Truth and Consequences

When I began losing weight with low-carb, my motivation was not the usual one. I knew that as an obese woman, I would have very little credibility as a scientist.

That sounds odd, doesn’t it? Why would obesity trump publications and other achievements in the professional world?

This week I came across an article in the journal Obesity, “The Stigma of Obesity: A Review and Update.” The authors, Rebecca Puhl and Chelsea Heuer, give numerous examples from the literature demonstrating that obese individuals are indeed the subjects of discrimination in many areas of life.

In the area of employment discrimination, the article states,

One study (N = 2,838) found that overweight respondents were 12 times more likely, obese respondents were 37 times more likely, and severely obese respondents were 100 times more likely than normal-weight respondents to report employment discrimination. In addition, women were 16 times more likely to report weight-related employment discrimination than men.

This discrimination took the form of derogatory humor, pejorative comments, lower pay, denial of promotions and firing.

Weight bias is also seen in health care settings. Physicans, medical students, nurses and dieticians all expressed negative attitudes toward obese patients. Common adjectives were “lazy,” “lacking self control” and “noncompliant.” Medical students reported that severely obese patients were most frequently the target of derogatory humor among attending physicians, residents and students, especially in surgical specialties. Obese women, in particular, pick up on these attitudes. The article discusses several studies indicating that women in the United States are more likely to delay or forego preventive care as their BMI increases.

The article also addresses obesity and interpersonal relationships, including sexual relationships. One study asked 449 college students to rate six pictures of hypothetical sex partners in order of preference. The top ranking went to a healthy partner. Second was an armless partner. Third was a partner with a history of STDs. Fourth was a partner with mental illness. Fifth was a partner in a wheelchair. And sixth? You guessed it. Sixth was an obese partner. Not only that, although both men and women ranked the obese potential partner to be least desirable, the men ranked obese female partners significantly lower than the women ranked obese male partners.

Is this fair? No, it isn’t. Nevertheless, as the authors go on to describe weight bias in the media, it seems that weight bias, and particularly weight bias against women is pervasive. They conclude their article by discussing research to decrease biases against obesity and even legislation to prohibit weight discrimination.

While both of these approaches might be helpful in the long-term, for whatever reason there seems to be an intrinsic stigma against obesity. If you doubt that you have it, take a look at the picture at the top of this post and be honest about your responses. Because of this stigma, and because we all live in the real world, it seems that low-carbers have yet another reason to achieve and maintain a weight loss. Not only is a normal weight more healthy, a normal weight will give us a better chance at achieving our maximum potential in employment, in receiving health care and in forming interpersonal relationships.

Thoughts on the China Study

There are about 2000 counties in China. In the 1980’s, Cornell University did a large ecological study in 65 of them and published the data as something called the China Study. The study measured 367 variables in about 6500 adults. It captured data on diet, lifestyle and disease and included analyses of blood and urine samples. The individual results were grouped geographically, by county, producing a data set with 65 (or fewer) observations for each variable that was measured.

T. Colin Campbell, Ph.D. was a researcher in this study. In 2005 he published a book, The China Study: Startling Implications for Diet, Weight Loss, and Long-Term Health, using data collected from the China Study, from his own published research and from several other sources. When all of this information was considered together, on page 7 of the 2004 edition of the book Dr. Campbell concluded that,

People who ate the most animal-based foods got the most chronic disease. Even relatively small intakes of animal-based food were associated with adverse effects. People who ate the most plant-based foods were the healthiest and tended to avoid chronic disease.

In light of what low-carbers know personally and know from the scientific literature about the benefits of eating animal-based foods, Dr. Campbell’s conclusion is quite surprising. Vegans and vegetarians commonly use The China Study as proof that their food choices are scientifically superior to those that incorporate animal products. (Take a look at the comments on Amazon.com for just a few examples.) What’s a low-carber to think?

In 2005 Chris Masterjohn wrote a critique of The China Study. Masterjohn pointed out that the data showed that intake of animal protein did not correlate with mortality for all cancers. Although Campbell had tried to connect animal protein intake to cancer mortality through a set of six biomarkers like plasma copper and urea nitrogen, the relationships between animal protein intake, the biomarkers and the eventual deaths from cancer were poorly documented. Masterjohn also showed that Campbell had taken his own research on the tumor-promoting activity of casein in cancer-prone rats to make the astounding statement on page 104 of the book that “casein, and very likely all animal proteins, may be the most relevant cancer-causing substances that we consume.” This seems to be a bit of a logical stretch.

