Photo by Irwin-Scott

I’ve had about a zillion people ask me about a new study that came out in the Archives of Internal Medicine this week linking red meat consumption to increased mortality.

Naturally some people are afraid their carne asada habit may be dooming them to an early death, and who could blame them with headlines like these?

On the other hand, I suspect many of you have dismissed the study out of hand because it conflicts with your world view that animal foods only make good things happen.

But in the interest of science and being grown ups, let’s take a look at the study and see what we can learn.

First, it is worth mentioning that the study was fairly well-designed and conducted by a respectable team of scientists at Harvard. They reanalyzed data from two large prospective cohort studies: The Health Professionals Follow-Up Study (HPFS, 1986-2008) and the Nurses Health Study (NHS, 1980-2008).

Both cohorts were large groups of health care professionals, which would presumably limit differences in education and income that can often confound health studies. The participants filled out regular food frequency questionnaires that have been previously validated as decently reliable (though food frequency questionnaires are notoriously unreliable).

Importantly, all the participants were eating Western diets during what have come to be known as the least healthy decades in US history. Also important, during the course of the study both red and processed meat consumption declined in both men and women.

“The mean daily intake of unprocessed red meat dropped from 0.75 to 0.63 servings from 1986 to 2006 in men and from 1.10 to 0.55 servings from 1980 to 2006 in women.”

The authors never comment on what this reduced consumption means for their analysis, however, since they “created cumulative averages of food intake from baseline to death from the repeated food frequency questionnaires.”

According to the report, people who ate the most red meat were more likely to smoke, drink, eat far more calories and be overweight. They were also less likely to exercise and eat healthy foods like fruits, vegetables, whole grains and fish. Basically they were less healthy people with less healthy habits.

The authors claim to have controlled for such lifestyle factors by doing statistical corrections for these variables, which is the industry standard for this type of analysis. They also performed a sensitivity analysis to see if any other dietary variable (including glycemic load) may have impacted their results. They did not detect any significant differences when controlling for these factors, which I admittedly find surprising.

To their credit, the authors made an effort to distinguish between processed and unprocessed meats. Given the time during which the study took place, however, it’s unlikely that any of the participants were eating non-industrial, grass-fed and pastured meat. I think this is an important point, particularly when considering cancer mortality, since toxic compounds tend to accumulate in the fat of animals.

In their analysis the authors estimated that for every one serving of red meat per day (defined as 3 oz), total mortality risk increased by 12% (20% for processed red meat alone, 13% for unprocessed). Heart disease risk increased by 16% for total red meat (21% for processed red meat, 18% for processed), and cancer risk increased 10% for total red meat (16% for processed, 10% unprocessed).

To help put this in perspective, in the Nurses Health Study (the larger of the two) the group that ate the least meat consumed about a 1.5 oz (half a deck of cards) of meat per day and the group that ate the most consumed around 6.5 oz of meat per day (here’s the data I’m pulling from, using the 3 oz serving size for conversion).

Remember, these numbers are for daily consumption. For the highest group, that’s nearly 3 pounds per week (45.5 oz). For the lowest group, under 1 pound (10.5 oz). Realistically, the lowest group probably ate red meat 1-2 times per week, while the highest group ate it once or twice a day. How we got from here to “all red meat will kill you” isn’t exactly clear.

Interestingly, when they did an analysis to see the specific effect of saturated fat in meat it accounted for only 4% of the 16% estimated risk. This is fairly low considering that saturated fat is supposedly what makes meat so bad for us by raising cholesterol. But since the authors say that saturated fat could account for some of the increased risk, can we at least assume that those eating the most meat were more likely to have higher cholesterol? Not so fast. It turns out that in both cohorts, those in the lowest group of meat consumption were the most likely to have high cholesterol. (Thanks Denise Minger for making this astute observation).

So what about the meat is killing us exactly? In addition to saturated fat, the authors also estimated that heme iron in meat (assumed to be a risk factor for some diseases) can account for another 5% of the risk, but they do not elaborate on how this might work. It is unclear what else about red meat may be increasing mortality risk, though preservation methods are suspected for the higher risk associated with processed meats.

The authors also used some fancy statistical magic to estimate what would happen if the participants theoretically replaced one “daily” meat serving with an equal portion of either fish, poultry, nuts, legumes, low-fat dairy or whole grains and determined that mortality risk would decline 7%, 14%, 19%, 10%, 10% and 14%, respectively. It is important to remember though that *ahem* these are not real experiments but merely estimations based on the numbers and statistical models used in this study. At best an analysis like this can generate a hypothesis that could then be tested in a controlled trial.

