Fast Food, Weight Gain and Insulin Resistance

CarbSane just posted an interesting new study that fits in nicely with what we're discussing here.  It's part of the US Coronary Artery Risk Development in Young Adults (CARDIA) study, which is a long-term observational study that is publishing many interesting findings.  The new study is titled "Fast-food habits, weight gain, and insulin resistance (the CARDIA study): 15-year prospective analysis" (1).  The results speak for themselves, loud and clear (I've edited some numbers out of the quote for clarity):
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Obesity and the Fluid-in, Fluid-out Therapy for Edema

I recently attended a lecture by Dr. Arya M. Sharma here at the University of Washington. Dr. Sharma is a Canadian clinician who specializes in the treatment of obesity. He gave the UW Science in Medicine lecture, which is a prestigious invited lecture.

He spent a little bit of time pointing out the fallacy behind conventional obesity treatment. He used the analogy of edema, which is an abnormal accumulation of fluid in the body.

Since we know that the amount of fluid contained in the body depends on the amount of fluid entering the body and the amount of fluid leaving the body, the treatment for edema is obvious: drink less, pee more.

Of course, this makes no sense. It doesn't address the underlying cause of edema and it will not help the patient. Yet we apply that exact same logic to fat loss. Since the amount of energy contained in the body (in the form of fat) depends on the amount entering and the amount leaving, the solution is easy: eat less, move more. Well, yes, if you can stick to that program it will cause fat loss. But that's equivalent to telling someone with edema to drink less water. It will cause a loss of fluid, but it won't correct the underlying problem that caused excessive fluid retention in the first place.

For example, if you have edema because your heart isn't pumping effectively (cardiac insufficiency), the heart is the problem that must be addressed. Any other treatment is purely symptomatic and is not a cure.

The same applies to obesity. If you don't correct the alteration in the system that causes an obese person to 'defend' his elevated fat mass against changes*, anything you do is symptomatic treatment and is unlikely to be very effective in the long term. My goal is to develop a method that goes beyond symptomatic treatment and allows the body to naturally return to a lower fat mass. I've been doing a lot of reading and I have a simple new idea that I feel confident in. It also neatly explains the results of a variety of weight loss diets. I've dropped a few hints here and there, but I'll be formally unveiling it in the next couple of months. Stay tuned.


* The body fat homeostasis system. The core element appears to be a negative feedback loop between body fat (via leptin, and insulin to a lesser degree) and the brain (primarily the hypothalamus, but other regions are involved). There are many other elements in the system, but that one seems to set the 'gain' on all the others and guides long-term fat mass homeostasis. The brain is the gatekeeper of both energy intake and energy expenditure, and unconscious processes strongly suggest appropriate levels for both factors according to the brain's perceived homeostatic needs. Those suggestions can be overridden consciously, but it requires a perpetual high degree of discipline, whereas someone who has been lean all her life doesn't require discipline to remain lean because her brain is suggesting behaviors that naturally defend leanness. I know what I'm saying here may seem controversial to some people reading this, because it's contrary to what they've read on the internet or in the popular press, but it's not particularly controversial in my field. In fact, you'll find most of this stuff in general neuroscience textbooks dating back more than 10 years (e.g., Eric Kandel and colleagues, Principles of Neuroscience).

Safflower Oil Study

A few people have sent me a new study claiming to demonstrate that half a tablespoon of safflower oil a day improves insulin sensitivity, increases HDL and decreases inflammation in diabetics (1). Let me explain why this study does not show what it claims.

It all comes down to a little thing called a control group, which is the basis for comparison that you use to determine if your intervention had an effect. This study didn't have one for the safflower group. What it had was two intervention groups, one given 6.4g conjugated linoleic acid (CLA; 50% c9t11 and 50% t10c12-CLA) per day, and one given 8g safflower oil. I have to guess that this study was originally designed to test the effects of the CLA, with the safflower oil group as the control group, and that the interpretation of the data changed after the results came in. Otherwise, I don't understand why they would conduct a study like this without a control group.

Anyway, they found that the safflower oil group did better than the CLA group over 16 weeks, showing a higher insulin sensitivity, higher HDL, lower HbA1c (a marker of average blood glucose levels) and lower CRP (a marker of inflammation). But they also found that the safflower group improved slightly compared to baseline, therefore they decided to attribute the difference to a beneficial effect of safflower oil. The problem is that without a control (placebo) group for comparison, there's no way to know if the improvement would have occurred regardless of treatment, due to the season changing, more regular check-ups at the doctor's office due to participating in a study, or countless other unforeseen factors. A control group is essential for the accurate interpretation of results, which is why drug studies always have placebo groups.

What we can say is that the safflower oil group fared better than the CLA group, because there was a difference between the two. However, what I think really happened is that the CLA supplement was harmful and the small dose of safflower oil had no effect. Why? Because the t10c12 isomer of CLA, which was half their pill, has already been shown by previous well-controlled studies to reduce insulin sensitivity, decrease HDL and increase inflammatory markers at a similar dose and for a similar duration (2, 3). The safflower oil group only looked good by comparison. We can add this study to the "research bloopers" file.

It's worth noting that naturally occurring CLA mixtures, similar to those found in pastured dairy and ruminant fat, have not been shown to cause metabolic problems such as those caused by isolated t10c12 CLA.

Gluten-Free January Survey Data, Part II: Health Effects of a Gluten-Free Diet

GFJ participants chose between three diet styles: a simple gluten-free diet; a "paleo light" diet diet that eliminated sugar and industrial seed (vegetable) oils in addition to gluten; and a "paleo full monty" diet that only included categories of food that would have been available to our pre-agricultural ancestors. The data in this post represent the simple gluten-free diet group, and do not represent the other two, which I'll analyze separately.

To get the data I'll be presenting below, first I excluded participants who stated on the survey that they did not adhere to the diet. Next, I excluded participants who were gluten-free before January, because they would presumably not have experienced a change from continuing to avoid gluten. That left us with 53 participants.

For each of these graphs, the vertical axis represents the number of participants in each category. They won't necessarily add up to 53, for several reasons. The most common reason is that for the questions asking about changes in health conditions, I didn't include responses from people who didn't have the condition in question at baseline because there was nothing to change.

Question #1: What is your overall opinion of the effect of gluten free January on you?

Participants had a very positive experience with the gluten-free diet. Not one person reported a negative overall experience.

Question #2: Did you note a weight change at the end of gluten free January?

And here are the data for people who described themselves as overweight at baseline:

Two-thirds of people who were overweight at baseline lost weight, and only one person out of 37 gained weight. That is striking. A number of people didn't weigh themselves, which is why the numbers only add up to 37.

Question #3: Before January 2011, did you have a problem with intestinal transit (frequent constipation or diarrhea)? If so, did your symptoms change during the month of January?


Responses are heavily weighted toward improvement, although there were a few instances where transit worsened. Transit problems are one of the most common manifestations of gluten sensitivity.

