939, the ratio of n-6 to n-3 fatty acids was reported to be 8.4:1. From 1935 to 1985, this ratio increased to 10.3:1 (a 23% increase). Other calculations put the ratio as high as 12.4:1 in 1985. Today, estimates of the ratio range from an average of 10:1 to 20:1, with a ratio as high as 25:1 in some individuals.

In fact, Americans now get almost 20% of their calories from a single food source – soybean oil – with almost 9% of all calories from the omega-6 fat linoleic acid (LA) alone! (PDF)

This reveals that our average intake of n-6 fatty acids is between 10 and 25 times higher than evolutionary norms. The consequences of this dramatic shift cannot be overestimated.

Omega-6 competes with omega-3, and vice versa

As you may recall from the last article, n-6 and n-3 fatty acids compete for the same conversion enzymes. This means that the quantity of n-6 in the diet directly affects the conversion of n-3 ALA, found in plant foods, to long-chain n-3 EPA and DHA, which protect us from disease.

Several studies have shown that the biological availability and activity of n-6 fatty acids are inversely related to the concentration of of n-3 fatty acids in tissue. Studies have also shown that greater composition of EPA & DHA in membranes reduces the availability of AA for eicosanoid production. This is illustrated on the following graph, from a 1992 paper by Dr. William Landis:

The graph shows the predicted concentration of n-6 in the tissue based on dietary intake of n-3. In the U.S. the average person’s tissue concentration of highly unsaturated n-6 fat is 75%. Since we get close to 10% of our calories from n-6, our tissue contains about as much n-6 as it possibly could. This creates a very inflammatory environment and goes a long way towards explaining why 4 in 10 people who die in the U.S. each year die of heart disease. (Note: the ratio of omega-6 to omega-3 matters, but so does the total amount of each.)

In plain english, what this means is that the more omega-3 fat you eat, the less omega-6 will be available to the tissues to produce inflammation. Omega-6 is pro-inflammatory, while omega-3 is neutral. A diet with a lot of omega-6 and not much omega-3 will increase inflammation. A diet of a lot of omega-3 and not much omega-6 will reduce inflammation.

Big Pharma is well aware of the effect of n-6 on inflammation. In fact, the way over-the-counter and prescription NSAIDs (ibuprofen, aspirin, Celebres, etc.) work is by reducing the formation of inflammatory compounds derived from n-6 fatty acids. (The same effect could be achieved by simply limiting dietary intake of n-6, as we will discuss below, but of course the drug companies don’t want you to know that. Less profit for them.)

As we discussed in the previous article, conversion of the short-chain n-3 alpha-linolenic acid (ALA), found in plant foods like flax and walnut, to DHA is extremely poor in most people. Part of the reason for that is that diets high in n-6 LA inhibit conversion of ALA to DHA. For example, one study demonstrated that an increase of LA consumption from 15g/d to 30g/d decreases ALA to DHA conversion by 40%.

Death by vegetable oil

So what are the consequences to human health of an n-6:n-3 ratio that is up to 25 times higher than it should be?

The short answer is that elevated n-6 intakes are associated with an increase in all inflammatory diseases – which is to say virtually all diseases. The list includes (but isn’t limited to):

• cardiovascular disease
• type 2 diabetes
• obesity
• metabolic syndrome
• irritable bowel syndrome & inflammatory bowel disease
• macular degeneration
• rheumatoid arthritis
• asthma
• cancer
• psychiatric disorders
• autoimmune diseases

The relationship between intake n-6 fats and cardiovascular mortality is particularly striking. The following chart, from an article entitled Eicosanoids and Ischemic Heart Disease by Stephan Guyenet, clearly illustrates the correlation between a rising intake of n-6 and increased mortality from heart disease:

As you can see, the USA is right up there at the top with the highest intake of n-6 fat and the greatest risk of death from heart disease.

On the other hand, several clinical studies have shown that decreasing the n-6:n-3 ratio protects against chronic, degenerative diseases. One study showed that replacing corn oil with olive oil and canola oil to reach an n-6:n-3 ratio of 4:1 led to a 70% decrease in total mortality. That is no small difference.

Joseph Hibbeln, a researcher at the National Institute of Health (NIH) who has published several papers on n-3 and n-6 intakes, didn’t mince words when he commented on the rising intake of n-6 in a recent paper:

The increases in world LA consumption over the past century may be considered a very large uncontrolled experiment that may have contributed to increased societal burdens of aggression, depression and cardiovascular mortality.

And those are just the conditions we have the strongest evidence for. It’s likely that the increase in n-6 consumption has played an equally significant role in the rise of nearly every inflammatory disease. Since it is now known that inflammation is involved in nearly all diseases, including obesity and metabolic syndrome, it’s hard to overstate the negative effects of too much omega-6 fat.

In the next article we’ll discuss three different methods for determining healthy intakes of n-3 that take background intake of n-6 into account.

I want to thank everyone for sending in their questions and voting on the next topic. The good news is that there’s a lot of interest in all of the topics I’m researching right now. The bad news is that there was no clear winner.

Finally, stay tuned for the first episode of The Healthy Skeptic audio podcast, coming up next week. I’ll be interviewing Stephan Guyenet, Ph.D, on the subject of obesity and weight regulation. Stephan is a senior fellow at the University of Washington studying the neurobiology of body fat regulation. He’s also the author of Whole Health Source, which is one of my favorite health related blogs.

Before we get into talking about the benefits of fish consumption, or how how much fish or fish oil you should eat, it’s probably a good idea to start with a basic review of the omega-3 fatty acids.

Essential Fatty Acids 101

A fatty acid is a chain of carbon, oxygen and hydrogen atoms with a carboxyl group on one end. Fatty acids are classified on the basis of how many carbon atoms are in the chain, as well as how many double bonds exist within the molecule.