The discussion lay more-or-less dormant until 2010 when Denise Minger, a 23 year old English major and self-described data junkie, happened upon the raw China Study data and wrote a lengthy description of her criticisms of the book. In a 2001 symposium Dr. Campbell had summed up some of the findings of the China Study and a subsequent China Study II. He said, “Plasma cholesterol in the 90-170 milligrams per deciliter range is positively associated with most cancer mortality rates. Plasma cholesterol is positively associated with animal protein intake and inversely associated with plant protein intake.” After spending 1 ½ months of working with the raw data from the China Study, Ms. Minger found that the data in fact showed no statistically significant relationship between the intake of animal protein and cancer. (It also showed no statistically significant relationship between the intake of plant protein and cancer.)

So, how could Dr. Campbell describe a positive correlation between increased intake of animal protein and cholesterol and between increased cholesterol and cancer, while the raw data showed that there was no one-to-one relationship between intake of animal protein and cancer? The answer: confounding factors. Schistosomiasis is a common disease in China. It is caused by a worm not normally found in plant-based food nor in animal-based food but in contaminated water. Ms. Minger found that as schistosomiasis increases, plasma cholesterol increases significantly. (This may be the result of negative effects of schistosomiasis on normal liver function.) As schistosomiasis increases, the rate of colorectal cancer also increases significantly.

In other words, in counties where schistosomiasis was present, one would expect that people who had high cholesterol would also tend to have more colorectal cancer. Hence the presumed relationship between high cholesterol and cancer mortality in China would actually reflect a factor that had nothing to do with diet. And when Chinese counties with zero schistosomiasis infection are compared with respect to the relationship between total cholesterol and the rate of mortality from colorectal cancer, the correlation between the two variables disappears. In other words, Dr. Campbell’s reasoning that eating animal protein is associated with high cholesterol is in turn associated with increased cancer mortality is invalid. The data was presented in a way that it implied a relationship, but the relationship disappears with a more detailed analysis.

From there, Ms. Minger went on to dismantle one after another of Dr. Campbell’s assertions regarding the use of animal-based foods and damage to health. Other laypeople with statistical experience (here and here) also did their own data analysis and reinforced her conclusions.

Dr. Campbell responded to Ms. Minger’s criticisms here. His main objections seemed to be that she used adjectives (!), that she used univariate correlations (so did he) and that she was probably unable to have made her analyses without outside help.

Ms. Minger’s very detailed response to Dr. Campbell is here.

If you have time to read all of these links, they provide fascinating insight into the analysis and potential applications of an important ecological study. If you don’t, the bottom line is this: when you encounter a scientific study that seems to contradict everything you know about a particular subject, be sure to take a very careful look at the data to see if it might have been cherry-picked, over-interpreted, or analyzed without reference to potential confounding factors. If anything like this has happened, the conclusions of the investigators may not necessarily reflect what the data actually shows.

Managing Hunger

(Warning: Most of my posts are science-based, but this one comes from my own experiences, i.e., n=1. Forewarned is forearmed, so here we go.)

One of the things I noticed before I began low-carbing was that after I ate a meal, I could only go a couple of hours before I had to have a snack. Hunger would overwhelm me, and since my willpower isn't great, I would give in. Eventually I became fat and prediabetic.

Then came low-carb. I could eat and leave the table satisfied. I could eat only at meals and not feel ravenously hungry between times. But as the years went by, I noticed that my between-meal hunger started to return. It wasn't as bad as before, but my willpower hadn't improved any and I would start snacking to the point that I was eating mass quantities of low-carb food almost every day. I found Dr. Atkins' Accel diet pills, and those seemed to help. Until the Atkins company quit making them. Next, somebody introduced me to the original formulation of Leptopril and that kept the hungries at bay fairly well. Until they changed the formula. Finally, the Country Life Diet Power pills seemed to help a bit, but eventually those became unavailable, too. And after that, I couldn't find another over-the-counter diet pill that worked for me.

