Magical, Mystical Coconut Oil

(This is another post referencing my own experiences. I present it in case someone else might want to give coconut oil a try for weight issues.)

The past
Coconut oil is the stuff that used to make movie popcorn taste like movie popcorn. When somebody realized that coconut oil is 90% saturated fat, things changed in a hurry. Movie popcorn began to taste more like the cardboard tub it comes in, and coconut oil became hard to find. Recently coconut oil has come back into favor in the low-carb world, and it can be purchased in health food stores and even in grocery stores.

I began using coconut oil several years ago and noticed that when I did so, I was better able to control my weight. I didn't mind the taste too much, but I was no particular fan of it either. (Nutiva seems to me to be the best-tasting brand so that's what I buy, but there are many other extra virgin organic coconut oils on the market.)

The present
About two months ago, as a sort of personal experiment, I began eating two tablespoons of coconut oil for breakfast. Just 250 calories of coconut oil, plus my supplements, seemed to hold me until lunch, which was a surprise. Not only that, I didn't seem to be quite as hungry during the rest of the day. Not only that, I seemed to do much better at weight maintenance than I have for many years. I was curious about why it worked, but didn't have the time to puzzle it out.

The explanation
Then one day as I was reading an article over at the Heart Scan Blog, I happened upon a comment by Might-o'chondri-AL (#23 in the list). He explained that coconut contains a 12-carbon saturated fat called lauric acid, and that lauric acid upregulates the secretion of glucagon-like peptide (GLP-1). GLP-1 in turn increases satiety by slowing stomach emptying.

I checked out the fatty acid profile of coconut oil and found that, sure enough, it contains about 50% lauric acid. Next I did a Google search and found a journal article that backed up the rest of Might-o'chondri-AL's statements: Effects of intraduodenal fatty acids on appetite, antropyloroduodenal motility and plasma CCK and GLP-1 in humans vary with their chain length.

The data
The article reported that in 2004 a group of investigators did a 90-minute duodenal infusion of water (control), capric acid (a saturated fatty acid with 10 carbon atoms) or lauric acid (a saturated fatty acid with 12 carbon atoms) into twelve healthy, normal-weight, male volunteers. They administered only 0.375 kcal/min in the treatment groups, but the contrast between the capric acid (C10) group and the lauric acid (C12) group was quite large.

By 45 minutes of infusion, plasma GLP-1 increased significantly and stayed high in subjects who received C12, while plasma GLP-1 in the C10 group was no different from control. (Remember, GLP-1 slows gastric emptying.) Cholecystokinin (CCK) is a peptide hormone that also produces satiety by decreasing the rate of gastric emptying. By 30 minutes, both C10 and C12 had increased CCK over control, but C12 did so to a greater extent. Gastro-duodenal motility was measured directly using a manometric catheter. Consistent with the GLP-1 and CCK levels, C12 suppressed both antral and duodenal pressure waves while C10 did not. Finally, at the conclusion of the infusion, subjects were offered a buffet meal. Subjects who had received C12 ate significantly less than those who had received C10 or water. In other words, intraduodenal infusion of lauric acid (C12) decreased gastric motility and suppressed the appetites of subjects who received it.

More data
A 2010 review article by Little and Feinle-Bisset confirmed these findings and added a few more. The presence of fatty acids like lauric acid in the intestine (and possibly even in the mouth) stimulates the secretion of hormones that suppress gastric emptying (GLP-1, CCK, and peptide YY) as well as down-regulating the hunger hormone ghrelin. A lauric acid infusion also appears to be able to signal the brainstem and hypothalamus directly via the vagus nerve and a CCK receptor mediated pathway. In addition to all of that, lauric acid is classified as a medium chain fatty acid. Unlike longer-chain fatty acids, it can be absorbed directly from the gut, transported to the liver, and there be readily converted into ketone bodies and used for energy rather than for fat storage. Both in suppressing energy intake and in improving energy utilization, the lauric acid found in abundance in coconut oil looks like a good candidate to help with weight loss and weight maintenance.

To be fair, the Little and Feinle-Bisset review article goes on to state that some studies have shown that a high-fat diet or the presence of obesity may attenuate the effects of fat intake on slowing gastric emptying and decreasing energy intake. However, none of the studies they cite were done in the context of a low carbohydrate intake.

