Stuck at the Starting Gate?

The Diet-Heart Hypothesis: Stuck at the Starting Gate?

The diet-heart hypothesis is the idea that (1) dietary saturated fat, and in some versions, dietary cholesterol, raise blood cholesterol in humans and (2) therefore contribute to the risk of heart attack. 

I'm not going to spend a lot of time on the theory in relation to dietary cholesterol because the evidence that typical dietary amounts cause heart disease in humans is weak.  Here's a graph from the Framingham Heart study (via the book Prevention of Coronary Heart Disease, by Dr. Harumi Okuyama et al.) to drive home the point. Eggs are the main source of cholesterol in the American diet. In this graph, the "low" group ate 0-2 eggs per week, the "medium" group ate 3-7, and the "high" group ate 7-14 eggs per week (click for larger image):The distribution of blood cholesterol levels between the three groups was virtually identical. The study also found no association between egg consumption and heart attack risk. Dietary cholesterol does not have a large impact on serum cholesterol in the long term, perhaps because humans are adapted to eating cholesterol. Most people are able to adjust their own cholesterol metabolism to compensate when the amount in the diet increases. Rabbits don't have that feedback mechanism because their natural diet doesn't include cholesterol, so feeding them dietary cholesterol increases blood cholesterol and causes vascular pathology. 

The first half of the diet-heart hypothesis states that eating saturated fat raises blood cholesterol. This has been accepted without much challenge by diet-health authorities for nearly half a century. In 1957, Dr. Ancel Keys proposed a formula (Lancet 2:1959. 1957) to predict changes in total cholesterol based on the amount of saturated and polyunsaturated fat in the diet. This formula, based primarily on short-term trials from the 1950s, stated that saturated fat is the primary dietary influence on blood cholesterol.

According to Keys' interpretation of the trials, saturated fat raised, and to a lesser extent polyunsaturated fat lowered, blood cholesterol. But there were significant flaws in the data from the very beginning, which were pointed out in this critical 1973 literature review in the American Journal of Clinical Nutrition (free full text).

The main problem is that the controlled trials typically compared saturated fats to omega-6 linoleic acid (LA)-rich vegetable oils, and when serum cholesterol was higher in the saturated fat group, this was most often attributed to the saturated fat raising blood cholesterol rather than the LA lowering it. When a diet high in saturated fat was compared to the basal diet without changing LA, often no significant increase in blood cholesterol was observed. Studies claiming to show a cholesterol-raising effect of saturated fat often introduced it after an induction period rich in LA. Thus, the effect sometimes had more to do with LA lowering blood cholesterol than saturated fat raising it. This is not at all what I was expecting to find when I began looking through these trials.

Reading through the short-term controlled trials, I was surprised by the variability and lack of agreement between them. Some of this was probably due to a lack of control over variables and non-optimal study design. But if saturated fat has a dominant effect on serum cholesterol in the short term, it should be readily and consistently demonstrable.  

The long-term data are not kind to the diet-heart hypothesis. Reducing saturated fat while greatly increasing LA certainly does lower blood cholesterol substantially. This was the finding in the well-controlled Minnesota Coronary Survey trial, for example (14% reduction). But in other cases where LA intake changed less, such as MRFIT, the Women's Health Initiative Diet Modification trial and the Lyon Diet-Heart trial, reducing saturated fat intake had little or no effect on total cholesterol or LDL (0-3% reduction).  The small changes that did occur could have been due to other factors, such as increased fiber and phytosterols, since these were multiple-factor interventions. 

Another blow to the idea that saturated fat raises cholesterol in the long term comes from observational studies. Here's a graph of data from the Health Professionals Follow-up study, which followed 43,757 health professionals for 6 years (via the book Prevention of Coronary Heart Diseaseby Dr. Harumi Okuyama et al.):What this graph shows is that at a relatively constant LA intake, neither saturated fat intake nor the ratio of LA to saturated fat were related to blood cholesterol in freely living subjects. This was true across a wide range of saturated fat intakes (7-15%). 

There's more. If saturated fat were important in determining the amount of blood cholesterol in the long term, you'd expect populations who eat the most saturated fat to have high blood cholesterol levels. But that's not the case. The Masai traditionally get a high proportion of their calories from milk fat, half of which is saturated. In 1964, Dr. George V. Mann published a paper showing that traditional Masai warriors eating practically nothing but very fatty milk, blood and meat had an average cholesterol of 115 mg/dL in the 20-24 year age group. For comparison, he published values for American men in the same age range: 198 mg/dL (J. Atherosclerosis Res. 4:289. 1964). Apparently, eating three times the saturated animal fat and several times the cholesterol of the average American wasn't enough to elevate their blood cholesterol. What does elevate the cholesterol of a Masai man?Junk food. 

Now let's swim over to the island of Tokelau, where the traditional diet includes nearly 50% of calories from saturated fat from coconut. This is the highest saturated fat intake of any population I'm aware of. How's their cholesterol? Men in the age group 20-24 had a concentration of 168 mg/dL in 1976, which was lower than Americans in the same age group despite a four-fold higher saturated fat intake. Tokelauans who migrated to New Zealand, eating half the saturated fat of their island relatives, had a total cholesterol of 191 mg/dL in the same age group and time period, and substantially higher LDL (J. Chron. Dis. 34:45. 1981). Sucrose consumption was 2% on Tokelau and 13% in New Zealand. Saturated fat seems to take a backseat to some other diet/lifestyle factor(s).  Body fatness and excess calorie intake are good candidates, since they influence circulating lipoproteins.

