Thursday, July 31, 2008

Jimmy Moore Is Losing Weight!

Jimmy Moore is one of the "stars" of the low-carb movement. In 2004 he followed Dr. Atkins' New Diet Revolution and took his weight from 410 down to 230 pounds.

He wrote a book about it, Livin' La Vida Low-Carb, and launched a blog with the same title. Since then, Jimmy has started many more blogs, interviewed the movers and shakers in the weight-loss community and served as an inspiration for people who want to experience the satisfaction of losing weight successfully.

But all was not perfect in the world of Jimmy Moore. In December 2007 he began to do resistance training. Long story short--in the process of building up strength and muscle mass, Jimmy gained 30 pounds and couldn't seem to get rid of it. He has kept a current account of these adventures in his Low-Carb Menus blog.

Fast-forward seven months. Jimmy finally seems to have found a method that works. Here it is:

1. He has stopped eating desserts and low-carb products. Even though Jimmy always ate strictly low-carb, he counted net carbs. That meant that he subtracted insoluble fiber, soluble fiber, sugar alcohols, glycerin, maltodextrin, and similar low-glycemic-impact carbohydrates. He ate Atkins bars and Dreamfields pasta, as well as low-carb brownies, cookies, muffins, ice cream, chips and wraps. Except for insoluble fiber and possibly erithritol, eventually all of these carbs have to be dealt with as carbs. In order to store or metabolise them, the pancreas must release insulin. And when insulin is released, fat stays trapped inside fat stores and is not available for burning.

2. He is eating much less protein. Protein is important for building and repairing muscles. But eating protein also causes insulin to be released. It's important to eat enough protein to keep the body in good shape, but if too much is eaten, insulin levels stay high, and the excess protein can be converted to glucose through gluconeogenesis.

3. He is waiting about six hours between meals and is doing very little snacking. Eating low-glycemic-impact carbohydrates and protein every few hours keeps insulin levels elevated continuously. Eventually the insulin signaling system down-regulates itself, and the muscles, liver and brain gradually become resistant to insulin. Waiting five to six hours between meals allows insulin levels to decline to baseline or near baseline. This in turn permits hormone-sensitive lipase to mobilize fatty acids from fat deposits. The body can use free fatty acids for fuel while the insulin signaling system has a chance to reset itself.

4. He is eating fewer calories. One of the best aspects of low-carbing is that it's easier to count carbs than calories. In the initial stages of low-carb weight loss, the anorectic effect of ketosis and the satiety-producing effects of moderate protein and high fat all work together to limit the number of calories consumed without requiring much conscious effort on the part of the dieter. However, in the words of Robert C. Atkins, "I never said calories don't count." As weight is lost and as the body becomes more efficent at low-carb living, eventually it becomes necessary to become aware of the number of calories eaten versus the number of calories used for resting energy expenditure, activity energy expenditure and thermogenesis. The advantage of dieting the low-carb way is that when fewer calories are eaten, the body does not have to slow down its metabolic rate to conserve energy. Low carbs mean a low insulin level, which gives the body ready access to the energy it has stored in adipose tissue.

Jimmy Moore's experiences are his own, and may or may not apply to others who are trying to lose weight or maintain a weight loss. But they do provide real-world insight into how low-carbing works on a practical basis.

An Update (October 12, 2008)

Jimmy followed this regimen until the middle of August and took his weight down to about 255. He then joined Isabeau Miller's FitCamp for two weeks and began doing all sorts of vigorous exercise, which he has faithfully continued during the subsequent weeks. To avoid muscle weakness and exhaustion during workouts, Jimmy experimented with adding in healthy extra carbs. He also returned to eating his favorite low-carb products and began eating more often. Bottom line: On October 3 and again on October 11 Jimmy weighed in at 270 pounds.

It is commonly believed that increased exercise results in weight loss. In Jimmy Moore's case, increased excercise has twice resulted in weight gain. Some of the weight gain is undoubtedly muscle, but the correlation between significantly increased exercise and significantly increased body weight is surely a cause for concern. As Jimmy continues to use various approaches to return to his 2004 weight of 230, it will be instructive to see which strategies work for him and which don't.

