Is Diabetes Caused by Refined Carbohydrates?

Last week we criticized Good Calories Bad Calories. This week we shall praise it. In chapter 6 of GCBC, Gary Taubes discusses Captain Thomas Latimore Cleave, a physician who believed that the common chronic diseases of Western civilization could be linked to the consumption of refined carbohydrates. Cleave had observed that non-Western societies tended to remain healthy even if they ate relatively large amounts of low glycemic index carbohydrates such as brown rice, wholemeal flour, non-starchy vegetables and nuts. But when a cultural group switched from traditional foods to white rice, white flour and sugar, the chronic diseases of civilization would begin to appear. To illustrate this, Cleave prepared the chart at the top of this post, which has been scanned from page 116 of GCBC. The dashed line shows per capita sugar consumption in England and Wales from just before 1905 to just after 1945. Sugar consumption increased during prosperous times and decreased during periods of wartime rationing. If diabetes had no relation to sugar intake, one would expect that deaths from diabetes (diabetic mortality) would gradually decrease as (1) injectable insulin was introduced and (2) medical treatments in general improved. Instead, until 1945 the index of diabetic mortality increased and declined in parallel with the consumption of sugar. Correlation is not causation, but the close relationship between sugar consumption and deaths from diabetes bears serious consideration.

Since 1945, the use of antibiotics to treat infection, the widespread use of home blood glucose monitors and the advent of new drugs to treat diabetes has dramatically reduced the death rate from diabetes. Nevertheless, there seems to be a steadily-increasing incidence of diabetes, particularly of type 2 diabetes. A recent article in Science Daily describes a study showing that type 2 diabetes has reached epidemic proportions in China. The scientists estimated that 9.7% of adult Chinese have diabetes and 15.5% have prediabetes. The prevalence of both conditions is higher in urban areas. Possible causes may include longer lifespans, increased smoking, decreased physical activity, increased air pollution, increased food consumption and decreased food quality.

Along the lines of Dr. Cleave's hypothesis about the relationship of refined carbohydrates and diabetes, in 2007 the Archives of Internal Medicine published an article suggesting one possible cause for the increase of diabetes in China. Its title was "Prospective Study of Dietary Carbohydrates, Glycemic Index, Glycemic Load, and Incidence of Type 2 Diabetes Mellitus in Middle-aged Chinese Women".

The study spent 4.6 years observing a cohort of about 64000 Chinese women with no history of diabetes or other chronic disease at baseline. These women were between 40 and 70 years old and lived in seven communities in urban Shanghai. They were divided into sets of quintiles according to several measures of carbohydrate intake. Adjustments were made for possible confounding factors including age, education, income, occupation, smoking status, alcohol consumption, total daily energy intake, physical activity, body mass index, waist-to-hip ratio and presence or absence of hypertension.

When confounding factors were eliminated, it was found that in middle-aged Chinese women, the percentage of carbohydrate in the diet was positively associated with the risk of developing type 2 diabetes. When glycemic index was considered, the higher the glycemic index of the food eaten, the more likely the women were to develop type 2 diabetes. In Shanghai, rice is a main staple food, contributing 73.9% of dietary glucose load (calculated by multiplying the total carbohydrate of a food by the glycemic index of the food and summing the values for all foods over a day). When women were stratified according to the amount of rice they ate, the group eating the most rice (over three cups of cooked rice per day) had a relative risk of 1.78 of developing diabetes as compared with those eating the least rice (less than two cups of rice per day).

For this group of Chinese women living in an urban area, carbohydrate intake averaged between about 260 and 340 grams per day. The largest part of their diet consisted of rice, which has a glycemic index of 55 (glucose=100). In this population, when adjusted for other factors predisposing to diabetes, a diet high in carbohydrates with a high glycemic index was associated with a higher risk of type 2 diabetes. Does this mean that diabetes is caused by refined carbohydrates? No, but once again, the close association between a higher intake of refined carbohydrates and a higher incidence of type 2 diabetes is worth serious consideration.

Good Calories Bad Calories Is Not Necessarily Infallible

When Good Calories Bad Calories (abbreviated here as GCBC) was published in 2007, the low-carb community was ecstatic. Dr. Robert Atkins and the Doctors Eades had discussed the scientific basis for the low-carb lifestyle, but their writings were usually presented in the context of clinical observations. With GCBC, Gary Taubes gave low-carbers 460 pages of tightly reasoned discussion and another 113 pages listing many specific citations from the scientific literature.

For a layperson, the book was not easy to read, but with effort it was comprehensible. At last low-carbers had access to information that cast doubt on the hypothesis that excessive consumption of fat raises cholesterol levels, which in turn causes heart disease and early death. Taubes presented plausible evidence for an alternative hypothesis--that excessive carbohydrate consumption, not fat consumption, is the cause of diabetes, heart disease, hypertension and even cancer.

Since the publication of GCBC, two interesting things have happened. (A) GCBC has moved into the position of holy writ in the eyes of many low-carbers and (B) several low-carb blogs and forums have arisen to discuss the scientific and practical aspects of low-carbing.

A rereading of GCBC in 2010 shows that many of its ideas have been supported by the subsequent publication of prospective dietary studies, including Weight Loss with a Low-Carbohydrate, Mediterranean, or Low-Fat Diet, published in the New England Journal of Medicine. However, recent discussions in the blogosphere show that some statements in GCBC may need to be reconsidered.