Fortunately controlled studies replacing meats (oh, and all the other crap in the Western diet) with other nutritious, whole foods have already been done. For example, in the Lyon Diet Heart Study (1988) a group of patients who had already had a heart attack were instructed to change their diets. One group went on the low-fat American Heart Association diet, the other group adopted a Mediterranean style diet that included lots of green and root vegetables, fruits, legumes, more fish and poultry, less red meat, olive oil and no cream. After only 3 years the study was stopped by the ethics and safety committee because the Mediterranean diet group had a 70% reduced risk of death compared to those on the low-fat diet.

Studies have consistently shown that replacing some dietary meat with fish and other sources of omega-3 fatty acids reduces the risk of heart disease. However, replacing red meat with anything else (even olive oil) seems to be pointless. For this reason I’ve always been skeptical that red meat is uniquely bad when the simpler explanation would be that eating more fish is uniquely good. I don’t see how this new analysis of old studies changes anything.

Lastly, although the authors included controls for lifestyle factors I’m highly suspicious that people with so many unhealthy habits are at an increased risk of death primarily because of meat consumption. Consequently, all that I’d feel comfortable concluding from the new analysis is that in the context of a Western diet, eating something other than meat every once in awhile is probably a good idea. Outside of the Western diet? It’s much harder to say.

What are your thoughts on the study?

Photo by Werwin15

The science of aging is among the most dynamic and provocative in modern biology. Over the past two decades we have seen a virtual explosion in research investigating the molecular and behavioral systems that control the aging process. But the more researchers uncover about the science of aging, the more questions emerge.

Dietary restriction has long been considered the most potent regulator of aging. Restricting food intake by any means induces a series of metabolic changes in organisms from yeast to primates that serve to extend life. Studies are currently underway to investigate the ability of dietary restriction to extend life in humans.

Several biological changes are known to occur upon the onset of dietary restriction including a decline in reproductive ability, increased stress resistance and a slowdown of some metabolic processes.

Insulin signaling was among the first molecular pathways to be identified in the regulation of aging, and offered a direct tie between diet and the aging process.  In 1998 UCSF scientist Cynthia Kenyon showed that removing an insulin receptor gene (daf-2) in worms could double their lifespan. Her lab later showed that removing another insulin signaling gene (daf-16) could extend life even longer. I spoke to Kenyon about the relationship between diet and aging for this article.

Blocking insulin signaling in these worms did not just prevent the worms from dying and allow them to age longer. Instead the aging process actually slows so that older worms continue to behave like young worms. Also, as these experiments were repeated in different animals, it was shown that lowering insulin signaling also helps protect animals from stress and diseases such as cancer and heart disease.

Insulin is released as a direct response to glucose in the blood. This means that any time you eat a meal with carbohydrates, you are increasing your insulin signaling and likely accelerating aging. But this does not mean that you will live forever if you stop eating carbohydrates.

Interestingly, protein metabolism also contributes to accelerated aging, but through a different mechanism. Even more intriguing is that restricting protein increases lifespan to a greater extent than restricting sugar.

So is it simply calories that promote aging?

Probably not. For one thing, the effect of a calorie from protein is greater than a calorie from carbohydrate, making it unlikely that a calorie is the basic unit of impact. Second, there is evidence that calories are not required to accelerate aging.

Recent studies have shown that the mere act of smelling food can reduce lifespan. The mechanism for this effect is still unknown, but seems to be tied to respiration.

According to Kenyon it is clear that “sensory perception influences lifespan,” at least in worms and flies.

Thus it is likely that aging is controlled by the interaction of several pathways, including metabolism, respiration and stress. Importantly, however, lifespan seems to be dependent on a handful of specific pathways rather than global changes in cellular function or breakdown. The idea that aging is an inevitable function of time must be put aside given the evidence that it is controlled at a genetic and environmental level.

This makes sense when you think about it. Different organisms exhibit vastly different lifespans and rates of aging that are too great to be explained by some kind of universal cellular breakdown. A more parsimonious hypothesis is that organisms differ in specific genetic factors that, combined with environmental influences, regulate lifespan.

So how should we mortal humans react to these findings?

The genes linking diet and aging are highly conserved through evolution, indicating that there is a great chance human aging is sensitive to diet. Indeed, insulin-related genes have been found to be important in long-lived human populations. This suggests that the pathways discovered in worms and other organisms have similar functions in humans.

What is not clear is how much influence diet has on lifespan and to what extent we are able to manipulate it. It is already known that abnormal insulin activity in humans is linked to higher disease rates, especially “diseases of civilization” such as heart disease, hypertension, type 2 diabetes and cancer. And these diseases are clearly associated with diets rich in processed foods, especially refined carbohydrates.

The effect of protein consumption on lifespan in humans has yet to be investigated. Envisioning an experiment that would test the influence of smelling food on human aging is difficult to even imagine.

