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Chinese Medicine Demystified (Part II): Origins of the “Energy Meridian” Myth

March 5, 2010 in Myths & Truths | 17 comments


energy meridiansNote: This is the second article in an ongoing series. Make sure to read the first article before reading this one, and check out the next articles in the series afterwards.

As an acupuncture student, I often like to ask people if they know what the word qi (sometimes spelled “chi”) means.

I get all kinds of answers. Some people don’t have any idea. Some guess it’s a kind of tea, like chai tea. Some say it has something to do with martial arts. Others say it means balance or flow. But those who’ve been to an acupuncturist, or at least know someone who has, say that qi means energy.

They say that because that’s what their acupuncturist told them. And their acupuncturist told them that because that’s what the acupuncturist was taught in school. That’s the definition of qi in the textbooks about Chinese medicine that we study in the west.

These textbooks teach that qi is an energy that moves through your body in meridians. A meridian is a metaphysical line “juxtaposed” on the body. It has no actual location inside of the body. In other words, it’s not really there. According to these textbooks this mysterious energy called qi flowing through these nonexistent lines called meridians forms the conceptual basis of Chinese medicine.

This is the definition of Chinese medicine that causes snickers, smirks and shaking heads amongst the scientific crowd – which is to say almost every doctor or medical professional trained in the west. But is this definition even accurate?

Much of what we know about Chinese medicine comes from a book called the Huangdi Neijing (HDNJ), or Yellow Emperor’s Internal Classic. There’s some controversy about when it was written, but most scholars agree that it was about 2,000 years ago, sometime between the second and first century BCE. The HDNJ is a massive encyclopedic text of Chinese medicine. You can think of it as their version of the Merck Manual.

The HDNJ had several sections. One was on anatomy. If you recall from the previous post in this series, the Chinese were performing detailed dissections 500 years before the birth of Christ. They listed the average weight, volume and measurements for all of the internal organs. They named the organs and described their functions. (In fact, they knew that the heart is the organ that pumps blood through the body more than 2,000 years ago. This wasn’t discovered in western medicine until the early 16th century.) They knew which vessels flowed away from the heart, which vessels flowed toward the heart, and which vessels supplied which organs.

The HDNJ also had detailed sections on pathology. They described how diseases develop and how to treat those diseases with acupuncture, herbal medicine, massage and dietary and lifestyle changes. In short, the Chinese were practicing truly preventative medicine 2,500 years before the term was even coined.

The HDNJ is a remarkable book. But early western scholars had a problem. The HDNJ is written in a dialect of Chinese that hasn’t been in common use in China for more than a thousand years. You could show it to a modern Chinese person and they wouldn’t be able to read it.

Several westerners took a crack at translating it. One of the first was a Dutch physician named Willem ten Rhijne. Ten Rhijne worked for the Dutch East India Company in Japan from 1683-1685. He reported clinical success by Chinese and Japanese practitioners in treating a wide range of disorders, including pain, internal organ problems, emotional disorders and infectious diseases prevalent at the time. Interestingly enough, Ten Rhijne accurately translated the Chinese character for qi as “air”, not energy, in his reports to the Dutch government.

But the translation we’re most familiar with, and the one that became the source for all of the textbooks used in western schools of Chinese medicine, was done by a man named Georges Soulie de Morant.

De Morant was a French bank clerk who lived in China from 1901 to 1917. He was enamored with Chinese culture and philosophy, and became interested in Chinese medicine during his stay. He decided to translate the HDNJ, in spite of the fact that he had no medical training nor any training in ancient Chinese language.

It was a huge undertaking for a French bank clerk to translate a 2,000 year old medical text written in an extinct Chinese dialect into a modern romance language (French). Under the circumstances, de Morant did well in many respects. But he made some huge mistakes that had serious consequences for how Chinese medicine has been interpreted in the west.

In the next post, we’ll look at those mistakes in more detail. We’ll also replace de Morant’s fictional “energy meridian” model with a new – or rather old – model of Chinese medicine that is both historically accurate and consistent with modern scientific principles of anatomy and physiology.

Continue to the next article.

References

Kendall, Donald, The Dao of Chinese Medicine, Oxford University Press, 2002

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Chinese Medicine Demystified (Part I): A Case of Mistaken Identity

March 4, 2010 in Myths & Truths | 43 comments


chinese physicianNote: This is the first article in an ongoing series. Make sure to check out the next articles when you’re finished with this one:

I’m sure you’re at least somewhat familiar with Chinese medicine and acupuncture by now.  It’s received a lot of media coverage over the last decade, and insurance companies are now covering it in many states. But even though an increasing number of people are using acupuncture to address their health problems, most still don’t understand how Chinese medicine works.

We’ve been told that Chinese medicine involves mysterious energy called “qi” circulating through invisible “meridians” in the body.  When the flow of qi through our meridians becomes blocked, illness results.  The purpose of acupuncture and other Chinese medical therapies (like herbal medicine and qi gong) is to promote the proper flow of qi through the meridians, thus restoring health.  Sound familiar?

If you’ve ever been to an acupuncturist in the west, I’m sure you’ve received some version of this explanation. After all, this is what they teach in acupuncture school. I know this because I’m in my final semester of studying Chinese medicine, and this is the explanation in our textbooks.

Understandably, these fundamental concepts of Chinese medicine have been difficult for western patients and doctors to accept.  If you sit a doctor down who has had ten years of post-graduate medical training and tell him that an unidentified energy called qi flowing through imaginary meridians is the key to health and disease, he’s going to look at you like you’re crazy.  And I don’t blame him.

What if I told you that nearly everything we’ve been taught in the West about how Chinese medicine works isn’t accurate?  What if I told you that Chinese medicine isn’t a woo-woo, esoteric “energy medicine” at all, but instead a functional, “flesh and bones” medicine based on the same basic physiology as western medicine?  And what if I told you I could explain the mechanisms of Chinese medicine in simple, familiar terms that any eight year-old could understand and even the most skeptical, conservative doctor couldn’t argue with?

Here’s the thing. The “energy meridian” model that has become the default explanation of Chinese medicine US is not only out of sync with our modern, scientific understanding of the body – it’s also completely inconsistent with classical Chinese medical theory.  In other words, we’ve made up our own western version of Chinese medicine that has little to do with how it was understood and practiced since it began more than 3,000 years ago in China.  

This gross mischaracterization has kept Chinese medicine on the fringes of conventional medical care since the 1930s and 1940s.  Most doctors and patients have simply been unable to accept the explanation they’ve been offered for how acupuncture works. The result is that acupuncture has come to be seen as either a mystical, psychic medicine or a foofy, relaxing spa-type treatment.

And that’s a big shame. Because Chinese medicine is in fact a complete system of medicine that has successfully treated many common health conditions for more than 2,500 years. Chinese medicine was passed through the ages in an unbroken lineage of some of the best minds of China. It was used by emperors and the royal courts to help them live into their 90s and stay fertile into their 80s at a time when the average life expectancy in the west was 30 years.

The Chinese were performing detailed human dissections where they carefully measured the blood vessels and weighed the internal organs at a time when western physicians thought the body was made up of “humors”. These dissections helped Chinese physicians to discover the phenomenon of continuous blood circulation 2,000 years before it was discovered in the west. The discovery of blood circulation is still considered the single most important event in the history of medicine.