Specifically, on page 394 of the hardbound edition of GCBC, Taubes states, "By the mid-1960s, four facts had been established beyond reasonable doubt: (1) carbohydrates are singularly responsible for prompting insulin secretion; (2) insulin is singularly responsible for inducing fat accumulation; (3) dietary carbohydrates are required for excess fat accumulation; and (4) both Type 2 diabetics and the obese have abnormally elevated levels of circulating insulin and a 'greatly exaggerated' insulin response to carbohydrates in the diet..."

Let's address these statements in order.

1. Although consumption of carbohydrates does prompt insulin secretion, it is a well-known physiological fact that consumption of proteins also prompts insulin secretion. The amount of insulin released in response to protein is about a third of that released in response to carbohydrate on a gram-for-gram basis, but the increase is still measurable. Dr. Mike Eades has an illustration of this on page 37 of the paperback edition of Protein Power. Scientific articles measuring the insulin release in response to protein can be found here and here. Insulin response to various foods in terms of 120 minute area under the curve can be found in Table 4 here.

2. Insulin release does promote the storage of fat in adipocytes, but it is not the only signaling protein that produces fat storage. Acylation Stimulating Protein (ASP) is secreted by fat cells and allows fat to be removed from chylomicrons and stored in fat cells. Acylation Stimulating Protein permits the body to store fat in the absence of insulin. The process is discussed here by Dave Dixon and here by Petro Dobromylskyj (Hyperlipid).

3. While it is difficult to accumulate excess fat in the absence of dietary carbohydrates, it is not impossible. On various discussion boards, a few zero-carbers have related anecdotal evidence that they gained weight while eating large amounts of protein and fat. From a theoretical perspecive, on pages 388-392 of GCBC Taubes goes into great detail about the necessity of glycerol phosphate for the storage of fat in adipose tissue. (Glycerol phosphate is the precursor to the molecule used as the backbone of a triglyceride, the storage form of fat.) On page 392 Taubes says, "Dietary glucose is the primary source of glycerol phosphate. The more carbohydrates consumed, the more glycerol phosphate available, and so the more fat can accumulate. For this reason alone, it may be impossible to store excess body fat without at least some carbohydrates in the diet and without the ongoing metabolism of these dietary carbohydrates to produce glucose and the necessary glycerol phosphate." This sounds logical. However, biochemists know that glycerol phosphate can readily be produced from protein via glyceroneogenesis. The absence of dietary carbohydrate in no way prevents the synthesis of triglycerides from a high-protein or even a high-fat diet.

(4) It is true that high insulin is often associated with type 2 diabetes, but it is important to remember that type 2 diabetics do not always have an excess of circulating insulin. Instead they have insulin resistance. If their body tries to control high blood glucose levels with excess insulin production by the pancreas, this can result in beta cell burnout and a patient who actually has less endogenous insulin production than a person without diabetes.

As described here the scientific method is an ongoing process. Good Calories Bad Calories is an excellent book and provides many good arguments for the low-carb lifestyle. But the scientific method requires that we keep testing and evaluating our hypotheses, and it is important to realize that not everything we read in GCBC will necessarily stand the test of time.

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.

Deadline

I have a project and a deadline in the real world, so I probably won't be able to blog for a while longer. Questions and comments on previous blogposts are still welcomed, however. (Be sure to include in the comment which specific post you're commenting on. Blogger doesn't provide that information and sometimes I can't find the comments after I've accepted them.)

In the meantime, I know you'll keep moving forward on your journey into good health.

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.

Essential Fatty Acids (Omega-3 and Omega-6)

Certain dietary deficiency diseases are quite straightforward. For instance, if we don't consume enough vitamin C for a long period of time, we will develop scurvy. Children who don't get enough vitamin D and/or calcium, will suffer from rickets. Adults with a persistent deficiency of vitamin D and/or calcium will eventually experience osteopenia and perhaps osteoporosis.

Other dietary deficiencies produce less obvious symptoms. As early as the 1920's, it was noted that a complete dietary deficiency of fatty acids produced impaired growth in animals. When this was investigated farther, it was found that the omega-3 and omega-6 fatty acids were particularly important for growth and development.

Now a detour to explain some nomenclature. Fatty acids are the carbon chains that are attached to glycerol backbones to form triglycerides. Illustrated above are three such fatty acids, alpha-linolenic acid (ALA), eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). The zig zag lines are a form of shorthand that circumvents the necessity of writing out all the carbons and hydrogens found in these molecules. Each inflection of the zig zag (plus the right end of the zig zag) represents a carbon atom. Count these points on ALA, and you will find 18 carbon atoms. On DHA there are 22. The straight lines between the points represent covalent bonds. A single straight line between two carbons is a single bond, also called a saturated bond. A double line between two carbons is a double bond, also called an unsaturated bond. You can see that all three of these fatty acids contain several unsaturated bonds, which is why they are called polyunsaturated fatty acids.

On the left of each fatty acid molecule is a carboxyl group, which is used to join the fatty acid to the glycerol backbone. On the extreme right is the omega (or final) carbon. In each of the fatty acids shown above, at carbon #3, there is a double bond. The presence of that bond means that these are omega-3 fatty acids. Fatty acids that have a double bond at carbon #6, but not at carbon #3 are called omega-6 fatty acids.