Monday, July 28, 2008

Reactive Hypoglycemia

When we think about blood glucose, we usually think about hyperglycemia, or excess blood glucose. But sometimes we can have too little glucose in our blood. The symptoms are lightheadedness, anxiety, and hunger. Low glucose can even produce shakiness and heart palpitations. This post discusses one of the causes of low blood glucose, reactive hypoglycemia.

Reactive hypoglycemia is important because it can be one of the steps on the path to type 2 diabetes. It is one of the possible responses to a six-hour glucose tolerance test, illustrated in the graph above. The normal person, represented by the red line, has ingested a large bolus of glucose at zero hours. The beta cells of his pancreas have released the appropriate amount of insulin, and while the amount of glucose in his blood has spiked a little, within 2.5 to 3 hours it has come back into the normal range of 70-110 mg/dl, which corresponds to a value between 4 and 6 mmol/L on the graph above. Once the extra glucose has been safely stored, insulin levels decline and the liver takes over.

As discussed in the previous post, the liver can release its stored glycogen in the the form of glucose, and it can also make glucose by gluconeogenesis. Between meals, the liver uses these two processes to keep blood glucose in the range between 70-100 mg/dl or 4-6 mmol/L.

After a person eats carbohydrates, his liver shuts down its production of glucose via glycogenolysis and gluconeogenesis. That makes sense. If the person is ingesting glucose, why would he want to add more glucose to that amount?

When a person eats protein, the situation is a little different. Insulin must be released to store the amino acids building blocks of the protein. But insulin is nonspecific. As it promotes the storage of amino acids, it will also drive glucose from the blood. Without some compensatory mechanism, the process of storing the amino acids would also produce severe hypoglycemia. In steps the pancreas. This time the alpha cells of the pancreas release the hormone glucagon. Glucagon tells the liver to release some of its glycogen in the form of glucose. The liver also begins to do gluconeogenesis to make more glucose. Thanks to the liver, glucose levels can be maintained while insulin is busy telling the body to store its new supply of amino acids. Once the nutrients are stored, the liver goes back to its baseline functions and enables the blood sugar to continue in its normal range.

So far, so good. But as diabetes develops, the liver is one of the organs that becomes insulin resistant. When the liver becomes insulin resistant, its production of glucose becomes dysregulated. The liver can no longer turn off its glucose output in response to carbs, or regulate its glucose output properly in response to protein.

Think about that. The person with insulin resistance may not be eating carbs, but his liver is making carbs (that is, glucose) all the time. In order to control the resultant high blood sugar, the pancreas must produce more insulin. That will get the blood sugar down in the short term, but in the long term it will make the liver more insulin resistant. Eventually, still more unwanted glucose will be produced by the liver, and even more insulin will need to be released by the pancreas.

In the process, the pancreas itself starts to suffer insulin resistance. It releases insulin erratically. Sometimes it allows the blood sugar to go too high. At other times the pancreas overshoots the required amount of insulin and the blood sugar drops too low. This leads to the phenomenon called reactive hypoglycemia, which is shown in the black line in the graph above. The person represented by the black line has ingested a large amount of glucose, but his pancreas has responded by releasing too much insulin, and his blood glucose has fallen below the normal range. Over time, reactive hypoglycemia can eventually progress and intensify to the condition of the person represented by the brown line, which is prediabetes.

We tend to think of type 2 diabetes as a condition characterized by high blood sugar. It is, but for many people, one of the steps on the road to type 2 diabetes is actually low blood sugar. If a person is not a diabetic but is experiencing episodes of low blood sugar, it might be time for him to consult a physician. It could be a important warning sign and an indication that he might need to make some changes in his lifestyle.

The figure is from the Hypoglycemic Health Association of Australia.

Wednesday, July 23, 2008

Glucose, Glycogen and Gluconeogenesis

We have glucose in our blood at all times. Where does it come from?

The first and most obvious source is from the carbohydrates in our food. Most of the complex carbs we eat, from sugar to pasta, can be broken down into glucose monosaccharides and will be absorbed into the circulation in that form. The illustration above is taken from page 329 of Lippincott's Illustrated Reviews-Biochemistry. It shows the effect of a meal of 100 grams of pure glucose. The large spike of glucose is metabolized or stored within about three hours.