In the world of weight loss and weight maintenace, calories don't count as much as carbs, but they do count. My weight was increasing slowly but surely and there seemed to be nothing I could do about it. I tried drinking lots of water. I tried different kinds of fiber. I tried zero-carb. I made charts of the ingredients of the diet pills that had worked to curb my hunger, and I couldn't figure out what the magic combination was.

When the between-meal hunger hit, I would look at the extra ten pounds of fat I was carrying and wonder--why, if I'm eating very low carb and if I have this stored fat available--why can't my body switch over and use some of that stored fat for energy?

A couple of weeks ago, when the hunger monster attacked about two hours after breakfast, for some reason I went to the kitchen and made a cup of regular coffee. No artificial sweetener and no whitener. Just black instant coffee in a cup. I sipped some of the coffee, put the cup on my desk and went back to work. The hunger abated for an hour or so, but then it returned. I sipped some more of the black coffee and the hunger went away again. I had lunch as usual, but sure enough, about two hours later the hunger monster came knocking. Again I sipped some coffee and it went away. I repeated this until dinner. After dinner I knew I couldn't drink caffeine or I wouldn't sleep, so I sipped on a diet soda instead and that seemed to work. I had eaten a reasonable amount of food at my three meals, and I didn't wake up hungry during the night.

The second day was easier. I knew that if the hunger monster hit, I would be able to switch my body into fat-burning mode by sipping the coffee. It worked, and it has worked ever since.

It's important to state that each day I have had a shake for breakfast, fatty meat, cheese and a few veggies for lunch and fatty meat, cheese and a few veggies for dinner. In other words, I've been careful to eat sufficient-but-not-too-much complete protein, to eat fat to provide energy, and to keep the carbs low. I don't eat until I'm full. I figure out what I need to eat and eat that. Then I stop. I have kept taking all my normal supplements and I've been drinking at least 60 ounces of water a day. The difference is that, by sipping black full-caffeine coffee whenever I start feeling between-meal hunger, I can put the hunger monster at bay. I hate the taste of the coffee, but the fact that I'm essentially using it as a drug seems to make that okay. I once again can eat three reasonable meals three times a day and be satisfied. Thoughts of food no longer rule my life.

In conclusion I'll do a little speculation. For some reason, my body seems to need a spike in epinephrine to switch from food-storage to fat-burning mode. And it seems to need several little spikes over time, rather than one big spike. That may be why certain over-the-counter (OTC) diet pills worked for me and others didn't. Most OTC diet pills contain caffeine in some form, but it may be that the three effective ones delivered the caffeine slowly enough to keep my fat burning process in motion. I've tried taking caffeine pills and those don't work for me. I've tried drinking cups of coffee and that doesn't work. There seems to be something about the slow ingestion of black coffee that makes the difference.

As I said, n=1. This may work for me and for nobody else. But I'm posting it in case somebody else is doing pure low-carb and finds it impossible to fight off between-meal hunger. Erasmus is a zero-carber who says his Satisfactometer is broken. I think my Satisfactometer is broken, too, but maybe, just maybe, I have found a way to cope with it. No guarantees, but in case this works for someone else, I thought I'd share.

Organic Food versus Conventional Food

After people have low-carbed for a while, they start to look better and feel better. As their health improves, one of the natural questions to ask is, "If I feel this good by dropping the carbs, wouldn't I feel even better if I ate organic food?" When this question is asked in the form of scientific studies, the short answer is, "Probably not."

To be sure, the alternative medicine community makes many claims for organic food. In Alternative Medicine Review, Walter J. Crinnion, a Nutritional Doctor, states that organic foods contain higher levels of certain nutrients, lower levels of pesticides, and may provide health benefits for the consumer. Please click the link for an extensive list of references.

On the other hand, in 2010 in the American Journal of Clinical Nutrition, Dangour et al. interviewed experts, searched bibliographies, and checked peer-reviewed articles with English abstracts. They found a total of 12 studies that evaluated health effects following the use of organic compared with conventionally produced foods. The authors reported that the largest study showed a 36% reduction in risk for allergic eczema when children under two consumed organic dairy products. Other than that, the majority of the studies showed no differences resulting from organic foods versus conventionally produced foods in nutrition-related health outcomes.