Although direct evidence is not available, there is good reason to suspect that a diet with low glycemic load may extend human lifespan. In November 2009, Kenyon’s lab reported that adding glucose to a worm’s normal diet shortens lifespan, but has no effect on the long-lived worms that lack insulin signaling genes daf-2 and daf-16. This discovery prompted Kenyon herself to adopt a low-carbohydrate diet.

Despite this there is still not sufficient evidence to recommend a calorie restricted diet for humans to extend life, largely because optimal nutrition levels for a given individual are unknown. However, most people would benefit vastly by eliminating processed foods and refined carbohydrates from their diets as much as possible.

Focusing on fresh, whole foods, enjoying an occasional glass of wine, avoiding smoking and getting regular exercise can add 14 years to the life of an average person. Maintain a healthy weight as well and your outlook gets even better.

Would you change your diet to be healthier and live longer?

Originally published February 3, 2010.

Photo by helgabj

Now you see me, now you don’t.

Today’s guest blogger Tim Harwood is a UK based optometrist who also writes for TreatmentSaver.com.

Top 5 Foods For Maintaining 20:20 Vision

by Tim Harwood

If you are lucky enough to have perfect vision, don’t assume it will last forever. As we get older the chances of us developing an eye disease increases dramatically–10% of people over the age of 65 have macular degeneration, and that increases to 30% over the next 10 years.

To preserve perfect vision, first you have to cover the basics:

• Get regular eye tests: Have your vision tested at least every 24 months, as early detection increases the likelihood a disease can be treated. Although not all diseases are treatable (e.g. macular degeneration), certain diseases such as glaucoma respond excellently to medication when detected early enough.
• Don’t ignore visual symptoms: Regardless of how recently you have had an eye test, you should never ignore visual symptoms. If you see flashing lights, floating specks or blind spots in your vision these could indicate an eye disease that needs urgent attention.

How can food help me maintain perfect vision?

The macula is in the center of our retina and is responsible for central vision, reading and recognizing faces. As we get older our macula shows signs of wear and tear, a process known as macular degeneration. There is no effective treatment for this age-related degeneration, which is why eating the right foods is extremely important.

Within the macula there are 2 key pigments:

1. Lutein
2. Zeaxanthin

Lutein and zeaxanthin are antioxidants found within the macula. These antioxidants reduce the amount of free radicals formed within our body as a natural consequence of our cells using oxygen (oxidation). These free radicals have degenerative effects on our eyes, which are thought to be the cause of macular degeneration. Lutein and zeaxanthin slow down this process and help preserve the macula.

Ophthalmologists are now recommending that people with early signs of macular degeneration take lutein and zeaxanthin supplements or change their diet accordingly.

What foods are high in lutein and zeaxanthin?

Here are the top 5 foods with the highest concentrations of these beneficial nutrients:

1. Kale
2. Spinach
3. Peas
4. Courgette / zucchini
5. Brussel sprouts

Studies show that 6 mg of lutein and zeaxanthin should be eaten daily as part of your diet to provide the maximum benefit to your macula. This equates to about one large bowl of spinach or kale daily. Even if you can’t eat this amont every day, it is worth the effort to eat as much of these vegetables as you can manage.

Though these nutrients do not guarantee protection against macular degeneration, evidence suggests they at least slow the progression of the disease. In any case these vegetables are extremely healthy and may also protect against other conditions caused by oxidation such as cancer, diabetes and heart disease.

How’s your vision?

Jeff Miller/University of Wisconsin Madison

Last week The New York Times published a story on the life prolonging effects of a low calorie diet in primates. The study in question found that like other organisms (from yeast to worms to mice), rhesus monkeys that eat 30% fewer calories age more slowly and develop fewer diseases than animals on a traditional diet. Those of us who follow the scientific literature on nutrition and aging are not surprised by this at all.

A few days after the story was published The Times published an op-ed questioning the value of the research. Roger Cohen argues that Canto, the healthier monkey, has suffered tremendously as a result of his restricted diet. He contends that it is far better to be fat and happy (and dead?) than thin and miserable.

To me it seems questionable why Cohen believes Canto is unhappy. If he is making his judgment solely on the image above, I must respectfully disagree with his assessment. To me both monkeys appear relatively miserable.

However, Cohen brings up a crucial question about diet and health. How far are we willing to go–how much are we willing to change our diets–in order to extend our lives?

Quality of life is a very important question.

To me one of the most interesting things about calorie restriction is that life extension is only one of many health benefits. Calorie restriction literally slows down the aging process. As a result the animals subject to a limited diet are able to maintain a high level of physical activity into old age. They are also relatively free of age-related diseases including cancer, heart disease, diabetes and neurodegenerative diseases.