Does dietary saturated fat influence total cholesterol and LDL over the long term?  I don't have the answers, but I do think it's interesting that the evidence is much less consistent than it's made out to be.  It may be that if dietary saturated fat influences total cholesterol or LDL concentration in the long term, the effect is is secondary to other factors.  That being said, it's clear that linoleic acid, in large amount, reduces circulating total cholesterol and LDL.

High-Fat Dairy, Obesity, Metabolic Health and Cardiovascular Disease.

New Review Paper by Yours Truly: High-Fat Dairy, Obesity, Metabolic Health and Cardiovascular Disease

My colleagues Drs. Mario Kratz, Ton Baars, and I just published a paper in the European Journal of Nutrition titled "The Relationship Between High-Fat Dairy Consumption and Obesity, Cardiovascular, and Metabolic Disease".  Mario is a nutrition researcher at the Fred Hutchinson Cancer Research Center here in Seattle, and friend of mine.  He's doing some very interesting research on nutrition and health (with an interest in ancestral diets), and I'm confident that we'll be getting some major insights from his research group in the near future.  Mario specializes in tightly controlled human feeding trials.  Ton is an agricultural scientist at the University of Kassel in Germany, who specializes in the effect of animal husbandry practices (e.g., grass vs. grain feeding) on the nutritional composition of dairy.  None of us have any connection to the dairy industry or any other conflicts of interest.

The paper is organized into three sections:

1. A comprehensive review of the observational studies that have examined the relationship between high-fat dairy and/or dairy fat consumption and obesity, metabolic health, diabetes, and cardiovascular disease.
2. A discussion of the possible mechanisms that could underlie the observational findings.
3. Differences between pasture-fed and conventional dairy, and the potential health implications of these differences.

 We wrote this paper because after reviewing the evidence, we found it to be surprising and fairly contradictory to conventional ideas on nutrition and health.  I wrote the sections on obesity, metabolic health and diabetes, Mario wrote the sections on cardiovascular disease and fatty acids, and Ton wrote the section on husbandry practices and dairy fat composition.  Mario was the lead author and did most of the editing/formatting, submitted the manuscript, etc.  Our paper went through a rigorous peer review process.

Here are our basic findings:

• High-fat dairy consumption is not associated with obesity, in fact, 11 out of 16 studies found that higher dairy fat intake is associated with lower body fat and/or less fat gain over time.  None identified an association between high-fat dairy consumption and fat gain, although some did find an association between low-fat dairy consumption and fat gain.
• High-fat dairy consumption is not associated with poorer metabolic health.  Six of 11 studies found that higher high-fat dairy consumption is associated with better metabolic health, while only one found that it was associated with one marker of poorer metabolic health (and this study used an odd design). 
• The association between high-fat dairy intake and diabetes risk is inconsistent.  Zero of eight studies found that high-fat dairy consumption is associated with diabetes risk, and three found that it was protective.  However, three studies also found that low-fat dairy intake was inversely associated with diabetes risk, compared to no association with high-fat dairy, suggesting by inference that the fat content of the dairy could be harmful.  These studies all adjusted for body fatness.  Since body fatness is a key risk factor for diabetes, and dairy fat intake is inversely associated with body fatness, this is obviously a major confound.  We discussed this and other potential confounds in the paper.
• The evidence on cardiovascular disease is inconsistent, with a number of studies suggesting a protective association, a few suggesting a harmful one, and several suggesting no association.
• Dairy fat is a complex substance.  There are major differences in the fatty acid composition of dairy from pasture-raised vs. conventionally raised cows, and many of these fatty acids are bioactive and could influence human health.
• We also discuss the limitations of observational studies in some detail, and many other issues that I won't touch on here.

What This Paper Means 

This is the first comprehensive review of studies on the association between high-fat dairy intake and obesity, metabolic, and cardiovascular health.  Typical dietary advice includes the recommendation to eat low-fat or skim dairy products.  This is based on the hypothesis that avoiding the (mostly saturated) fat in dairy will reduce the risk of obesity, metabolic problems, and cardiovascular disease.  This idea is logical, but not every idea that is logical is correct when tested scientifically, particularly when it pertains to a complex natural food.  We asked the question "what does the evidence say about this hypothesis?"

The research to date suggests that high-fat dairy overall does not have a negative impact on obesity risk, metabolic problems, diabetes risk, or cardiovascular disease.  In fact, these studies offer fairly strong support to the hypothesis that high-fat dairy may protect against obesity.  However, there was variability between studies and this may be explained by factors such as a) differences in the quality of dairy products between countries/regions, b) the form in which dairy is consumed (e.g., traditional cheeses vs. ice cream and pizza), and c) other confounding factors discussed in the paper. 

Please keep in mind that these studies are observational and therefore can not establish cause and effect. They're best viewed as a springboard for future research.

What This Paper Doesn't Mean

I want to be very clear about this.  This paper does not mean that adding butter to all your food will make you lose fat or become healthier.  In fact, if you do that you will most likely gain fat and become less healthy.  Say what??  The studies we reviewed examined the role of high-fat dairy in the context of normal varied diet patterns.  They did not compare people eating normally to people who put extra butter on everything, which is an excellent way to increase your calorie intake.  Essentially they compared people eating high-fat dairy to people eating other types of fats as part of a mixed diet.  The difference is subtle but critical to understand: addition vs. replacement. 