Question #4: Before January 2011, did you have frequent digestive discomfort (pain, bloating, etc.)? If so, did your symptoms change during the month of January?


Digestive discomfort was common, and the gluten-free diet improved it in nearly everyone who had it at baseline. I find this really impressive.

Question #5: Before January 2011, did you have acid reflux? If so, did your symptoms change during the month of January?

Acid reflux responded well to a gluten-free diet.

Question #6: Before January 2011, did you have a problem with tiredness/lethargy? If so, did your symptoms change during the month of January?
Lethargy was common and generally improved in people who avoided gluten. This doesn't surprise me at all. The recent controlled gluten study in irritable bowel syndrome patients found that lethargy was the most reliable consequence of eating gluten that they measured (1, 2). That has also been my personal experience.

Question #7: Before January 2011, did you have a problem with anxiety? If so, did your symptoms change during the month of January?

Anxiety tended to improve in most participants who started with it.

Question #8: Before January 2011, did you have a problem with an autoimmune or inflammatory condition? If so, did your symptoms change during the month of January?

Autoimmune and inflammatory conditions tended to improve in the gluten-free group, although one person experienced a worsening of symptoms.

Question #9: If you ate gluten again or did a gluten challenge after gluten free January, what was the effect?

Just under half of participants experienced moderate or significant negative symptoms when they re-introduced gluten at the end of the month. Two people felt better after re-introducing gluten.


Conclusion

I find these results striking. Participants overwhelmingly improved in every health category we measured. Although the data may have been somewhat biased due to the 53% response rate, it's indisputable that a large number of participants, probably the majority, benefited from avoiding gluten for a month. At some point, we're going to compile some of the comments people left in the survey, which were overwhelmingly positive. Here's a typical comment in response to the question " In your own words, how would you describe your January 2011 experience" (used with permission):

Amazing! I would recommend the experiment to anyone. I felt completely more alert, and less bloated. When I ate some gluten at the close of the experiment, I felt gross, bloated, and lethargic.

I think it's worth mentioning that some participants also eliminated other starches, particularly refined starches. Judging by the comments, the diet was probably lower in carbohydrate for a number of participants. We may try to assess that next year.

Flu Season is Here

I've noticed everyone around me getting sick lately (I seem to have become mostly immune to colds and the flu in the last couple of years), so I took a look at Google Flu Trends. Lo and behold, the United States is currently near peak flu incidence for the 2010-2011 season. Here's a graph from Flu Trends. This year's trend is in dark blue:


Flu Trends also has data for individual US states and a number of other countries.

It's time to tighten up your diet and lifestyle if you want to avoid the flu this year. Personally, I feel that eating well, managing stress effectively, and taking 2,000 IU of vitamin D3 per day in winter have helped me avoid colds and the flu.

Polyphenols, Hormesis and Disease: Part II

In the last post, I explained that the body treats polyphenols as potentially harmful foreign chemicals, or "xenobiotics". How can we reconcile this with the growing evidence that at least a subset of polyphenols have health benefits?

Clues from Ionizing Radiation

One of the more curious things that has been reported in the scientific literature is that although high-dose ionizing radiation (such as X-rays) is clearly harmful, leading to cancer, premature aging and other problems, under some conditions low-dose ionizing radiation can actually decrease cancer risk and increase resistance to other stressors (1, 2, 3, 4, 5). It does so by triggering a protective cellular response, increasing cellular defenses out of proportion to the minor threat posed by the radiation itself. The ability of mild stressors to increase stress resistance is called "hormesis." Exercise is a common example. I've written about this phenomenon in the past (6).

The Case of Resveratrol

Resveratrol is perhaps the most widely known polyphenol, available in supplement stores nationwide. It's seen a lot of hype, being hailed as a "calorie restriction mimetic" and the reason for the "French paradox."* But there is quite a large body of evidence suggesting that resveratrol functions in the same manner as low-dose ionizing radiation and other bioactive polyphenols: by acting as a mild toxin that triggers a hormetic response (7). Just as in the case of radiation, high doses of resveratrol are harmful rather than helpful. This has obvious implications for the supplementation of resveratrol and other polyphenols. A recent review article on polyphenols stated that while dietary polyphenols may be protective, "high-dose fortified foods or dietary supplements are of unproven efficacy and possibly harmful" (8).

The Cellular Response to Oxidants

Although it may not be obvious, radiation and polyphenols activate a cellular response that is similar in many ways. Both activate the transcription factor Nrf2, which activates genes that are involved in detoxification of chemicals and antioxidant defense**(9, 10, 11, 12). This is thought to be due to the fact that polyphenols, just like radiation, may temporarily increase the level of oxidative stress inside cells. Here's a quote from the polyphenol review article quoted above (13):

We have found that [polyphenols] are potentially far more than 'just antioxidants', but that they are probably insignificant players as 'conventional' antioxidants. They appear, under most circumstances, to be just the opposite, i.e. prooxidants, that nevertheless appear to contribute strongly to protection from oxidative stress by inducing cellular endogenous enzymic protective mechanisms. They appear to be able to regulate not only antioxidant gene transcription but also numerous aspects of intracellular signaling cascades involved in the regulation of cell growth, inflammation and many other processes.

It's worth noting that this is essentially the opposite of what you'll hear on the evening news, that polyphenols are direct antioxidants. The scientific cutting edge has largely discarded that hypothesis, but the mainstream has not yet caught on.

Nrf2 is one of the main pathways by which polyphenols increase stress resistance and antioxidant defenses, including the key cellular antioxidant glutathione (14). Nrf2 activity is correlated with longevity across species (15). Inducing Nrf2 activity via polyphenols or by other means substantially reduces the risk of common lifestyle disorders in animal models, including cardiovascular disease, diabetes and cancer (16, 17, 18), although Nrf2 isn't necessarily the only mechanism. The human evidence is broadly consistent with the studies in animals, although not as well developed.

One of the most interesting effects of hormesis is that exposure to one stressor can increase resistance to other stressors. For example, long-term consumption of high-polyphenol chocolate increases sunburn resistance in humans, implying that it induces a hormetic response in skin (19). Polyphenol-rich foods such as green tea reduce sunburn and skin cancer development in animals (20, 21).

Chris Masterjohn first introduced me to Nrf2 and the idea that polyphenols act through hormesis. Chris studies the effects of green tea on health, which seem to be mediated by polyphenols.

A Second Mechanism

There is a place in the body where polyphenols are concentrated enough to be direct antioxidants: in the digestive tract after consuming polyphenol-rich foods. Digestion is a chemically harsh process that readily oxidizes ingested substances such as polyunsaturated fats (22). Oxidized fat is neither healthy when it's formed in the deep fryer, nor when it's formed in the digestive tract (23, 24). Eating polyphenol-rich foods effectively prevents these fats from being oxidized during digestion (25). One consequence of this appears to be better absorption and assimilation of the exceptionally fragile omega-3 polyunsaturated fatty acids (26).

What does it all Mean?

