The Fiber Hypothesis

Today's question is: What if you know that the dietary-saturated-fat-and-cholesterol hypothesis doesn't work very well to explain heart disease, but at the same time you don't want to admit that eating too many refined carbohydrates might be the cause?

Answer: You put the blame on fiber. Or rather on not eating enough fiber.

In 1972, Peter Cleave tried to explain to a U.S. Senate Select Committee that when primitive cultures adopted Western eating patterns, they also began to experience the diseases of Western civilization, including diabetes, heart disease and hypertension. Cleave pointed out that the fat and cholesterol hypothesis of heart disease did not explain this transition, but that the adoption of a diet rich in refined carbohydrates did account for it rather elegantly. The Senators reached the only logical conclusion. They refused to believe Dr. Cleave. Dr. Ancel Keys had so completely won the argument that dietary fat was the cause of heart disease, that any alternative hypothesis had to be rejected out of hand.

The Senators were left with the problem of how to explain the increased incidence of heart disease in transitioning cultures. Enter a famous medical missionary, Denis Burkitt. While working in Uganda, Dr. Burkitt had noticed that Africans produced several times more feces than people in Western countries. He hypothesized that the presence of dietary fiber produced the absence of the diseases of Western civilization. Burkitt collected over 800 anectodal reports showing that primitive peoples ate high fiber foods, while Westernized cultures tended to eat foods that were nutritionally dense and low in bulk, not providing enough volume to allow the intestines to remain healthy. This idea made sense to the granola-eating counterculturalists of the time. More importantly, it did not contradict Ancel Keys' diet-heart hypothesis.

Forty years later, the need for high fiber in the diet has become received wisdom. Some studies show that eating more dietary fiber is associated with lower all-cause mortality, for example Dietary fiber intake in relation to coronary heart disease and all-cause mortality over 40 y: the Zutphen Study. Other studies show no relationship between fiber intake and all-cause mortality, including this one, The long-term effect of dietary advice in men with coronary disease: follow-up of the Diet and Reinfarction trial (DART).

For the purposes of low-carbers, several of the studies on the relationship of glycemic load with the risk of type 2 diabetes may be instructive. The glycemic load is the glycemic index of each food eaten, multiplied by the number of carbohydrate grams of that food eaten, summed for all items consumed during a day. In two studies (here in women and here in men), Salmerón et al. showed that the combination of a high glycemic load and a low cereal fiber intake increased the risk of type 2 diabetes when compared with a low glycemic load and high cereal fiber intake. The figure below is taken from the women's study.Looking at the X axis, at all levels of intake of cereal fiber, the relative risk of diabetes decreases as the glycemic load goes from high to medium to low. On the Z axis, at all levels of glycemic load the relative risk of diabetes decreases as the cereal fiber intake goes from low to medium to high.

Let's say that two low-carbers eat an identical number of carbs. One eats high-glycemic foods and has a high glycemic load. The other eats low-glycemic foods and has a low glycemic load. Both of them will need to release insulin to dispose of the carbs, but the first low-carber will have to release insulin in spikes to counteract the rapid rise of his blood glucose, while the second low-carber will be able to get by with a more gradual release of insulin. As Sullivan et al. have shown here, there is reason to believe that insulin spikes contribute to the development of insulin resistance.

How does fiber fit into the equation? The traditional explanation is that fiber fills us up. However, experiments done with caloric dilution show that when low-calorie foods are subsituted for higher-calorie ones, humans are well able to adjust their consumption of food to maintain their customary caloric intake. Another function of fiber is that it slows the absorption of nutrients from food. In other words, the addition of fiber can be expected to lower the effective glycemic index of high-, medium- and low-glycemic index carbohydrates. The relationship of the total amount of fiber to the total number of carbs to the glycemic index is probably quite complex, which may explain why many of the fiber-health studies do not show clearcut relationships between fiber intake and outcomes such as heart disease, type 2 diabetes, obesity and cancer.