If we do not eat any more food after that 100 grams of glucose, our blood glucose levels nevertheless must be maintained. If we are well-fed, our livers store about 80-100 grams of glucose as glycogen. The liver is able to convert glycogen back into glucose by means of a process called glycogenolysis. The blue line on the graph shows that, over the next few hours, the liver releases glucose back into the blood on an as-needed basis.

What if we continue to fast? Eventually, we run out of liver glycogen. If you look at the green line in the graph, you'll see that it gradually rises. This line represents gluconeogenesis, which we have discussed before. In the absence of ingested carbohydrates, and even after our liver glycogen is depleted, our liver is able to make glucose out of glycogenic amino acids and the glycerol backbones of fatty acids. It takes several hours or even days for this process to ramp up.

What if we are not fasting but are simply low-carbing? The ramping-up of gluconeogenesis is one of the reasons that people who are new to low-carbing experience something called the "Atkins flu" when they start eating 20 grams of carbs or less per day for the first time. They are not starving, but their bodies have to get used to manufacturing new glucose out of amino acids and glycerol rather than absorbing ready-made glucose from the gut. Once gluconeogenesis is established, our bodies can readily make glucose from the protein we eat.

However, even when it is well established, gluconeogenesis is not a quick-response system. Because it takes us several hours to digest a protein meal into its constituent amino acids, followed by more time to convert the amino acids into glucose, the process of gluconeogenesis is relatively slow. However, the glucose we produce can be used to replenish the glycogen in the liver, and liver glycogen is a quick-response system.

Once we are adapted to a low intake of carbohydrates, we have two means of stabilizing our blood sugar. Gluconeogeneis provides a baseline of glucose production from the protein we eat. Because the fuel needed for gluconeogenesis ebbs and flows, the new glucose made by this process ebbs and flows. Fortunately our stored liver glycogen is available to make up the difference, assuring a steady stream of glucose for baseline functions for our brain, red blood cells and other tissues that require glucose as fuel. If we need an extra burst of energy, or if a big protein meal causes our insulin to spike and our glucose to plummet, our stored liver glycogen is also there to step in the gap and provide the glucose necessary to keep our blood glucose within normal limits.

When we first start low-carbing, it's hard to understand that (if we choose to) we never need to eat another gram of carbohydrate again. But once our good friend the liver is adapted to the process, it can provide all the carbs we need through gluconeogenesis and glycogenolysis.

Tuesday, July 22, 2008

Comfort Food

Even though the media and the medical commmunity have generally been skeptical of the low-carb lifestyle, many people now know that low-carbing is a healthy way to live and an excellent way to lose weight.

But what about people who know that low-carbing is a healthy lifestyle and DON'T choose to follow it, even though the consequences are significant? Why would they go ahead and indulge in food that is high in carbohydrate and low in nutrition instead of being careful about their food choices? Specifically, how can a person deliberately choose:

  • Comfort food plus diabetic retinopathy (i.e.,blindness)?

  • Comfort food plus erectile dysfunction?

  • Comfort food plus a lifetime of diabetes medication?

  • Comfort food plus death from heart disease?

  • Comfort food plus a degree of obesity that puts their livelihood in jeopardy?

People who understand low-carbing, understand that low-carbing has a good track record of improving all of those health conditions. In light of that, why do so many of them either not follow or stop following the low-carb lifestyle? The answer could be serotonin. Serotonin is a neurotransmitter, or signaling molecule, found in the brain. It has many actions, but one of them is modulation of mood. If we don't have enough serotonin, one result is that we can become depressed.

Serotonin is manufactured in our bodies from a large neutral amino acid called tryptophan. Tryptophan is one of the amino acids found in the protein we eat. So if we're depressed, why can't we just eat more tryptophan to drive the production of more serotonin?