Chinese medicine has been around for a very, very long time. The first evidence of the type of medicine that led to the Chinese Medicine in use today dates back to about 6,000 BC, which was during the neolithic (new stone age) period. Stone tools from this period have been found that were specially shaped for making small incisions in the skin, which was the early form of acupuncture. That’s 8,000 years of uninterrupted use. To put this in perspective, western medicine as we’ve come to recognize it today wasn’t even invented until the 1350s (the middle ages), which makes it less than 700 years old. Ah hem.

Let me ask you this. Do you think Chinese medicine would have survived for more than 3,000 years and spread to every corner of the globe if it wasn’t a powerful, complete system of medicine?

The reason Chinese medicine isn’t more popular in the west is that it’s completely misunderstood even by the people who practice it. And as long as acupuncturists continue to promote the “energy meridian” model as the explanation for how Chinese works, it’s destined to remain a fringe alternative modality.

In the next article I’m going to give you an explanation for how Chinese medicine works that is not only historically accurate, but also consistent with the principles of anatomy and physiology as we understand them today. I’m also going to tell you how this blatant mischaracterization of Chinese medicine in the west came about.

Read the next post in the series: Chinese Medicine Demystified (Part II): Origins of the “Energy Meridian” Myth

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The most important thing you probably don’t know about cholesterol

January 20, 2010 in Food & Nutrition, Heart Disease, Myths & Truths | 22 comments


important

Summary:

  • The simplified view of cholesterol as “good” (HDL) or “bad” (LDL) has contributed to the continuing heart disease epidemic
  • Not all LDL cholesterol is created equal. Only small, dense LDL particles are associated with heart disease, whereas large, buoyant LDL are either benign or may protect against heart disease.
  • Replacing saturated fats with carbohydrates – which has been recommended by the American Heart Association for decades – reduces HDL and increases small, dense LDL, both of which are associated with increased risk of heart disease.
  • Dietary cholesterol has a negligible effect on total blood LDL cholesterol levels. However, eating eggs every day reduces small, dense LDL, which in turn reduces risk of heart disease.
  • The best way to lower small, dense LDL and protect yourself from heart disease is to eat fewer carbs (not fat and cholesterol), exercise and lose weight.

Not all cholesterol is created equal

By now most people have been exposed to the idea of “good” and “bad” cholesterol. It’s yet another deeply ingrained cultural belief, such as the one I wrote about last week, that has been relentlessly driven into our heads for several decades.

But once we’ve put on our Healthy Skeptic goggles, which I know all of you fair readers have, we no longer simply believe what we’re told by the medical establishment or mainstream media. Nor are we impressed or in any way swayed by the number of people that tell us something is true. After all, as Anatole France said, “Even if fifty million people say a foolish thing, it is still a foolish thing.”

Words to live by.

The oversimplified view of HDL cholesterol as “good” and LDL cholesterol as “bad” is not only incomplete, it has also directly contributed to the continuing heart disease epidemic worldwide.

But before we discover why, we first have to address another common misconception. LDL and HDL are not cholesterol. We refer to them as cholesterol, but they aren’t. LDL (low density lipoprotein) and HDL (high density lipoprotein) are proteins that transport cholesterol through the blood. Cholesterol, like all fats, doesn’t dissolve in water (or blood) so it must be transported through the blood by these lipoproteins. The names LDL and HDL refer to the different types of lipoproteins that transport cholesterol.

In addition to cholesterol, lipoproteins carry three fat molecules (polyunsaturated, monounsaturated, saturated – otherwise known as a triglyceride). Cholesterol is a waxy fat particle that almost every cell in the body synthesizes, which should give you some clue about its importance for physiological function.

You do not have a cholesterol level in your blood, because there is no cholesterol in the blood. When we speak of our “cholesterol levels”, what is actually being measured is the level of various lipoproteins (like LDL and HDL).

Which brings us back to the subject at hand. The consensus belief, as I’m sure you’re aware, is that LDL is “bad” cholesterol and HDL is “good” cholesterol. High levels of LDL put us at risk for heart disease, and low levels of LDL protect us from it. Likewise, low levels of HDL are a risk factor for heart disease, and high levels are protective.

It such a simple explanation, and it helps drug companies to sell more than $14 billion dollars worth of “bad” cholesterol-lowering medications to more than 24 million American each year.

The only problem (for people who actually take the drugs, rather than sell them, that is) is the idea that all LDL cholesterol is “bad” is simply not true.

In order for cholesterol-carrying lipoproteins to cause disease, they have to damage the wall of an artery. The smaller an LDL particle is, the more likely it is to do this. In fact, a 1988 study showed that small, dense LDL are three times more likely to cause heart disease than normal LDL.

On the other hand, large LDL are buoyant and easily move through the circulatory system without damaging the arteries.

Think of it this way. Small, dense LDL are like BBs. Large, buoyant LDL are like beach balls. If you throw a beach ball at a window, nothing happens. But if you shoot that window with a BB gun, it breaks.

Another problem with small LDL is that they are more susceptible to oxidation. Oxidized LDL, or oxLDL, is formed when the fats in LDL particles react with oxidation and break down.

Researchers have shown that the smaller and denser LDL gets, the more quickly it oxidizes when they subject it to oxidants in a test tube.

Why does this matter? oxLDL is a far greater risk factor for heart disease than normal LDL. A large prospective study by Meisinger et al. showed that participants with high oxLDL had more than four times the risk of a heart attack than patients with lower oxLDL.

I hope it’s clear by now that the notion of “good” and “bad” cholesterol is misleading and incomplete. Not all LDL cholesterol is the same. Large, buoyant LDL are benign or protect against heart disease, whereas small, dense LDL are a significant risk factor. If there is truly a “bad” cholesterol, it is small LDL. But calling all LDL “bad” is a dangerous mistake.

Low-fat, high-carb diets raise “bad” cholesterol and lower “good” cholesterol

Here’s where the story gets even more interesting. And tragic.

Researchers working in this area have defined what they call Pattern A and Pattern B. Pattern A is when small, dense LDL is low, large, buoyant LDL is high, and HDL is high. Pattern B is when small, dense LDL is high, HDL is low, and triglycerides are high. Pattern B is strongly associated with increased risk of heart disease, whereas Pattern A is not.

It is not saturated fat or cholesterol that increases the amount of small, dense LDL we have in our blood. It’s carbohydrate.

Dr. Ronald Krauss has shown that reducing saturated fat and increasing carbohydrate intake shifts Pattern A to Pattern B – and in the process significantly increases your risk of heart disease. Ironically, this is exactly what the American Heart Association and other similar organizations have been recommending for decades.

In Dr. Krauss’s study, participants who ate the most saturated fat had the largest LDL, and vice versa.

Krauss also tested the effect of his dietary intervention on HDL (so-called “good” cholesterol). Studies have found that the largest HDL particles, HDL2b, provide the greatest protective effect against heart disease.

Guess what? Compared to diets high in both total and saturated fat, low-fat, high-carbohydrate diets decreased HDL2b levels. In yet another blow to the American Heart Association’s recommendations, Berglund et al. showed that using their suggested low-fat diet reduced HDL2b in men and women of diverse racial backgrounds.

Here’s what the authors said about their results:

The results indicate that dietary changes suggested to be prudent for a large segment of the population will primarily affect [i.e., reduce] the concentrations of the most prominent antiatherogenic [anti-heart attack] HDL subpopulation.