So does this mean that replacing other types of fats with dairy fat (pasture-raised in particular), in the context of a normal varied diet, could lead to less fat gain and perhaps even better health over time?  Perhaps.  That is what the studies suggest overall.  But again, these are observational studies with major limitations, so we'll have to wait for more evidence before we can hang our hats on the idea.  In the meantime, it's clear that typical dietary recommendations to favor low-fat dairy over high-fat dairy are on thin ice.

The Eocene Diet

The Eocene Diet

65 million years ago, a massive asteroid slammed into the Yucatan peninsula, creating a giant dust cloud that contributed to the extinction of terrestrial dinosaurs.  In the resulting re-adjustment of global ecosystems, a new plant tissue evolved, which paved the way for the eventual appearance of humans: fruit.  Fruit represents a finely crafted symbiosis between plants and animals, in which the plant provides a nourishing morsel, and the animal disperses the plant's seeds inside a packet of rich fertilizer.

Fruit was such a powerful selective pressure that mammals quickly evolved to exploit it more effectively, developing adaptations for life in the forest canopy.  One result of this was the rapid emergence of primates, carrying physical, digestive and metabolic adaptations for the acquisition and consumption of fruit and leaves.  Primates also continued eating insects, a vestige of our early mammalian heritage. 

The Eocene epoch began 55.8 million years ago, just after the emergence of primates.  For most of the time between the beginning of the Eocene and today, our ancestors ate the archetypal primate diet of fruit, leaves and insects, just as most primates do today. 

In contrast, the Paleolithic era, marked by the development of stone tools and a dietary shift toward meat and cooked starches, began only 2.6 million years ago.  The Paleolithic era represents only 5 percent of the time that shaped our primate genome-- 95 percent of primate evolutionary history occurred prior to the Paleolithic.  The Neolithic period, since humans domesticated plants roughly 10,000 years ago, accounts for only 0.02 percent.

Therefore, we are not well adapted to eating grains, legumes and dairy, and we aren't well adapted to eating meat and starch either.  Our true, deepest evolutionary adaptations are to the foods that sustained our primate ancestors for the tens of millions of years prior to the Paleolithic.  That's why I designed the Eocene Diet (TM). 

The Eocene Diet is easy.  You simply eat these three foods:

• Raw fruit
• Raw leaves (no dressing!)
• Live insects

Once a week, you also get to eat a two ounce portion of raw meat or liver, to mimic the occasional meat consumption of chimpanzees and other primates.  

Here's a photo of a sample meal:

Fruit and leaves are easy to find, but what about insects?  With a little practice, you'll see that they're easy to find too, often for free.  Here are some tips:

• Pet stores.  They usually sell crickets and mealworms.
• Look under rotting logs.
• Find a long, flexible stem and stick it into a termite mound.  Termites will grab onto it and you can eat them off the stem. 

How well does the Eocene Diet work?  Here's a photo of WHS reader Cristina B. after only three weeks on the diet:

She looks pleased.

The Eocene Diet is so effective for weight loss and general health that I've come up with this slogan for it:

"You WILL lose weight on the Eocene Diet (TM).  Even if you don't want to.  I guarantee it!"

April Fools!

Full-fat Dairy for Cardiovascular Health??

Full-fat Dairy for Cardiovascular Health??

[2013 update: a few colleagues and I have published a comprehensive review paper on the association between full-fat dairy consumption and obesity, metabolic health, and cardiovascular disease.  You can find it here.]

I just saw a paper in the AJCN titled "Dairy consumption and patterns of mortality of
Australian adults". It's a prospective study with a 15-year follow-up period. Here's a quote from the abstract:

There was no consistent and significant association between total dairy intake and total or cause-specific mortality. However, compared with those with the lowest intake of full-fat dairy, participants with the highest intake (median intake 339 g/day) had reduced death due to CVD (HR: 0.31; 95% confidence interval (CI): 0.12–0.79; P for trend = 0.04) after adjustment for calcium intake and other confounders. Intakes of low-fat dairy, specific dairy foods, calcium and vitamin D showed no consistent associations.

People who ate the most full-fat dairy had a 69% lower risk of cardiovascular death than those who ate the least. Otherwise stated, people who mostly avoided dairy or consumed low-fat dairy had more than three times the risk of dying of coronary heart disease or stroke than people who ate the most full-fat diary.  This result is an outlier, and also observational so difficult to interpret, but it certainly is difficult to reconcile with the idea that dairy fat is a significant contributor to cardiovascular disease.

Contrary to popular belief, full-fat dairy, including milk, butter and cheese, has never been convincingly linked to cardiovascular disease. What has been linked to cardiovascular disease is milk fat's replacement, margarine. In the Rotterdam study, high vitamin K2 intake was linked to a lower risk of fatal heart attack, aortic calcification and all-cause mortality. Most of the K2 came from full-fat cheese.

From a 2005 literature review on milk and cardiovascular disease in the EJCN:

In total, 10 studies were identified. Their results show a high degree of consistency in the reported risk for heart disease and stroke, all but one study suggesting a relative risk of less than one in subjects with the highest intakes of milk.

...the studies, taken together, suggest that milk drinking may be associated with a small but worthwhile reduction in heart disease and stroke risk.

...All the cohort studies in the present review had, however, been set up at times when reduced-fat milks were unavailable, or scarce.