I think that overall, the evidence suggests that polyphenol-rich foods are healthy in moderation, and eating them on a regular basis is generally a good idea. Certain other plant chemicals, such as suforaphane found in cruciferous vegetables, and allicin found in garlic, exhibit similar effects and may also act by hormesis (27). Some of the best-studied polyphenol-rich foods are tea (particularly green tea), blueberries, extra-virgin olive oil, red wine, citrus fruits, hibiscus tea, soy, dark chocolate, coffee, turmeric and other herbs and spices, and a number of traditional medicinal herbs. A good rule of thumb is to "eat the rainbow", choosing foods with a variety of colors.

Supplementing with polyphenols and other plant chemicals in amounts that would not be achievable by eating food is probably not a good idea.


* The "paradox" whereby the French eat a diet rich in saturated fat, yet have a low heart attack risk compared to other affluent Western nations.

** Genes containing an antioxidant response element (ARE) in the promoter region. ARE is also sometimes called the electrophile response element (EpRE).

The Diabetes Epidemic

The CDC just released its latest estimate of diabetes prevalence in the US (1):

Diabetes affects 8.3 percent of Americans of all ages, and 11.3 percent of adults aged 20 and older, according to the National Diabetes Fact Sheet for 2011. About 27 percent of those with diabetes—7 million Americans—do not know they have the disease. Prediabetes affects 35 percent of adults aged 20 and older.

Wow-- this is a massive problem. The prevalence of diabetes has been increasing over time, due to more people developing the disorder, improvements in diabetes care leading to longer survival time, and changes in the way diabetes is diagnosed. Here's a graph I put together based on CDC data, showing the trend of diabetes prevalence (percent) from 1980 to 2008 in different age categories (2):

These data are self-reported, and do not correct for differences in diagnosis methods, so they should be viewed with caution-- but they still serve to illustrate the trend. There was an increase in diabetes incidence that began in the early 1990s. More than 90 percent of cases are type 2 diabetics. Disturbingly, the trend does not show any signs of slowing.

The diabetes epidemic has followed on the heels of the obesity epidemic with 10-20 years of lag time. Excess body fat is the number one risk factor for diabetes*. As far as I can tell, type 2 diabetes is caused by insulin resistance, which is probably due to energy intake exceeding energy needs (overnutrition), causing a state of cellular insulin resistance as a defense mechanism to protect against the damaging effects of too much glucose and fatty acids (3). In addition, type 2 diabetes requires a predisposition that prevents the pancreatic beta cells from keeping up with the greatly increased insulin needs of an insulin resistant person**. Both factors are required, and not all insulin resistant people will develop diabetes as some people's beta cells are able to compensate by hypersecreting insulin.

Why does energy intake exceed energy needs in modern America and in most affluent countries? Why has the typical person's calorie intake increased by 250 calories per day since 1970 (4)? I believe it's because the fat mass "setpoint" has been increased, typically but not always by industrial food. I've been developing some new thoughts on this lately, and potentially new solutions, which I'll reveal when they're ready.


* In other words, it's the best predictor of future diabetes risk.

** Most of the common gene variants (of known function) linked with type 2 diabetes are thought to impact beta cell function (5).

Eating Wheat Gluten Causes Symptoms in Some People Who Don't Have Celiac Disease

Irritable bowel syndrome (IBS) is a condition characterized by the frequent occurrence of abdominal pain, diarrhea, constipation, bloating and/or gas. If that sounds like an extremely broad description, that's because it is. The word "syndrome" is medicalese for "we don't know what causes it." IBS seems to be a catch-all for various persistent digestive problems that aren't defined as separate disorders, and it has a very high prevalence: as high as 14 percent of people in the US, although the estimates depend on what diagnostic criteria are used (1). It can be brought on or exacerbated by several different types of stressors, including emotional stress and infection.

Maelán Fontes Villalba at Lund University recently forwarded me an interesting new paper in the American Journal of Gastroenterology (2). Dr. Jessica R. Biesiekierski and colleagues recruited 34 IBS patients who did not have celiac disease, but who felt they had benefited from going gluten-free in their daily lives*. All patients continued on their pre-study gluten-free diet, however, all participants were provided with two slices of gluten-free bread and one gluten-free muffin per day. The investigators added isolated wheat gluten to the bread and muffins of half the study group.

During the six weeks of the intervention, patients receiving the gluten-free food fared considerably better on nearly every symptom of IBS measured. The most striking difference was in tiredness-- the gluten-free group was much less tired on average than the gluten group. Interestingly, they found that a negative reaction to gluten was not necessarily accompanied by the presence of anti-gluten antibodies in the blood, which is a test often used to diagnose gluten sensitivity.

Here's what I take away from this study:

1. Wheat gluten can cause symptoms in susceptible people who do not have celiac disease.
2. A lack of circulating antibodies against gluten does not necessarily indicate a lack of gluten sensitivity.
   
3. People with mysterious digestive problems may want to try avoiding gluten for a while to see if it improves their symptoms**.
4. People with mysterious fatigue may want to try avoiding gluten.
   

A previous study in 1981 showed that feeding volunteers a large dose of gluten every day for 6 weeks caused adverse gastrointestinal effects, including inflammatory changes, in relatives of people with celiac disease, who did not themselves have celiac (3). Together, these two studies are the most solid evidence that gluten can be damaging in people without celiac disease, a topic that has not received much interest in the biomedical research community.

I don't expect everyone to benefit from avoiding gluten. But for those who are really sensitive, it can make a huge difference. Digestive, autoimmune and neurological disorders associate most strongly with gluten sensitivity. Avoiding gluten can be a fruitful thing to try in cases of mysterious chronic illness. We're two-thirds of the way through Gluten-Free January. I've been fastidiously avoiding gluten, as annoying as it's been at times***. Has anyone noticed a change in their health?


* 56% of volunteers carried HLA-DQ2 or DQ8 alleles, which is slightly higher than the general population. Nearly all people with celiac disease carry one of these two alleles. 28% of volunteers were positive for anti-gliadin IgA, which is higher than the general population.

** Some people feel they are reacting to the fructans in wheat, rather than the gluten. If a modest amount of onion causes the same symptoms as eating wheat, then that may be true. If not, then it's probably the gluten.

*** I'm usually about 95% gluten-free anyway. But when I want a real beer, I want one brewed with barley. And when I want Thai food or sushi, I don't worry about a little bit of wheat in the soy sauce. If a friend makes me food with gluten in it, I'll eat it and enjoy it. This month I'm 100% gluten-free though, because I can't in good conscience encourage my blog readership to try it if I'm not doing it myself. At the end of the month, I'm going to do a blinded gluten challenge (with a gluten-free control challenge) to see once and for all if I react to it. Stay tuned for more on that.