Extended life would arguably not be as desirable if these diseases maintained the same progression as they do in those with normal diets. But freedom from these diseases and preserved physical and mental capacities may indeed be worth some dietary alteration.

The next question is how must the diet be changed?

In the monkey experiment, the calorie-restricted group received 30% fewer calories than the control monkeys, who were allowed to eat what they wanted. It is still unknown if a 30% reduction in calories will extend human life in a similar manner, but short-term experiments have indicated that at least some benefits are immediately apparent when calories are limited, such as lower triglycerides, body fat and blood pressure.

Interestingly, however, there may be alternatives to a strict low calorie diet. Cynthia Kenyon, a scientist at UCSF, was the first to show that the key to the life extending properties of calorie restriction is the insulin signaling pathway. A decrease in insulin signaling slows the aging process and extends life.

In the laboratory, organisms like worms, mice and monkeys always receive a uniform diet that has a consistent effect on insulin signaling. But humans do not eat lab food (at least not usually).

Extensive research over the past several decades has made it clear that different foods impact insulin signaling differently in humans. For example, refined carbohydrates have a large, rapid impact on blood sugar, insulin secretion and insulin signaling. By contrast, fat, protein and fiber have next to zero impact on blood sugar and subsequent insulin signaling.

The implication of the diverse human diet is that we are able to alter insulin levels and signaling in our bodies without undergoing severe calorie restriction. Whether or not a diet that promotes less insulin signaling can slow aging in humans is still unknown, but there are many other benefits associated with a diet that lacks refined carbohydrates.

Insulin signaling is not only tied to the aging process, it is also the primary cause of metabolic syndrome–high triglycerides, insulin resistance, hyperinsulinemia, abdominal obesity, low HDL cholesterol and high blood pressure–as well as type 2 diabetes and heart disease.

A diet that improves these symptoms may or may not slow the aging process directly, but it can certainly promotes a higher quality of life by lowering the risk of many debilitating and life threatening diseases.

Going to farmers markets and eating delicious meals isn’t so bad either.

What are your thoughts on health, diet and quality of life?

Collards, Carrots and Lentils

There is much debate among nutrition scientists over whether meat eating is healthy. On one side there are the hardcore low-fat vegetarian advocates like Dr. Colin Campbell, author of The China Study, who believe all animal fat and protein is dangerous. On the other side are those who point to refined carbohydrates as the biggest threat to public health, citing studies that suggest meat alone is harmless or even helpful (for more information read Good Calories, Bad Calories, by Gary Taubes).

I tend to agree somewhat with both.

For heart disease, the evidence certainly seems to indicate that refined carbohydrates are the worst culprit. Though health advocates once pointed to saturated fat as the cause, this suggestion has not stood up to rigorous scientific testing. In fact, dietary fat (particularly from plants) seems to be protective against heart disease.

Refined carbohydrates are also the cause of type 2 diabetes and metabolic syndrome (a combination of insulin resistance, high blood pressure, heart disease and obesity), which is arguably the biggest health threat of our time.

For these reasons and many others, I avoid refined sugar and flour as much as possible in my daily life.

Heart disease and metabolic syndrome are not the only diseases that concern me, however. Cancer is another modern ailment that has been linked to diets high in both carbohydrates and meat. Though the studies are not perfectly consistent in showing harm or no harm regarding meat consumption and cancer, rarely does anything suggest meat eating is actually beneficial (though studies are almost always confounded because meat eaters also tend to eat the most sugar and refined grains).

Fish is another story entirely. Although fish is technically a meat, its properties are very different from land animals. For one thing, fish eating has consistently proven beneficial in scientific studies of heart disease and metabolic syndrome. It also seems to play a role in protecting the brain against degenerative diseases.

I am an avid fish eater and try to include seafood in my diet several times per week.

Until now, however, I have not read much about the role of fish in cancer. A new meta-analysis published in the British Journal of Cancer (part of the Nature publishing group) suggests that vegetarians have significantly less cancer than meat eaters, and that cancer rates are even lower in fish eaters.

The researchers analyzed data from two British studies of vegetarians from the early 80s and early 90s that includes over 60,000 individuals, mostly women but some men. The participants were followed until the end of 2006.

Incidence of malignant tumors was compiled for all the subjects and the relative risks were calculated. Vegetarians and fish eaters had significantly lower risk for stomach cancer, ovarian cancer, lymphatic and bone marrow cancers, and bladder cancer. Vegetarians had a higher risk of cervical cancer than meat eaters. Fish eaters had a lower risk of prostate cancer than meat eaters.

Overall vegetarians had 8% fewer cancers than meat eaters and fish eaters had 20% fewer.

Interestingly, no difference was found in breast cancer or colorectal cancer incidence, which have both been tied to meat consumption. The authors speculate that this study could be lacking in statistical power to observe a difference. However, the current data is inconsistent and no conclusions can be drawn.