High-Fat Dairy, Obesity, Metabolic Health and Cardiovascular Disease

New Review Paper by Yours Truly: High-Fat Dairy, Obesity, Metabolic Health and Cardiovascular Disease

My colleagues Drs. Mario Kratz, Ton Baars, and I just published a paper in the European Journal of Nutrition titled "The Relationship Between High-Fat Dairy Consumption and Obesity, Cardiovascular, and Metabolic Disease".  Mario is a nutrition researcher at the Fred Hutchinson Cancer Research Center here in Seattle, and friend of mine.  He's doing some very interesting research on nutrition and health (with an interest in ancestral diets), and I'm confident that we'll be getting some major insights from his research group in the near future.  Mario specializes in tightly controlled human feeding trials.  Ton is an agricultural scientist at the University of Kassel in Germany, who specializes in the effect of animal husbandry practices (e.g., grass vs. grain feeding) on the nutritional composition of dairy.  None of us have any connection to the dairy industry or any other conflicts of interest.

The paper is organized into three sections:

1. A comprehensive review of the observational studies that have examined the relationship between high-fat dairy and/or dairy fat consumption and obesity, metabolic health, diabetes, and cardiovascular disease.
2. A discussion of the possible mechanisms that could underlie the observational findings.
3. Differences between pasture-fed and conventional dairy, and the potential health implications of these differences.

 We wrote this paper because after reviewing the evidence, we found it to be surprising and fairly contradictory to conventional ideas on nutrition and health.  I wrote the sections on obesity, metabolic health and diabetes, Mario wrote the sections on cardiovascular disease and fatty acids, and Ton wrote the section on husbandry practices and dairy fat composition.  Mario was the lead author and did most of the editing/formatting, submitted the manuscript, etc.  Our paper went through a rigorous peer review process.

Here are our basic findings:

• High-fat dairy consumption is not associated with obesity, in fact, 11 out of 16 studies found that higher dairy fat intake is associated with lower body fat and/or less fat gain over time.  None identified an association between high-fat dairy consumption and fat gain, although some did find an association between low-fat dairy consumption and fat gain.
• High-fat dairy consumption is not associated with poorer metabolic health.  Six of 11 studies found that higher high-fat dairy consumption is associated with better metabolic health, while only one found that it was associated with one marker of poorer metabolic health (and this study used an odd design). 
• The association between high-fat dairy intake and diabetes risk is inconsistent.  Zero of eight studies found that high-fat dairy consumption is associated with diabetes risk, and three found that it was protective.  However, three studies also found that low-fat dairy intake was inversely associated with diabetes risk, compared to no association with high-fat dairy, suggesting by inference that the fat content of the dairy could be harmful.  These studies all adjusted for body fatness.  Since body fatness is a key risk factor for diabetes, and dairy fat intake is inversely associated with body fatness, this is obviously a major confound.  We discussed this and other potential confounds in the paper.
• The evidence on cardiovascular disease is inconsistent, with a number of studies suggesting a protective association, a few suggesting a harmful one, and several suggesting no association.
• Dairy fat is a complex substance.  There are major differences in the fatty acid composition of dairy from pasture-raised vs. conventionally raised cows, and many of these fatty acids are bioactive and could influence human health.
• We also discuss the limitations of observational studies in some detail, and many other issues that I won't touch on here.

What This Paper Means 

This is the first comprehensive review of studies on the association between high-fat dairy intake and obesity, metabolic, and cardiovascular health.  Typical dietary advice includes the recommendation to eat low-fat or skim dairy products.  This is based on the hypothesis that avoiding the (mostly saturated) fat in dairy will reduce the risk of obesity, metabolic problems, and cardiovascular disease.  This idea is logical, but not every idea that is logical is correct when tested scientifically, particularly when it pertains to a complex natural food.  We asked the question "what does the evidence say about this hypothesis?"

The research to date suggests that high-fat dairy overall does not have a negative impact on obesity risk, metabolic problems, diabetes risk, or cardiovascular disease.  In fact, these studies offer fairly strong support to the hypothesis that high-fat dairy may protect against obesity.  However, there was variability between studies and this may be explained by factors such as a) differences in the quality of dairy products between countries/regions, b) the form in which dairy is consumed (e.g., traditional cheeses vs. ice cream and pizza), and c) other confounding factors discussed in the paper. 

Please keep in mind that these studies are observational and therefore can not establish cause and effect. They're best viewed as a springboard for future research.

What This Paper Doesn't Mean

I want to be very clear about this.  This paper does not mean that adding butter to all your food will make you lose fat or become healthier.  In fact, if you do that you will most likely gain fat and become less healthy.  Say what??  The studies we reviewed examined the role of high-fat dairy in the context of normal varied diet patterns.  They did not compare people eating normally to people who put extra butter on everything, which is an excellent way to increase your calorie intake.  Essentially they compared people eating high-fat dairy to people eating other types of fats as part of a mixed diet.  The difference is subtle but critical to understand: addition vs. replacement. 

So does this mean that replacing other types of fats with dairy fat (pasture-raised in particular), in the context of a normal varied diet, could lead to less fat gain and perhaps even better health over time?  Perhaps.  That is what the studies suggest overall.  But again, these are observational studies with major limitations, so we'll have to wait for more evidence before we can hang our hats on the idea.  In the meantime, it's clear that typical dietary recommendations to favor low-fat dairy over high-fat dairy are on thin ice.

Weight Gain and Weight Loss in a Traditional African Society

Weight Gain and Weight Loss in a Traditional African Society

The Massas is an ethnic group in Northern Cameroon that subsists mostly on plain sorghum loaves and porridge, along with a small amount of milk, fish and vegetables (1, 2).  They have a peculiar tradition called Guru Walla that is only undertaken by men (2, 1):

This social institution, aimed at prestige acquisition, includes a massive overfeeding representing twice or threefold the habitual daily intake.