Dairy Fat and Diabetes

Introduction

Having access to embargoed news from the Annals of Internal Medicine is really fun. I get to report on important studies at the same time as the news media. But this week, I got my hands on a study that I'm not sure will be widely reported (Mozaffarian et al. Trans-palmitoleic Acid, Metabolic Risk Factors, and New-Onset Diabetes in US Adults. Ann Internal Med. 2010). Why? Because it suggests that dairy fat may protect against diabetes.

The lead author is Dr. Dariush Mozaffarian, whose meta-analysis of diet-heart controlled trials I recently criticized (1). I think this is a good opportunity for me to acknowledge that Dr. Mozaffarian and his colleagues have published some brave papers in the past that challenged conventional wisdom. For example, in a 2005 study, they found that postmenopausal women who ate the most saturated fat had the slowest rate of narrowing of their coronary arteries over time (2). It wasn't a popular finding but he has defended it. His colleague Dr. Walter Willett thinks dietary fat is fine (although he favors corn oil), whole eggs can be part of a healthy diet, and there are worse things than eating coconut from time to time. Dr. Willett is also a strong advocate of unrefined foods and home cooking, which I believe are two of the main pillars of healthy eating.

Let's hit the data

Investigators collected two measures of dairy fat intake in 3,736 Americans:

1. 24 hour dietary recall questionnaires, six times. This records volunteers' food intake at the beginning of the study.
2. Blood (plasma phospholipid) content of trans-palmitoleate. Dairy fat and red meat fat are virtually the only sources of this fatty acid, so it reflects the intake of these foods. Most of the trans-palmitoleate came from dairy in this study, although red meat was also a significant source.

After adjustment for confounding factors, trans-palmitoleate levels were associated with a smaller waist circumference, higher HDL cholesterol, lower serum triglycerides, lower C-reactive protein, lower fasting insulin and lower calculated insulin resistance. Furthermore, people with the highest trans-palmitoleate levels had 1/3 the risk of developing diabetes over the three years volunteers were followed. Keep in mind, however, that this is an observational study and does not prove that dairy fat prevents diabetes.

Even though certain blood fatty acids partially represent food intake, they can also represent metabolic conditions. For example, people on their way to type II diabetes tend to have more saturated blood lipids, independent of diet (3, 4)*. So it's reassuring to see that dietary trans-palmitoleate intake was closely related to the serum level. The investigators also noted that "greater whole-fat dairy consumption was associated with lower risk for diabetes," which increases my confidence that serum trans-palmitoleate is actually measuring dairy fat intake to some degree. However, in the end, I think the striking association they observed was partially due to dairy fat intake, but mostly due to metabolic factors that had nothing to do with dairy fat**.

Here's a nice quote:

Our findings support potential metabolic benefits of dairy consumption and suggest that trans-palmitoleate may mediate these effects***. They also suggest that efforts to promote exclusive consumption of low-fat and nonfat dairy products, which would lower population exposure to trans-palmitoleate, may be premature until the mediators of the health effects of dairy consumption are better established.

Never thought I'd see the day! Not bad, but I can do better:

Our findings support eating as much butter as possible****. Don't waste your money on low-fat cream, either (half-n-half). We're sorry that public health authorities have spent 30 years telling you to eat low-fat dairy when most studies are actually more consistent with the idea that dairy fat reduces the risk obesity and chronic disease.

What are these studies suggesting that dairy fat may be protective, you ask? That will be the topic of another post, my friends.


*Probably due to uncontrolled de novo lipogenesis because of insulin resistance. Many studies find that serum saturated fatty acids are higher in those with metabolic dysfunction, independent of diet. They sometimes interpret that as showing that people are lying about their diet, rather than that serum saturated fatty acids don't reflect diet very well. For example, in one study I cited, investigators found no relationship between dietary saturated fat and diabetes risk, but they did find a relationship between serum saturated fatty acids and diabetes risk (5). They then proceeded to refer to the serum measurements as "objective measurements" that can tease apart "important associations with diabetes incidence that may be missed when assessed by [food questionnaires]." They go on to say that serum fatty acids are "useful as biomarkers for fatty acid intake," which is true for some fatty acids but not remotely for most of the saturated ones, according to their own study. Basically, they try to insinuate that dietary saturated fat is the culprit, and the only reason they couldn't measure that association directly is that people who went on to develop diabetes inaccurately reported their diets! A more likely explanation is that elevated serum saturated fatty acids are simply a marker of insulin resistance (and thus uncontrolled de novo lipogenesis), and had nothing to do with diet.

**Why do I say that? Because mathematically adjusting for dairy and meat fat intake did not substantially weaken the association between phospholipid trans-palmitoleate and reduced diabetes risk (Table 4). In other words, if you believe their math, dairy/meat fat intake only accounted for a small part of the protective association. That implies that healthy people maintain a higher serum phospholipid trans-palmitoleate level than unhealthy people, even if both groups eat the same amount of trans-palmitoleate. If they hadn't mentioned that full-fat dairy fat intake was directly associated with a lower risk of diabetes, I would not find the study very interesting because I'd have my doubts that it was relevant to diet.

***I find it highly doubtful that trans-palmitoleate entirely mediates the positive health outcomes associated with dairy fat intake. I think it's more likely to simply be a marker of milk fat, which contains a number of potentially protective substances such as CLA, vitamin K2, butyric acid, and the natural trans fats including trans-palmitoleate. In addition, dairy fat is low in omega-6 polyunsaturated fat. I find it unlikely that their fancy math was able to tease those factors apart, because those substances all travel together in dairy fat. trans-palmitoleate pills are not going to replace butter.

****That's a joke. I think butter can be part of healthy diet, but that doesn't mean gorging on it is a good idea. This study does not prove that dairy fat prevents diabetes, it simply suggests that it may.

Can a Statin Neutralize the Cardiovascular Risk of Unhealthy Dietary Choices?

The title of this post is the exact title of a recent editorial in the American Journal of Cardiology (1). Investigators calculated the "risk for cardiovascular disease associated with the total fat and trans fat content of fast foods", and compared it to the "risk decrease provided by daily statin consumption". Here's what they found:

The risk reduction associated with the daily consumption of most statins, with the exception of pravastatin, is more powerful than the risk increase caused by the daily extra fat intake associated with a 7-oz hamburger (Quarter Pounder®) with cheese and a small milkshake. In conclusion, statin therapy can neutralize the cardiovascular risk caused by harmful diet choices.

Routine accessibility of statins in establishments providing unhealthy food might be a rational modern means to offset the cardiovascular risk. Fast food outlets already offer free condiments to supplement meals. A free statin-containing accompaniment would offer cardiovascular benefits, opposite to the effects of equally available salt, sugar, and high-fat condiments. Although no substitute for systematic lifestyle improvements, including healthy diet, regular exercise, weight loss, and smoking cessation, complimentary statin packets would add, at little cost, 1 positive choice to a panoply of negative ones.

Wow. Later in the editorial, they recommend "a new and protective packet, “MacStatin,” which could be sprinkled onto a Quarter Pounder or into a milkshake." I'm not making this up!