Back to the dietary deficiency story. In a review article, William Lands describes how further research showed that omega-3 and omega-6 fatty acids are somewhat interchangeable, but that omega-6 fatty acids are particularly important for maintaining skin integrity, renal function and the process of birth. Omega-3 fatty acids may be more important in the support of visual and neural functions.

As Lands describes it, in 1963 it was discovered that one of the omega-6 fatty acids could be converted to a signaling molecule called a prostaglandin. Prostaglandins act on the vascular system, affect platelet aggregation and regulate inflammation. Further research revealed that omega-3 and omega-6 fatty acids could be converted to a large set of short-lived locally-acting signaling molecules called eicosanoids. Along with the prostaglandins, these include thromboxanes, leukotrienes and prostacyclins. Representative examples are illustrated below. (Both figures in this post are modified from figures found at Wikipedia.)


There are dozens of eicosanoid molecules, and each of them has many actions. Because of this, there is no simple relationship between a deficiency of omega-3 and omega-6 fatty acids and a defined profile of symptoms. When taken in optimal amounts, the eicosanoids promote the health of the cardiovascular system, the central nervous system, and the immune system. For scientific citations, please see the extensive Notes and References section at the end of the Wikipedia article on Omega-3 Fatty Acid. Positive effects have been shown for lowering blood pressure, improving blood lipid profiles, decreasing the risk of stroke and preventing psychotic disorders.

In a practical sense, a Westernized diet provides an abundant supply of omega-6 fatty acids and a relatively poor supply of omega-3 fatty acids. During the past few decades, healthy eating recommendations have caused us to transition from animal fats, rich in omega-3 fatty acids, to corn oil, safflower oil, cottonseed oil, peanut oil and soybean oil, which are all rich in omega-6 fatty acids and poor in omega-3 fatty acids. This is important because, when it comes to omega-6 fatty acids, we cannot say that if a little is good, a lot is better. An excess of omega-6 fatty acids causes these molecules to form inflammatory intermediates which are relevant to processes such as asthma, arthritis and atherosclerosis.

A review article by Artemis Simopoulos describes how these inflammatory intermediates can be counteracted by decreasing our intake of omega-6 fatty acids and increasing our intake of omega-3 fatty acids. Unfortunately, in the modern world, it takes some thought and financial resources to balance our intake of omega-6 and omega-3 fatty acids. That will be the subject of the next blog post.

Caffeine and Weight Loss

In 2004 the Food and Drug Administration banned the sale of dietary supplements containing ephedra in the United States. Although studies had shown a beneficial effect of the combination of ephedra and caffeine for weight loss in trials of six months or less, there were many reports of heart attacks, strokes, seizures and death caused by ephedra. This caused the FDA to discourage and finally to prohibit the sale of dietary supplements containing ephedrine alkaloids.

Caffeine, however, remains readily available in the form of coffee, tea, chocolate and over-the-counter pills. Does caffeine alone have a beneficial effect on weight loss?

It may, but if it does, the effect is slight. By inhibiting an enzyme that degrades intracellular cyclic AMP, caffeine is able to promote thermogenesis and stimulate fat oxidation. However, the long-term effect of these changes is not dramatic. From 1986 to 1998, Lopez-Garcia et al. studied the effect of changes in caffeine intake in a total of 58,000 health care professionals. Caffeine intake was calculated from the self-reported weekly consumption of coffee, tea, soft drinks and chocolate. Participants were divided into quintiles according to the amount that their caffeine intake had varied, from a net decrease to a net increase over the twelve years of the study. Each quintile gained weight during the study, but in the quintile that had increased its caffeine intake the most, less weight was gained. How much less? Slightly under a pound. Over twelve years. It is also important to note that this was a correlational study, and as we have learned, correlation does not equal causation.

One of the interesting aspects of caffeine consumption is that it is associated with an increase in insulin resistance. In this 2005 article in Diabetes Care, Lee et al. show that lean, obese and type 2 diabetic men experienced a 33-37% reduction in insulin sensitivity immediately following ingestion of a capsule containing caffeine equivalent to about 2-3 cups of coffee. The references in the article confirm that other investigators found similar results in single-dose administration of caffeine, but none of these the addressed the effect of chronic caffeine ingestion on insulin resistance.

This is important because in their discussion Lee et al. point out a paradox. The consumption of coffee (as opposed to consumption of pure caffeine) has an inverse relationship with the incidence with type 2 diabetes. Van Dam et al. saw a dose-response relationship between increasing coffee consumption and a declining risk of type 2 diabetes in younger and middle-aged women. This was true both for caffeinated and decaffeinated coffee. Granted, this was another correlational study, but it does raise the interesting possibility that there is a non-caffeine component of coffee that provides a protective effect against type 2 diabetes. Potassium, magnesium, chlorogenic acid, quinic acid, trigonelline and lignan secoisolariciresinol have all been proposed as possible agents for improved glucose metabolism in coffee drinkers, but the association is mostly speculative.