The result
In any case, after reading these articles, I now understand why coconut oil seems to be such a help to me in weight maintenance. Whether that will hold true in the long term or whether it will work for other people is not certain, but for now personal experience seems to be backed by a fair amount of science.

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.

Eat Fat for Weight Loss

As most low-carbers already know, eating fat produces satiety. But in some cases, eating fat also helps a dieter lose weight.

It turns out that the chain length of the fatty acids in the triglyceride is an important factor in choosing a fat that promotes weight loss. Most of the fats found in a normal diet will contain long-chain fatty acids. That is, most of the triglycerides we eat will have fatty acids that contain between 13 and 22 carbons. These long-chain fatty acids are digested in the gut, where they are packaged into chylomicrons. The chylomicrons are moved into the lymphatic system and eventually enter the blood at the left subclavian vein in the upper chest. (A review of the process can be found here.)

When the chylomicrons reach the blood, the long-chain fatty acids in them can be absorbed by any cell, including fat cells, that contain lipoprotein lipase. Once these fatty acids are absorbed into a fat cell, they are still available for later mobilization into the blood via hormone-sensitive lipase. But in insulin-resistant individuals, the activity of hormone-sensitive lipase is down-regulated by high insulin levels. In those people, stored fat tends to remain in storage.

Medium-chain fatty acids contain from 6 to 12 carbons. (In a normal diet, the most common source is probably butter, which contains about 10% medium-chain fatty acids. For those who shop the health food aisles, another source is coconut oil, containing about 66% medium chain fatty acids.) Medium-chain fatty acids are processed differently in the gut. Because they are more water-soluble, they tend not to be packaged into chylomicrons. Instead, they are absorbed from the gut directly into the blood as free fatty acids. Medium-chain fatty acids are bound to serum albumin in the blood, and in that form they travel to the liver where they are used primarily for energy production. Some are converted to ketones that are in turn used for energy by many of the cells of the body.

A 1996 review article by Bach et al. discussed the fact that, compared with long-chain triglycerides, medium-chain triglycerides have more rapid delivery to the liver, higher oxidation rates, poorer rates of incorporation into fat cells, and greater control of satiety. However, there were some counteracting factors that suggested that eating medium-chain fatty acids might not produce the expected reduction in body weight.

After that review article was published, Marie-Pierre St-Onge and her colleagues began studying the effect of human diets that were either rich in medium-chain triglycerides or rich in long-chain triglycerides. The medium-chain triglyceride oil contained primarily caprylic (8 carbons, saturated) and capric (10 carbons, saturated) fatty acids. The long-chain triglyceride oil was olive oil, which contains primarily oleic acid (18 carbons, monounsaturated).


In a randomized crossover controlled feeding trial published in 2003, energy expenditure was measured before and up to 5.5 hours after eating a breakfast meal. Although both groups saw increases in fat oxidation and energy expenditure following the meal, the medium-chain triglyceride group saw larger increases at some though not all of the timepoints after the breakfast meal. The medium-chain triglyceride group also saw a trend toward lower energy intake at the subsequent lunch meal. Not surprisingly, over the four-week duration of the study, the medium-chain triglyceride group saw a significant loss of total adipose tissue of about 1.8 pounds. The reduction in adipose of the olive oil group did not reach significance.

In 2008 Dr. St-Onge and colleagues performed a 16-week double-blind non-crossover weight loss study in overweight men and women. Once again, the groups were divided according to diets containing either medium-chain triglycerides or olive oil. Women consumed 1500 calories per day and men consumed 1800 calories per day, with about 12% of these calories as the prescribed study oil. At the end of the study, those who consumed medium-chain triglyceride oil had lost about 3.7 more pounds of body weight than those in the olive oil group. The loss of total fat mass was also about 3.2 pounds greater in the medium-chain triglyceride group compared with the olive oil group.

These findings are consistent with those of other investigators, both for animal models of obesity and for humans. In 2007 a group in China performed a pilot study to see if other health parameters are affected with the ingestion of medium-chain triglycerides. For ninety days, forty moderately overweight type 2 diabetic patients were given either 18 grams per day of medium-chain triglycerides or 18 grams per day of corn oil. The medium-chain triglyceride group showed a reduction in body weight, a reduction in waist circumference, a decline in serum cholesterol, an increase in serum C-peptide and a reduction of insulin resistance.