Translation: following the advice of the American Heart Association is hazardous to your health.

Eating cholesterol reduces small LDL

The amount of cholesterol in the diet is only weakly correlated with blood cholesterol levels. A recent review of the scientific literature published in Current Opinion in Clinical Nutrition and Metabolic Care clearly indicates that egg consumption has no discernible impact on blood cholesterol levels in 70% of the population. In the other 30% of the population (termed “hyperresponders”), eggs do increase both circulating LDL and HDL cholesterol.

Why is this? Cholesterol is such an important substance that its production is tightly regulated by the body. When you eat more, the body produces less, and vice versa. This is why the amount of cholesterol you eat has little – if any – impact on the cholesterol levels in your blood.

Eating cholesterol is not only harmless, it’s beneficial. In fact, one of the best ways to lower small, dense LDL is to eat eggs every day! Yes, you read that correctly. University of Connecticut researchers recently found that people who ate three whole eggs a day for 12 weeks dropped their small-LDL levels by an average of 18 percent.

If you’re confused right now I certainly don’t blame you.

Let’s review what we’ve been told for more than 50 years:

  1. Eating saturated fat and cholesterol in the diet raises “bad” cholesterol in the blood and increases the risk of heart disease.
  2. Reducing intake or saturated fat and cholesterol protects us against heart disease.

Now, let’s examine what credible scientific research published in major peer-reviewed journals in the last decade tells us:

  1. Eating saturated fat and cholesterol reduces the type of cholesterol associated with heart disease.
  2. Replacing saturated fat and cholesterol with carbohydrates lowers “good” (HDL) cholesterol, raises triglyceride levels, and increases our risk of heart disease.

Dr. Krauss, the author of one of the studies I mentioned above, recently said in an interview published in Men’s Health, “Everybody I know in the field — everybody — recognized that a simple low-fat message was a mistake.”

In other words, the advice we’ve been given by medical “authorities” over the past half century on how to prevent heart disease is actually causing it.

I don’t know about you, but that makes me very angry. Heart disease is the #1 cause of death in the US. Almost 4 in 10 people who die each year die of heart disease. It directly affects over 80 million Americans each year, and indirectly affects millions more.

We spend almost half a trillion dollars treating heart disease each year. To put this in perspective, the United Nations has estimated that ending world hunger would cost just $195 billion.

Yet in spite of all this money spent, the best medical authorities can do is tell us the exact opposite of what we should be doing? And they continue to give us the wrong information even though researchers have known that it’s wrong for at least the past fifteen years?

Really?

Sometimes it seems like everything is backwards.

How to reduce small LDL

Eating fewer carbs is perhaps the best place to start. Reducing carbs has several cardio-protective effects. It reduces levels of small, dense LDL, reduces triglycerides, and increases HDL levels. A triple whammy.

Exercise and losing weight also reduce small, dense LDL. In fact, weight loss has been shown to reverse the evil Pattern B all by itself.

As we saw above, eating three eggs a day can reduce our small LDL by almost 20%. Interestingly, alcohol has also been shown to reduce small LDL by 20%.

In other words, if you want to reduce your risk of heart disease, do the opposite of the American Heart Association (and probably your doctor) tells you to do. Eat butter. Eat eggs. Eat traditional animal fats. Reduce your intake of carbs, vegetable oils and processed foods, and stay active and within a healthy weight range.

Testing your small LDL level

I’m not a fan of arbitrary testing. Our medical system is obsessed with testing. But where has testing has brought us with cholesterol and heart disease? Has it improved outcomes? On the contrary, we test for a number (total LDL) that tells us very little, and then medicate it downwards recklessly and expensively.

If you’re worried about your small LDL level, my advice would be to eat fewer carbohydrates, eat plenty of saturated fat and cholesterol (instead of vegetable oils), exercise, lose weight if you need to, and have a drink every now and then! Since this is the same advice I’d give you if you took a test that actually showed high levels of small LDL, I don’t see much value in doing the test.

However, if you need to see the test results to get motivated to make the changes I suggested above, by all means do the test. There are a few ways to go about it.

First, keep in mind that a regular cholesterol test at your doctor won’t tell you anything about your small LDL level. The standard tests measure your total cholesterol, LDL and HDL. But they don’t distinguish between the dangerous small LDL and benign or protective large LDL.

The fastest and cheapest, albeit most indirect, route is to test your blood sugar both before and then 60 minutes after a meal (this is called a “post-prandial” glucose test). The reason a post-prandial blood glucose test can be a rough indicator for small LDL is the same foods that trigger a rise in blood sugar also increase small LDL. Namely, carbohydrates.

Blood glucose monitors are readily available at places like Walgreens and cost about $10. You’ll also need lancets and test strips, which aren’t expensive either. If your post-prandial glucose is higher than 120 mg/dl, that may be suggestive of a higher than desired small LDL level. This test is not a perfect approximation of small LDL, but it’s the cheapest and and easiest way to get a sense of it.

If you want to get more specific, there are two tests I recommend for small LDL that use slightly different methodology:

  1. LDL-S3 GGE Test. Proteins from your blood are spread across a gel palette. As the molecules move from one end to the other, the gel becomes progressively denser. Large particles of LDL cholesterol can’t travel as far as the small, dense particles can, Dr. Ziajka says. After staining the gel, scientists determine the average size of your LDL cholesterol particles. Berkeley Heart Lab. About $15 with insurance.
  2. The VAP Test. Your sample is mixed into a solution designed to separate lipoproteins by density. Small, dense particles sink, and large, fluffy particles stay at the top. The liquid is stained and then analyzed to reveal 21 different lipoprotein subfractions, including dominant LDL size. The Vap Test. Direct cost is $40.

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Breakfast of champions (with 88 grams of fat!)

December 17, 2009 in Food & Nutrition, Myths & Truths | 31 comments


smoothieA friend of mine was observing me making my breakfast the other day. She’s been hip to the dangers of low-fat diets and the benefits of saturated fat for some time now, but even so she was pretty surprised with just how much fat I was plowing into my smoothie. We thought it might be fun to actually measure the amount and do a full nutritional analysis on my breakfast.

Here’s the recipe:

  • 1.5 cups of whole, raw milk
  • 8 oz. of whole, plain yogurt made with raw milk
  • 1/4 cup of cream
  • 3 TBS of extra virgin coconut oil (melted)
  • 1 TBS of raw, grass-fed butter(melted)
  • 1/2 cup of strawberries (frozen or fresh, depending on season)
  • 1/2 cup of blueberries (frozen or fresh, depending on season)
  • 1/2 cup of raspberries (frozen or fresh, depending on season)
  • 2 raw egg yolks (from pastured chickens)

And here’s the nutrition breakdown:

nutrition data

calorie breakdown

The results are enough to give a cardiologist a heart attack. My morning fruit smoothie contains 88 grams of fat and 1,097 calories. 66% of those calories are coming from fat. According to the calorie calculators (that I normally pay no attention to), a person of my height and weight that is very active should consume approximately 2500 calories per day and no more than 83 grams of fat in a day (at 30% of calories). As you can see, I’m blowing right past that in my first meal of the day!

Of course the powers that be suggest that only 1/3 of those fat calories come from saturated fat. Oops! A full 62 of those 88 grams of fat in my smoothie are saturated. Yum!

