Monday, May 28, 2012

How Bad is Fructose? David Despain Interviews Dr. John Sievenpiper

In my article "Is Sugar Fattening?", I discussed a recent review paper on fructose, by Dr. John Sievenpiper and colleagues (1).  It was the most recent of several review papers to conclude that fructose is probably not inherently fattening in humans, but that it can be fattening if it's consumed to excess, due to the added calories.  Dr. Sievenpiper and colleagues have also written other papers addressing the metabolic effects of fructose, which appear to be fairly minor unless it's consumed to excess (2, 3, 4, 5).  The senior author on these studies is Dr. David Jenkins at McMaster University.  David Despain, a science and health writer who publishes a nice blog called Evolving Health, recently interviewed Dr. Sievenpiper about his work.

It's an interesting interview and very timely, due to the recent attention paid to fructose in the popular media. This has mostly been driven by a couple of high-profile individuals-- an issue they discuss in the interview.  The interview, recent papers, and sessions at scientific conferences are part of an effort by researchers to push back against some of the less well founded claims that have received widespread attention lately.

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Monday, May 21, 2012

Lower Blood Pressure Naturally

Recently, Chris Kresser published a series on dietary salt (sodium chloride) and health (1).  One of the issues he covered is the effect of salt on blood pressure.  Most studies have shown a relatively weak relationship between salt intake and blood pressure.  My position overall is that we're currently eating a lot more salt than at almost any point in our evolutionary history as a species, so I tend to favor a moderately low salt intake.  However, there may be more important factors than salt when it comes to blood pressure, at least in the short term. 

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Rice consumption and health

Carbohydrate-rich foods lead to the formation of blood sugars after digestion (e.g., glucose, fructose), which are then used by the liver to synthesize liver glycogen. Liver glycogen is essentially liver-stored sugar, which is in turn used to meet the glucose needs of the human brain – about 5 g/h for the average person.

(Source: Wikipedia)

When one thinks of the carbohydrate content of foods, there are two measures that often come to mind: the glycemic index and the glycemic load. Of these two, the first, the glycemic index, tends to get a lot more attention. Some would argue that the glycemic load is a lot more important, and that rice, as consumed in Asia, may provide a good illustration of that importance.

A 100-g portion of cooked rice will typically deliver 28 g of carbohydrates, with zero fiber, and 3 g of protein. By comparison, a 100-g portion of white Italian bread will contain 54 g of carbohydrates, with 4 g of fiber, and 10 g of protein – the latter in the form of gluten. A 100-g portion of baked white potato will have 21 g of carbohydrates, with 2 g of fiber, and 2 g of protein.

As you can see above, the amount of carbohydrate per gram in white rice is about half that of white bread. One of the reasons is that the water content in rice, as usually consumed, is comparable to that in fruits. Not surprisingly, rice’s glycemic load is 15 (medium), which is half the glycemic load of 30 (high) of white Italian bread. These refer to 100-g portions. The glycemic load of 100 g of baked white potato is 10 (low).

The glycemic load of a portion of food allows for the estimation of how much that portion of food raises a person's blood glucose level; with one unit of glycemic load being equivalent to the blood glucose effect of consumption of one gram of glucose.

Two common denominators between hunter-gatherer groups that consume a lot of carbohydrates and Asian populations that also consume a lot of carbohydrates are that: (a) their carbohydrate consumption apparently has no negative health effects; and (b) they consume carbohydrates from relatively low glycemic load sources.

The carbohydrate-rich foods consumed by hunter-gatherers are predominantly fruits and starchy tubers. For various Asian populations, it is predominantly white rice. As noted above, the water content of white rice, as usually consumed by Asian populations, is comparable to that of fruits. It also happens to be similar to that of cooked starchy tubers.

An analysis of the China Study II dataset, previously discussed here, suggests that widespread replacement of rice with wheat flour may have been a major source of problems in China during the 1980s and beyond ().

Even though rice is an industrialized seed-based food, the difference between its glycemic load and those of most industrialized carbohydrate-rich foods is large (). This applies to rice as usually consumed – as a vehicle for moisture or sauces that would otherwise remain on the plate. White rice combines this utilitarian purpose with a very low anti-nutrient content.

It is often said that white rice’s nutrient content is very low, but this problem can be easily overcome – a topic for the next post.

Thursday, May 17, 2012

Beyond Ötzi: European Evolutionary History and its Relevance to Diet. Part III

In previous posts, I reviewed some of the evidence suggesting that human evolution has accelerated rapidly since the development of agriculture (and to some degree, before it).  Europeans (and other lineages with a long history of agriculture)  carry known genetic adaptations to the Neolithic diet, and there are probably many adaptations that have not yet been identified.  In my final post in this series, I'll argue that although we've adapted, the adaptation is probably not complete, and we're left in a sort of genetic limbo between the Paleolithic and Neolithic state. 