The studies discussed in this blogpost are not definitive, and much more research will be necessary to see if medium-chain triglycerides are an effective tool for reducing obesity. Nevertheless, it is encouraging to see that, at least in an experimental setting, these fats are able to decrease fat mass in both overweight men and women over time.

To Eat Saturates or Not to Eat Saturates?

As we discussed in the previous post, saturated fats are not fats that are saturated with calories or saturated with cholesterol. "Saturated" is a chemical term that can be thought of as a measure of the stability of a particular fat in the presence of heat, light and oxygen. Saturated fats are more stable than monounsaturated fats and much more stable than polyunsaturated fats. Saturated fats are generally solid at room temperature. The richest sources are from animals (lard, butter, tallow) or from tropical plants (coconut oil, palm oil).

When heart disease began to become prevalent in the 20th century, scientists looked for a cause and decided that saturated fats were a good candidate. By the end of the 20th century most people thought that the science was settled--eating saturated fats causes heart disease. But studies are starting to accumulate that suggest that this isn't necessarily so.

Two articles (abstracts here and here) by Ronald Krauss and colleagues were recently published in the American Journal of Clinical Nutrition. They did an analysis of twenty one prospective cohort studies (i.e., these were actual clinical studies, not just correlational number crunching) and examined the relationship between intake of saturated fat and the risk of coronary heart disease, stroke and cardiovascular disease. This type of analysis depends on the integrity of the authors in selecting the studies to be analyzed, especially if the authors have a bias toward a particular outcome. With that caveat, it is noteworthy that the authors concluded that "there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD [coronary heart disease] or CVD [coronary vascular disease]." (There was also no significant association with stroke, and the authors stated that results were not affected by age, sex or the quality of a particular study.)

The authors noted that when studies replaced saturated fat with a higher carbohydrate intake, this resulted in increased triglycerides, smaller LDL particles and reduced HDL cholesterol. In the studies that replaced saturated fat with mono- or polyunsaturated fat, patients saw a reduction in their LDL cholesterol, but they also reduced their "good" HDL cholesterol.

But these were the only studies that showed no relationship between saturated fat and cardiovascular disease, right? Not exactly.

In his blog, Dr. Michael Eades describes a group of 264 men who entered a study after experiencing their first heart attack. From 1957 to 1963 the treatment group ate a diet with about 13.5% saturated fat. The control group continued to eat their normal diet, which probably contained about 25% saturated fat according to Dr. Eades' ballpark estimate. After six years, both groups had the same heart attack relapse rate and the same death rate.

Eades also describes a study in which patients with ischemic heart disease ate either a high-saturated fat diet, a diet in which most of the fat was olive oil or a diet in which most of the fat was corn oil. After two years, 75% of the high-saturated fat group was alive and free from a second heart attack. Fifty seven percent of the olive oil group was alive and heart attack free at the completion of the study. And the corn oil group had only 52% alive and heart attack free at the end of two years.

Finally, a 2004 study by Mozaffarian et al. examined the progression of coronary atherosclerosis in postmenopausal women with established coronary heart disease. Comparing the intake of saturated fatty acid among these women over three years, they found that the intake of saturated fat was inversely related to the rate of progression of coronary atherosclerosis, and was unrelated both to unstable angina and to death from myocardial infarction. Unexpectedly, investigators saw a positive association between polyunsaturated fat intake and the rate of narrowing of the coronary arteries. This was particularly true in women with diabetes, lower HDL cholesterol, a lower protein intake and a higher carbohydrate intake. (It is important to note that this was a correlational study and the outcome could be affected by confounding factors that were not identified.)

To eat or not to eat saturated fat? It appears that it is up to the individual. Some studies have shown a slightly increased risk of heart disease with consumption of saturated fats, but many studies show no correlation at all. On the other hand, the increased consumption of carbohydrates, particularly refined carbohydrates, is associated with increased triglycerides, decreased LDL particle size, and decreased HDL cholesterol, all of which are associated with increased risk of cardiovascular disease. If we have to choose between fat and carbohydrate for heart health, it appears that fat may be the better choice.

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.