While the results of this study are very compelling, there are several caveats that must be addressed. First, the number of cancers at individual sites were relatively few, meaning that findings may be exaggerated or due to chance. For me the most convincing numbers are of the overall cancer rates (the largest numbers and strongest statistics), but this leaves many questions about the causes of the different cancers.

Another issue is that vegetarians and fish eaters in the study tended to be younger and get more exercise than the meat eaters, so there may be important confounding factors that could influence the results. Likewise, studies that rely on self-reported dietary patterns have well-documented flaws (basically everyone believes they eat healthier than they really do).

It is not clear what is causing the differences in cancer incidence among vegetarians, fish eaters and meat eaters. Vegetables and fruits have been suspected of actively protecting against cancers, but so far the mechanisms are only speculative and not concrete. Recent studies have suggested vitamin D can be protective against certain cancers. Since some fish can be very high in vitamin D, this may explain some of the benefit seen in fish eaters.

The higher incidence of cervical cancer among vegetarians is also compelling and warrants further research.

Despite the flaws in this study it is mostly consistent with other research suggesting that an optimal diet is primarily fresh, unprocessed plants, some fish and little meat.

Moderation is usually the best policy.

What is your take on this study? How do you feel about health vs the ethics of fish consumption?

1 lb Fat

Last week the New York Times and many other reputable news sources reported on a Canadian study that claims people with a normal body mass index (BMI) had a slightly increased risk of dying over a 12-year period than those with a BMI in the overweight range (25-29).

The use of the phrase “overweight was protective” landed this article just a hair’s width from being labeled Summer Tomato’s B.S. of the week on Friday. An observational study cannot determine cause and effect, as implied by the word “protective.” This study does not prove that extra body weight protects against all cause mortality, and saying so is irresponsible.

Studies (and reporting) like this have instigated wide-spread confusion about health and body weight. First people are told they are too heavy and should lose weight for health, then in the same breath they are told a little extra weight might not be so bad.

What is the average person supposed to believe? How should we act?

If you want to understand the facts it important to know exactly what the data does and does not say. Indeed, some studies (including one on Japanese men reported in the same issue of Obesity) have reported lower or equal risk of mortality for people with an overweight BMI compared to people of normal BMI (18.5-24). However, this is not the whole story.

First, the alleged benefit of being overweight has only been found in older individuals and does not apply to healthy, young people. Second, although it appears in some cases that overall mortality may be reduced, disease incidence is notably higher in overweight individuals compared to people of normal weight.

To point, a study in the most recent issue of Obesity (same journal, 2 weeks later) examines the relationship of BMI with many measures of cardiovascular disease in healthy, athletic men. In this study, those on the lowest end of BMI in the normal range (18.5-22.5) had a much lower risk of dying from or developing cardiovascular disease than normal weight men with a slightly higher BMI (22.5-25).

Men with the lowest healthy BMIs also had lower risk of hypertension, lower cholesterol and half the risk of diabetes. While the length of this study was only 7.7 years (compared to the 12 years reported in the Times story), there were more than double the number of participants (28,776 vs. 11,834).

(Why did this story not make the news? My guess is that it makes for a less compelling storyline and people would rather not hear it.)

Mortality is certainly an important measure in any study, but it is arguably not the most relevant endpoint. Disease and excess body weight can severely impact quality of life, particularly for older individuals (as illustrated by another study in the latest issue of Obesity). While I cannot speak for everyone, it seems probable that quality of life is equally if not more important than longevity alone. Thus it is questionable how much stock to put into studies that ignore these other factors.

It is also critical to remember that BMI is a measure that was designed to describe people at a population level, not as individuals. While large cohort studies can tell us useful things about relative risk, they are not directly applicable to individual people.

The inconsistency of the data related to BMI and mortality may in fact be an indication of its inadequacy as a general measurement. Remember that BMI represents a ratio between height and weight, making it possible to compare people of various body sizes. Normalizing for height may, however, be deceptive.

Decades of data on caloric restriction consistently show that smaller body size (irrespective of body fat levels and, possibly, BMI) is associated with longer life and decreased risk of nearly all diseases. This is true in all animals from yeast, to worms and flies, to mice and monkeys. While humans are certainly different from all these model organisms, there is tremendous evolutionary precedent indicating smaller body size as the best for health.

The principle of parsimony tells us the simplest hypothesis–that smaller body size is beneficial–is probably correct. Substantial evidence must be accumulated before this hypothesis can be rejected, and I have yet to see that data.