To summarize, from the literature, it appears that caffeine does not provide much help with weight loss, but on the average it does not hinder it either. Caffeine increases insulin resistance in the short term, but it may or may not do so in the long term. For those who get their caffeine fix by drinking coffee, it is possible but by no means certain that the coffee itself contains one or more compounds that have a beneficial effect on glucose metabolism. As of this writing, the use of caffeine on a low-carb diet is up to the dieter. The science is far from settled.

Cinnamon and Blood Glucose

The other day I was at Sam's Club, pushing my cart past the supplement section on the way to the meat counter. As I glanced at the shelves, I noticed something new. There was a bottle containing 500 mg capsules of cinnamon (specifically, ground Cinnamomum cassia bark). On the one hand, I had heard that cinnamon was able to improve blood glucose levels, but I hadn't read any of the papers. On the other hand, my fasting blood glucose levels had been in the 100 mg/dl range for a while, even though I eat less than 10 grams of carbs per day. I had been taking chromium supplements, but they didn't seem to have much of an effect. Since the cinnamon capsules weren't particularly expensive, I decided to take a chance and I bought them.

When I got home, I pulled up some of the scientific papers on cinnamon and saw that a reasonable dose would be about 1.5 grams per day. I took a capsule at breakfast, lunch and bedtime and the next morning my blood glucose was 95. To my amazement, the readings continued near that value throughout the week. I told a prediabetic friend about this, and she decided to try it as well. She too noticed a drop of about 5-10 mg/dl in her blood glucose levels. Next, my husband told one of the people at work about my experience. She has type 2 diabetes and is taking both oral hypoglycemic agents and a bit of insulin. She tried the cinnamon capsules and her blood glucose levels fell by 50 mg/dl.

Alrighty then. I decided it was time to read the scientific papers and see if there was anything to these anecdotal experiences. This blogpost will summarize my findings, such as they are.

In 2003 a paper by Khan et al. appeared in Diabetes Care. It described a group of 60 people who had type 2 diabetes and were being treated with sulfonylurea drugs. They were divided into six groups, with the first three taking 1, 3 or 6 grams of cinnamon daily while the second three were given placebo capsules of 1, 3 or 6 grams of wheat flour. After 40 days of treatment, the placebo groups experienced no change in fasting serum glucose, but the three treatment groups experienced decreases of 25%, 18% and 29%. There did not appear to be a dose-response because all three levels of cinnamon intake produced similar results.

This result was not totally unexpected because cinnamon had been observed to have insulin-enhancing activity in laboratory studies. With that in mind, several groups performed prospective clinical trials with cinnamon in human beings. Five of these studies were reviewed by Baker et al. in 2008. They concluded that the use of cinnamon did not significantly alter hemoglobin A1c or fasting blood glucose in patients with type 1 or type 2 diabetes.

However, other studies showed that there was an improvement in blood glucose with cinnamon. Zeigenfuss et al. used an aqueous cinnamon extract to treat prediabetic subjects and saw no effect at six weeks, but at twelve weeks observed an 8.4% drop in fasting blood glucose. In 2007 Wang et al. studied women with polycystic ovary syndrome (PCOS), a hormone disorder associated with insulin resistance. After eight weeks of treatment with a cinnamon extract, these women experienced significant declines both in fasting blood glucose and in two measures of insulin resistance. In 2009 Paul Crawford studied a heterogenous group of poorly controlled type 2 diabetics in a primary care setting. Their medications and dietary recommendations were left unchanged, but the treatment group received an add-on dose of 1 gram of cinnamon per day in an open-label study. After 90 days, the treatment group had significantly lowered its hemoglobin A1c from 8.47 to 7.64.

A 2008 lecture by Richard A. Anderson gives some insight into the possible mechanisms of cinnamon enhancement of insulin sensitivity. When insulin binds to its receptor, it starts a signaling cascade that begins with the autophosphorylation of the insulin receptor. In the presence of cinnamon extracts, this autophosphorylation is more robust. Not only that, cinnamon inhibits the dephosphorylation of the insulin receptor, which further enhances the signal. Cinnamon also increases the amount of insulin receptor proteins and of other proteins in the insulin signaling pathway. Cinnamon is not a substitute for insulin, but it does make insulin signaling more sensitive to the insulin that is present in the blood.

In summary, it appears that supplementation with cinnamon may provide a small but significant improvement in insulin sensitivity. It appears to have a greater influence in people with poorly controlled blood sugar, especially in those who are taking drugs that enhance insulin secretion by the pancreas. In people who are pre-diabetic, the glucose-lowering effect seems to be less. In fact, when cinnamon is given to normal subjects, it does not decrease their blood glucose, but instead reduces their postprandial serum insulin. Although the anecdotal experiences I related at the beginning would suggest that cinnamon has an immediate effect on blood glucose, from the scientific literature, it appears that it may take up to 12 weeks to exert its actions.

Even though cinnamon is found in practically every kitchen in the Western world, it is important to note that some people are allergic to cinnamon. If you decide to try cinnamon supplementation, be careful to look for rashes, inflammation of the mucous membranes or even trouble with breathing. Be sure to discontinue the cinnamon if any of these symptoms occur.

That said, it appears that supplementation with cinnamon may be helpful as part of a strategy to normalize blood glucose levels.