In other words, if low-carb is good and low-glycemic index carb is good, the addition of fiber to all of that might be better. Low-glycemic-index foods like broccoli and nuts do tend to contain more fiber, so perhaps the point is moot for low-carbers who are careful about the type of carbs they consume. In any case, there is good evidence that lowering carbohydrate intake and lowering the glycemic index of those carbs is protective against the diseases of Western civilization. The data on the benefits of fiber intake is not overwhelming, so use your own judgment to decide what level of fiber intake might be right for you.

Fun with Graphs

For the next few weeks, I will be on an overseas vacation. In the meantime, I've been searching on Google and have come up with a set of graphs that should be interesting to look at and consider in the context of low-carbing. Most, but not all, of the data comes from the United States. These graphs are provided without any context to describe how the data was collected or how valid it might be. They just provide something to think about. If you want to enlarge any graph, just click on it, and it will open in a larger version.

One of the more interesting graphs shows that there is not much of a relationship between average cholesterol and rates of death from heart disease. Ancel Keys used seven carefully selected countries to "prove" the opposite, but the countries used for this graph tell another story.



Here's a graph that should be completely unsurprising to a low-carber. It shows a steadily increasing consumption of sugar in the United Kingdom and the United States and, beginning about 1900, a dramatic increase in rates of obesity.



Starting in about 1970, people in the United States began substituting high fructose corn syrup (HFCS) for table sugar. Interestingly, there was also an increase in the incidence of diabetic end stage renal disease during that time. Correlation is not causation, but the values do increase in a similar manner.



End stage renal disease is one of the complications of diabetes, which has also been increasing in the United States.



Sugar consumption, and in recent years HFCS consumption, has been increasing. Has anything else been increasing? Yes, we have been using more wheat flour per capita in the United States.



We are also eating more carbohydrates as a percentage of our total calories.



Not only are we eating a higher percentage of carbs, we are also eating more total calories per person every day.



All of these observations are consistent with (but do not prove) the hypothesis that eating refined carbohydrates can result in the diseases of civilization. However, other factors may also contribute to the increase in metabolic diseases during the past century, and here are some more graphs to consider in that regard.

It is possible that insufficient fiber can be blamed for an increase in health problems. I couldn't find a graph that described fiber consumption over time, but did find one on vegetable consumption. It appears that we are eating more vegetables (and presumably more fiber) than we used to.



It's possible that products that are subject to "sin taxes" could contribute to health problems. Although the introduction of cigarette smoking could be associated with the arrival of Western civilization and its diseases, it is interesting to note that the per capita consumption of cigarettes has actually declined since 1977.



Total alcohol consumption has decreased, too.



As discussed in a previous post, a high intake of omega-6 fats promotes the formation of inflammatory intermediates. Another possible explanation for the increased incidence of the diseases of Western civilization is the increased use of omega-6 rich vegetable oils in place of animal fats. As usual, correlation is not causation, but as shown in the graph below, the production of soybean oil for food consumption went from close to zero in 1935 to 25 pounds person per year in 1999.



Consumption of canola oil has also increased dramatically, from zero in 1984 to seven pounds per person per year in 2004, while the consumption of olive oil went to about two pounds per person per year and the consumption of butter declined.



What do all of these graphs prove? Not a thing. Although they show associations, they cannot prove causation. But I present them for your consideration because they do give us some things to think about as we enjoy a low-carb summer. Have a happy, healthy June!

What Causes Coronary Artery Disease?

In January 1961 a physiologist named Ancel Keys was featured on the cover of Time magazine. His appearance marked the victory of the idea that heart disease is caused by high blood cholesterol. Beginning in the 1940's, Dr. Keys had noted correlations between dietary fat intake and heart disease. He believed that high dietary fat produced high blood cholesterol, which in turn produced coronary artery disease. When the data Dr. Keys used is examined more carefully, the causal relationships between dietary fat, blood cholesterol and heart disease are less persuasive. In spite of that, by December 1960, the American Heart Association was willing to state that cholesterol is the leading risk factor for heart disease and that Americans should reduce their intake of fat, particularly of saturated fat.