As you might expect, it is not that simple. Tryptophan is too large to diffuse into the cells in our brain by itself. For our brain cells to take it up, tryptophan must be carried into the cells by means of a transporter. The problem is, tryptophan has to compete for transport with the other large neutral amino acids--phenylalanine, tyrosine, isoleucine, leucine and valine. Tryptophan tends to get lost in the shuffle.

How, then, can we get extra tryptophan into our brain? Amazingly, the answer is insulin. If we eat a meal or a food high in carbohydrate, insulin will be released and will sweep the other large neutral amino acids out of the blood and into our muscles. However, tryptophan is different. It will tend to stay behind and bind to albumin in the blood. But once the albumin-bound tryptophan reaches the capillaries of the brain, the transporters there will be ready to take up the tryptophan, increase the brain concentration of it, and drive the synthesis of serotonin. The result? A pervasive feeling of sleepiness and contentment.

For people who are anxious or depressed, this is a hard feeling to walk away from. What if we knew that a temporary fix for our bad feelings was right inside the freezer or refrigerator or cupboard? No prescription necessary. The comfort food found in our pantries might not be the best choice for us in the long run, but we have to realize that sometimes our eyes won't stay focused on the long run. The bad feelings will come. The comfort foods will always be available. Recognizing that, this might be a time for all of us good low-carbers to sit down and plan a strategy that provides comfort when we need it, but doesn't rely on comfort food.

Saturday, July 19, 2008

Is the Tide Turning?

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

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

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

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

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

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

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

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

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

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

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

Wednesday, July 16, 2008

Fructose II

Sucrose, also known as table sugar, is a disaccharide. In the gut, it is split into its constituent monosaccharides--glucose and fructose. Sucrose is frequently replaced by high fructose corn syrup (HFCS) in commercially prepared foods and soft drinks. High fructose corn syrup is a mixture of about 45% glucose and 55% fructose. You probably knew all of that already.

The important thing about sucrose and HFCS is that they are the main sources of fructose in the American diet. As we saw in the previous post, when fructose is metabolized in the liver, it is most likely to be broken down into glycerol 3-phosphate and acyl-coA, which are then assembled into triglycerides, i.e., fat.

Eat fructose, create fat. But that's not the end of the story. Fructose increases glucose metabolism in the liver by mobilizing an enzyme called glucokinase. The liver takes up more glucose than it normally would, and the excess glucose is also synthesized into fat.

In addition to fructose-induced lipogenesis, other long-term effects of fructose have been observed in experimental animals and in humans. Although fructose produces a very small insulin response, long-term use of fructose nevertheless induces insulin resistance, which eventually results in fructose-induced hypertension. Somewhat surprisingly, the low concentration of insulin released after fructose ingestion also means that there is a low satiety response to fructose. It is possible to consume a great deal of fructose without feeling full. Finally, fructose is 10-17 times more effective than glucose in producing Advanced Glycation Endproducts--the crosslinked matrix of proteins and sugars that accumulates in our tissues and stiffens them.

In 1960, the average American consumed approximately 110 pounds of sweeteners per year, mostly in the form of cane and beet sugar. Since then, the use of table sugar has declined, but the use of high fructose corn syrup has more than replaced it. Americans now consume an average of over 140 pounds of sweeteners per year. Because half of those sweeteners by weight is composed of fructose, the potential negative health effects are worth serious consideration.

If you're interested in learning more about fructose metabolism:

Sunday, July 13, 2008

Fructose--Not as healthy as it appears to be

What if there was a food that could easily be converted to fat in your body? You would think that that food would be on the list of substances to avoid among those who are weight-conscious. You would be wrong.

Fructose is the sugar is found in most fruits. Like glucose, it is a simple sugar, but our bodies handle fructose in a special way. Look at the diagram below, which appears in Fructose, weight gain, and the insulin resistance syndrome by Sharon Elliot and coauthors.

The metabolic pathways for glucose are on the right side of the diagram. Note that there are many steps between glucose and the final product in this figure--acyl glycerols (triglycerides) which are packaged into VLDL (Very Low Density Lipoproteins) and sent out into the body for storage as fat. Depending on the body's needs, glucose can be used for energy via glycolysis and the citric acid cycle, and it can be stored as glycogen. If glucose is present in excess, it can be converted to triglycerides in the liver, but that is only one of many options.