I can't be sure, but I think there's a pretty good chance the authors were being facetious in this editorial, in which case I think a) it's hilarious, b) most people aren't going to get the joke. If they are joking, the editorial is designed to shine a light on the sad state of mainstream preventive healthcare. Rather than trying to educate people and change the deadly industrial food system, which is at the root of a constellation of health problems, many people think it's acceptable to partially correct one health risk by tinkering with the human metabolism using drugs. To be fair, most people aren't willing to change their diet and lifestyle habits (and perhaps for some it's even too late), so frustrated physicians prescribe drugs to mitigate the risk. I accept that. But if our society is really committed to its own health and well-being, we'll remove the artificial incentives that favor industrial food, and educate children from a young age on how to eat well.

I think one of the main challenges we face is that our current system is immensely lucrative for powerful financial interests. Industrial agriculture lines the pockets of a few large farmers and executives (while smaller farmers go broke and get bought out), industrial food processing concentrates profit among a handful of mega-manufacturers, and then people who are made ill by the resulting food spend an exorbitant amount of money on increasingly sophisticated (and expensive) healthcare. It's a system that effectively milks US citizens for a huge amount of money, and keeps the economy rolling at the expense of the average person's well-being. All of these groups have powerful lobbies that ensure the continuity of the current system. Litigation isn't the main reason our healthcare is so expensive in the US; high levels of chronic disease, expensive new technology, a "kitchen sink" treatment approach, and inefficient private companies are the real reasons.

If the editorial is serious, there are so many things wrong with it I don't even know where to begin. Here are a few problems:

1. They assume the risk of heart attack conveyed by eating fast food is due to its total and trans fat content, which is simplistic. To support that supposition, they cite one study: the Health Professionals Follow-up Study (2). This is one of the best diet-health observational studies conducted to date. The authors of the editorial appear not to have read the study carefully, because it found no association between total or saturated fat intake and heart attack risk, when adjusted for confounding variables. The number they quoted (relative risk = 1.23) was before adjustment for fiber intake (relative risk = 1.02 after adjustment), and in any case, it was not statistically significant even before adjustment. How did that get past peer review? Answer: reviewers aren't critical of hypotheses they like.
   
2. Statins mostly work in middle-aged men, and reduce the risk of heart attack by about one quarter. The authors excluded several recent unsupportive trials from their analysis. Dr. Michel de Lorgeril reviewed these trials recently (3). For these reasons, adding a statin to fast food would probably have a negligible effect on the heart attack risk of the general population.
   
3. "Statins rarely cause negative side effects." BS. Of the half dozen people I know who have gone on statins, all of them have had some kind of negative side effect, two of them unpleasant enough that they discontinued treatment against their doctor's wishes. Several of them who remained on statins are unlikely to benefit because of their demographic, yet they remain on statins on their doctors' advice.
   
4. Industrial food is probably the main contributor to heart attack risk. Cultures that don't eat industrial food are almost totally free of heart attacks, as demonstrated by a variety of high-quality studies (4, 5, 6, 7, 8, 9). No drug can replicate that, not even close.
   

I have an alternative proposal. Rather than giving people statins along with their Big Mac, why don't we change the incentive structure that artificially favors the Big Mac, french fries and soft drink? If it weren't for corn, soybean and wheat subsidies, fast food wouldn't be so cheap. Neither would any other processed food. Fresh, whole food would be price competitive with industrial food, particularly if we applied the grain subsidies to more wholesome foods. Grass-fed beef and dairy would cost the same as grain-fed. I'm no economist, so I don't know how realistic this really is. However, my central point still stands: we can change the incentive structure so that it no longer artificially favors industrial food. That will require that the American public get fed up and finally butt heads with special interest groups.

Interview with Jimmy Moore

About two months ago, I did an interview with Jimmy Moore of the Livin' la Vida Low Carb internet empire. I hardly remember what we talked about, but I think it went well. I enjoyed Jimmy's pleasant and open-minded attitude. Head over to Jimmy's website and listen to the interview here.

I do recall making at least one mistake. When discussing heart attacks,I said "atrial fibrillation" when I meant "ventricular fibrillation".

Nitrate: a Protective Factor in Leafy Greens

Cancer Link and Food Sources

Nitrate (NO3) is a molecule that has received a lot of bad press over the years. It was initially thought to promote digestive cancers, in part due to its ability to form carcinogens in the digestive tract. As it's used as a preservative in processed meats, and there is a link between processed meats and gastric cancer (1), nitrate was viewed with suspicion and a number of countries imposed strict limits on its use as a food additive.

But what if I told you that by far the greatest source of nitrate in the modern diet isn't processed meat-- but vegetables, particularly leafy greens (2)? And that the evidence specifically linking nitrate consumption to gastric cancer has largely failed to materialize? For example, one study found no difference in the incidence of gastric cancer between nitrate fertilizer plant workers and the general population (3). Most other studies in animals and humans have not supported the hypothesis that nitrate itself is carcinogenic (4, 5, 6). This, combined with recent findings on nitrate biology, has the experts singing a different tune in the last few years.

A New Example of Human Symbiosis

In 2003, Dr. K. Cosby and colleagues showed that nitrite (NO2; not the same as nitrate) dilates blood vessels in humans when infused into the blood (7). Investigators subsequently uncovered an amazing new example of human-bacteria symbiosis: dietary nitrate (NO3) is absorbed from the gut into the bloodstream and picked up by the salivary glands. It's then secreted into saliva, where oral bacteria use it as an energy source, converting it to nitrite (NO2). After swallowing, the nitrite is reabsorbed into the bloodstream (8). Humans and oral bacteria may have co-evolved to take advantage of this process. Antibacterial mouthwash prevents it.

Nitrate Protects the Cardiovascular System

In 2008, Dr. Andrew J. Webb and colleagues showed that nitrate in the form of 1/2 liter of beet juice (equivalent in volume to about 1.5 soda cans) substantially lowers blood pressure in healthy volunteers for over 24 hours. It also preserved blood vessel performance after brief oxygen deprivation, and reduced the tendency of the blood to clot (9). These are all changes that one would expect to protect against cardiovascular disease. Another group showed that in monkeys, the ability of nitrite to lower blood pressure did not diminish after two weeks, showing that the animals did not develop a tolerance to it on this timescale (10).

Subsequent studies showed that dietary nitrite reduces blood vessel dysfunction and inflammation (CRP) in cholesterol-fed mice (11). Low doses of nitrite also dramatically reduce tissue death in the hearts of mice exposed to conditions mimicking a heart attack, as well as protecting other tissues against oxygen deprivation damage (12). The doses used in this study were the equivalent of a human eating a large serving (100 g; roughly 1/4 lb) of lettuce or spinach.

Mechanism

Nitrite is thought to protect the cardiovascular system by serving as a precursor for nitric oxide (NO), one of the most potent anti-inflammatory and blood vessel-dilating compounds in the body (13). A decrease in blood vessel nitric oxide is probably one of the mechanisms of diet-induced atherosclerosis and increased clotting tendency, and it is likely an early consequence of eating a poor diet (14).