However, there is an alternative hypothesis for the cause of coronary artery disease. As we have seen, insulin is a storage hormone. When insulin is released, it promotes the storage of fat in our adipose tissue. It also promotes the storage of cholesterol and fat in our arterial walls. Not only that, insulin promotes the synthesis of cholesterol and fat in the lining of our arteries. Although we haven't discussed this, another role of insulin is as a growth factor--it causes an increase in the number of smooth muscle cells lining our arteries, which in turn causes the artery walls to thicken.

Insulin is released in response to elevated glucose in the blood. When blood sugar is high, cells will preferentially burn glucose for fuel. In certain tissues, the burning of glucose produces reactive oxygen species, which include oxygen ions, free radicals, and peroxides. If the body does not have sufficient antioxidant protection, the reactive oxygen species will interact with cells and cause cellular breakdown. Another cause of breakdown was discussed in a previous post. Advanced Glycation Endproducts (AGEs) are produced when sugar molecules attach to proteins and crosslink them, eventually making our tissues, including our arteries, stiff and inelastic.

The two hypotheses for the cause of coronary artery disease suggest two very different lines of treatment. The cholesterol-lipid hypothesis implies that we should cut back on dietary cholesterol and fat, taking cholesterol-lowering medication if necessary, which will reduce cholesterol deposits, which will produce fewer heart attacks. The carbohydrate hypothesis implies that we should cut back on carbohydrates, which will lower blood glucose and blood insulin, which will cause less damage to arterial walls, which will produce fewer heart attacks. It appears that Tim Russert's physician believed the cholesterol-lipid hypothesis, and Tim Russert followed his advice. At age 58, Tim Russert died of sudden caradiac arrest. Tim was only one man, and his medical history might not be representative of the American population as a whole. On the other hand, Tim's unexpected death might signal that it is time for us to reconsider our approach to heart disease. It might be time for the medical community to do some long-range studies to see if the cholesterol-lipid hypothesis or the carbohydrate hypothesis produces better outcomes in the prevention and treatment of coronary artery disease.

Saturated Fats/Unsaturated Fats

Since Dr. Ancel Keys and his colleagues formulated and promulgated the diet-heart hypothesis in the 1960's, the idea of eating saturated fat has become anathema in most nutritional circles. When Americans were told that that consumption of saturated fat was positively correlated with the incidence of heart disease, they began to eat more of the "heart-healthy" mono- and polyunsaturated fats and fewer of the saturated ones. In spite of that, the number of hospital discharges with cardiovascular disease as the first listed diagnosis has continued to increase in the U.S. This is especially surprising in light of the fact that the percentage of U.S. adults who smoke has declined from over 40% in 1965 to about 20% in 2007. Is it possible that saturated fats are not as evil as they have been portrayed?

To begin the discussion, it is important to understand that a saturated fat is not saturated with calories or with cholesterol. In this case, "saturated" is a chemical term, and it means that the molecule in question is saturated with hydrogens--that is, it contains the maximum number of hydrogens it can hold. Here are two fatty acids, one saturated and the other unsaturated:


In the fatty acid at the top, the carbon-carbon bond between the two green C's is a single bond. Each green carbon holds two hydrogens, and they are saturated with hydrogen. In the fatty acid at the bottom, there is a double bond between the two green C's. Each of those carbons holds one hydrogen. The carbons do not hold as many hydrogens as they possibly could and they are therefore unsaturated. This particular fatty acid has only one unsaturated carbon-carbon bond, so it is monounsaturated. If it had two or more unsaturated bonds, it would be polyunsaturated.

The important thing about unsaturated fatty acids is that the presence of a double bond weakens the carbon-hydrogen bonds on the carbons next to the double bond. In the picture above, those carbon-hydrogen bonds are marked with green asterisks. That doesn't sound particularly interesting until we understand what happens when those hydrogens are removed by something like oxygen, heat or metal ions. As soon as we remove one of the vulnerable hydrogens, our heart-healthy unsaturated fatty acid becomes a free radical. In other words, it contains an unpaired electron and it becomes extremely chemically reactive.