Anyone still laboring under the delusion that eating saturated fat makes you fat might think I weigh 300 pounds eating a breakfast like this every day. On the contrary, I have to struggle to keep the weight on. I am 6’2 and weigh about 170 pounds. Yes, I am relatively active but nothing extreme. I commute by bicycle almost everywhere, and that makes a big difference. I go to the climbing gym once or twice a week, surf and kiteboard when I can, and practice martial arts occasionally. But we’re not talking about 1.5 hour workouts on the Stairmaster or running half-marathons every day.

What’s great about this breakfast is that it fills me up until lunch (because of all the fat, of course) and gives me all the nutrition I need for the morning. As you can see from the following chart, the smoothie is almost meeting (and in one case exceeding) the US RDA of several vitamins and minerals:

vitamin data

I should also point out that this is generally the only sweet thing I eat each day. I have completely lost my craving for sugar. I mean completely. No deprivation, no rules – I just don’t want it anymore. This is coming from a guy who started cooking at a very young age just so he could make his own chocolate chip cookies!

How did I lose my craving for sugar? By eating a lot of fat. Fat creates satiety, which is the feeling of being satisfied after eating. When we don’t eat enough fat, we crave carbs and sugar because we don’t feel satisfied. And ironically, eating carbs and sugar cause hormonal changes that stimulate more cravings for carbs and sugar. It’s a vicious cycle. So if you want to reduce your cravings for sugar, eat more fat! Saturated, animal fats of course.

In case you’re wondering, lunch and dinner are usually some kind of grass-fed meat along with a cooked vegetable and a salad. And of course the vegetables are covered with butter or cheese, and the salad has nuts, avocado, cheese and olive oil. Why? Read my recent article “Have some butter with your veggies!” to find out.

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Where's the beef?

March 26, 2009 in Cancer, Food & Nutrition, Myths & Truths | 22 comments


roast beefYou might have seen an article in your newspaper or online touting a recent study published in the Archives of Internal Medicine that “strongly” linked red meat consumption with cancer and an increased risk of death. Heck, how could you miss it? Google shows 547 new articles about the study, and it was mentioned in just about every major newspaper in the U.S.

(That’s not an accident, by the way. It’s an intentional attack by the tyrannical meat-hating scientific majority, the same folks who brought us the “cholesterol causes heart disease” and “saturated fat is bad for you” myths.)

Trouble is – as is so often the case – the study is deeply flawed. In fact, anyone with training in research methodology might find themselves wondering “where’s the beef?” after they read it. In the end it’s just another piece of worthless propaganda parading as medical research. It tells us a lot more about the biases and motives of the researchers, and the incompetence of the media reporting on it, than it does about the effect of red meat consumption on human health.

Here are my “top 10″ reasons to ignore this study and continue to eat your grass-fed, organic red meat:

  1. It was an observational study. Observational studies can show an association between two variables (i.e red meat consumption and death), but they can never show causation (i.e. that eating red meat caused the deaths). A simple example of the difference between correlation and causation is that elevated white blood cell count is correlated with infections. But that doesn’t mean elevated white blood cell counts cause infections!
  2. The relative risk reduction (RRR) was slightly over 1.0. Most researchers don’t pay attention to an RRR under 2.0, due to the notorious difficulties involved with this type of research.
  3. Two articles were published in the American Journal of Clinical Nutrition at around the same time that directly contradicted these results. The first study pooled data from 13 studies and found that risk of colorectal cancer was not associated with saturated fat or red meat intake. The second study found that there was no difference in mortality between vegetarians and meat eaters.
  4. The authors didn’t adequately control for other dietary factors known to increase morbidity and mortality. As another commentator pointed out in her analysis of this study, “Americans get their “cancer causing” red meat served to them on a great big white bun with a load of other carbohydrates (soda, chips, fries) and inflammation-causing n-6 vegetable oils (chips, fries, salad dressings) on the side.” It’s more likely (based on other studies, including the two mentioned above) that the increase in deaths was caused by the junk food surrounding the red meat and not by the meat itself.
  5. The basis of measurement is a “detailed questionnaire”. Questionnaires about one’s diet are always error prone as remarkably few people remember accurately what they eat on any given day, let alone over a period of years. Furthermore, most people lie about what they actually eat, especially now that proper diet has been given a quasi-religious significance and eating poorly is equated with being morally inferior.
  6. Check out this quote from the Archives of Internal Medicine study:

    “Red meat intake was calculated using the frequency of consumption and portion size information of all types of beef and pork and included bacon, beef, cold cuts, ham, hamburger, hotdogs, liver, pork, sausage, steak, and meats in foods such as pizza, chili, lasagna, and stew”.

    In other words, even those people who ate things like hot dogs and hamburgers (with buns made of refined white flour), and who ate pizza (on refined white flour crusts) were included in the ‘red meat’ group. Also, those who ate processed or cured meats, such as ham, bacon, sausage, hot dogs, or cold cuts (with possible nitrates) were included in the ‘red meat’ group. And those who ate prepared food (with unknown additives and preservatives) such as pizza, chili, lasagna, and stew were also included in the ‘red meat’ group. Therefore, this study does absolutely nothing to prove that red meat, and not these processed and highly refined foods, is the culprit.

  7. The quality of the meat consumed in the study was not taken into account. Highly processed and adulterated “factory-farmed” meats like salami and hot dogs are lumped together with grass-fed, organic meat as if they’re the same thing. It’s likely that very little of the meat people ate in the study was from pasture-fed animals. Factory fed animals are fed corn (high in polyunsaturated, omega-6 fat), antibiotics, and hormones, all of which negatively impact human health.
  8. We don’t know anything about the lifestyles of the different study groups. Were they under stress? Did they lose their jobs? Did they have other illnesses? Did they live in a toxic environment? All of these factors contribute significantly to disease and mortality.
  9. We don’t know if the people in the study ate more sugar, processed food, artificial sweeteners, preservatives, additives or fast food – all of which are known to cause health problems.
  10. We don’t know if the people who ate more red meat were better off financially than the people who ate less red meat, and thus had more exposure to the “medical industrial complex” – which, as you know from my previous article, kills more than 225,000 people per year and is the 3rd leading cause of death in this country.

I could go on, but I think you get the idea. Nothing to see here, folks. Move along.

Me? I’m gonna go have a big, juicy, grass-fed steak.

Further recommended reading

  1. Meat and Mortality. A great critique of the study by Dr. Michael Eades, author of Protein Power.
  2. More on Meat & Sustainability. A Challenge to Environmentalists.
  3. The Red Scare. Another insightful analysis over at Mark’s Daily Apple.

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The failure of U.S. healthcare

February 28, 2009 in Medical Industrial Complex, Myths & Truths | 6 comments


failureThe U.S. spent 16 percent of its Gross Domestic Product (GDP) – a cool $2 trillion – on health care in 2005.1 Considering this enormous expenditure, we should have the best medicine in the world. We should be reversing disease, preventing disease, and doing minimal harm. However, careful and objective review shows the opposite.

The U.S. ranks just 34th in the world in life expectancy and 29th for infant mortality. Of 13 countries in a recent comparison, the United States ranks an average of 12th (second from bottom) for 16 available health indicators.2

40 million people in this country do not have health insurance. The exorbitant cost of health care seems to be tolerated based on the assumption that better health results from more expensive care, despite studies that as many as 20% to 30% of patients receive contraindicated care.3

Even worse, a recent study by Dr. Barbara Starfield published in 2000 in the prestigious Journal of the American Medical Association demonstrated that iatrogenic incidents (events caused by medical intervention) are the 3rd leading cause of death in this country, causing more than 250,000 deaths per year. Only heart disease and cancer kill more people.