The Long View

Leafy greens were one of the "protective foods" emphasized by the nutrition giant Sir Edward Mellanby (15), along with eggs and high-quality full-fat dairy. There are many reasons to believe greens are an excellent contribution to the human diet, and what researchers have recently learned about nitrate biology certainly reinforces that notion. Leafy greens may be particularly useful for the prevention and reversal of cardiovascular disease, but are likely to have positive effects on other organ systems both in health and disease. It's ironic that a molecule suspected to be the harmful factor in processed meats is turning out to be one of the major protective factors in vegetables.

Vitamin D: It's Not Just Another Vitamin

If I described a substance with the following properties, what would you guess it was?

-It's synthesized by the body from cholesterol
-It crosses cell membranes freely
-It has its own nuclear receptor
-It causes broad changes in gene transcription
-It acts in nearly every tissue
-It's essential for health

There's no way for you to know, because those statements all apply to activated vitamin D, estrogen, testosterone and a number of other hormones. Vitamin D, as opposed to all other vitamins, is a steroid hormone precursor (technically it's a secosteroid but it's close enough for our purposes). The main difference between vitamin D and other steroid hormones is that it requires a photon of UVB light for its synthesis in the skin. If it didn't require UVB, it would be called a hormone rather than a vitamin. Just like estrogen and testosterone, it's involved in many processes, and it's important to have the right amount.

The type of vitamin D that comes from sunlight and the diet is actually not a hormone itself, but a hormone precursor. Vitamin D is converted to 25(OH)D3 in the liver. This is the major storage form of vitamin D, and thus it best reflects vitamin D status. The kidney converts 25(OH)D3 to 1,25(OH)D3 as needed. This is the major hormone form of vitamin D. 1,25(OH)D3 has profound effects on a number of tissues.

Vitamin D was originally identified as necessary for proper mineral absorption and metabolism. Deficiency causes rickets, which results in the demineralization and weakening of bones and teeth. A modest intake of vitamin D is enough to prevent rickets. However, there is a mountain of data accumulating that shows that even a mild form of deficiency is problematic. Low vitamin D levels associate with nearly every common non-communicable disorder, including obesity, diabetes, cardiovascular disease, autoimmune disease, osteoporosis and cancer. Clinical trials using vitamin D supplements have shown beneficial and sometimes striking effects on cancer, hypertension, type 1 diabetes, bone fracture and athletic performance. Vitamin D is a fundamental building block of health.

It all makes sense if you think about how humans evolved: in a tropical environment with bright sun year-round. Even in many Northern climates, a loss of skin pigmentation and plenty of time outdoors allowed year-round vitamin D synthesis for most groups. Vitamin D synthesis becomes impossible during the winter above latitude 40 or so, due to a lack of UVB. Traditional cultures beyond this latitude, such as the Inuit, consumed large amounts of vitamin D from nutrient-rich animal foods like fatty fish.

The body has several mechanisms for regulating the amount of vitamin D produced from sunlight exposure, so overdose from this source is impossible. Sunlight is also the most effective natural way to obtain vitamin D. To determine the optimal blood level of vitamin D, it's instructive to look at the serum 25(OH)D3 levels of people who spend a lot of time outdoors. The body seems to stabilize between 55 and 65 ng/mL 25(OH)D3 under these conditions. This is probably near the optimum. 30 ng/mL is required to normalize parathyroid hormone levels, and 35 ng/mL is required to optimize calcium absorption.

Here's how to become vitamin D deficient: stay inside all day, wear sunscreen anytime you go out, and eat a low-fat diet. Make sure to avoid animal fats in particular. Rickets, once thought of as an antique disease, is making a comeback in developed countries despite fortification of milk (note- it doesn't need to be fortified with fat-soluble vitamins if you don't skim the fat off in the first place!). The resurgence of rickets is not surprising considering our current lifestyle and diet trends. In a recent study, 40% of infants and toddlers in Boston were vitamin D deficient using 30 ng/mL as the cutoff point. 7.5% of the total had rickets and 32.5% showed demineralization of bone tissue! Part of the problem is that mothers' milk is a poor source of vitamin D when the mother herself is deficient. Bring the mothers' vitamin D level up, and breast milk becomes an excellent source.

Here's how to optimize your vitamin D status: get plenty of sunlight without using sunscreen, and eat nutrient-rich animal foods, particularly in the winter. The richest food source of vitamin D is high-vitamin cod liver oil. Blood from pasture-raised pigs or cows slaughtered in summer or fall, and fatty fish such as herring and sardines are also good sources. Vitamin D is one of the few nutrients I can recommend in supplement form. Make sure it's D3 rather than D2; 3,000- 5,000 IU per day should be sufficient to maintain blood levels in wintertime unless you are obese (in which case you may need more and should be tested). I feel it's preferable to stay on the low end of this range. Vitamin D3 supplements are typically naturally sourced, coming from sheep lanolin or fish livers. A good regimen would be to supplement every day you get less than 10 minutes of sunlight.

People with dark skin and the elderly make less vitamin D upon sun exposure, so they should plan on getting more sunlight or consuming more vitamin D. Sunscreen essentially eliminates vitamin D synthesis, and glass blocks UVB so indoor sunlight is useless. Vitamin D toxicity from supplements is possible, but exceptionally rare. It only occurs in cases where people have accidentally taken grotesque doses of the vitamin. As Chris Masterjohn has pointed out, vitamin D toxicity is extremely similar to vitamin A deficiency. This is because vitamin A and D work together, and each protects against toxicity from the other. Excess vitamin D depletes vitamin A, thus vitamin D toxicity is probably a relative deficiency of vitamin A.

I know this won't be a problem for you because like all healthy traditional people, you are getting plenty of vitamin A from nutrient-dense animal foods like liver and butter. Vitamin K2 is the third, and most overlooked, leg of the stool. D, A and K2 form a trio that act together to optimize mineral absorption and use, aid in the development of a number of body structures, beneficially alter gene expression, and affect many aspects of health on a fundamental level.

Thanks to horizontal.integration for the CC photo.

The Kitavans: Wisdom from the Pacific Islands

There are very few cultures left on this planet that have not been affected by modern food habits. There are even fewer that have been studied thoroughly. The island of Kitava in Papua New Guinea is host to one such culture, and its inhabitants have many profound things to teach us about diet and health.

The Kitava study, a series of papers produced primarily by Dr. Staffan Lindeberg and his collaborators, offers a glimpse into the nutrition and health of an ancient society, using modern scientific methods. This study is one of the most complete and useful characterizations of the diet and health of a non-industrial society I have come across. It's also the study that created, and ultimately resolved, my cognitive dissonance over the health effects of carbohydrate.

From the photos I've seen, the Kitavans are beautiful people. They have the broad, attractive faces, smooth skin and excellent teeth typical of healthy non-industrial peoples.