Recent Genetic Adaptations are Often Crude

It may at first seem strange, but many genes responsible for common genetic disorders show evidence of positive selection.  In other words, the genes that cause these disorders were favored by evolution at some point because they presumably provided a survival advantage.  For example, the sickle cell anemia gene protects against malaria, but if you inherit two copies of it, you end up with a serious and life-threatening disorder (1).  The cystic fibrosis gene may have been selected to protect against one or more infectious diseases, but again if you get two copies of it, quality of life and lifespan are greatly curtailed (2, 3).  Familial Mediterranean fever is a very common disorder in Mediterranean populations, involving painful inflammatory attacks of the digestive tract, and sometimes a deadly condition called amyloidosis.  It shows evidence of positive selection and probably protected against intestinal disease due to the heightened inflammatory state it confers to the digestive tract (4, 5).  Celiac disease, a severe autoimmune reaction to gluten found in some grains, may be a by-product of selection for protection against bacterial infection (6).  Phenylketonuria also shows evidence of positive selection (7), and the list goes on.  It's clear that a lot of our recent evolution was in response to new disease pressures, likely from increased population density, sendentism, and contact with domestic animals.

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Monday, May 7, 2012

Beyond Ötzi: European Evolutionary History and its Relevance to Diet. Part II

In previous posts, I described how Otzi was (at least in large part) a genetic descendant of Middle Eastern agriculturalists, rather than being purely descended from local hunter-gatherers who adopted agriculture in situ.  I also reviewed evidence showing that modern Europeans are a genetic mixture of local European hunter-gatherers, incoming agricultural populations from the Middle East, neanderthals, and perhaps other groups.  In this post, I'll describe the evidence for rapid human evolution since the end of the Paleolithic period, and research indicating that some of these changes are adaptations to the Neolithic (agricultural/horticultural/pastoral) diet.

Humans have Evolved Significantly Since the End of the Paleolithic

Evolution by natural selection leaves a distinct signature in the genome, and geneticists can detect this signature tens of thousands of years after the fact by comparing many genomes to one another.  A landmark paper published in 2007 by Dr. John Hawks and colleagues showed that humans have been undergoing "extraordinarily rapid recent genetic evolution" over the last 40,000 years (1).  Furthermore:
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The 2012 Arch Intern Med red meat-mortality study: The “protective” effect of smoking

In a previous post () I used WarpPLS () to analyze the model below, using data reported in a recent study looking at the relationship between red meat consumption and mortality. The model below shows the different paths through which smoking influences mortality, highlighted in red. The study was not about smoking, but data was collected on that variable; hence this post.


When one builds a model like the one above, and tests it with empirical data, the person does something similar to what a physicist would do. The model is a graphical representation of a complex equation, which embodies the beliefs of the modeler. WarpPLS builds the complex equation automatically for the user, who would otherwise have to write it down using mathematical symbols.

The results yielded by the complex equation, partly in the form of coefficients of association for direct relationships (the betas next to the arrows), have a meaning. Some may look odd, and require novel interpretations, much in the same way that odd results from an equation describing planetary motions may have led to the development of the theory of black holes.

Nothing is actually "proven" by the results. They are part of the long and painstaking process we call "research". To advance new knowledge, one needs a lot more than a single study. Darwin's theory of evolution is still being tested. Based on various tests and partial refutations, it has itself evolved a great deal since its original formulation.

One set of results that are generated based on the model above by WarpPLS, in addition to coefficients for direct relationships, are coefficients of association called "total effects". They aggregate all of the effects, via multiple paths, between each pair of variables. Below is a table of total effects, with the total effects of smoking on diabetes incidence and overall mortality highlighted in red.


As you can see, the total effects of smoking on diabetes incidence and overall mortality are negative, but small enough to be considered insignificant. This is interesting, because smoking is definitely not health-promoting. Among hunter-gatherers, who often smoke tobacco, it increases the incidence of various types of cancer (). And it may be at the source of many of the health problems suggested by analyses on the China Study II data ().

So what are these results telling us? They tell us that smoking has an intermediate protective effect, very likely associated with its anorexic effect. Smoking is an appetite suppressor. Its total effect on food intake is negative, and strong. As we can see from the table of total effects, just below the two numbers highlighted in red, the total effect of smoking on food intake is -0.356.

Still, it looks like smoking is nearly as bad as overeating to the point of becoming obese (), in terms of its overall effect on health. Otherwise we would see a positive total effect on overall mortality of comparable strength to the negative total effect on food intake.

Smoking may make one eat less, but it ends up hastening one’s demise through different paths.

Saturday, May 5, 2012

Media Appearances

Last October, I participated in a panel discussion organized by the Harvard Food Law Society in Boston.  The panel included Drs. Walter Willett, David Ludwig, Robert Lustig, and myself, with Corby Kummer as moderator.  Dr. Willett is the chair of the Harvard Department of Nutrition; Dr. Ludwig is a professor of nutrition and pediatrics at Harvard; Dr. Lustig is a professor of clinical pediatrics at UCSF; and Kummer is a food writer and senior editor for The Atlantic
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