In one sense, this is not surprising. A 2009 literature review by the same group showed that there were very few differences in nutrients between organic and conventionally produced foods. In crops, eleven nutrient categories were analyzed. Conventionally produced crops had a significantly higher content of nitrogen, while organically produced crops had a significantly higher phosphorus and more acidity. The other eight categories were not different between the two groups. An analysis of the database on livestock products found no differences in nutrients between organic and conventionally produced products.

This finding is supported by the UK Food Standards Agency which found that nutrient levels vary as a result of freshness, storage conditions, crop variety, soil conditions, weather conditions and how animals are fed, rather than as a function of whether the food is produced in an organic or a conventional manner. They caution that while single papers may show differences in the nutritional content of a particular food, it is important to evaluate the weight of evidence across a range of published papers.

An important consideration favoring organic food is that organically grown foods have about one third the pesticide residues as do conventionally grown foods. A study in elementary age children found that their urinary organophosphorus pesticide metabolites were significantly lower when a conventional diet was replaced by one with organic food items. However, chemical pesticides are not the only ones available. It is important to note that while organic farming does not allow the use of synthetic pesticides, it does permit the use of plant-derived pesticides including Bt, pyrethrins and rotenone, and all of these exhibit varying degrees of toxicity in humans.

Another concern is ecological rather than health-related. Organic farming requires more land per unit of food produced. Repeated use of soil for growing crops makes it necessary to use fertilizer. In place of chemical nitrates and ammonia, organic farmers must obtain and apply manure and use crop rotation with leguminous plants to return nitrogen to the soil. When soils are phosphate-depleted, conventional farmers can use highly soluble chemically-made superphosphate while organic farmers must use poorly soluble rock phosphate. These practices, along with the poorer efficiency of organic pesticides and the need to till the land frequently to prevent weeds, means that the production of food is up to 50% less efficient when it is done organically. (See Reference 15 here.)

Even if a country has plenty of land to devote to food production, there are a couple of other items that should be considered. The use of manure rather than chemicals as fertilizer introduces the presence of bacteria, especially in fruits and vegetables that are eaten fresh. Because organic food production does not use antibacterial techniques such as food irradiation or chemical washes, it is very important to wash organic foods before they are consumed. Finally, organic foods tend to spoil more quickly than their conventionally produced counterparts, which makes it necessary to buy them when they are fresh and to use them up quickly. This is especially important with grains, seeds and nuts which are liable to produce mold and its associated toxins.

As is frequently the case, I can't come down on one side or the other in the case of organic versus conventional food. Sometimes people have worries about the possible effects of agricultural chemicals. Sometimes they prefer the taste and smell of organically produced food. Sometimes they simply want to get back to a more natural way of living. If that's the case, and if they are aware that eating natural foods is not completely risk-free, then they should go ahead and buy organic food. But speaking from a scientific perspective, and looking at groups of people rather than at individuals, it's probably fine to buy and eat food that is produced in conventional ways.

Cheating

No, this blogpost won't address the ethics of writing out the answers for an exam on your hand. In the context of low-carb, cheating means going off the diet for a short time or for a long time.

One of the hardest concepts about low-carb dieting is that it's for life. Those of us who have dieted all our lives are used to losing weight, regaining it, and losing it one more time. We may have sets of "fat" and "skinny" clothes in our closets to accommodate this lifestyle. Unfortunately, low-carb doesn't work that way.

When we follow the low-carb lifestyle, we learn to eat meat, eggs and cheese for protein, green vegetables and berries for vitamins, and lots of delicious fat to give us energy. If we stay away from the carbs we find that our appetites are satisfied and we start to to lose weight. Our skin and hair improve, our HDL increases and our triglycerides decrease, our elevated blood sugars become less of a problem, and gradually even our blood pressure starts to come into a normal range.

But what if we step out of our normal routine? What if we go to a restaurant? It's easy to take a roll out of the bread basket or eat a few chips with the salsa that's on the table. And after the meal is over, it's hard to resist dessert, especially if there is a sugar-free version available.

The body is able to adapt to all sorts of things, and an indulgence once in a while probably doesn't hurt. Our paleo ancestors no doubt ran onto the odd honeycomb or patch of blueberries and were able to stuff themselves with no ill effects. The difference, however, is that in the paleo world, when the honey or the berries were gone, they were gone. In the 21st century, the restaurant is available several times a week and so are the rolls, chips and desserts.