Dr. Starfield estimates that, each year, medical errors and adverse effects of the health care system are responsible for:

  • 116 million extra physician visits
  • 77 million extra prescriptions
  • 17 million emergency department visits
  • 8 million hospitalizations
  • 3 million long-term admissions
  • 199,000 additional deaths
  • $77 billion in extra costs

As grim as they are, these statistics are likely to be seriously underestimated as only about 5 to 20% of iatrogenic incidents are even recordedanalyses which have taken these oversights into consideration estimate that medical care is in fact the leading cause of death in the U.S. each year.

Starfield believes that a major contributor to the poor performance of the United States on health indicators is the high degree of income inequality in this country. Countless studies in the medical literature document the adverse effects of low socioeconomic position on health. New research suggests the adverse effects not only of low social position but, especially, low relative social position in industrialized countries.6

Perhaps the words “health care” have given us the illusion that medicine is about health. In fact, western medicine is not a purveyor of healthcare but of disease-care. When the number one killer in a society is the health care system, that system has no excuse except to address its own urgent shortcomings. Unfortunately, until this happens partaking in allopathic medicine itself is one of the highest causes of death as well as one of the most expensive ways to die.

  1. Park, A. America’s Health Check Up. 11/20/2008. Time Magazine Online. ↩
  2. Starfield B. Primary Care: Balancing Health Needs, Services, and Technology. New York, NY: Oxford University Press; 1998. ↩
  3. Schuster M, McGlynn E, Brook R. How good is the quality of health care in the United States? Milbank Q. 1998;76:517-563 ↩
  4. Leape LL. Error in medicine. JAMA . 1994 Dec 21;272(23):1851-7. ↩
  5. injuryboard.com. General Accounting Office study sheds light on nursing home abuse. July 17, 2003 . Available at: http://www.injuryboard.com/view.cfm/Article=3005. Accessed December 17, 2003 ↩
  6. Wilkinson R. Unhealthy Societies: The Afflictions of Inequality. London, England: Routledge; 1996. ↩

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How to increase your risk of heart disease

August 5, 2008 in Food & Nutrition, Heart Disease, Myths & Truths | 13 comments


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.

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Low-carb diet best for weight loss

July 16, 2008 in Food & Nutrition, Myths & Truths | 9 comments


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

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

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

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

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

This certainly causes me to wonder how much more dramatic the results of this study might have been if the low-carb subjects were encouraged to significantly restrict their consumption of omega-6 fats (which cause water retention, and thus weight gain) and replace them with saturated fats (which do not cause water retention). What is remarkable is that in spite of the consumption of omega-6 fats, the low-carb group still lost more weight than both the low-fat and Mediterranean groups. That’s a strong endorsement for the benefits of a low-carb diet for weight loss.

The low-carb and Mediterranean (to a lesser degree) diet also had other benefits beyond promoting weight loss and improving cholesterol measures. The level of high-sensitivity C-reactive protein decreased significantly only in the Mediterranean and ow-carb group, with the low-carb group again showing the greatest decrease (29% vs. 21%). C-reactive protein is a measure of inflammation that has been positively correlated with heart disease in recent studies. Once again, one must wonder if the reduction would have been even greater in the low-carb group had the subjects been told to restrict their intake of omega-6 fats, which are known to promote inflammation.

Another interesting finding is that although caloric intake was only restricted in the low-fat and Mediterranean diet groups, the low-carb group also ended up eating fewer calories during the diet. Many people who follow a low-carb, high protein/high fat diet find that they spontaneously eat less because additional protein, and in particular fat, leads to greater levels of satiety (satisfaction).

One limitation of the study is that it relied on self-reported dietary intake (this is true of almost every dietary study except those performed in tightly controlled conditions, such as an inpatient facility). However, the study was somewhat unique in that it was conducted in a workplace at a research center with an on-site medical clinic. It also had several other strengths. The drop-out rate was exceptionally low for a study of this kind; all participants started simultaneously; the duration was relatively long (2 years); the study group was relatively large; and the monthly measurements of weight remitted a better understanding of the weight-loss trajectory than other studies.

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The "chemical imbalance" myth

June 30, 2008 in Depression, Myths & Truths | 61 comments


serotonin illustration“A theory that is wrong is considered preferable to admitting our ignorance.” – Elliot Vallenstein, Ph.D.

The idea that depression and other mental health conditions are caused by an imbalance of chemicals in the brain is so deeply ingrained in our psyche that it seems almost sacrilegious to question it.

Direct-to-consumer-advertising (DCTA) campaigns, which have expanded the size of the antidepressant market (Donohue et al., 2004), revolve around the claim that SSRIs (the most popular class of antidepressants) alleviate depression by correcting a deficiency of serotonin in the brain.

For example, Pfizer’s television advertisement for Zoloft states that “depression is a serious medical condition that may be due to a chemical imbalance”, and that “Zoloft works to correct this imbalance.”

Other SSRI advertising campaigns make similar claims. The Effexor website even has a slick video explaining that “research suggests an important link between depression and an imbalance in some of the brain’s chemical messengers. Two neurotransmitters believed to be involved in depression are serotonin and norepinephrine.” The video goes on to explain that Effexor works by increasing serotonin levels in the synapse, which is “believed to relieve symptoms of depression over time.”

These days serotonin is widely promoted as the way to achieve just about every personality trait that is desirable, including self-confidence, creativity, emotional resilience, success, achievement, sociability and high energy. And the converse is also true. Low serotonin levels have been implicated in almost every undesirable mental state and behavioral pattern, such as depression, aggressiveness, suicide, stress, lack of self-confidence, failure, low impulse control, binge eating and other forms of substance abuse.

In fact, the idea that low levels of serotonin cause depression has become so widespread that it’s not uncommon to hear people speak of the need to “boost their serotonin levels” through exercise, herbal supplements or even sexual activity. The “chemical imbalance” theory is so well established that it is now part of the popular lexicon.

It is, after all, a neat theory. It takes a complex and heterogeneous condition (depression) and boils it down to a simple imbalance of two to three neurotransmitters (out of more than 100 that have been identified), which, as it happens, can be “corrected” by long-term drug treatment. This clear and easy-to-follow theory is the driving force behind the $12 billion worth of antidepressant drugs sold each year.

However, there is one (rather large) problem with this theory: there is absolutely no evidence to support it. Recent reviews of the research have demonstrated no link between depression, or any other mental disorder, and an imbalance of chemicals in the brain (Lacasse & Leo, 2005; (Valenstein, 1998).

The ineffectiveness of antidepressant drugs when compared to placebo cast even more doubt on the “chemical imbalance” theory. (See my recent articles Placebos as effective as antidepressants and A closer look at the evidence for more on this.)

Folks, at this point you might want to grab a cup of tea. It’s going to take a while to explain the history of this theory, why it is flawed, and how continues to persist in light of the complete lack of evidence to support it. I will try to be as concise as possible, but there’s a lot of material to cover and a lot of propaganda I need to disabuse you of.

Ready? Let’s start with a bit of history.