For fructose, there are fewer choices. Fructose by itself does not stimulate insulin release. If insulin is low and glucagon is high, fructose can enter the gluconeogenesis pathway and be turned into glucose. But we seldom eat pure fructose. If we eat fructose with other carbohydrates, or if we eat it in the form of table sugar, the more likely situation is that insulin will be high and glucagon will be low. This will direct the fructose to be converted into the intermediates for fatty acid synthesis, and then into triglycerides. The result will be a phenomenon called fructose-induced lipogenesis.

Photo of apples:

Thursday, July 10, 2008

Reversing Insulin Resistance

It is commonly thought that weight loss is required to reverse insulin resistance. A small study of obese type 2 diabetics indicates that this may not be the case. Ten diabetic patients, seven of whom were on diabetes medications, checked into a hospital with an average weight of 252 pounds. For seven days they acted as their own Control group. They ate their normal diets, averaging 3111 calories and 309 grams of carbohydrate a day. On day 7 their blood glucose and blood inuslin levels were measured over a 24 hour period. The time course of glucose and insulin is represented by the black circles in the graphs below.

On day 8 the patients remained in the hospital and became the Low-carbohydrate diet group. They were switched to a low-carbohydrate diet which included 21 daily grams of carbohydrate, plus as much fat and protein as they desired. Adherence to the low-carbohydrate diet was confirmed by measurement of urinary ketones. After two weeks on this diet, blood glucose and blood insulin levels were again measured over a 24 hour period. The time course of glucose and insulin after two weeks of eating low-carb is represented by the blue circles in the graphs above. (For the sake of reference, the 6mmol/L Glucose Level is roughly equivalent to a glucometer reading of 100 and the 8 mmol/L Glucose Level is roughly equivalent to a reading of 150.)

There were no set mealtimes, so all of the curves are fairly flat. Nevertheless, it is easy to see that a diet of 309 grams of carbohydrate a day produced high glucose levels around the clock and high insulin levels during waking hours. By contrast, just two weeks of eating 21 grams of carbohydrate a day brought blood glucose levels to a normal range and kept insulin levels low both during waking hours and at night.

Other measures of insulin resistance reflected the values shown in the graphs. In just two weeks on the low-carbohydrate regimen, glycosylated hemoglobin fell from 7.3% to 6.8%. Insulin sensitivity improved by approximately 75%, while plasma triglycerides decreased by 35% and cholesterol levels decreased by 10%.

During the last two weeks of the study, patient weights also decreased by an average of 1.8%. Although it might be possible to attribute the large improvement in lab values to this small decrement in weight, it seems more likely that both the weight loss and the rapid improvement in insulin resistance was attributable to the patients' adherence to a low-carbohydrate diet.

Monday, July 7, 2008

Low-Carb at the Movies

Analyst Maxwell Smart is briefing agents at the secret U.S. government spy agency CONTROL. What does it mean, he asks rhetorically, that agents at the enemy terrorist organization KAOS have been overheard discussing muffins?

His answer: "Muffins are comfort food. Why would they eat comfort food unless they were nervous about something?"

Hmmm. Where did that come from? In this summer's theater version of the old TV series, "Get Smart," we learn that that the handsome and heroic secret agent Maxwell Smart was once very fat. When his partner, Agent 99, tells him that she used to look like her mom, Max responds, "I used to look like two of my moms, put together."

Flashbacks show us that, in order to advance from analyst to agent, Smart had to lose 150 pounds. And how did he do it? By low-carbing. References to low-carbing and to the fact that big people have feelings, too, abound throughout the movie.

Would-you-believe that low-carbing has again reached the mainstream? Probably not, but seeing it discussed in a serious way on the big screen is certainly is an encouraging development.

Friday, July 4, 2008

Metabolic Syndrome

In several recent posts we've mentioned something called "metabolic syndrome." What is metabolic syndrome?