More on Omega-3 and Omega-6

Omega-3 and omega-6 fatty acids are long-chain polyunsaturated fatty acids. They cannot be synthesized by the human body, but are important for growth, for cardiovascular health and for immune function. They may also be involved in a variety of other health-related issues including the prevention of cancer and of central nervous system disorders. Their effects are somewhat non-specific, but because the omega-3s in particular have shown positive effects in many controlled double-blind prospective scientific studies, people who are interested in nutrition are also interested in the omega-3 and omega-6 fatty acids. This blogpost, and the previous one, attempt to explain a few principles that may make it easier for readers to evaluate their own use of these essential fatty acids.

The omega-3 and omega-6 fatty acids are unbranched molecules ranging from 16 to 24 carbons in length and carrying from two to six unsaturated bonds. The most common forms are illustrated above. When they are ingested in the diet, these polyunsaturated fatty acids gradually become incorporated into the phospholipid bilayers that form the cell walls of most of the cells in our bodies. As phospholipids, the omega-3 and omega-6 fatty acids affect the flexibility and permeability of the membrane surrounding each cell. They also exist in equilibrium with the unsaturated free fatty acids that circulate in our blood. It is this pool of free fatty acids that is used by the body as precursors for the eicosanoid signaling molecules, i.e., the prostaglandins, thromboxanes, leukotrienes and prostacyclins.

From a survey of the omega-3 literature, it appears that the longer the molecule, the more biologically potent it is. (An example is found here.) The body is able to convert one form of omega-3 fatty acid to another, but it is not particularly efficient at it. For instance, although flax seed oil is rich in alpha-linolenic acid (ALA), ALA (18 carbons) is converted into EPA (20 carbons) at an efficiency of about 5-10% and into DHA (22 carbons) at an efficiency of about 2-5%. Recent studies indicate that in some individuals the conversion rates may be less than 1%. By contrast, EPA and DHA can be obtained directly from fish oil and require no modification to provide maximum protection against conditions such as coronary artery disease. Vegetarians and those who are allergic to fish will be able to eat extra ALA to compensate for the poor conversion rate to EPA and DHA, but they must bear in mind that not all omega-3s are created equal.

Another consideration in omega-3 and -6 fatty acid intake is the interchangeability of the omega-3 and omega-6 fatty acids in the eicosanoid synthesis pathways. Take a look at the figure above. EPA (eicosapentaenoic acid) is an omega-3 fatty acid with 20 carbons and five double bonds. AA (arachidonic acid) is an omega-6 fatty acid with 20 carbons and four double bonds. Superficially, they look very similar. These molecules also look similar to the enzymes involved in eicosanoid synthesis and, as such, they compete with one another. Metabolites of omega-6 fatty acids, particularly metabolites of arachidonic acid (20 carbons), are significantly more inflammatory than those of omega-3 fatty acids. This becomes important because the Westernized diet has a fatty acid ratio of omega-6 to omega-3 that falls between 10:1 and 30:1. If our dietary raw material is almost all omega-6 fatty acids, the metabolites will be predominately pro-inflammatory. For some interesting lists of omega-6 sources, see here. I can't vouch for the accuracy of the lists, but in general they provide some surprising insights.

One way to decrease the omega-6-derived inflammatory intermediates is simply to replace omega-6 polyunsaturated fats with saturated and monounsaturated fats. (A recent journal article suggests that eating saturated fat is not as dangerous as previously thought.) Saturated and monounsaturated fats provide energy, but they cannot be converted into eicosanoid signaling molecules. Another strategy is to take advantage of the metabolic competition between omega-3 and omega-6 fatty acids by replacing the intake of omega-6s with omega-3s. Although the omega-3 fatty acids can be pro-inflammatory when eaten to excess (probably more than three grams per day), in general they will form less-inflammatory signaling intermediates and will also decrease the omega-6-stimulated production of small pro-inflammatory proteins called cytokines.

A review article on omega-3 fatty acids suggests setting a goal of an omega-6 to omega-3 ratio between 1:1 to 1:4, though it gives no rationale for these numbers other than speculation that that was the ratio consumed by our ancestors. The article also recommends consuming fatty fish three times per week. Unfortunately the oceans are no longer pristine, and fish tend to contain pollutants such as mercury, PCBs and dioxin. For those who prefer not to take the risk, purified fish oil supplements are available from manufacturers who use high-vacuum, low-temperature molecular distillation to purify their fish oils. Another source of EPA and DHA is krill oil, which comes from animals that are low on the food chain and therefore low in pollutants. Krill oil is quite expensive, however. Meat, eggs and plant sources also contain omega-3s in varying amounts. For the obsessive-compulsive, here is a list of the total omega-3 content of 200 calories' worth of various foods.