For low-carbers, especially low-carbers with insulin resistance, this spells trouble. Eating moderate protein and relatively high fat does not protect a person from the effects of insulin unless that eating is done in the relative absence of carbs. Add carbs (and the rolls, chips and sugar-free desserts do have carbs) and insulin will be released. And as long as insulin is present, any excess calories will be converted to fat, which will be stored our fat cells and then kept trapped there until our blood insulin comes back to a low level. Even if a low-carber is able to convince himself that the cheat didn't count, that he "deserved" the cheat or that he really eats very few carbs on most days, his body will tell the tale.

The scale always fluctuates day-to-day, but as the rolls, chips and desserts become a more constant feature, eventually the fluctuations will start to trend upward. The low-carber may be able to brag that he fits into a certain size, and his mirror may lie to him about it for a while, but eventually the signs of "Dunlap's disease" (the belly done-laps over the belt) will become undeniable. Excellent lab values will start to return to their previous levels. It may be possible to get away with low-carb cheating in the short term, but not in the long term. Unlike the proctor on a test, the body is always paying attention.

What to do? That depends on the low-carber. First of all, we have to decide if sticking to the program is worth the effort. Were we happier when we were fatter but had fewer food restrictions? Are we able to live with a loss in overall health if that gives us the opportunity to eat certain types of food?

If the answer to both questions is yes, then it's our body and our life. Low-carbing is an individual decision, not a regime to be imposed on unwilling participants by a group of food Nazis.

If the answer to one or both questions is no, then it might be time to go back and remind ourselves why we've chosen this way of eating. We can make lists of what life was like before low-carb and what changes happened after. We can re-read the books by Dr. Atkins and the Drs. Eades as a reminder of what does and doesn't work on low-carb. We can get involved in one or more low-carb bulletin boards. We might search around the internet to find new blogs about low-carb and paleo eating to get a new infusion of energy. Or we could even start a blog to help give back to others what low-carb has given us.

Cheating happens. But it's within our power to decide if it continues to happen. I'm hoping that any readers who find themselves in a cheating situation will use this reminder to take the steps they need to, to get back on a happy healthy low-carb path, and to keep on keeping on.

Vacation!

Fun with Graphs

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

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



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



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



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



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



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



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



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

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



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



Total alcohol consumption has decreased, too.



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



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



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

Cortisol Versus Insulin

The man in the picture has insulin resistance and what the Heart Scan Blog" calls "wheat belly," right? Wrong. He has a hormone problem, but in this case the hormone isn't insulin, it's cortisol.

Insulin, which we discuss frequently on this blog, is a storage hormone. In response to ingestion of carbohydrates, and to a lesser degree of amino acids, the pancreas releases insulin. As a result, within minutes to hours, carbohydrates, amino acids and fats are stored after each meal.

Cortisol is a glucocorticoid hormone that is released from the adrenal glands in response to stress. The stress can be physical or emotional. The effects of cortisol in the body occur over hours to days and include suppression of the immune system, suppression of inflammation and an increase in blood glucose. When people survived by hunting, or when they were involved in combat, elevated cortisol would allow a person to ignore pain and illness in order to concentrate on the task at hand. It would also provide excess glucose in the blood, allowing the person additional energy to fuel the brain and muscles in extreme situations.

Both insulin and cortisol are powerful hormones. Too much insulin for too long will eventually result in insulin resistance, a condition in which more and more insulin must be secreted to produce normal insulin responses in tissues such as muscle, brain and liver. Too much cortisol for too long produces an increased risk of infection, reduced bone density, increased muscle weakness and excess glucose in the blood. Cushing's syndrome is the result of having excessively high cortisol for several years. Take another look at the picture at the beginning of this post. The patient looks like a person with metabolic syndrome, doesn't he? But this person actually has Cushing's syndrome.

Cushing's syndrome can be caused by an adrenal or pituitary tumor, or it may be the result of taking high doses of glucocorticoids for a long period of time. People who do not have these tumors and who do not take exogenous glucocorticoids do not have to worry about Cushing's syndrome, but the man in the picture does illustrate the point that there may be metabolic side effects from stress-induced hypercortisolism.