Metabolic syndrome is not a disease, but rather a set of symptoms that frequently appear together in patients as they grow older. Typically these symptoms include obesity, low HDL cholesterol levels, high triglyceride levels, high glucose and insulin levels, and high blood pressure. As these symptoms worsen, patients with metabolic syndrome frequently progress to type 2 diabetes and cardiovascular disease. If we could somehow prevent or reverse the symptoms of metabolic syndrome, it seems logical that we could correspondingly decrease the incidence of type 2 diabetes and cardiovascular disease.

Obesity is one of the characteristics of metabolic syndrome. Because obesity is easy to observe, it is commonly assumed that metabolic syndrome is caused by obesity. However, a careful inspection of the markers associated with metabolic syndrome reveals that they are all related to insulin resistance.

While weight loss will relieve some of the symptoms of metabolic syndrome, weight loss is notoriously difficult to accomplish and even harder to maintain. The good news is that carbohydrate restriction, even in the absence of dramatic weight loss, is effective in alleviating all of the aspects of metabolic syndrome.

In a study published in the New England Journal of Medicine, 63 obese patients were assigned to a low-carb/high-fat/high-protein diet or to a high-carb/low-fat/low-calorie conventional diet. They were given little follow-up to mimic typical dieting conditions. The graph above summarizes the findings. Light blue bars represent low-carbers at 6 months and dark blue bars represent low-carbers at 12 months. Light red bars represent high-carbers at 6 months and dark red bars represent high-carbers at 12 months.

Although the low-carb group lost more weight than the high-carb group, at 12 months the difference was not significant. The low-carb group experienced a slight decline in systolic blood pressure while the high-carb group experienced a slight increase. HDL cholesterol was significantly higher and triglycerides were significantly lower and in the low-carb group at 12 months. Finally, there was less insulin released in the low-carb group at 6 months, though the difference was no longer significant at 12 months.

Jeff Volek and Richard Feinman have compiled a review of over 30 dietary studies, tabulating the effects of carbohydrate restriction on the markers associated with metabolic syndrome. As we might expect, some studies show great differences and other show little or none. However, taken together, the studies show that while both low-carb diets and conventional diets are associated with an overall decrease in weight, low-carb diets also typically produce the following
  • an increase in HDL cholesterol
  • a decrease in triglycerides
  • a decrease in glucose levels
  • a decrease in insulin levels
  • a decrease in blood pressure

In other words, a review of the scientific literature shows that dietary carbohydrate restriction is a reproducible way to improve the features of metabolic syndrome.

Tuesday, July 1, 2008

Roots and Branches

What are the diseases of civilization? Measles? Whooping cough? AIDS?

No--you can get all of those diseases without being civilized!

The diseases of civilization are conditions that appear in indigenous populations within about 20 years of significant contact with Western culture. They include dental caries, ulcers, gallstones, appendicitis, diverticulitis, constipation, obesity, asthma, varicose veins, diabetes, high blood pressure, cardiovascular disease, stroke and cancer. Early twentieth century missionaries from Albert Schweitzer in Africa to Samuel Hutton in Labrador noticed that prior to Western contact, these populations experienced such diseases rarely if at all. However, as decades passed and the local people began to adopt Western culture, inevitably Western diseases would gradually appear and eventually become prevalent.

Western civilization brought modern medicine and good public health practices. Why should it also bring poor health? It is possible that an increase in smoking, a decrease in physical activity, high fat consumption and resultant obesity explain why local populations became progressively less healthy over time. However, another explanation is that arriving Westerners brought with them foods that would not spoil over long ocean voyages. White flour, white rice and sugar do not provide much in the way of vitamins and minerals, but they keep well, are fairly cheap, contain necessary calories, and taste very good. They are also rich in easily digestible carbohydrates.

(Illustration inspired by Dave Hatch of Green Bay, Wisconsin)

Look at the tree above. In the branches are many of the diseases of Western civilization. Conventional wisdom says that obesity is at the root of the tree, and that obesity results from too much food and too little exercise. In the tree above, however, we see refined carbohydrates as the root cause. Too much carbohydrate leads to too much insulin release and too much insulin leads to a host of symptoms which eventually manifest themselves as the diseases of civilization. What is the root cause of these diseases--obesity or an excessive intake of carbohydrates? A lot depends on which answer is the correct one.