Like the Kuna, Kitavans straddle the line between agricultural and hunter-gatherer lifestyles. They eat a diet primarily composed of tubers (yam, sweet potato, taro and cassava), fruit, vegetables, coconut and fish, in order of calories. This is typical of traditional Pacific island cultures, although the relative amounts differ.

Grains, refined sugar, vegetable oils and other processed foods are virtually nonexistent on Kitava. They get an estimated 69% of their calories from carbohydrate, 21% from fat, 17% from saturated fat and 10% from protein. Most of their fat intake is saturated because it comes from coconuts. They have an omega-6 : omega-3 ratio of approximately 1:2. Average caloric intake is 2,200 calories per day (9,200 kJ). By Western standards, their diet is high in carbohydrate, high in saturated fat, low in total fat, a bit low in protein and high in calories.

Now for a few relevant facts before we really start diving in:

• Kitavans are not particularly active. They have an activity level comparable to a moderately active Swede, the population to which Dr. Lindeberg draws frequent comparisons.
  
• They have abundant food, and shortage is practically unknown.
  
• Their good health is probably not related to genetics, since genetically similar groups in the same region are exquisitely sensitive to the ravages of industrial food. Furthermore, the only Kitavan who moved away from the island to live a modern life is also the only fat Kitavan.
  
• Their life expectancy at birth is estimated at 45 years (includes infant mortality), and life expectancy at age 50 is an additional 25 years. This is remarkable for a culture with limited access to modern medicine.
  
• Over 75% of Kitavans smoke cigarettes. Even the most isolated societies have their modern vices.

The first study in the series is provocatively titled "Apparent absence of stroke and ischaemic heart disease in a traditional Melanesian island: a clinical study in Kitava." In it, Dr. Lindeberg presents data from interviews and electrocardiograms (ECG) suggesting that heart disease and stroke are absent or extremely rare on Kitava. The inhabitants are entirely unfamiliar with the (characteristic) symptoms of heart attack and stroke, despite the sizable elderly population. This is confirmed by the ECG findings, which indicate remarkable cardiovascular health. It also agrees with data from other traditional cultures in Papua New Guinea. Lindeberg states:

For the whole of PNG, no case of IHD or atherothrombotic stroke has been reported in clinical investigations and autopsy studies among traditionally living Melanesians for more than seven decades, though an increasing number of myocardial infarctions [heart attacks] and angina pectoris in urbanized populations have been reported since the 1960s.

Dementia was not found except in in two young Kitavans, who were born handicapped. The elderly remained sharp until death, including one man who reached 100 years of age. Kitavans are also unfamiliar with external cancers, with the exception of one possible case of breast cancer in an elderly woman.

Overall, Kitavans possess a resistance to degenerative diseases that is baffling to industrialized societies. Not only is this typical of non-industrial cultures, I believe it represents the natural state of existence for Homo sapiens. Like all other animals, humans are healthy and robust when occupying their preferred ecological niche. Our niche happens to be a particularly broad one, ranging from complete carnivory to plant-rich omnivory. But it does not include large amounts of grains or modern industrial foods.

In the next few posts, I'll discuss more specific data about the health of the Kitavans, including their body composition, serum lipids, and hormone profile. These data challenge the theory of an "atherogenic lipid profile", the idea that certain blood lipid patterns cause heart disease.

Vitamin Deficiency

I'm going to do some speculating today. More than usual. What are some of the deficiency symptoms of A, D and K2? Another way of putting the question is, what problems can you prevent or cure by giving people the right fat-soluble vitamins? If you read my last post, you know that cardiovascular disease, osteoporosis (and resulting fractures) and tooth decay are all strongly linked to fat-soluble vitamin status, probably in a causal way. There's also a strong suggestion that they could be involved in diabetes, kidney stones, resistance to infection and cancer. Well, we've just about covered all the major modern health problems, haven't we?

What if the 'disease of civilization' is simply a deficiency of fat-soluble vitamins? What if the only reason we haven't realized it yet is because we haven't understood the critical importance of K2 MK-4, and its synergy with A and D? I'm not totally convinced it's true, but it does make sense. I'm interested to hear other peoples' opinions on this.

There are two mechanisms that could cause deficiency. The first is the obvious: reduced intake. In general, we have a lower intake of A, D (from sunlight) and especially K2 than non-industrial populations past and present that did not suffer from the disease of civilization. Most Westerners fall short of optimal serum vitamin D, and K2 deficiency is nearly ubiquitous.

Reading Nutrition and Physical Degeneration, as well as other accounts of non-industrial groups transitioning from their traditional diets to a more Westernized one, it struck me how badly these people were being affected. Even when they were still eating some nutrient-dense traditional foods, their development and health suffered tremendously. I asked myself this question: could the Western food they were eating have actively interfered with their vitamin status, and could it be doing the same to us?

The most common foods that replaced traditional diets in Weston Price's studies were white wheat flour and sugar. Wheat contains a lot of gluten, which in some people causes celiac disease. Celiac is an immune response to gluten that causes the degeneration of the intestinal lining, which is responsible for absorbing nutrients, among other things. Celiac patients are often deficient in many nutrients, including fat-soluble vitamins. So there's clearly a link between gluten damage and fat-soluble vitamin status.

The interesting thing about celiac is it may actually be a spectrum, with nearly everyone showing some degree of gluten damage, but only severe cases being diagnosed. The diagnosis involves looking for antibodies against gluten, but there is evidence that some people may mount an immune response without producing antibodies (through the innate immune system). Peter pointed this out a while back.

So the hypothesis goes: the disease of civilization is caused by a deficiency of fat-soluble vitamins, due to both a lower intake and inefficient absorption through a damaged intestinal lining. Comments?

Vitamin K2, menatetrenone (MK-4)

Weston Price established the importance of the MK-4 isoform of vitamin K2 (hereafter, K2) with a series of interesting experiments. He showed in chickens that blood levels of calcium and phosphorus depended both on vitamin A and K2, and that the two had synergistic effects on mineral absorption. He also showed that chickens preferred eating butter that was rich in K2 over butter low in K2, even when the investigators couldn't distinguish between them. Young turkeys fed K2-containing butter oil along with cod liver oil (A and D) also grew at a much faster rate than turkeys fed cod liver oil alone.

He hypothesized that vitamin A, vitamin D and vitamin K2 were synergistic and essential for proper growth and subsequent health. He particularly felt that the combination was important for proper mineral absorption and metabolism. He used a combination of high-vitamin cod liver oil and high-vitamin butter oil to heal cavities, reduce oral bacteria counts, and cure numerous other afflictions in his patients. He also showed that the healthy non-industrial groups he studied had a much higher intake of these fat-soluble, animal-derived vitamins than more modern cultures.