Fish contain a variety of fatty acids, but the ones that are believed to confer the majority of the benefits are the long-chain omega-3 fats eicosapentanaenoic acid (EPA) and docosahexaenoic acid (DHA). These omega-3 fats are found exclusively in seafood and marine algae.

As you can see from the chart below, it is also possible for the body to synthesize EPA and DHA from the short-chain omega-3 alpha-linolenic acid (ALA). ALA is found in plant foods such as flax, hemp and pumpkin seeds and walnuts.

Click thumbnail for a larger version

However, research clearly indicates that the conversion of ALA to EPA and DHA is extremely limited. Less than 5% of ALA gets converted to EPA, and less than 0.5% (one-half of one percent) of ALA is converted to DHA.

A common misconception, especially amongst vegetarians and vegans, is that our need for EPA and DHA can be met by consuming flax oil and other plant sources of ALA. But the conversion numbers above clearly indicate that this isn’t the case.

Studies have shown that ALA supplements (like flax oil) are unable to raise plasma DHA levels in vegans, despite low DHA levels at baseline. (ref) So unless they are supplementing with an algae-derived source of DHA, it is likely that most vegetarians and vegans are deficient.

This is significant because researchers now believe that the majority of the health benefits we get from dietary omega-3 fats come from the longer chain derivatives (especially DHA, as I will explain below).

Is DHA essential?

In fact, some researchers have proposed that DHA is essential. When scientists label a nutrient as “essential”, they they’re not just saying that it’s “very important”. In the context of nutrition essential means that the nutrient cannot be synthesized in the human body, and must be derived from dietary sources.

According to today’s nutrition textbooks, there are only two essential fatty acids, omega-6 linoleic acid (LA) and omega-3 alpha-linolenic acid (ALA). It is believed that as long as these fats are present in the diet, all of the longer-chain omega-3 and omega-6 derivatives can be synthesized in the body.

As I pointed out above, while this is theoretically possible, in reality the conversion doesn’t work well. This is true even for healthy people, but it’s especially true for those with nutrient deficiencies, because the conversion of ALA to DHA depends on zinc, iron and pyridoxine.

The bioavailability of iron in plant sources is poor compared to animal sources, so iron deficiency is common in vegans and vegetarians. This is another reason why they tend to be poor converters of ALA to DHA.

Several other observations support the hypothesis that DHA is essential:

• DHA content in the tissues of all mammals is very similar despite widely varying intakes of omega-3 fatty acids. ¹
• DHA and AA, but not other omega-3 or omega-6 fatty acids, are selectively transferred across the placenta (PDF).
• 60% of the dry matter of the brain is lipid, and DHA and AA are the most abundant fatty acids of brain phospholipids (PDF)
• DHA status in newborns is much lower in those receiving formula with LA and ALA, than in those receiving milk or formula with pre-formed DHA (PDF)

It is possible that the primarily carnivorous diet of our ancestors, which ensured a consistently high dietary intake of DHA and AA, precluded the need to evolve efficient conversion mechanisms.

In other words, since we were eating a lot of meat and fish with pre-formed DHA and AA, our bodies didn’t need to be experts at converting ALA and LA in plants to DHA and AA. It is far easier for the body to assimilate pre-formed DHA and AA than it is to synthesize them from precursors.

What about EPA? Isn’t it essential too?

EPA is another long-chain omega-3 fatty acid that is conventionally believed to be responsible for the benefits of fish consumption.

EPA is often referred to as “anti-inflammatory”. However, according to this report on essential fatty acids by Masterjohn, EPA’s effect seems to be more of an interference with the metabolism of omega-6 arachidonic acid (AA) than the performance of any essential role itself.

Take a look at the chart again that I linked to in the beginning of the post. The fatty acids in blue boxes are less inflammatory, and those in pink boxes are more inflammatory. The chart shows that AA is used to synthesize prostaglandins that cause inflammation (indicated by the pink box on the chart). Because it has the same number of carbon atoms, EPA competes with AA for the enzymes that metabolize it. Since the prostaglandins made by EPA are less inflammatory than those made by AA (indicated by the blue box), EPA is often referred to as “anti-inflammatory”.

But while EPA is certainly less inflammatory than AA, it doesn’t make sense that the body would require an essential fatty acid just to block the inflammatory effects of of another fatty acid.

By contrast, DHA is used to synthesize compounds that play an active role in resolving inflammation. EPA only makes these compounds in the presence of aspirin (PDF). EPA is thus likely to simply be a byproduct of compromised DHA synthesis.

What does this mean to you?

Putting all of this information together yields the following conclusions:

1. DHA is the most important of the omega-3 fatty acids, and is primarily responsible for the benefits we get from consuming them.
2. DHA is likely to be essential, which means that you must consume it in the diet to prevent disease and ensure optimal function.
3. The conversion of plant sources of ALA, such as flax seed oil, to DHA is poor in healthy people and even worse in people deficient in certain nutrients. Vegans and vegetarians are especially prone to be poor converters of ALA to DHA.
4. If you’ve been buying flax oil in the hopes that it will help, you’d be far better off putting that money towards some fish or fish oil capsules.

Dietary changes over the past century have lowered the DHA status to a state of subclinical deficiency in many people. Countless studies show that this deficiency is at least in part to blame for the rising incidence of cardiovascular disease, inflammatory disease, mental and psychiatric disorders and suboptimal neurodevelopment.

DHA is not the only reason to eat fish, which is also rich in selenium and vitamin D. However, DHA is likely to be the primary reason why populations that eat fish on a regular basis have consistently been shown to healthier than those that don’t. We’ll discuss this further in the next article.

From the documentary Fat Head