Photo by markhillary

Last month The American Journal of Clinical Nutrition published a meta-analysis of 21 studies concluding that saturated fat is not linked to heart disease–a finding that flies in the face of 20th century nutrition dogma.

Despite the tremendous impact such information would have on the field of nutrition however, the research was largely ignored by mainstream media outlets.

The meta-analysis performed by scientists at the Children’s Hospital Oakland Research Institute was funded by the National Dairy Council and the Unilever corporation, two institutions with a vested interest in selling food products to consumers. The study was also funded by the National Institute of Health.

Technically funding source should not impact scientific outcomes, but analyses have repeatedly shown that industry sponsorship can strongly predict research conclusions that favor the source of funding.

I asked Marion Nestle, professor in the Department of Nutrition, Food Studies and Public Health at NYU, about the specific impact of industry funding on a meta-analysis of this nature.

“Meta-analyses are particularly subject to investigator bias (conscious or unconscious) because of the selection criteria for inclusion.”

So while this study may provide another clue about the relationship between saturated fat and heart disease, caution should be taken when interpreting the results.

Conflict of interest is a serious concern in science that is used to guide health policy and consumer behavior. In this case the influence of industry sponsorship would be especially unfortunate since an impartial evaluation of the link between saturated fat and heart disease is greatly needed.

Saturated fat is most commonly associated with animal products like beef and pork, and is known to raise cholesterol. Since high cholesterol is considered a biomarker of heart disease, it has long been assumed that saturated fat contributes directly to America’s number one killer.

But while this argument seems to make intuitive sense, a direct causal relationship between saturated fat and heart disease has never been established. Moreover, evidence is accumulating that cholesterol in general is not the best predictor of heart disease and that refined carbohydrates are a bigger problem.

Thus there is a real need for rigorous science regarding the role of saturated fat in heart health and other diseases.

“My take on this one is that it is one more piece of evidence that saturated fat may not be AS important a determinant of heart disease risk as is sometimes believed-at least in the kinds of studies included in the analysis.  These, of course, do not paint a complete picture of the situation.”

Saturated fat is unlikely to make or break any diet in terms of overall health, let alone heart disease in particular. General dietary patterns consistently prove to be better predictors of long-term health than any single food or nutrient, and anything we discover about saturated fat is unlikely to change this.

“In any case, this is another example of what happens when you look at single nutrients outside of their dietary context.”

While we’re waiting for science and industry to battle it out in the lab, focus on eating real, unprocessed foods most of the time and don’t get too hung up on the details.

What do you think of industry sponsorship in nutrition studies?

Update: After speaking with readers and colleagues I have made some revisions to this article to clear up my stand on this research. I do not intend to imply that the investigators of this study were influenced by their funding source, only that caution should be used when interpreting the results of any meta-analysis where there is a potential conflict of interest.

Tags: American Journal of Clinical Nutrition, dietary pattern, food industry, heart disease, Marion Nestle, saturated fat

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?

Tags: aging, calorie restriction, carbs, Cynthia Kenyon, diseases of civilization, glycemic load, insulin, low-carb, protein, refined carbohydrates

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?) then 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?

Tags: caloric restriction, insulin

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.

For these reasons I am cautious about eating meat and make a moderate effort to limit my intake, in both portion size and frequency.

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?

Tags: cancer, fish, vegetarian

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?

Tags: BMI, body fat, body mass index, caloric restriction, mortality