Induction Flu

Those of us who have done low-carb for years are happy to sing the praises of the low-carb lifestyle--decreased weight and increased energy, plus improvements in blood pressure, triglycerides, HDL and blood glucose numbers. But in much the same way that the joy of having a new baby diminishes our memory of the pain of childbirth, we find it easy to forget that one of the aspects of low-carbing is very hard. It's called Induction flu, or Atkins flu.

On the Standard American Diet (very aptly named the SAD diet) we are used to eating low fat, moderate protein and high carbohydrate. Our body's primary source of energy comes from the burning of hundreds of grams of carbohydrates we consume every day. When we change from a SAD diet to a low-carb diet, we abruptly remove the macronutrient that has provided most of our energy. Eventually our energy will come from the fat we eat, but in the meantime our bodies have a huge transition to make.

Every nucleated cell in our body contains 46 chromosomes with over 3 billion base pairs of DNA. In that DNA is the information needed to make the enzymes required for us to metabolize both carbohydrates and fats into energy. Although the information is there, it is not translated into enzymes unless those enzymes are actually needed. A person eating a SAD diet will have all the enzymes he or she needs to convert carbohydrates into energy, but very few of the enzymes needed to convert fat into energy.

Typically a low-carb diet is begun at a level of 20 to 30 grams of carbohydrate a day. Suddenly the carbohydrate conversion enzymes no longer have a substrate. They initiate Plan B, which is to utilize the glycogen stored in the liver and muscle tissue. Glycogen is converted to glucose, which is converted to energy. After about a day, glycogen is depleted, and the body moves to Plan C. It notices that fat is available in abundance, and it upregulates the machinery to transcribe the necessary codes from the DNA into RNA, and then to translate that into the enzymes that are required to metabolize the fat into energy. Unfortunately this takes a day or two, and in the meantime the new low-carb dieter starts to experience Induction flu.

The symptoms of Induction flu are not those that are normally associated with dieting. Instead of ravening hunger and cravings, there is a headache and nausea. The dieter may be irritable and lack energy and concentration. Chills and fever are not typical symptoms, but other than that, it feels like the flu and will last for about two days.

What to do? First of all, recognize that this is a transitional state and that it will end. Second, pamper yourself. This does not mean that you dive headfirst back into the carbs, but drink plenty of water, sleep, take a hot bath, take NSAIDs or acetaminophen, watch a good video or read a good book. One of the best strategies is to find a supportive friend either on the low-carb boards or in real life to commiserate with. Simply knowing that this stage is coming and planning for it is one of the keys to getting through it.

Sometimes new low-carbers try to change everything all at once. If you're a caffeine addict, you might want to wait until Induction is over before you give up the caffeine. If you are resolved to start an exercise regime along with the low-carb diet, it might be better to wait until you have recovered from the Atkins flu before you hit the pavement or go to the gym. If you are lightheaded or start having muscle cramps, consider taking a potassium supplement or using Lite Salt or a KCl salt supplement on your food. Low-carb diets have a diuretic effect and tend to make the kidneys excrete potassium.

It takes several weeks for the body to become fully keto-adapted, that is, to complete the conversion from from carb utilization to fat utilization for energy. However, the worst of the process should be over by the end of Day 3. At that point the benefits of low-carbing (increased energy, decreased appetite and a sense of freedom from the enslavement to rising and falling insulin) should start to predominate. Low-carbing is a continuous learning process, but once the Induction flu is over, it's a worthwhile journey into good health.

Glyceroneogenesis, and Other Reasons for Fat Storage on Zero Carb

This week I have an extra set of responsibilities in real life and have had a hard time finding time for a new blog post. Fortunately I recently learned of an excellent article by LynMarie Daye, Is the Fable of Unfettered Fat Burning Derailing Your Low Carb Diet?

The author explains in clear and well-referenced terms how the body is able to store fat in the relative absence of insulin. As she says, only type-1 diabetics have a total absence of insulin, and it is true that they cannot store fat. However, the rest of us have a low baseline level of insulin at all times, and in that situation, Acylation Stimulating Protein is able to promote fat storage even when blood insulin levels remain low.

It is also true that fat storage requires the presence glycerol 3-phosphate to form the backbone of the triglyceride molecule. However, simply refraining from eating carbs is not sufficient to stop the synthesis of glycerol 3-phosphate. Even in a state of prolonged fasting, the body is able to use its own muscle protein to synthesize glycerol 3-phosphate. This metabolic pathway is called glyceroneogenesis, and it is illustrated in the figure above.

If you have ever wondered how it is possible to eat no carbs whatsoever and still gain weight, LynMarie Daye provides a thorough treatment of the issue. I highly recommend her article.

Ghrelin, the Hunger Hormone

A hormone is a chemical that is produced in one part of the body, is released into the blood, and is able to regulate activities in other parts of the body. One example would be insulin, which is produced in the pancreas, but affects the function of tissues throughout the body, including muscles, brain and liver.

Insulin is important for food storage and satiety. Another hormone that plays a role in energy homeostasis is ghrelin, a 28-amino acid peptide discovered in 1999. Its name includes the Proto-Indo-European root word "ghre," meaning "to grow." Ghrelin is produced in the hypothalamus, kidney and pituitary gland, but most of it is synthesized in and released by the stomach. The picture below (credit to Rae Silver, Joseph LeSauter and Donald Pfaff) shows a photomicrograph of the stomach wall. The hormone ghrelin has been specifically tagged and can be seen in the form of black dots.