It lasts two months, during which they are overfed on sorghum, milk, fish and vegetables (mostly sorghum, but with an increased ration of milk as well).  They eat beyond the point of nausea, day and night, and expend as little energy as possible.  Calorie intake exceeds 8,000 kcal per day.  According to two detailed studies of nine Massas, by the end of Guru Walla, they had gained about 37 pounds (17 kg), mostly as fat* (2, 3).

What happened after they stopped overeating?  When they returned to their typical diet, which contains 75% carbohydrate, 11% fat, and 15% protein, the investigators found something interesting (3):

Rapid and substantial decreases in body weight and fat were observed in all subjects during the first 3.5 mo after the cessation of overfeeding. Subsequently, a more progressive decrease was noted up to the last measurement session. Thirty months after the end of Guru, the group had lost all of the overfeeding-induced weight gain.

This supports two ideas that may be starting to sound familiar:

1. Body fat mass is regulated in both directions (i.e., both increases and decreases are opposed)**.  This is supported by numerous overfeeding and underfeeding studies in both humans and rodents. 
2. Plain, repetitive starchy foods do not lead to fat gain and can support fat loss.

* This is less fat gain than expected due to the energy intake, suggesting "substantial thermogenesis" in response to the overfeeding.  Their bodies appeared to have mounted a compensatory response aimed at countering fat gain. 

** According to this hypothesis, obesity represents an increase in the "setpoint" around which fat mass in regulated.  This Guru Walla study is especially interesting because it looks at body fat regulation in a non-industrial society, which should have well functioning homeostasis mechanisms that have not been damaged by industrial living.  As fatness is prized in this society, they had no incentive to deliberately lose fat after Guru Walla.

High-Fat Diets, Obesity and Brain Damage

High-Fat Diets, Obesity and Brain Damage

Many of you have probably heard the news this week:

High-fat diet may damage the brain
Eating a high-fat diet may rapidly injure brain cells
High fat diet injures the brain
Brain injury from high-fat foods

Your brain cells are exploding with every bite of butter!  Just kidding.  The study in question is titled "Obesity is Associated with Hypothalamic Injury in Rodents and Humans", by Dr. Josh Thaler and colleagues, with my mentor Dr. Mike Schwartz as senior author (1).  We collaborated with the labs of Drs. Tamas Horvath and Matthias Tschop.  I'm fourth author on the paper, so let me explain what we found and why it's important.  

The Questions

Among the many questions that interest obesity researchers, two stand out:

1. What causes obesity?
2. Once obesity is established, why is it so difficult to treat?

Our study expands on the efforts of many other labs to answer the first question, and takes a stab at the second one as well.  Dr. Licio Velloso and collaborators were the first to show in 2005 that inflammation in a part of the brain called the hypothalamus contributes to the development of obesity in rodents (2), and this has been independently confirmed several times since then.  The hypothalamus is an important brain region for the regulation of body fatness, and inflammation keeps it from doing its job correctly.

The Findings 

Inflammation occurs in many tissues when rodents are placed on a fattening diet, but this usually takes weeks or months to develop, and therefore it is often considered secondary to the development of obesity.  One of the things we were able to show in this study is that in rodents, we can detect signs of inflammation in the hypothalamus within one day of exposure to a fattening diet, making it the earliest known inflammatory event during the development of obesity.  This is consistent with the idea that dysfunction of other tissues is the result, at least partially, of dysfunction that occurs first in the brain.

Our study also addresses the second question: why is obesity so difficult to treat?  We know that brain inflammation contributes to obesity in rodents, so one possibility is that the hypothalamus sustains damage during this process, which durably elevates the "setpoint" around which body fat mass is defended by the body.  In other words, damage to the part of the brain that regulates body fatness makes the body "want" to carry more fat and resist fat loss attempts.

This is the hypothesis we began to test in this study, and we found evidence that supports it.  Rodents placed on a fattening diet show evidence of neuron injury in as little as three days.  Our study was not able to say that neuron injury causes obesity or resistance to fat loss, only that obesity and neuron injury are associated with one another.  This is the first step in this line of investigation, and we are currently following up with related studies that will expand the findings. 

The most striking finding in the paper was contributed by our collaborator Dr. Ellen Schur, who showed by MRI that obesity is associated with a marker of neuron injury in the hypothalamus of live humans. As you might imagine, this increased the impact of the study considerably!  It is important to point out that we found the suggestion of neuron injury specifically in the hypothalamus, not in other brain regions.  We did not find changes in brain regions responsible for thought, language, movement, etc., that might be expected to impact a person's ability to think and function.

The Diet

The "high-fat diet" that was used in this study is Research Diets D12492 (3), and the comparison diet was normal unpurified rodent chow.  Normal rodent chow is a whole food based pellet that is mostly composed of unrefined corn, soybeans, a small amount of meat and animal fat, and added micronutrients.  It is very low in fat, typically ~14 percent of calories.  They do just fine on this food, particularly if they are given a running wheel and other forms of environmental enrichment. 

D12492 is a "purified" diet that is fundamentally different from unrefined rodent chow.  It is one of the many rodent diets that were created because investigators needed a highly consistent food to minimize experimental variability.  Whereas unrefined chow can have a different composition based on the variety of corn/soybeans used, the terroir, the particular growing conditions of that year, etc., purified diets are composed entirely of highly refined ingredients so they are much less variable.  However, it rapidly became clear that rodents don't do as well on these diets, even if macronutrients and micronutrients are approximately matched to the unrefined chow diets.  D12492 is composed of non-hydrogenated lard, soybean oil, maltodextrin, sucrose, casein for protein, cellulose for fiber, and added vitamins and minerals.  It does contain sugar, but the amount is modest (6.8 percent of calories).