The history of the “chemical imbalance” theory

The first antidepressant, iproniazid, was discovered by accident in 1952 after it was observed that some tubercular patients became euphoric when treated with this drug. A bacteriologist named Albert Zeller found that iproniazid was effective in inhibiting the enzyme monoamine oxydase. As its name implies, monoamine oxydase plays an essential role in inactivating monoamines such as epinephrine and norepinephrine. Thus, iproniazid raised levels of epinephrine and norepinephrine which in turn led to stimulation of the sympathetic nervous system – an effect thought to be responsible for the antidepressant action of the drug.

At around the same time, an extract from the plant Rauwolfia serpentina was introduced into western psychiatry. This extract had been used medicinally in India for more than a thousand years and was thought to have a calming effect useful to quite babies, treat insomnia, high blood pressure, insanity and much more. In 1953 chemists at Ciba, a pharmaceutical company, isolated the active compound from this herb and called it reserpine.

In 1955 researchers at the National Institutes of Health reported that reserpine reduces the levels of serotonin in the brains of animals. It was later established that all three of the major biogenic amines in the brain, norepinephrine, serotonin, and dopamine, were all decreased by reserpine (again, in animals).

In animal studies conducted at around the same time, it was found that animals administered reserpine showed a short period of increased excitement and motor activity, followed by a prolonged period of inactivity. The animals often had a hunched posture and an immobility that was thought to resemble catatonia (Valenstein, 1998). Since reserpine lowered levels of serotonin, norepinephrine and dopamine, and caused the effects observed in animals, it was concluded that depression was a result of low levels of biogenic amines. Hence, the “chemical imbalance” theory is born.

However, it was later found that reserpine only rarely produces a true clinical depression. Despite high doses and many months of treatment with reserpine, only 6 percent of the patients developed symptoms even suggestive of depression. In addition, an examination of these 6 percent of patients revealed that all of them had a previous history of depression. (Mendels & Frazer, 1974) There were even reports from a few studies that reserpine could have an antidepressant effect (in spite of reducing levels of serotonin, norepinephrine and dopanmine).

As it turns out, that is only the tip of the iceberg when it comes to revealing the inadequacies of the “chemical imbalance” theory.

The fatal flaws of “chemical imbalance” theory

As Elliot Valenstein Ph.D., Professor Emeritus of psychology and neuroscience at Michigan University, points out in his seminal book Blaming the Brain, “Contrary to what is often claimed, no biochemical, anatomical or functional signs have been found that reliably distinguish the brains of mental patients.” (p. 125)

In his book, Valenstein clearly and systematically dismantles the chemical imbalance theory:

  1. Reducing levels of norepinephrine, serotonin and dopamine does not actually produce depression in humans, even though it appeared to do so in animals.
  2. The theory cannot explain why there are drugs that alleviate depression despite the fact that they have little or no effect on either serotonin or norepinephrine.
  3. Drugs that raise serotonin and norepinephrine levels, such as amphetamine and cocaine, do not alleviate depression.
  4. No one has explained why it takes a relatively long time before antidepressant drugs produce any elevation of mood. Antidepressants produce their maximum elevation of serotonin and norepinephrine in only a day or two, but it often takes several weeks before any improvement in mood occurs.
  5. Although some depressed patients have low levels of serotonin and norepinephrine, the majority do not. Estimates vary, but a reasonable average from several studies indicates that only about 25 percent of depressed patients actually have low levels of these metabolites.
  6. Some depressed patients actually have abnormally high levels of serotonin and norepinephrine, and some patients with no history of depression at all have low levels of these amines.
  7. Although there have been claims that depression may be caused by excessive levels of monoamine oxydase (the enzyme that breaks down serotonin and norepinephrine), this is only true in some depressed patients and not in others.
  8. Antidepressants produce a number of different effects other than increasing norepinephrine and serotonin activity that have not been accounted for when considering their activity on depression.

Another problem is that it is not now possible to measure serotonin and norepinephrine in the brains of patients. Estimates of brain neurotransmitters can only be inferred by measuring the biogenic amine breakdown products (metabolites) in the urine and cerebrospinal fluid. The assumption underlying this measurement is that the level of biogenic amine metabolites in the urine and cerebrospinal fluid reflects the amount of neurotransmitters in the brain. However, less than one-half of the serotonin and norepinephrine metabolites in the urine or cerebrospinal fluid come from the brain. The other half come from various organs in the body. Thus, there are serious problems with what is actually being measured.

Finally, there is not a single peer-reviewed article that can be accurately cited to support claims of serotonin deficiency in any mental disorder, while there are many articles that present counterevidence. Furthermore, the Diagnostic and Statistical Manual of Mental Disorders (DSM) does not list serotonin as the cause of any mental disorder. The American Psychiatric Press Textbook of Clinical Psychiatry addresses serotonin deficiency as an unconfirmed hypothesis, stating “Additional experience has not confirmed the monoamine depletion hypothesis” (Lacasse & Leo, 2005).

When all of this evidence is taken in full, it should be abundantly clear that depression is not caused by a chemical imbalance.

But, as Valenstein shrewdly observes, “there are few rewards waiting for the person who claims that “the emperor is really nude” or who claims that we really do not know what causes depression or why an antidepressant sometimes helps to relieve this condition.”

How have we been fooled?

There are several reasons the idea that mental disorders are caused by a chemical imbalance has become so widespread (and none of them have anything to do with the actual scientific evidence, as we have seen).

It is known that people suffering from mental disorders and especially their families prefer a diagnosis of “physical disease” because it does not convey the stigma and blame commonly associated with “psychological problems”. A “physical disease” may suggest a more optimistic prognosis, and mental patients are often more amenable to drug treatment when they are told they have a physical disease.

Patients are highly susceptible to Direct-to-Consumer-Advertising (DCTA). It has been reported that patients are now presenting to their doctors with a self-described “chemical imbalance” (Kramer, 2002). This is important because studies show that patients who are convinced they are suffering from a neurotransmitter defect are likely to request a prescription for antidepressants, and may be skeptical of physicians who suggest other interventions such as cognitive behavioral therapy (DeRubeis et al., 2005). It has also been shown that anxious and depressed patients “are probably more susceptible to the controlling influence of advertisements (Hollon MF, 2004).

The benefit of the chemical imbalance theory for insurance companies and the pharmaceutical industry is primarily economic. Medical insurers are primarily concerned with cost, and they want to discourage treatments (such as psychotherapy) that may involve many contact hours and considerable expense. Their control over payment schedules enables insurance companies to shift treatment toward drugs and away from psychotherapy.

The motivation of the pharmaceutical companies should be fairly obvious. As mentioned previously, the market for antidepressant drugs is now $12 billion. All publicly traded for-profit companies are required by law to increase the value of their investor’s stock. Perhaps it goes without saying, but it is a simple fact that pharmaceutical companies will do anything they legally (and sometimes illegally) can to maximize revenues.

Studies have shown that the advertisements placed by drug companies in professional journals or distributed directly to physicians are often exaggerated or misleading and do not accurately reflect scientific evidence (Lacasse & Leo, 2005). While physicians deny they are being influenced, it has been shown repeatedly that their prescription preferences are heavily affected by promotional material from drug companies (Moynihan, 2003). Research also suggests that doctors exposed to company reps are more likely to favor drugs over non-drug therapy, and more likely to prescribe expensive medications when equally effective but less costly ones are available (Lexchin, 1989). Some studies have even shown an association between the dose and response: in other words, the more contact between doctors and sales reps the more doctors latch on to the “commercial” messages as opposed to the “scientific” view of a product’s value (Wazana, 2000).