In a May 2010 review in the American Journal of Physiology-Endocrinology and Metabolism, Dake Qi and Brian Rodrigues described the effects of glucocorticoids on insulin-responsive tissues. Many of the studies in the review used dexamethasone, a synthetic glucocorticoid that is about 50 times as potent as cortisol and produces robust reactions in a short period of time. However, clinical experience with excess cortisol secretion supports these observations. At any rate, excess glucocorticoids will produce:

• Decreased glucose uptake and utilization in muscle and adipose tissue.
  
• Increased gluconeogenesis and glucose output by the liver.
  
• Increased triglyceride storage in the liver.
  
• Increased fatty acid uptake, fat synthesis and fat storage in adipose cells.

Readers of the previous post will recognize that these symptoms are consistent with insulin resistance. What makes it complicated is that there are many different molecules involved in insulin signaling, and each of these can be regulated on several levels. Any of the signaling intermediates can be synthesized more slowly or more rapidly, degraded more slowly or more rapidly, and activated or inactivated through phosphorylation or dephosphorylation by various kinases or phosphatases at numerous sites. These multiple levels of regulation mean that insulin resistance can be achieved through one mechanism when excess cortisol is involved and through another mechanism when excess insulin is involved. Consequently it is possible that both hormones working together can achieve more damage to insulin signaling pathways than one hormone acting alone.

Stress is able to produce a ten-fold increase in cortisol secretion. If the stress is chronic, it is possible that this alone could result in insulin resistance and eventually in the symptoms of the metabolic syndrome. This has been postulated by Anagnostis et al. in The Pathogenetic Role of Cortisol in the Metabolic Syndrome: A Hypothesis.

As we have noted, when primitive cultures adopt Western lifestyles, within about twenty years they can expect to begin experiencing the chronic diseases of Western civilization. While the carbohydrate hypothesis postulates that a diet of refined carbohydrates is the chief cause of insulin resistance and ultimately of the metabolic syndrome, it is also possible that the stress associated with the Western lifestyle is a contributor to insulin resistance. Stress and cortisol secretion are unavoidable, but in the absence of mammoth hunts and hand-to-hand warfare, those of us who wish to avoid the symptoms of insulin resistance would do well to avoid stress while also minimizing our intake of refined carbohydrates.

Insulin Resistance and the Metabolic Syndrome

The metabolic syndrome is a symptom set that includes the following: increased truncal obesity, high blood pressure, high blood glucose, low HDL cholesterol and high triglycerides. As anyone who has observed adults and even children in Western countries can confirm, the metabolic syndrome is becoming more and more prevalent. In Good Calories Bad Calories, Gary Taubes uses several lines of argument to show that one unifying explanation for the development of the metabolic syndrome is the prior development of insulin resistance.

Interestingly, one of the arguments Taubes does not use for his hypothesis is something called the "knockout mouse." The knockout mouse is not a small pugilist with boxing gloves. Instead, it is a genetically engineered mouse in which one or more genes have been turned off (knocked out) through targeted deletions. If we want to know what the effect of insulin is on a particular tissue, one approach is to delete the expression of the insulin receptor in that tissue.

The first attempt at an insulin receptor knockout mouse was to remove insulin receptor expression from the entire mouse. These mice were smaller than normal but were born alive at term. Shortly after birth they developed diabetic ketoacidosis and died. This was not helpful to the investigation of the relationship of insulin receptor signaling to various metabolic conditions, and the investigators moved on.

Because muscle insulin resistance is thought to be important in the development of type 2 diabetes, the next group of knockout studies involved mice that lacked insulin receptors specifically on muscle tissue. These mice had normal levels of blood glucose and plasma insulin. However, they had a 74% decrease in insulin-stimulated glucose transport into their muscle tissue. This caused blood glucose to be preferentially taken up by adipose tissue. Although these mice did not develop overt symptoms of diabetes, they demonstrated two of the features of the metabolic syndrome: increased fat mass and high triglycerides.

Another tissue targeted for insulin receptor deletion was the liver. By two months of age, the mice lacking liver insulin receptors had high levels of serum insulin but were were hyperglycemic in the fed state. To a great extent this was found to be attributable to the fact that insulin was unable to suppress the production of glucose by the liver. This suggests that hepatic insulin resistance is necessary for the onset of overt diabetes.