Ghrelin has many actions, but the most prominent one is that it increases hunger by stimulating neurons in the arcuate nucleus of the hypothalamus, especially the neurons that express neuropeptide Y and agouti-related protein. Neuropeptide Y and agouti-related protein are both potent stimulators of appetite. Not only that, neuropeptide Y and agouti-related protein also enhance appetite by reducing the action of the appetite inhibitor proopiomelanocortin. As might be expected, people who are given injections of ghrelin become voraciously hungry and eat more than they otherwise would.

Ghrelin does have a specific role in the energy management of the body. Researchers at Columbia and Rockefeller Universities have shown that ghrelin is released in a circadian manner, prior to the onset of mealtimes. This pattern is illustrated in the graph below.

Just before mealtime, ghrelin is released from the stomach and acts on the hypothalamus to induce food-seeking behavior. In some ways this is a very adaptive mechanism. Rather than allowing a person to continue various activities and deplete energy stores, ghrelin acts to remind us to start seeking food and begin preparing for a meal. As soon as food reaches the stomach, ghrelin levels drop dramatically and stay low until an hour or so before the next meal is normally eaten.

Because of ghrelin's role in enhancing hunger, it is a prominent target of anti-obesity strategies. However, counteracting ghrelin has proved harder than one might expect. When a large part of the stomach is removed in weight loss surgery, ghrelin levels do drop in the short term. However, within a year post-surgery, ghrelin production recovers and patients tend to have higher blood levels of ghrelin than they did before the surgery. Even when mice are bio-engineered to lack the ability to produce any ghrelin whatsoever, their body weight gain and 24-hour food intake remain unaffected, suggesting that there are redundant appetite control systems that promote food intake in spite of the fact that ghrelin levels have been reduced to zero.

Although ghrelin-related strategies for hunger control do not look promising at this time, knowing about this hormone can still help us on a cognitive level. When the clock is moving toward lunch or dinner-time and we find ourselves obsessing about food, it's good to know that we aren't actually starving. We are simply getting a signal from our stomachs that it is time to start foraging for food. Because most of us live in a situation where food is as close as the nearest refrigerator or pantry, we can smile and tell ourselves that all is well. Thanks to modern civilization, we won't have to pick up a spear and run down an unsuspecting wild animal or rush out to gather roots and berries. The food will be there when it's needed, and we can calmly go back to our activities until it is time to eat.

Essential Carbohydrates

The most obvious characteristic of a low-carb diet is that it is low in carbohydrates. The original Atkins diet recommends that dieters start its Induction phase with essentially zero grams of carbohydrates. The 2002 version of the Atkins diet allows dieters to do Induction with up to twenty grams of carbohydrates. The Protein Power diet begins its Phase I Intervention stage at thirty grams of carbohydrates. As all of these diets progress, additional carbohydrates are introduced in a controlled manner, but even at maintenance, most low-carbers eat no more than 100 grams of carbohydrate per day.

By contrast, the US Department of Agriculture recommends that both children and adults eat 45-65% of their daily calories as carbohydrates. That can mean well over 300 grams of carbohydrates per day for a person consuming a 2000 calorie diet.

What happens if we ignore the USDA guidelines and don't eat enough carbs every day? Carbohydrates are popularly thought to be essential for providing energy. Specifically they are thought to be necessary to provide fuel for the brain and to refill stores of glycogen in muscles and in the liver.

The American Diabetes Association tells us that the brain and central nervous system normally have a daily requirement of about 130 grams of carbohydrate in the form of glucose. However, after a period of adaptation, most of these tissues are also able to use ketones as an energy source. This reduces the carbohydrate requirement to about 30 grams of glucose per day. As low-carbers with Ketostix already know, ketones are produced in abundance from the fats and amino acids consumed on a low-carb diet. The remaining need for thirty grams of glucose can easily be met through a metabolic pathway called gluconeogenesis, which allows the body to use amino acids from proteins and the glycerol backbones from fats to synthesize glucose in the absence of any carbohydrate intake.

Glycogen, which is a storage form of glucose, can similarly be replenished by the glucose made through gluconeogenesis. As far as the general energy requirements of the body, these can be met very efficiently both by the utilization of dietary fat and by the mobilization of stored fat.

Carbohydrates, therefore, are not an essential element of a healthy diet. There are essential fats, which include the omega-3 and omega-6 fatty acids. Because they are not produced by the body, omega-3 and omega-6 fatty acids must be consumed in order to ensure the normal function of the nervous system, heart and immune system. There are essential amino acids, including isoleucine, leucine, lysine, methionine, phenylalanine, threonine, tryptophan and valine. Although some amino acids can be synthesized by the body, these eight cannot. Unless they are ingested, and ingested in the proper amounts, the body is unable to assemble all of the structural and enzymatic proteins that are needed to sustain life.

By contrast, there is no disease state associated with an insufficient intake of carbohydrates. It is true that the body needs carbohydrates for energy within certain types of tissues, for synthesis of the backbones of DNA and RNA, and for signaling purposes, but it is well able to synthesize all of these from the raw materials provided by the amino acids in the proteins we eat.