D12492 is 60 percent fat by calories.  Although rodents love the taste of it, it is not good for their health-- susceptible strains of rats and mice will begin gaining fat in as little as a week on the diet, become morbidly obese by three months, sometimes develop diabetes, and live less than half a typical rodent lifespan if they are allowed to age (generally they are not). Personally, I refer to this diet as a "purified high-fat diet", because that acknowledges that not only is it high in fat, it is also composed of refined ingredients.  In our study, there is no way for us to know if what we observed in rodents was due to the dietary fat per se, some other aspect of the diet, or both.  Based on other findings, I strongly suspect that it is both.

We deliberately use rodent strains that are susceptible to obesity on this diet.  Some strains are more resistant to obesity than others, but a comprehensive look at the literature reveals that high-fat diets are generally not good for rodents, and most strains tend to gain some amount of fat and develop long-term health problems on high-fat feed.  There are a few exceptions in the literature if you look hard enough for them, but they are drowned out by the much greater number of studies showing harm.

So if we're deliberately selecting rodent strains that are particularly sensitive to fat gain on a purified high-fat diet, how can we generalize from this and say that dietary fat causes damage in the brain and obesity?  The answer is that we can't, and we haven't.   Nowhere in the paper does it say that dietary fat per se causes damage to the brain, or even causes obesity, and Drs. Thaler and Schwartz were careful not to say that in interviews either.  We choose rodent strains that are susceptible to obesity on purified high-fat diets simply because we're studying obesity, and we know that feeding this diet to the right strains of rats and mice produces it readily.  

The fact is, we don't know what aspects of D12492 cause injury to neurons and obesity in rodents, and we don't know if those are the same factors that cause obesity in humans.  That was not the point of the study!  The point was to try to understand what's happening in the brain during the development of obesity.  Based on previous studies, the dietary fat itself is probably an important component that makes D12492 fattening in rodents, but whether high dietary fat would lead to obesity in the context of a well-composed whole food-based high fat diet, and a running wheel, is not known. 

The Implications

This study once again highlights the importance of the brain in the development of obesity, and shows directly for the first time that similar changes occur in humans.  Our findings also raise the possibility that injury to the hypothalamus may contribute to the fact that obesity is so difficult to durably reverse.  That does not mean that fat loss efforts are hopeless!  I believe that with the right techniques, many obese people can lose a substantial amount of fat and keep it off.  But realistically, we already know that it is rare for a long-term obese person to attain a totally lean state.  Persistent changes in the function of the hypothalamus are a logical way to explain this, although more research will be required before we can say it conclusively. 

I do not think this study suggests that dietary fat is inherently fattening or causes damage to neurons in humans.  The question of whether or not dietary fat is inherently fattening is controversial, but our study did not address it.  Based on my reading, studies show overall that dietary fat is not fattening in humans as long as total calorie intake remains appropriate.  However, adding fat to food that is otherwise low in fat does facilitate overconsumption of calories in some people, by increasing energy density and food palatability/reward, and this has been demonstrated many times.  I think the fact that low-carbohydrate diets cause fat loss in many obese people offers support to the idea that dietary fat is not inherently fattening in humans. 

This was not a diet study, but if there is a dietary message in it, it is this: eat a whole food based diet that allows you to reach or maintain a healthy weight naturally.

"The American Diet: a Historical Perspective"

My TEDx Talk, "The American Diet: a Historical Perspective"

On October 21st, I spoke at the Harvard Food Law Society's TEDx conference, Forum on Food Policy.  The conference kicked off with three talks on nutrition, by Drs. Walter Willett, David Ludwig and myself.  My talk is only 17 minutes long as per TED format, but it's packed with research on both quantitative and qualitative changes in the US diet over the last two centuries.  It contains surprises for almost anyone, and I can guarantee you've never learned this much about the history of the US diet in 17 minutes.  The talk was titled "The American Diet: a Historical Perspective"; you can access it by following that link.


My talk has been online for a while, but I didn't post a link to it due to the fact that the slides were not synched properly and many of the graphs did not appear at all.  I've been working with a gentleman at Harvard to fix these problems, and he recently finished a new version, which was posted online to replace the old one thanks to Food Law Society president Krista DeBoer.

There are two problems with the talk I want to point out right away.  The first problem is an error in one of my slides that a WHS reader recently pointed out.  At 8:10, I have a slide showing changes in dietary fat composition over the last century in the US.  I stated that polyunsaturated fat consumption has increased by 300 percent, but actually it has increased by 200 percent.  It was a math error on my part.  

The second problem is a residual issue with the synching.  At 8:39, when I'm talking about the accumulation of omega-6 linoleic acid in human body fat over the last 50 years due to increased seed oil consumption, the first graph doesn't show up in the synched version (it did appear in the live talk).  I'm reproducing it here:

Each dot represents an individual study spanning 1961 to 2008 (1, 2, 3, 4, 5, 6).  The increase has been extraordinary and corresponds closely to the large increase in dietary linoleic acid.

The talk was better live, because it contained a lot of animations that don't appear in the synched version.  But the video is a pretty good substitute.  Enjoy!

Understanding the Relationship Between Yoga and Ayurveda

Reflections by Melina Meza

by Ram

A lot of questions/comments are being raised in this blog regarding Ayurveda and yoga, so Nina asked me to address these issues. While I think that the science of Ayurveda and yoga is better addressed and understood in a verbal format—akin to a didactic exchange of information—through this article I will try to lay out the main principles that govern both these sciences.