Because insulin receptors are widely distributed in the brain, investigators also developed a neural insulin receptor knockout mouse. The brains of these mice were normally developed, but the mice showed increased food intake and moderate diet-dependent obesity. It is known that the brain is able to regulate hepatic glucose production. When these neural-knockout mice were given exogenous insulin, they were only about half as effective as normal mice at suppressing hepatic glucose output.

Finally, the insulin receptor was uniquely deleted in the pancreatic beta cells of another group of mice. The investigators were expecting the pancreas to sense glucose concentrations directly rather than to use insulin signaling as an intermediary. To their surprise, mice that lacked pancreatic beta cell insulin receptors showed both a decreased ability to sense glucose and an insufficient secretion of insulin in response to glucose. Some, but not all, of the mice developed diabetes.

For those who would like to read more about these experiments, additional information can be found here and here. The use of insulin receptor knockout mice is a rather blunt instrument to determine whether insulin resistance can be implicated as the cause of the development of the metabolic syndrome. And mice are not people. Nonetheless, it is interesting to note that the deletion of insulin signaling in various tissues can produce obesity, high triglycerides, poor suppression of glucose output by the liver and both impaired pancreatic production of insulin and insufficient release of insulin in response to glucose.

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.

Food Nazis?

When low-carbers begin following the low-carb lifestyle, they start to feel free. Free of the hunger that forces them to eat every few hours even though they are morbidly obese. Free of enslavement to particular foods that they have never been able to resist. And after a while, free of many, many pounds of fat that they have been hauling around everywhere, all the time.

Low-carbing is an odd way to eat, but the freedom makes it worth the trouble of figuring out a new way to shop and a new way to eat out in restaurants. There are many low-carb bulletin boards and blogs for support. There is more and more scientific evidence demonstrating the superiority of low-carbing in the control of diabetes and heart disease and its efficacy in weight loss as well. The recent appearance of the paleolithic approach to low-carbing has given a common-sense aspect to the low-carb lifestyle. When observers object to low-carb food choices, low-carbers can point out that this is the way humans have eaten for millennia. It's only recently that humans began to eat lots of refined carbohydrates, and with that change in diet, perhaps not coincidentally, humans also began to experience the diseases of Western civilization.

So far, so good. But as I look back on my recent blogposts and those of other bloggers, I have started to notice a more rigid, regimented (shall we say Nazi-like?) aspect to the world of low-carbing. Some examples:

• It's good to eat fat, but be sure the fat has the right omega-3 to omega-6 ratio.
  
• It's good to eat nonstarchy vegetables, but remember that broccoli has goitrogens and tomatoes are nightshades. And wheat, even whole wheat, contains many compounds that can damage the human digestive tract.
  
• It's good to eat meat, but it should be grass fed, not grain fed.
  
• It's good to eat eggs and chicken, but they need to be free range.
  
• It's good to eat seafood, but watch out for the mercury.
  
• It's good to avoid sugar, but it's better to avoid artificial sweeteners as well.

The list could go on and on.

In the last couple of days I've noticed one low-carber who seems to be on the edge of dropping out because of the difficulty of following all the extra rules all at once. Another works 60 hours a week and is not sure he has the time required to be sure all his food meets the higher standards for healthy low-carb eating. A third concern is that, although low-carb foods tend to cost more than the Standard American Diet, the more strict versions of low-carbing become prohibitively expensive for people on a limited budget.

Low-carbing is literally a lifesaver for people who are on their way to diabetes, heart disease, and morbid obesity. Some people have additional health issues, and it is fine to refine the low-carb lifestyle to help address those needs.

However, it's important for low-carbers to remember that we don't need to sacrifice the good for the sake of the perfect. For those who are new to the low-carb lifestyle, or for those who don't have the concentration, the time or the money to pursue all the ins and outs of healthy eating, can I make a plea for mercy?

Let's not become low-carb food Nazis. Low-carbing is a gift. Please let people enjoy the freedom it provides. If they want to add additional aspects to it, fine. If not, we can rejoice that they are at least doing something that will significantly improve the quality of their lives. With that knowledge, we can follow our own set of dietary rules while giving other low-carbers the freedom to choose what additional modifications they will or will not follow.

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.