Once the first free radical is formed, the generation of free radicals from unsaturated fatty acids happens in a self-propagating manner. One free radical can interact with other unsaturated fatty acids to produce more free radicals, which in turn produce even more free radicals, and so on. Besides damaging the fatty acids, these free radicals can also destroy other molecules, including vitamins and proteins. In addition, the free radicals are able to react with oxygen to produce hydroperoxides. These eventually break down into aldehydes, which produce the odors and flavors associated with rancidity.

The reactivity of fatty acids increases with the number of double bonds they contain. Stearic acid is an 18-carbon saturated fatty acid. If we add one double bond, it becomes one hundred times more likely to form a free radical. If we add three double bonds, it becomes 2500 times more likely to form a free radical. The health effects of saturated versus unsaturated fatty acids won't be addressed until the next blogpost, but it is certain that saturated fatty acids are far more stable than their unsaturated counterparts.

There are several ways to decrease the likelihood of free radical formation and rancidification in fatty acids. One is to be sure that heat is not used to extract the fatty acid from its source. In the case of unrendered animal fats, this is not a problem. In the case of vegetable fats, cold pressing ensures (at least it does in the EU) that the oil will not be heated above about 80 degrees Fahrenheit. Unfortunately the U.S. definition of cold pressed is not particularly rigorous, so it may be necessary to check websites or make telephone calls to the manufacturer to determine the temperature a particular brand of oil reaches as it is extracted. When fat is used for cooking, it is important to realize that the higher it is heated and the longer it is heated, the more likely it will be to form free radicals.

Another strategy to avoid free radical formation and rancidification in fats and oils is to be sure that they are kept away from light, particularly UV light. It is also helpful to keep fats and oils away from oxygen. They should not be stored for long periods, and once a container is opened, it should be used up as quickly as possible.

As we have already seen, some polyunsaturated fats are necessary for growth and for optimal health. However it pays to know which fats are which and to be careful with respect to the amounts and types of dietary fats we consume. In closing, here is a table that presents the approximate composition of some common fats, arranged from the lowest to the highest percentage of polyunsaturated fatty acids.

High Carbs/Low Fat--Not Such a Good Idea

A book that has changed my life is Gary Taubes's Good Calories, Bad Calories. In this book, Taubes explains how Ancel Keyes hypothesized that high fat and high cholesterol produce heart disease. By carefully picking their data, and controlling who was allowed to be influential in the scientific discussion, Keyes and his colleagues were able to persuade the American medical community that carbohydrate should constitute 70% of our diets and we should eat no more than 15% fat.


When Americans began increasing carbs and decreasing fat, heart disease did not decrease. Obesity, however, increased. Experts said that Americans were exercising too little. Americans started exercising more, but as they continued to eat high carb/low fat diets, they continued to get fatter. The graph above comes from the Centers for Disease Control, National Center for Health Statistics. Look at the line labeled "Obese, 20-74 years." In the 1970's, about 13% of adult Americans were obese. By the early 1990's it was about 21%. By 2000, about 31% of adult Americans were obese. In subsequent posts, we may be able to gain some insights into the reasons for this trend.

Scientists Behaving Badly

The premise of this blog is that the scientific method can be used to support or invalidate the tenets of the low-carb lifestyle. While science can never claim to establish the final truth of a particular hypothesis, it is the best instrument we have to approximate the truth of something that is falsifiable, that is, something that is capable of being tested by experiment or observation.

Although science is an excellent tool, we must be careful to remember that science is performed by human beings who are not perfect. Low-carbers are already aware of the problematic work of Dr. Ancel Keys. Among Dr. Keys' most important publications was the Seven Countries Study. This study helped establish the diet-heart hypothesis when it found that in seven specific countries, the cardiovascular disease rate was positively correlated with average serum cholesterol and per capita intake of saturated fatty acids. In 1957 two scientists, Jacob Yershalmy and Herman Hilleboe, noted that data were available from 22 countries, not just seven. They published a paper showing that when all 22 countries were analyzed, the cholesterol/saturated fat correlation to heart disease became much weaker, and the incidence of heart disease was more strongly related to sugar intake. Even though it seemed that Dr. Keys might have cherry picked his data, his diet-heart hypothesis has nonetheless prevailed over the years.