Thanks to Swami Vivekananda, yoga came to the West in 1893 and was welcomed by a very receptive audience. While people embraced yoga, its counterpart Ayurveda, was left behind in India. This despite the fact that both yoga and Ayurveda are two very similar paths sharing a close relationship, so closely related that they are often described as two sides of the same coin. Both these sciences, which have their origin in the Vedic texts, address health and health practices. If Ayurveda is the healing aspect, yoga is the spiritual/practical side of the Vedic teachings. Together they emphasize a complete approach to the wellbeing of the body, the mind, and the spirit. In fact, their close relationship has even led to some scholars arguing that Patanjali, considered by many to be the father of yoga, and Charaka, often considered as the father of Ayurveda, may have in fact been one and the same person known in Vedic India by different names during his travels to spread the teachings of these ancient sciences.

Both sciences have common underlying principles: the well being of an individual at the level of body and mind and the aim of helping an individual re-connect to their true nature through direct and personal experience (pratyeksha in Sanskrit). While yoga prepares the body and mind of the individual for eventual liberation and enlightenment, Ayurveda describes the various ways to keep the body and mind healthy. Both sciences emphasize our close relationship with the environment and how to alter our environment in such a way that it is harmonious with our deepest nature.

In today’s world, yoga is often thought of as “asanas only,” something like a stretching tool to keep the body limber and agile. People are drawn to yoga as a way to keep fit even though the idea behind the physical practice of yoga is to help the mind to become clear or pure and develop deeper mind-body awareness. A clear mind is not affected by stress and a clear mind produces a healthy body thus creating a greater connection with one's own pure, essential nature. Similarly, Ayurveda brings with it the knowledge of how to keep the physical body healthy and how this relates to one's spiritual journey. It addresses our entire lifestyle, including exercise and yoga. However, Ayurveda is highly individualistic and sees each individual as unique and an individual's path toward perfect health as a unique path. Hence, what is right for each individual is unique to that individual alone. This could be described as person’s unique genetic background or constitution or dosha in Sanskrit. An individual’s constitution describes who the person is at the most fundamental level.

The above concept is remarkable because as a result of this understanding, Ayurveda prescribes a unique, “tailor-made” program to each individual based upon his/her constitution and the nature of the imbalance, and avoids the “one size-fits all” concept that is followed in many systems of healing. As Dr Marc Halpern, director of the California College of Ayurveda, points out:

While Ayurveda does not agree with the "Fits all" concept, it subscribes to the philosophy that “nothing is right for everyone and everything is right for someone.”

Thus, Ayurveda is based upon understanding individualized needs and what is right only for the individual - not the masses - and fulfilling those needs to bring complete harmony.

As with diet, herbs, colors, aromas, etc, Ayurveda sheds light on which specific yoga asanas are best for each individual based on his/her constitution. With the knowledge of Ayurveda, a practitioner of hatha yoga can refine his/her practice so that it is in harmony with their internal balance of energy. Some yoga postures are best for one person while others can cause greater imbalance. By knowing one's constitutional balance, an individual can use constitution-specific asanas to reverse their imbalances and improve their health and wellbeing. Indeed, if we can understand our constitution, we can control our choices and choose only those that will lead us toward optimal health.

How does one get to know their inherent constitution? There are several alternative health journals or web sites that analyze your constitution based on your answers to a specific set of questions. Chances are that your alternative health practitioner (who does not hold a proper certification in Ayurveda studies) may have made a passing remark about your constitution. Do not rely solely on this analysis, instead take it all with a grain of salt. Before jumping to any conclusion about your constitution and changing your diet, asanas or lifestyle, it is always best to consult with an Ayurvedic health professional who will help to determine your constitution, help you to understand the nature of any imbalance, and establish a plan to bring you to balance thus providing guidance toward success in establishing a disease-free lifestyle.

Despite my opposition to separating these two sciences, let me emphasize that when it comes to the Yoga for Healthy Aging blog, we have a general policy against writing about anything except yoga and the science of aging. Not all the staff of Yoga for Healthy Aging are trained in the area of Ayurevdic sciences and we would like to keep this subject off limits. So we’re going to have to decline to address questions on specific diet, herbs, or general Ayurvedic medical advice as it is a highly individualized system. Besides we cannot provide Ayurvedic advice without examining you in person in a private setting and this, after all, is a yoga blog! So, we hope you understand.

Namaste.

Mission Statement

by Nina

Above the Fog by Brad Gibson

Recently I received a question from a reader asking two questions; the first question was yoga related. The second, which was not yoga related, asked which supplements we recommended for a certain condition. After letting our reader know we would be happy to address the first question (and in fact, an answer to her question will be coming this very week), I wrote:

But regarding the second question, we don't address nutrition and supplements on the blog. None of us are trained in that area, and recommending supplements is a very tricky issue for a number of reasons. So, from the beginning, we established a general policy against writing about anything except yoga and the science of aging. So we're going to have to decline to address that one. I hope you understand!

The reader graciously—we love our readers!—wrote back saying that she did understand. But as we have a number of new readers since we published our original mission statement (see In the Kitchen), I thought I’d take a moment to let you all know a little bit more about our mission. Of course, we’re blessed here at Yoga for Healthy Aging to have an extraordinary staff, including two MDs (Dr. Baxter Bell and Dr. Timothy McCall), two scientists who study aging (Dr. Bradford Gibson and Dr. Rammohan Rao) and a practicing physical therapist (Shari Ser, P.T.). Naturally with so much available expertise, you might assume that we’d be able and willing to address subjects other than yoga that know quite a bit about, especially if they are related to the aging. But even we were first discussing the blog, we understood that for differing reasons, some subjects needed to be off limits. So without further ado....