Furthermore, while the research on the risk of overweight may be slightly ambiguous, the data on obesity is not. It is painfully clear that the dangers of obesity are profound and on par with those of smoking cigarettes. Overweight is a necessary step to becoming obese, and according to the National Population Health Survey nearly a quarter of Canadians who were overweight in 1994/1995 were obese by 2002/2003. Since overweight is still a substantial risk factor for becoming obese, misleading public health messages about the benefits of body fat are especially dangerous.

As a consumer of information, the most important thing you can do is be skeptical of what you read. Just because something is printed in the New York Times does not make it true. In fact, many of our most trusted sources of health information do not base their recommendations on rigorous scientific thinking, which is probably the reason for the health disaster we are currently facing.

Thanks to Jan from Quest for Health for sparking this discussion.

What does your gut tell you about the relationship between health and body fat?

Collards, Carrots and Lentils

A new study published yesterday in the Archives of Internal Medicine suggests that both weight loss and risk factors for heart disease can be improved following a vegan version of the low-carb, high-protein Atkins diet.

The “Eco-Atkins” diet focuses primarily on soy, nuts and wheat proteins (gluten) to increase the amount of vegetarian protein in the diet. Carbohydrates were restricted to 130 g/day, which is on the higher end of most low-carb diets. All starchy foods such as bread, baked goods, potatoes and rice were eliminated. Carbohydrates were provided in the form of whole, intact grains (barley and oats) and low-starch vegetables.

In a small (47 participants), short-term randomized controlled trial, this diet lowered bad LDL cholesterol by 20%, without negatively impacting good HDL cholesterol (statin drugs improve cholesterol levels by 30%). The diet also substantially lowered blood pressure and other markers of cardiovascular disease, such as triglycerides and apolipoprotein B.

The original meat-based Atkins diet has been shown to be effective for temporary weight loss (after 1 year the effects of the Atkins diet are diminished), but cardiovascular risk factors such as LDL cholesterol and blood pressure are not substantially improved under the traditional Atkins regimen.

Interestingly, a traditional Atkins-style diet based on animal protein was not used as a control in this study, so a true comparison of the diets cannot be made using the present data. Instead the researchers chose a control diet representative of a typical high-carb, low-fat vegetarian diet that included eggs and dairy products. Both diets tested in this study represented a 60% decrease in total calories.

Because of the study design, we cannot conclude that this diet is more effective than the Atkins diet for health, though you would predict it would be if future studies made this comparison. On the other hand, it does seem that a plant-based high-protein diet is more effective at improving health than a high-carbohydrate lacto-ovo vegetarian diet, at least in the short-term in a highly controlled environment.

This study took place over the course of 4 weeks, and all the food was provided for the particpants by the researchers. Thus, compliance in the program was very high. It is not clear if the participants would have had the same level of success if they were instructed to provide their own food to comply with the dietary programs.

Despite this, satiety levels were notably improved in the high-protein group and it would be expected that the increase in satiety would encourage greater compliance in a free living situation.

A small four week study, however, tells us very little about the effectiveness of this diet. While it is possible to improve risk factors such as cholesterol and blood pressure in such a short period of time, disease outcome is the true measure of a successful diet. Also, this study did not test the feasibility of the Eco-Atkins diet in the long-term, and it is likely many dieters would object to a strictly vegan regimen.

Interesting points raised by this preliminary study include:

• Plant-based, high-protein diets may be more effective at improving cholesterol and other cardiovascular measures than traditional lacto-ovo vegetarian diets.
• Short-term weight loss is primarily determined by the number of calories consumed, not macronutrient content.
• Low-carb diets that include intact whole grains and plant-based protein can be effective at improving both weight and cardiovascular risk factors in the short-term.
• Plant-based high-protein diets can increase satiety compared to high-carb vegetarian diets.

However, many questions must be addressed before this diet can be recommended to individuals trying to improve cardiovascular measures and lose weight.

New questions:

• Can the Eco-Atkins diet be maintained in the long-term by normal individuals?
• Does the Eco-Atkins diet continue to improve cardiovascular risk factors including weight loss after 4 weeks?
• What would result from this study if beans and lentils were used instead of soy and gluten?
• Does the Eco-Atkins diet improve disease outcome?
• Does the Eco-Atkins diet extend life?
• Does the Eco-Atkins diet affect quality of life?
• Can these effects be attained through other diets that include some animal protein, more whole grains or more fat?
• Is the effectiveness of the Eco-Atkins diet affected by an individual’s level of insulin resistance?
• Can adding fish further improve the results of the Eco-Atkins diet?
• Can a further reduction in carbohydrates improve the results?
• Will you get these same results if the study is NOT funded by the soy industry?

In summary, the results of this study are interesting and encouraging, especially for those of us who think both carbohydrates and meat should be limited in a healthy diet. I very much look forward to future studies exploring this idea.