The motivation of psychiatrists to accept the chemical imbalance theory is somewhat more subtle. Starting around 1930, psychiatrists became increasingly aware of growing competition from nonmedical therapists such as psychologists, social workers and counselors. Because of this, psychiatrists have been attracted to physical treatments like drugs and electroshock therapy that differentiate them from nonmedical practitioners. Psychiatry may be the least respected medical specialty (U.S. General Accounting Office report). Many Americans rejected Fruedian talk therapy as quackery, and the whole field of psychiatry lacks the quality of research (randomized, placebo-controlled, double-blind experiments) that serves as the gold-standard in other branches of medicine.

Dr. Colin Ross, a psychiatrist, describes it this way:

“I also saw how badly biological psychiatrists want to be regarded as doctors and accepted by the rest of the medical profession. In their desire to be accepted as real clinical scientists, these psychiatrists were building far too dogmatic an edifice… pushing their certainty far beyond what the data could support.”

Of course there are also many “benefits” to going along with the conventional “chemical imbalance” theory, such as free dinners, symphony tickets, and trips to the Caribbean; consultancy fees, honoraria and stock options from the pharmaceutical companies; and a much larger, growing private practice as the $20 billion spent by drug companies on advertising brings patients to the office. Psychiatrists are just human, like the rest of us, and not many of them can resist all of these benefits.

In sum, the idea that depression is caused by a chemical imbalance is a myth. Pharmaceutical ads for antidepressants assert that depression is a physical diseases because that serves as a natural and easy segue to promoting drug treatment. There may well be biological factors which predispose some individuals toward depression, but predisposition is not a cause. The theory that mental disorders are physical diseases ignores the relevance of psychosocial factors and implies by omission that such factors are of little importance.

Stay tuned for future articles on the psychosocial factors of depression, the loss of sadness as a normal response to life, and the branding of new psychological conditions as a means of increasing drug sales.

Recommended resources

  • Blaming the Brain, by Elliot Valenstein Ph.D.
  • Rethinking Psychiatric Drugs, by Grace Jackson M.D.
  • America Fooled: The truth about antidepressants, antipsychotics and how we’ve been deceived, by Timothy Scott Ph.D.
  • The Loss of Sadness, by Alan Horwitz and Jerome Wakefield
  • The Myth of the Chemical Cure, by Joanna Moncrieff

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A closer look at antidepressants

June 26, 2008 in Depression, Myths & Truths | 15 comments


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

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

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

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

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

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

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

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

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

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

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

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

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

  • Why do antidepressants work
  • How do antidepressants work?
  • Whom do they work for?

Why are these questions important? Because if it turns out that antidepressants do not have any specific drug effects (raising serotonin, for example), and work only because people expect or desire them to work (like placebos), or because of non-specific drug effects (such as sedation or stimulation), then the logic behind prescribing antidepressants at all becomes quite tenuous to say the least – especially when their side effects and risks are taken into consideration.

Now let’s consider each point in turn.

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

What Stephan says about the dangers of meta-analysis are true. However, the same danger applies to overestimating the efficacy of antidepressants. There may be some people who are “responders” who have a response to the drug that is significantly higher than placebo; however, there may also be “nonresponders” whose response to the drug was significantly lower than placebo. There is no indication that antidepressants work on a particular subset of people, and no one has identified who this subset is and why they are helped by antidepressants when others are not.

Kirsch’s analysis that antidepressants do not have a clinically meaningful advantage over placebo (“The Emperor’s New Drugs“) has been almost universally accepted within the scientific community. Kirsch’s and his colleagues invoked the Freedom of Information Act to obtain access to the FDA database of controlled trials used in the initial approval for the most popular antidepressants. According to researcher David O. Antonuccio in his article “Antidepressants: A Triumph of Marketing Over Science?“, it is difficult to imagine a database that would offer a more fair opportunity to evaluate the efficacy of antidepressants.

The fact that Kirsch found that antidepressants were no more effective than placebo is surprising, in a way, because these results come from studies that were underwritten and designed by the drug companies themselves under conditions most favorable to the active drug condition. In other words, the deck was stacked from the start in favor of the drugs, and they still didn’t come out ahead.

Since a drug must be shown to be superior to placebo in order to be approved, placebo effects are incredibly annoying to drug companies and they do everything they can to minimize the impact of placebo in their studies. The fact that the FDA allows them to use these techniques is, in my mind, blatant corruption. Consider the following methods used in the studies Kirsch analyzed (and most studies, for that matter):

  1. Placebo washout period: During the first two weeks of the study, everyone is on a placebo. The subjects that respond best to placebo are eliminated from the study. This potentially removes both antidepressant nonresponders (i.e. those that were on an antidepressant before the study starts who get better when they are taken off of it) and placebo resopnders (i.e. those that are not on antidepressants before the study and who respond to placebo). Imagine the converse: an antidepressant washout procedure that eliminates all of the antidepressant responders before a study begins! Such a procedure would surely be considered bias.
  2. Penetration of the blind: the double-blind in these studies (where neither the patients nor doctors are supposed to know who is taking the drug and who is taking the placebo) is likely to be unintentionally broken because of the pattern of side effects in the active and inactive drug conditions (Greenberg & Fisher, 1997). When efforts are made to ensure the integrity of the blind, drug effects are diminished. For example, a recent review of the Cochrane database of antidepressant studies using “active placebos” (making side effects more difficult to detect) found very small, non-significant differences between drug and placebo, suggesting that trials using inert placebos overestimate drug effects (Moncrieff, Wessely & Hardy, 2001)
  3. Replacement of non-responders: at least six of the studies Kirsch reviewed (of 38) allowed replacement of nonresponders. This means that during the first two weeks of the study, those that were not responding to the drug were removed from the study!
  4. Use of sedative medication: Most studies allowed the prescription of a sedative concurrent with the antidepressant. Since other studies have shown that sedatives are as effective in treating depression as antidepressants, how can we possibly know whether the antidepressant effect obtained (if there was one) in these studies was due to the antidepressant drug or the sedative? There are at least 6 points on the 52-point HAM-D scale that the doctors use to determine whether a patient is depressed or not that are related to sleep and favor medications with sedative properties. Since the mean difference between patients taking drugs and patients taking placebos in the studies Kirsch analyzed was only 2 points, it is entirely possible that this small difference is only due to the effects of the sedatives used in the studies and has nothing to do with a true antidepressant drug effect.
  5. Reliance on clinician ratings: Given that patients tend to report smaller differences than clinicians (Moncrieff, 2001) one certainly wonders how the pattern of results would change using self-report measures like the Beck Depression Inventory.

Frankly, considering the bias against placebo described above, it is simply amazing that placebo still nearly matched the effects of the drug. Imagine what the results might look like if the trials had been performed without these “anti-placebo” measures!

Also, Kirsch et al. pointed out that the overall active drug effects may have been further inflated because mean results were not reported from several studies that found nonsignificant differences between placebo and active drugs.