Price found an inverse correlation between the levels of K2 in butter and mortality from cardiovascular disease and pneumonia in a number of different regions. A recent study examined the relationship between K2 (MK-4 through 10) consumption and heart attack risk in 4,600 Dutch men. They found a strong inverse association between K2 consumption and heart attack mortality risk. Men with the highest K2 consumption had a whopping 51% lower risk of heart attack mortality and a 26% lower risk of death from all causes compared to men eating the least K2! Their sources of K2 MK-4 were eggs, meats and dairy. They obtained MK-5 through MK-10 from fermented foods and fish. The investigators found no association with K1, the form found in plants.

Perigord, France is the world's capital of foie gras, or fatty goose liver. Good news for the bon vivants: foie gras turns out to be the richest known source of K2. Perigord also has the lowest rate of cardiovascular mortality in France, a country already noted for its low CVD mortality.

Rats fed warfarin, a drug that inhibits K2 recycling, develop arterial calcification. Feeding the rats K2 completely inhibits this effect. Mice lacking matrix Gla protein (MGP), a vitamin K-dependent protein that guards against arterial calcification, develop heavily calcified aortas and die prematurely. So the link between K2 and cardiovascular disease is a very strong one.

Mammals can synthesize K2 MK-4 from K1, but humans seem to be bad at it since most of us are K2 deficient despite eating ample K1. This suggests that through evolution, we lost the ability to synthesize K2 in sufficient amounts because we always obtained it abundantly in our diets from nutrient-dense animal tissues.

The synergism Weston Price observed between vitamins A, D and K2 now has a solid mechanism. In a nutshell, vitamins A and D signal the production of some very important proteins, and K2 is required to activate them once they are made. Many of these proteins are involved in mineral metabolism, thus the effects Price saw in his experiments and observations in non-industrialized cultures. For example, osteocalcin is a protein that organizes calcium and phosphorus deposition in the bones and teeth. It's produced by cells in response to vitamins A and D, but requires K2 to perform its function. This suggests that the effects of vitamin D on bone health could be amplified greatly if it were administered along with K2. By itself, K2 is already highly protective against fractures in the elderly. It works out perfectly, since K2 also protects against vitamin D toxicity.

I'm not going to go through all the other data on K2 in detail, but suffice it to say it's very very important. I believe that K2 is a 'missing link' that explains many of our modern ills, just as Weston Price wrote. Here are a few more tidbits to whet your appetite: K2 may affect glucose control and insulin release (1, 2). It's concentrated in the brain, serving an as yet unknown function.

Hunter-gatherers didn't have multivitamins, they had nutrient-dense food. As long as you eat a natural diet containing some vegetables and some animal products, and lay off the processed grains, sugar and vegetable oil, the micronutrients will take care of themselves.

Vitamin K2, MK-4 is only found in animal products. The best sources known are grass-fed butter from cows eating rapidly growing grass, and foie gras. K2 tends to associate with beta-carotene in butter, so the darker the color, the more K2 it contains (also, the better it tastes). Fish eggs, other grass-fed dairy, shellfish, insects and other organ meats are also good sources. Chris Masterjohn compiled a list of food sources in his excellent article on the Weston Price foundation website. I highly recommend reading it if you want more detail. K2 MK-7 is found abundantly in natto, a type of fermented soybean, and seems to have some of the same effects as MK-4 on bone health in clinical trials. However, it is not the from of K2 that mammals synthesize for themselves so I'm not convinced it's the real thing.

Finally, you can also buy K2 supplements. The best one is butter oil, the very same stuff Price used to treat his patients. I have used this one personally, and I noticed positive effects on my skin overnight. Thorne research makes a synthetic liquid K2 MK-4 supplement that is easy to dose drop-wise to get natural amounts of it. Other K2 MK-4 supplements are much more concentrated than what you could get from food so I recommend avoiding them. I am generally against supplements, but I've ordered the Thorne product for a little self-experimentation. I want to see if it has the same effect on my skin as the butter oil (update- it does).

Nature's Laws

Last night I was watching a little video clip of the Jack LaLanne show. LaLanne was an advocate of strength training and whole foods nutrition whose TV show ran from the 1950s through the 1980s. In the clip, he describes how his father died an early death due to heart and liver disease. A quote that really stuck with me was when he said his father died due to "disregarding nature's laws". That pretty much sums up my philosophy. Live in a way that generally mimics what our genes evolved to thrive on. Why did our paleolithic ancestors have strong, healthy bodies? Why are there still cultures that are free of chronic disease to this day, even into old age? Because they are following nature's laws. Break the law at your own risk.

Jack LaLanne and I do differ a bit on what constitutes a natural diet. For example, I don't throw out my egg yolks... But hey, the man is 94 and going strong. Here's another quote of his: "If man made it, don't eat it". Words to live by. Quite literally.

Genetics and Disease

There is a lot of confusion surrounding the role of genetics in health. It seems like every day the media have a new story about gene X or Y 'causing' obesity, diabetes or heart disease. There are some diseases that are strongly and clearly linked to a gene, such as the disease I study: spinocerebellar ataxia type 7. I do not believe that genetics are the cause of more than a slim minority of health problems however. Part of this is a semantic issue. How do you define the word 'cause'? It's a difficult question, but I'll give you an example of my reasoning and then we'll come back to it.

A classic and thoroughly studied example of genetic factors in disease can be found in the Pima indians of Arizona. Currently, this population eats a version of the American diet, high in refined and processed foods. It also has the highest prevalence of type II diabetes of any population on earth (much higher than the US average), and a very high rate of obesity. One viewpoint is that these people are genetically susceptible to obesity and diabetes, and thus their genes are the cause of their health problems.

However, if you walk across the national border to Mexico, you'll find another group of Pima indians. This population is genetically very similar to the Arizona Pima except they have low rates of obesity and diabetes. They eat a healthier, whole-foods, agriculture-based diet. Furthermore, 200 years ago, the Arizona Pima were healthy as well. So what's the cause of disease here? Strictly speaking, it's both genetics and lifestyle. Both of these factors are necessary for the health problems of the Arizona Pima. However, I think it's more helpful to think of lifestyle as the cause of disease, since that's the factor that changed.

The Pima are a useful analogy for the world in general. They are an extreme example of what has happened to many if not all modern societies. Thus, when we talk about the 'obesity gene' or the 'heart disease gene', it's misleading. It's only the 'obesity gene' in the context of a lifestyle to which we are not genetically adapted.

I do not believe that over half of paleolithic humans were overweight, or that 20% had serious blood glucose imbalances. In fact, studies of remaining populations living naturally and traditionally have shown that they are typically much healthier than industrialized humans. Yet here we are in the US, carrying the very same genes as our ancestors, sick as dogs. That's not all though: we're actually getting sicker. Obesity, diabetes, allergies and many other problems are on the rise, despite the fact that our genes haven't changed.

I conclude that genetics are only rarely the cause of disease, and that the vast majority of health problems in the US are lifestyle-related. Studies into the genetic factors that predispose us to common health problems are interesting, but they're a distraction from the real problems and the real solutions that are staring us in the face. These solutions are to promote a healthy diet, exercise, and effective stress management.