What concerns me most is the lack of marine omega-3 fatty acids (fish) in the Eco-Atkins diet, which could potentially improve cardiovascular measures even further. Fish is also important for cognitive health and may lower cancer risk.

I am also worried that a strictly vegan diet would not be feasible in the long-term for many Americans. Moreover, it is not necessarily the healthiest option available. Vitamin B12 deficiency is a particular concern, but could be addressed with supplements. Generally, however, I do not recommend relying on supplements for optimal nutrition.

Finally, this study was funded by a company that makes soy and gluten products. Personally I would have prefered to see these protein sources used in combination with other things such as beans and lentils. Many people question how much soy can be safely consumed and gluten intolerance is more common than ever, so wouldn’t it be interesting to know if there were safer alternatives? It really annoys me to see science being influenced by industry funding.

What do you think of the Eco-Atkins diet?

Vegetables

Most scientists agree that diet plays an important role in heart disease, but until now there has been no comprehensive analysis of which dietary factors most strongly affect disease outcome. A new meta-analysis published in the Archives of Internal Medicine reviews six decades of research (1950-2007) to assess how different dietary factors affect heart disease. Vegetables, nuts, “Mediterranean” and high-quality dietary patterns are strongly protective, while trans-fat, foods with high glycemic index or load and a “Western” dietary pattern were shown to be harmful.

The Study

This new study is unique for several reasons. First, the authors were only interested in factors that influenced heart disease directly, not simply heart disease risk factors such as cholesterol levels. Also, emphasis was placed on high-quality studies designed to identify strong dietary associations (cohort studies and randomized controlled trials) with long periods of follow up (at least one year). They asked whether the studies they reviewed were consistent with other data such as epidemiological reports, and sought to establish a causal link between diet and heart disease outcomes. Another important goal of the analysis was to identify factors that lack sufficient evidence to be conclusive and require further research.

Results

In addition to identifying vegetables, nuts, high-quality and Mediterranean dietary patterns as being strongly protective against heart disease, they also found monounsaturated fats (e.g. olive oil), dietary folate (e.g. whole grains, not supplements), dietary vitamins C and E (not supplements), alcohol consumption (in any form) and omega-3 fatty acids from fish (not plants, e.g. flax) to be moderately protective.

Factors that were not associated with heart disease in this study were dietary supplements (e.g. vitamins C and E), total fat, saturated fats, polyunsaturated fats (from plants), meat, eggs and milk. It is important to note, however, that negative findings in this analysis are not necessarily indicative of a lack of causality. Rather, it may indicate insufficient data to observe a significant positive association.

Dietary Patterns

The authors point out that “only overall healthy dietary patterns are significantly associated with coronary heart disease” in the controlled trials, while “evidence for most individual nutrients or foods is too modest to be conclusive.” They suggest that the reason an association exists for dietary patterns and not individual nutrients is that patterns “have the advantage of taking into account the complex interactions and cumulative effects of multiple nutrients within the entire diet.” The authors recommend future trials test various dietary patterns for disease outcome, including cardiovascular disease and cancer.

Taking this further, most dietary factors that were shown to be protective when consumed as part of a healthy diet were not protective when taken in supplement form. This finding bolsters the argument that overall diet rather than individual foods or nutrients are the best strategy for protecting against heart disease. The authors conclude that their findings suggest “investigating dietary patterns in cohort studies and randomized controlled trials for common and complex chronic diseases such as coronary heart disease.”

Based on their analysis, the dietary pattern that best protects against heart disease is rich in vegetables, nuts, fish, healthy fats, whole grains, and fruit. Likewise, the worst dietary pattern consists of refined carbohydrates and artificial trans-fats. The lesson: the best diet consists of plants, fish and whole foods, while processed foods contribute to heart disease.

What about red meat and saturated fats?

Interestingly, there was insufficient data to conclude that red meat or saturated fats are harmful for the heart. This is not terribly surprising, since the data has always been inconsistent. However, I would point out that many studies have looked at the role of red meat and saturated fat in coronary risk and the outcome always shows either harm or no result. And as explained above, no result can be indicative of a lack of statistical power rather than lack of causation. Importantly however, I cannot recall a single study suggesting that red meat and saturated fat is actually good for you.

From this the best we can conclude is that red meat or saturated fat may be involved in promoting heart disease, but if they are the effect is likely to be less harmful than a diet of processed foods. Practically this means small doses of saturated fat may not do much harm when eaten as a part of an overall healthy diet. This is a fairly compelling argument for exercising moderation.

Conclusions

Before you run out and order a ribeye, keep in mind that heart disease is not the only debilitating chronic disease that plagues our culture. Red meat is also associated with several kinds of cancer. Likewise, refined carbohydrates are highly correlated with type 2 diabetes. Vegetables and whole grains are protective against these other diseases as well, and fish may play a role in protecting against neurodegenerative diseases.