The science of Anthropogenic Global Warming (AGW) doesn't have much to do with low-carbing, but it does have a great deal to teach us about the practical aspects of whether to believe or disbelieve a particular scientific finding. In November 2009, a series of e-mails was made available on the internet, purporting to be from the Climate Research Unit (CRU) at the University of East Anglia in Norwich, England. As of this writing, their authenticity has not yet been denied, and these e-mails now form the heart of what has been termed Climategate.

What does Climategate have to tell us about how to evaluate scientific claims with a skeptical eye?

First, if the scientists refuse to release their raw data, it's not a good sign.

Phil Jones (head of the CRU) and Tom Wigley (University Corporation for Atmospheric Research in Boulder, Colorado) discuss here how to avoid releasing data in response to a Freedom of Information request. Dr. Jones is so averse to scrutiny of his data that he admits to clearing e-mails off his computer here and advises his colleagues to do the same here. (AR4, referenced in this link, is the Fourth Assessment Report of the UN's Intergovernmental Panel on Climate Change (IPCC), released in 2007. The AR4 allowed AGW supporters to claim a consensus in favor of anthropogenic global warming.)

Second, if the scientists select or massage their data to make it obey their hypothesis, it's a bad sign.

Dr. Jones has a problem because his data shows declining recent temperatures rather than rising ones. Here he tells three of his colleagues, "I've just completed Mike's Nature trick of adding in the real temps to each series for the last 20 years (ie from 1981 onwards) amd from 1961 for Keith's to hide the decline." Trick? Hide the decline? What might that mean?

"Mike" is Michael Mann, the creator of the Hockey Stick graph that used tree ring data to show no warming in the Medieval Warm Period, but a sudden, dramatic increase in global temperature in the late 20th century. In this article, Stephen McIntyre and Ross McKitrick show that the hockey stick graph is the result of overweighting data from American bristlecone pines and from using a non-centered principal component analysis that will almost always produce a hockey stick endpoint, even from random numbers.

"Keith" is Keith Briffa, whose tree ring data from the Yamal Peninsula of Siberia also showed a hockey stick pattern of recent global temperatures. Except that when Briffa's 12 tree cores (the red line on the graph below) are compared with 34 cores from the same area analyzed by Stephen McIntyre (the black line), the larger sample does not show the hockey stick pattern, suggesting that Briffa's 12 tree cores were unrepresentative of the local tree growth patterns and should not have been used to infer patterns of climate change for the Yamal region of Siberia, let alone for the whole planet.




Finally, if the scientists collude to allow some points of view to pass the peer review process while preventing other points of view from being expressed, it's a very bad sign.

Scientific journal editors decide which submitted papers will get reviewed, who the reviewers are, and whether the papers eventually get published. Here Tom Wigley tells Timothy Carter that they must get rid of an editor of the journal Climate Research. The man subsequently resigned. Here Tom Wigley and Michael Mann discuss a troublesome editor at Geophysical Research Letters (GRL) and whether he could be ousted because his presence may bring other AGW skeptics on board. Several months later the editor has left his post and here Michael Mann says, "The GRL leak may have been plugged up now w/ new editorial leadership there." Here Phil Jones is also having trouble with a new editor of the journal Weather, published by the Royal Meteorological Society (RMS). Dr. Jones says he has complained about the editor to the RMS chief executive, but if that doesn't work, he will not send any more papers to the RMS and will resign from the organization. When a group of scientists consciously engages in encouraging some editors and intimidating others, it's not particularly surprising if their papers tend to get published in the peer-reviewed journals while those of the scientists with opposing views do not.


Presumably scientists who hide data, who change data to fit their preconceived ideas and who conspire to see that only their data is published may nevertheless have reached correct conclusions. That would be the "fake but accurate" defense. However, it is much more likely that scientists who behave in this way have something to hide. Whenever you learn that a scientist in any field has engaged in one or more of these questionable activities, be very careful of whatever that scientist has to say.