Omega-3 and omega-6 fatty acids are essential for life. They also affect the quality of life in positive and negative ways. Because they are stored in the phospholipid bilayers of our cell membranes, they take a long time to act. They must build up, reach an equilibrium with their free fatty acid form in the blood and then be converted to intermediates. For that reason, it may take weeks or months before a negative effect starts to decline or a positive effect is noticed. However, there are many scientific articles that indicate that it may be worth the time, effort and expense of attending to our intake of these essential fatty acids.

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.

The Scientific Method

Aristotle was a Greek philosopher who lived from 384 BC to 322 BC. His works contain the first known formal study of logic, which he applied in many areas of life, including the field of science. Aristotle made extensive observations of natural phenomena and then applied logic to these observations in an effort to systematize them. Sometimes these logical inferences were correct, for example his deduction that the Milky Way is not shaded by the earth from illumination by the sun because the sun is too large and the stars are too distant for this to occur. Sometimes Aristotle's reasoning led to incorrect conclusions, such as his belief that the sun, stars and planets circle the earth. And occasionally Aristotle's conclusions were incorrect because his observations were not as careful as they might have been--for instance, he believed that men have more teeth than women, and that heavier objects fall faster than lighter ones.

Aristotle believed that observations coupled with reasoning could decipher the laws of the universe. He discounted experiments as artificial contrivances with little relevance to the natural world. When isolated events contradicted the laws of the universe as he understood them, they were regarded as "monsters" that could be ignored. Because Aristotle was very highly thought of as a philosopher and logician, it was regarded as a form of heresy to contradict the laws of science Aristotle had deduced from his observations. For that reason, his incorrect scientific ideas carried a great deal of weight at least until the 1500's.

In the 1500's, men such as Francis Bacon and Galileo Galilei brought changes to the study of science. Bacon rejected the idea of science by logical reasoning and syllogism. He advocated the use of observation, hypothesis and experiment leading to a gradual and systematic formulation of general axioms which could be disproven if evidence came forth to contracdict them (the scientific method, illustrated above). Galileo, as every schoolchild knows, availed himself of technology that had not been available to Aristotle. His telescope revealed that satellites orbited the planet Jupiter and that the planet Venus had phases just like the moon. While logic dictated that the earth was the center of the universe, experimental observations made by an Italian physicist indicated that this could not be the case.

When science was dominated by the application of deductive reasoning, scientific progress was slow to nonexistent. Even highly educated people believed in such things as phlogiston and spontaneous generation. Thanks to the scientific method, experiments were performed by Antoine Lavoisier, one of the men who discovered oxygen, and we now realize that burning is not a process of releasing an invisible, weightless substance called phlogiston, but a process of oxidation. Thanks to the scientific method in the hands of Louis Pasteur, we know that flasks of broth do not become cloudy by creating bacteria on their own, but that microscopic organisms can reproduce and multiply in a broth that initially appears clear.

With all of this in mind, it is surprising that some 21st century health experts wish to return to the days of science by deductive reasoning. While certain phenomena may appear to be true by anecdote or under certain conditions, without a systematic comparison of different interventions, there is no way to know for sure if eating a particular type of diet is good for weight loss, weight maintenance or (more importantly) the avoidance of the diseases of Western civilization. As Gary Taubes says at the conclusion of Good Calories, Bad Calories, "What's needed now are randomized trials that test the carbohydrate hypothesis as well as the conventional wisdom. ...it's hard to imagine that this controversy will go away if we don't do them, that we won't be arguing about the detrimental role of fats and carbohydrates in the diet twenty years from now. ...it's hard to imagine that the cost of such trials, even a dozen or a hundred of them won't ultimately be trivial compared with the societal cost."