The take home lesson is that both diet and disease are complex systems that involve innumerable factors in several different regions of the body. When choosing what to eat it is important that you consider the context of your overall diet and do not get caught up is single foods or a single disease threat.

The Centers for Disease Control and Prevention (CDC) just released their 2005 report on cancer statistics. The web-based report contains official federal government statistics for cancer incidence in 96% of the United States population and mortality statistics for 100%. This is the seventh time the CDC’s National Program of Cancer Registries and the National Cancer Institute’s Surveillance, Epidemiology and End Results Program have combined registries to offer official federal statistics on cancer incidence and mortality for a single year.

Rates of cancer incidence are reported as the number of newly reported cases per 100,000 people. In 2005, the top four most common cancer diagnoses have not changed since 2000 and represent diseases strongly associated with lifestyle factors.

The number one diagnosed cancer in the US is prostate cancer (142.4), followed by breast (117.7), lung (67.7) and colorectal (48.3) cancers. The deadliest cancer is of the lung (52.8), while the mortality rates from prostate (24.7) and breast (24.0) cancer are nearly identical. Colorectal cancer is the fourth deadliest cancer (17.4).

Cancer is the second leading cause of death in the US, with heart disease being the first. Though most of us associate heart disease with lifestyle factors, cancer is usually regarded more fatalistically as being random or due primarily to genetics. While genetics does play a factor in some cancer cases, vast amounts of epidemiological data indicate that lifestyle factors, particularly diet and smoking, can largely account for high cancer rates in affluent countries such as the US.

There is abundant evidence that diets high in animal products and refined carbohydrates, and low in vegetables contribute to cancers of the prostate, breast and colon. A similar dietary pattern is responsible for cardiovascular disease, diabetes and neurodegenerative diseases. What is striking about cancer, however, is that there are no known drugs that stymie its development. Statins do not protect against cancer, nor do multivitamins.

The best diet to prevent all these diseases of affluence is a plant-based, whole foods diet.

Does fear of cancer impact your eating habits?

Vitamin D

Both environmental and genetic factors seem to play a role in the development of multiple sclerosis (MS), but determining an exact cause of the disease has been elusive. Now new evidence suggests that vitamin D may play a direct role in regulating a gene known to be associated with MS. This finding helps bridge the gap between environmental and genetic risk factors, and strengthens the hypothesis that vitamin D could be instrumental in MS prevention.

MS is an autoimmune disease that attacks myelin, a component of the nervous system essential for the conduction of neural impulses. Onset of MS usually occurs between the ages 18 and 35, and is more prevalent in females than males.

One of the most interesting epidemiological findings associated with MS is that it is more common in regions farthest from the equator, with a few notable exceptions. Climate, sunlight and vitamin D are all suspected candidates in the occurrence of MS, as are genetics and diet. Importantly, the relationship between geographical location and MS risk seems to be most significant in early childhood years. After age 15, risk of MS for immigrants is closer to that of their home country than to that of their new country.

Sunshine is the most common source of vitamin D for humans. Vitamin D is created when ultraviolet B (UVB) light contacts skin. Dietary vitamin D is rare, though it can be obtained at significant levels with certain foods, particularly oily fish (e.g. sardines and salmon). Notably, Norway and many Asian countries have relatively low prevalence of MS. It has been suggested that fish consumption is the reason for these regional discrepancies that cannot be explained by sun exposure. This makes vitamin D a particularly strong candidate for MS prevention.

In addition to environmental factors, certain genetic risks are linked to MS. In particular, proteins associated with the body’s immune cells are mutated in many MS cases. Mutations in these proteins disrupt the ability of immune cells to determine which particles in the body are foreign and which are “self.” When this happens, the cells get confused and begin to attack their own body’s tissues.

A new article published last week in PLoS Genetics investigated the relationship between vitamin D and the genetic variants associated with MS. They found that vitamin D directly interacts with these genes at a molecular level, providing insight into the mechanism by which vitamin D may affect the disease. Though it is still not clear what specific role vitamin D plays in its interaction with MS genes, a new avenue of exploration has opened up into MS etiology.

The tie between vitamin D and MS is still vague, but it is a good idea to ensure your vitamin D levels are adequate. People living at latitudes greater than 40 degrees from the equator (San Francisco is on the border) should be taking vitamin D supplements. This is true for many reasons; MS is not the only disease that is linked to low vitamin D levels.

Vitamin D pills are now easy to find, and can be obtained at both Trader Joe’s and Whole Foods. Take one or two oil-based 1000IU vitamin D supplements daily. Men should avoid vitamin D supplements that contain calcium, because excess calcium increases risk of prostate cancer.

Do you take vitamin D supplements?

UPDATE: This article can also be found in Synapse.