The advantage to using the FDA database for analysis is considerable. It contains all of the data from initial trials, published or not, and therefore is not subject to the usual publication bias. (As I mentioned earlier in the article, drug companies simply don’t publish negative results. This is known as the “file drawer” phenomenon, since they probably just stuff those studies in some file drawer hoping they will never be found). Antidepressants are significantly more effective than inert placebos in about two-thirds of published trials. However, in the FDA database which includes unpublished trials, Kirsch found that medication outperformed placebo less than half of the time (in 20 of 46 trials).

Although Kirsch’s study is a meta-analyses, he is also looking directly at the results of individual trials. When less than half of individual trials show any advantage for the active drug over placebo, one must really wonder whether these drugs have any specific “antidepressant” effects.

Now on to the next point.

“I don’t have a problem believing that antidepressants work for some people. They certainly work in animal models of depression, where there is no placebo effect.”

Actually, it’s not the case that antidepressants work in animal models. According to Joanna Moncrieff in her book The Myth of the Chemical Cure, it is rarely mentioned that all animal models of depression produce variable results according to where they are conducted. “In other words,” she says, “they are unreliable.” In addition to this, they fail to select specifically for antidepressants and responses are obtained with drugs that are not generally considered to be antidepressants (i.e. amphetamines, opiates, antihistamines, antipsychotics, atropine, pentobarbital, zinc and antibiotics).

Also, the SSRIs (the most popular class of antidepressant drugs) typically fail to have any response in the forced swim test, which is one of the most common antidepressant screening tests. In this test, rats are placed in a tank of water from which they cannot escape. The time until they give up trying to escape is measured, on the assumption that the state of giving up is akin to depression. It is thought that antidepressants should prolong the time to giving up. However, the SSRIs have no such effect.

Finally, other tests for depression also frequently show that non-antidepressant drugs (sedatives, stimulants, antihistamines, etc) yield “false positive” results.

“I don’t think we should banish them from planet Earth. But I do think the fact that we use them so much points to a bigger problem that we should be addressing by other means.”

I’m not so sure we shouldn’t banish them from planet Earth, to tell you the truth.

Longitudinal follow-up studies (which study the effects of antidepresants over the long term – not just the 6-8 week periods the clinical trials look at) show very poor outcomes for people treated for depression both in the hospital and in the community, and the overall prevalence of depression is rising despite increased use of antidepressants (Moncrieff & Kirsch, 2006). Two studies that assessed outcome in depressed patients treated with and without drugs found that people prescribed antidepressants had a slightly worse outcome than those not prescribed them, even after baseline severity had been taken into account (Brugha TS et al, 1992; Ronalds C et al., 1997). No comparable studies exist that show a better outcome in people prescribed antidepressants.

Outside short-term randomized clinical trials there is virtually no evidence that antidepressants have changed the outcome of depression. The evidence that does exist suggests that they may have possibly made it worse. Depression is more common today than before antidepressants were introduced and the outcome has not improved. Epidemiological trends show that the more antidepressants are prescribed, the more prevalent depression is. Sharply rising levels of antidepressant prescribing since the 1990s have been accompanied by increased prevalence of depressive episodes (Patten 2004) and by rising levels of sickness absence for depression (Moncrieff & Pomerleau 2000).

Finally, there is a growing body of research suggesting that antidepressants worsen the chronicity, if not severity, of depression in many patients. Even relatively short-term exposure to antidepressants has been shown to cause chemical and even anatomical changes in the body and brain that could predispose patients to further depressive episodes (Jackson, “Rethinking Psychiatric Drugs“)

Some might argue that antidepressants are important to stave off suicide in very depressed patients. However, there is no evidence that antidepressants reduce the risk of suicide or suicide attempts in comparison with a placebo in clinical trials (Kahn et al. 2000). In fact, rates have actually increased in some age groups and in some countries despite increased antidepressant prescribing (Moncrieff & Kirsch 2006), and when antidepressant trials have been re-analyzed to compensate for erroneous methodologies, the SSRIs have consistently revealed a risk of suicide (completed or attempted) of between two to four times higher than placebo (ackson, “Rethinking Psychiatric Drugs“)

And we haven’t even talked about side effects yet! Since this article is already very long, I’ll save that for another day. Suffice to say that these are not harmless drugs and the side effects can be severe and potentially fatal.

So I ask you, fair readers, when you add all of this up, should doctors continue to prescribe antidepressants? Let’s see what researchers who have been studying antidepressants and depression for decades have to say:

“The SSRIs produce no effects that look likely to be useful in depression. They cause unpleasant agitation in a proportion of patients and, although it is difficult to prove conclusively, an increase in suicidal and violent tendencies may be associated with this effect. Therefore, I can think of no goo reason to prescribe them at all.” – Joanna Moncrieff, 2008

Moncrieff has actually suggested that the term “antidepressant” is a misnomer, because the drugs have not been demonstrated to have a consistent and specific effect against depression.

“There is no doubt that antidepressants have a biochemical impact on the brain, but the valence of that impact is open for considerable debate, and whether it corrects a chemical imbalance is in grave doubt… One day we may look back and marvel at the stroke of marketing genius that led to calling these medications antidepressants in the first place. Kirsch et al. have demonstrated that just because a pill is called an antidepressant, it doesn’t necessarily make it so.” – David Antonuccio, 2002

If antidepressant drugs were the only option for treating depression, one might still be able to make an argument for their use in spite of their lack of efficacy and risks. However, it has repeatedly been shown that aerobic exercise, light therapy, Cognitive Behavioral Therapy, St. John’s Wort, bibliotherapy (prayer) and perhaps acupuncture (more studies are needed) are just as effective for treating depression as antidepressants – with few, if any, adverse effects. In fact, in the case of exercise many of the side effects produced are beneficial (e.g. better overall health and wellness).

Considering that antidepressants are likely no more effective than placebos, have not improved (and perhaps worsened) long-term outcomes, may increase the risk of suicidal and violent behavior and have significant many other significant side effects and risks, including potentially permanent changes in the brain which predispose patients to further depression… and considering that there are well-established alternatives that are just as effective, if not more so, in treating depression with almost no adverse effects and significantly fewer costs, I see no compelling reason to continue prescribing antidepressants.

Obviously many other people are posing this question, particularly in the medical community. Kirsch’s research has been so widely accepted that the debate has not centered around his conclusions, but on the implications of those conclusions. Ironically, it has been suggested by more than one commentator that although we now know that antidepressants aren’t effective, we should continue to prescribe them – if only in an attempt to elicit a placebo effect.

Huh? Let me explain. One major reason people respond to placebo in antidepressant trials is that they expect the drug to work. They expect it to work because of all of the promotion they’ve seen, newspaper and magazine articles they’ve read, and personal testimonials they’ve heard. What would happen if it became known that antidepressants are, in fact, not effective and that they could actually make depression worse. Bye bye placebo effect.

So some researchers and doctors have actually suggested that we should go on promoting the delusion that antidepressants are effective so that people who are taking them will continue to believe that they are working, which of course significantly increases the chance that they will work.

If these drugs were not so potentially dangerous and harmful, and if there were not proven alternatives, I could almost go along with this deception – although it does raise some very interesting ethical questions. However, the drugs are potentially dangerous and harmful, and there are proven alternatives, so I cannot agree with this approach.

In closing, I just want to remind anyone who is currently taking an antidepressant and thinking about stopping that it is essential you do so under your doctor’s supervision. You will have to gradually taper off of your medication – do not stop abruptly!

As always, I welcome your comments and questions.

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