What we will take on: 

1. Yoga asana, meditation, pranayama, and other practices, especially as they relate to healthy aging.
2. Yoga philosophy and yoga history.
3. The science of aging and various theories of aging.
4. Scientific studies regarding yoga.
5. Medical conditions in general and how you can use yoga to address them.

What we won't take on:

1. Diet
2. Supplements.
3. Medical advice. (Yes, we have doctors here, but as with any doctor, our doctors cannot dispense medical advice without examining you in person. Besides, this is a yoga blog!)

Even after declaring those three topics off limits, we can assure you, we've still got an enormous wealth of useful and inspiring information to share with you. Plus, we've added three new regular contributors (Timothy, Ram, and Shari) since we first started the blog, who have even more ideas and new points of view. During the very first discussion Baxter, Brad and I had about the idea of the blog (we were in the kitchen, preparing a meal together), Baxter was initially concerned that we might not have enough material, but Brad said, "No way. We'll never run out of topics!"  

Got Mindfulness?

by Nina

Yesterday I read an Op-Ed piece by Mark Bittman in the NY Times Got Milk? You Don't Need It and I was very surprised to read the following:

“This in a country where as many as 50 million people are lactose intolerant, including 90 percent of all Asian-Americans and 75 percent of all African-Americans, Mexican-Americans and Jews.

Seventy five percent of all Jews are lactose intolerant? Wow! I’m Jewish and I never even heard this before! When I was a kid, I hated drinking milk. But my mother was so convinced that it was imperative for my health that I was not allowed to leave the table until I forced down my entire (totally yucky) serving. When I was old enough to stop drinking milk as a beverage, I did, although I continued to eat dairy products in their many tempting forms (cheese, butter, ice cream, yoghurt, in lattes and on cereal, etc.). Meanwhile, I always had a rather delicate digestive system, but I tended to blame it on other things (soy, garlic, etc.) Then several years ago my digestive problems got worse, and I finally consulted my doctor about it. She suggested that perhaps it was just the aging process and added there was little I could do about that (to her credit, she did ask me if I was lactose intolerant, but I said that I wasn’t).  Hope I’m not boring you with all this, but there’s a point, I promise.

Anyway, I had noticed that when I spent a week or two eating a vegan diet (because my two kids took turns being vegan during different periods) I felt great. But I still wasn’t connecting the dots. It wasn’t until a few years ago when my husband and I decided to experiment by giving up diary products entirely for other reasons (the environment, global warming, a new theory of inflammation, consideration of dairy cows) that I noticed, hey, my digestive problems are gone! And all the plant foods I thought I couldn’t digest well now made me happy and healthy. Because I felt so much better, it became easy for me to pass up the tempting treats I used to indulge in, even to give them up for life (though with the occasional splurge—hey, my daughter is a pastry chef).

Above the Fog Again by Brad Gibson

You see, last week’s interview with Dayna Macy Yoga for Healthy Eating about mindfulness and healthy eating really made me think, especially the following: 

"Most people don't just sit in Lotus, they work to open their hips and one day, maybe, they get there. It's the same with food. You are discovering who you are in your relationship with eating. You don't just wake up one day and say, "ah ha! This is the perfect way to eat! Now I will do this perfectly from now on!" Knowledge is earned and learned, one day at a time. The truth must resonate and live in your body to become real change."

I just realized this morning that I had been practicing exactly what she described, and that mindfulness about my eating led me to healthier eating habits for my particular body, even though I never heard that fact about Jews being lactose intolerant. My long-time yoga practice no doubt helped me tune into how my body was reacting to different foods, and that ultimately brought me to a decision about my diet that is not only going to have the short-term benefit of making me feel better on a daily basis but will also help my health in the long run.

Have any of you used mindfulness about your eating to move yourself toward a healthier diet? We’d love to hear from you.

Diet....The Dirty Word

Hi Readers…..

How have you been doing? Checking in with you to see how your “ME TIME” is going. Did you incorporate fun moving, healthy eating, and increased water????? Just a little food for thought and speaking of food, that is just what I want to address today.

DIET…THE DIRTY WORD

I developed an acronym for the word DIET and how it affects each and everyone of us.

D: Depressing
I: Illogical
E: Extreme
T: Taxing

How many times have you heard someone say they are on a DIET!!!! The media has once again hit us with sooooo many to choose from….Low Carb, No Carb, High Protein, Low Protein, No Protein, No Carb, No Fat, High Fat, Low Fat, All Soup, All Vegie, All Meat, No Meat, All Fruit, All Shake, No Sugar, Fake Sugar, Low Calorie, High Calorie, Eat for the blood type, Eat for the body type, Eat for the hormones, and for goodness sake…do not mix carbs, proteins, and fats together! Wow, this makes even my head spin. No wonder we as people are so confused about how to eat, what to eat, and when. Friends…..eat for health…how easy is that? Throw the DIRTY WORD out the window and implement a healthy NUTRITION PLAN that says YES…EATING IS GOOD! It is all about food selection. Eating 5/6 small meals per day is key to keeping your metabolism on fire. Restriction of the GOOD STUFF (FOOD) means Retention of FAT!!!

Stay Healthy!

Darla