For those of us raised on the dogma of eating low-fat and high-carb, this is hard to believe. But if we think about our caveman ancestors, we realize that they didn't have access to pasta, potatoes or rice, or even high-carb fruits and vegetables on a regular basis. They were able to survive and reproduce without a high carbohydrate intake because, amazingly enough, there is no such thing as an essential carbohydrate.

Welcome, New Low-Carbers!

You'd been hoping to lose weight all through 2009, but never quite managed it. Then came Thanksgiving. After the big meal and the family time, you washed the dishes, put away the leftovers, dug out the Christmas decorations, and as you made the house ready for the season you hoped to do better in December. Of course, you had forgotten about the holiday goodies that would be brought into your office as treats for everybody. They sat there in all their deliciousness, and it was just too hard to resist them.

Christmas arrived. Only Scrooge would decline the traditional foods that various relatives and friends had prepared. A week of polishing off the remaining treats has left you with a closet of clothes that no longer fit and a temptation to try a weight-related New Year's resolution one more time.

What makes your 2010 resolution different from your previous weight-loss resolutions? This time you're doing low-carb! You have gone to the Internet to investigate low-carbing and to make contact with people who can encourage and advise you. You have a book (Dr. Atkins' Diet Revolution or Mike and Mary Dan Eades' Protein Power), and you have decided to read it and follow what it says.

What's different about low-carbing? Low-carbing allows us to work with the way our body works rather than fighting against it. When we eat foods with lots of carbs (bread, pasta, potatoes, most desserts and snacks), our bodies can't use all of those calories at once. Our pancreas releases the hormone insulin to store the nutrients in our cells. Between meals, the nutrients are released and are used for energy.

However, as we age, the store-and-release cycle sometimes starts to break down. We eat the carbs and store the nutrients, but when it comes time for our cells to release the nutrients, they resist doing so. The body needs energy but the cells don't want to release it. So the body moves to plan B. It commands us, "EAT MORE." Sure enough, we load up on more carbs and for a little while we have the energy we need. The excess energy from our snack is stored in our cells, but once again the cells resist releasing it when we need more energy a few hours after we've eaten. As this vicious cycle deepens, we notice that we are eating, getting hungry, eating again, getting hungry again and steadily gaining weight. We can try ignoring our appetite, but our bodies are clever. They will make the drive for food relentless. If our willpower holds, our bodies will assume they are in a starvation situation and will retaliate. They will throttle down our core temperature and make us less energetic. Sound familiar?

Low-carb eating circumvents the broken store-and-release cycle. Eating low-carb food means we will be eating mostly protein and fat. Both protein and fat are stored after meals, but the process is more gradual. With very few carbs, less insulin is needed, and this means that body's cells are more likely to make the switch from storage mode to release mode between meals. The presence of dietary fat (in the absence of carbs) will signal the cells that starvation is not imminent, and will tell the body that there is no need to lower body temperature and energy level.

What about calories? When our body is utilizing its own stored energy, it will naturally adjust our appetite to be content with a lower calorie intake. That's hard to believe, but most people will spontaneously start eating less as they become adapted to a low-carb way of eating. They are no longer putting a part of each meal into permanent storage, and are actually able to mobilize the energy their body has been hoarding against what it thinks is a famine. With low-carbing, self control is necessary when it comes to food choices, but the constant battle against raging hunger is over.

That's it in a nutshell. The practice is harder than the theory, but that's why the books by Dr. Atkins and the Eades are there. Psychological support is available from online bulletin boards such as Low Carb Friends.

You can do it. Your body will actually help you when you work with it rather than against it. And those clothes in your closet will soon be too big rather than too small. Happy Low-Carb Year!

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.

Narcissism: When Low-Carbers Hurt Other People

Narcissus, a young hero in Greek mythology, saw his image in a pool of water, fell in love with it and was unable to leave the beauty of his own reflection. He has given his name to an Axis II personality disorder described in the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV), narcissistic personality disorder.

There is no laboratory test for the diagnosis of narcissistic personality disorder. Typically a trained psychiatrist or psychologist will evaluate a patient who, by early adulthood, demonstrates grandiose thinking or behavior, has an unusual need for admiration, and shows a lack of empathy for other people. These maladaptive patterns must be present in a variety of contexts.

In addition, a person with narcissistic personality disorder will demonstrate five or more of the following criteria (taken from the DSM-IV):

1. Has a grandiose sense of self-importance (e.g., exaggerates achievements and talents, expects to be recognized as superior without commensurate achievements)
   


2. Is preoccupied with fantasies of unlimited success, power, brilliance, beauty, or ideal love
   


3. Believes that he or she is "special" and unique and can only be understood by, or should associate with, other special or high-status people (or institutions)
   


4. Requires excessive admiration
   


5. Has a sense of entitlement, i.e., unreasonable expectations of especially favorable treatment or automatic compliance with his or her expectations
   


6. Is interpersonally exploitative, i.e., takes advantage of others to achieve his or her own ends
   


7. Lacks empathy: is unwilling to recognize or identify with the feelings and needs of others
   


8. Is often envious of others or believes that others are envious of him or her
   


9. Shows arrogant, haughty behaviors or attitudes

While it is tempting to do amateur psychology, that is not the point of this blogpost. Only a professional can diagnose and treat narcissistic personality disorder. Nevertheless, it is important for laypeople to be aware that this condition exists, and that it exists in the low-carb community in particular.