Some investigators are doing randomized clinical trials, such as the A TO Z Weight Loss Study to compare diets such as Atkins, Ornish, Zone and a standard low-fat/high-carbohydrate diet. More of these studies need to be done, so that we can understand the specific health effects of eating various types of diets in various types of people over extended periods of time. And even in the context of low-carbing, it would also be helpful to have studies that examine the effect of eating saturated fats vs. polyunsaturated fats; eating at least 12-15 carbs' worth of vegetables per day vs. eating very few plant foods; including dairy vs. avoiding dairy in our diets; and taking various supplements vs. using no supplements. Until we have the studies to confirm or disprove our presuppostions, we are on shaky ground, just like Aristotle. Most of the time he was correct. Some of the time he was not. Without the scientific method, it's hard to know which is which.

Is the Tide Turning?

See that logo? The New England Journal of Medicine is one of the premier scientific journals in the world. It is in the top tier of the top tier of medical journals.

Contrary to popular opinion, it is possible to get mediocre research published. You can present a preliminary poster of your findings at a scientific meeting and it will appear in a volume summarizing all the posters from that meeting. You can submit your manuscript to a journal that will simply print it for you without any pesky review by your scientific peers.

But if you want credibility for your work, you send it to a respected journal where two or more qualified scientists will analyze it, tear it apart and ask you many questions about how you can back up your claims. The more respected the journal, the more likely that your submission will not pass muster and will be returned to you for submission elsewhere. In the scientific world, it's not just "publish or perish." The quality of the journals in which you publish is also extremely important.

For that reason, it is very significant that on July 17, 2008, the New England Journal of Medicine published an article entitled Weight Loss with a Low-Carbohydrate, Mediterranean, or Low-Fat Diet. The study enrolled 322 Israelis (men and women, average age 52, diabetic and non-diabetic) who worked at a nuclear research facility and were moderately obese. They were divided into three groups.

The Low-Fat group adhered to the guidelines of the American Heart Association (AHA). They ate 30% fat, and were permitted very little saturated fat and cholesterol. Men were limited to 1800 calories per day and women were limited to 1500 calories per day.

The Mediterranean Diet group ate 35% fat, mostly in the form of olive oil. They ate lots of vegetables and were instructed to get their protein from chicken and fish. Men were limited to 1800 calories per day and women were limited to 1500 calories per day.

The Low-Carbohydrate group ate 20 grams of carbohydrates per day for two months, followed by a gradual increase to a maximum of 120 grams of carbs per day. Participants were told to choose vegetarian sources of fat and protein. Daily calories were not limited.

The results were not unequivocally in favor of the Low-Carb group. They had the poorest long-term adherence rate to their diet (78%). Their fasting plasma glucose levels did not improve. Their blood pressure, LDL cholesterol, insulin and leptin levels and high molecular weight adiponectin all improved, but there was no significant difference in the degree of improvement among the three diet groups.

Compared with the other two groups, the Low-Carb group did see a significant drop in their weight, in their glycosylated hemoglobin, and in their ratio of total cholesterol to HDL cholesterol. In several other markers, the Low-Carb and the Mediterranean diet groups were not different from each other, but showed significant improvement over the group following the AHA-recommended Low-Fat diet.

One of the criticisms made against the low-carb diet is that it might not be safe or effective in the long term when compared with the standard American Heart Association low-fat diet. This study specifically addressed that question. It is notable that in the Discussion, the authors of this article state, "In this 2-year dietary-intervention study, we found that the Mediterranean and low-carbohydrate diets are effective alternatives to the low-fat diet for weight loss and appear to be just as safe as the low-fat diet." The wobble you just felt was the tide turning.

This study has received wide publicity in print and on television. It is possible that, at long last, the medical community and the media are beginning to question the dogma that the only healthy diet is a low-fat diet.

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.

Good Fats, Good Proteins

Carbohydrates, fats and protein are all macronutrients, i.e., the part of our diet that provides energy and the building blocks our bodies use for growth and maintenance. If we don't need to eat carbs, what macronutrients DO we need to eat?

Good fats and good proteins.

Good fats are (obviously) not the transfats. We also have to be careful with mono- and polyunsaturated fats, found in liquid vegetable oils. These become rancid within days to weeks and turn into forms that cause oxidative damage to our bodies. A better choice is the saturated fat found in animal fat and butter. An even better choice is the medium chain triglycerides found in coconut oil.

Good proteins are complete proteins. Proteins are made of long chains of amino acids. We can make some of the amino acids through intermediary metabolism, but some are essential amino acids and must be taken in as food. Excellent souces of complete protein include eggs, whey protein, cheese, meat and fish.