Low-carbers are vulnerable. Typically they have been overweight for many years and have a poor self-image as a result. Many have tried and failed at various weight loss schemes. Couple those experiences with the societal stigma against overweight people, and self-worth becomes almost nonexistent.

Along comes low-carb. For once, these formerly-obese people find themselves successful at something. They are able to move their bodies, to buy clothes, and to go out in public without a sense of shame. And, in some cases, they find a mentor who is able to take advantage of all their vulnerabilities.

The mentor provides a diet outline that seems to work. The mentor creates an internet community that gives support and a place to belong to people who were formerly outsiders. All of that is good.

But if the mentor has narcissistic personality disorder, the mentor starts to overstate the benefits of his or her diet plan without commensurate proof (Point #1). The mentor sets himself or herself up as the ideal example of the diet plan (Points #2 and #4). The mentor begins to lay down specific rules that require either automatic compliance or, failing that, expulsion from the community (Points #3 and #5). The mentor may show friendliness, charm and empathy when it provides an advantage (Point #6), but in the end will behave in an arrogant, abusive manner toward people who have disappointed him or her in any way (Point #9).

In my experience, low-carbers tend to think the best of people, even of people who abuse them. When they encounter a person with narcissism, they often hope that by careful reasoning or sympathetic friendship, they can help that person see his or her problem, deal with it, and adopt a more successful style of living. Unfortunately, the treatment of narcissism requires psychotherapy (see this PDF for a fascinating outline of what's involved), and even then the treatment is unlikely to be successful if the patient is not a willing participant in the therapy.

In the meantime, when you encounter another low-carber who is self-absorbed, who believes himself or herself to be superior to others, who belittles others, and who is willing to manipulate others to achieve his or her own ends, recognize that this is a person who can derail your journey into good health. It may be difficult, but if the person is harming you while he or she claims to be helping you, it may be time to end this relationship and develop new ones in the low-carb community.

Water

For low-carbers, the design of an eating plan often focuses on carb counts, calories, and essential vitamins and minerals. With the array of tasty and nutritious foods that are available to low-carbers, it's easy to overlook another important aspect of low-carbing--water intake.

Water keeps our tissues hydrated, provides an environment for enzymatic reactions to occur, and in the form of blood, water carries vital nutrients to cells that need them. Water also dissolves and removes the toxins from our bodies in the form of urine--1.5 quarts a day in the average adult.

One of the interesting aspects of Dr. Atkins' New Diet Revolution and Protein Power by the Drs. Eades is that both call for the daily intake of at least eight 8-ounce glasses of water per day. In Dr. Atkins' case, he says that only water counts as water for the purposes of the diet (page 230 of the paperback version of the book). The Eades say that any water-based fluid will work, as long as it doesn't contain calories (pp.103-105 of the paperback version of the book). Their counsel is, in fact, "Drink Till You Float." Whichever guideline you choose, if you decide to drink coffee or tea, remember that caffeine is a diuretic, and you will need to drink extra fluid to compensate for this. Both caffeine and artificial sweeteners can slow weight loss in some people, and if you are one of them you may wish to make other choices for your fluid intake.

One of the unique reasons for monitoring water intake during low-carb dieting is that most low-carb weight loss comes from the breakdown of body fat. Some of the body fat is burned to create ATP through the TCA cycle and oxidative phosphorylation, as was described in the previous post. However, some of the fat will be burned incompletely and will be converted to molecules called ketones. Ketones are also able to be used for the production of ATP, but if an individual is not totally keto-adapted, the body will allow some of them to be breathed out, or excreted in the urine and the stool. Drinking plenty of water makes it easier for the body to get rid of the excess ketones.

As the body adapts to a ketogenic diet, or as carb intake increases, fewer ketones will be produced. Even so, long-time low-carbers will continue to spill ketones if their fat intake is high and their carb intake is low, and they will benefit from an increased water intake.

Water has a few other properties that make it an important part of a low-carb diet. If plenty of water is ingested every day, less water will need to be reabsorbed from the colon, making it easier to have bowel movements. Some people have a propensity toward urinary tract infections. Drinking lots of water prevents urinary stasis and makes these infections much less likely. Similarly, although kidney stones have many causes and many treatments, in a person with a history of kidney stones, a universal preventive strategy includes drinking well over three quarts of water per day. Finally, low-carb dieters freqently begin to do more exercise as a result of having enough energy to resume physical activity, or in order to improve their overall health. Because less water is retained on a low-carb diet, those who engage in strenuous exercise programs need to be sure that they drink plenty of water so that they do not inadvertently become dehydrated.

Often, thirst alone is not a good indicator for drinking water. This is especially true as people age and their bodies are less able to sense dehydration. In order to keep water intake at an optimal level, it may be necessary to fill a container or a set of containers in the morning and consume the water throughout the day, so that by bedtime all that day's water has been consumed. It may take a while, but drinking lots of water will eventually become a habit. Be sure to drink extra water when you engage in vigorous exercise, on days that are hot and humid, during the winter heating season, when you are at high altitude, and when you are sick.

Water is an important part of a low-carb diet. And the best news of all? It doesn't contain a single carb!