Weight Regain

You've worked hard. You've lost all that weight on a low-carb lifestyle, and now you're going to gain it all back, right? Not necessarily.

A couple of studies indicate that those who stick to a low-carb lifestyle have a reasonable chance of maintaining at least part of their weight loss. The National Weight Control Registry (NWCR) tracks over 5,000 individuals who have lost significant amounts of weight and kept it off for long periods of time. Most of these people have lost weight on low-calorie diets, but some have lost it on low-carb. In 2007 the NWCR reported a comparison of 96 low-carbers with 795 others, all of whom had lost at least 30 pounds and had maintained a weight loss for a year. At three years the low-carbers regained an average of 15.4 pounds and the others had regained 12.5 pounds, which was not a significant difference.

In 2005, AV Nielson and colleagues compared the efficacy of a low-carb versus a high-carb diet in the control of body weight in diabetic patients. At six months the low-carb group had lost an average of 25 pounds and the low-calorie group had lost an average of 4 pounds. In a followup paper published in 2006, Nielson reported that 7 of the 16 original low-carb patients retained the same bodyweight from 6 to 22 months or reduced it further, and all but one of the sixteen had lower weight at 22 months than at their entry into the study, even though they were not being closely monitored after the initial study was completed. For people who have lost weight successfully on low-carb, that's a very encouraging result.

Low-Carb Is Also Good for Weight Loss

People who follow the low-carb lifestyle report that they feel better when they are doing low-carb. But do they also lose weight?

A study published in March 2007 in the Journal of the American Medical Association says that they do. The A to Z Weight Loss Study, where "A" represents Atkins and "Z" represents Zone, compared those two diets as well as the standard American diet (called LEARN) and the Ornish diet. 311 free-living, overweight/obese (body mass index, 27-40) nondiabetic, premenopausal women were randomized into the four diets and were followed for a year.

The graph above shows clearly that the group doing the Atkins low-carb diet had significantly greater weight loss at 6 months and 12 months than all of the other three groups.

Two other items are interesting. The first is that at 12 months, the Atkins low-carb group had lower systolic and diastolic blood pressures, lower blood glucose, lower triglycerides and higher HDL (good) cholesterol than the other groups, although the differences did not always reach statistical significance. To see a table of the actual numbers, look here.

The second interesting item is that 88% of the women who did the Atkins low-carb diet completed the study. By contrast, the 12-month retention rate among each of the other three groups was about 77%. One of the commonly-used objections to low-carb dieting is that people won't stick with it. In the A-Z Study, over the course of a year, the Atkins low-carb group retained more of its subjects than the groups following the Zone diet, the LEARN diet or the Ornish diet.

Why Should We Low-Carb?

This post is not about science. It's about anecdotes. But occasionally anecdotes can give us valuable insights.

Many of us think that low-carb eating is primarily a way of losing weight. Anybody who has tried a low-fat low-calorie diet is aware of how hard it is to stay on such a diet. We get hungry, we lose energy, and very often we don't lose much weight.

By contrast, in most cases a dedicated low-carber can lose significant amounts of weight without a great deal of hunger. However, the sad truth is that no matter how we may have lost our weight, statistically we are almost sure to regain it. If that's true, why should we bother with a low-carb diet at all?

I'm a member of an Atkins-related board on Yahoo. Over the years I have noticed that most of the members of this board have lost some weight by doing Atkins, but very few of them have actually reached and maintained their goal weights. When I asked the members of the board why they continue to do low-carb I received these answers.

• One woman said that she had lost 70 pounds. She is still 30 pounds from her goal weight, but she has maintained the 70 pound loss for 5 years. Her back problems and reflux have vanished, and she doesn't get sick all the time. She says she has energy and has never been this healthy.
  
  
• Another said that she has lots of hormonal problems, and by doing low-carb, she is at least not gaining weight.
  
  
• A third woman said, "I am no longer considered a diabetic (no more meds for it either!) I no longer have high blood pressure (no more meds for that either), I no longer have any signs of sleep apnea (no more c-pap), I CAN (don't like it) do some exercising... I will never be a runner- I don't want to, don't like it and that is my choice so I will never run in a marathon. :) But I do walk - a lot, which I couldn't do before."
  
  
• Almost everybody said that they feel better when they do low-carb.

Next I went to a bulletin board called Low Carb Friends. They saw similar benefits from following the low-carb lifestyle, and added a few more to the list.

• Lowered cholesterol, triglycerides and blood pressure
  
• Stabilized blood sugar
  
• Better skin, hair and nails
  
• Fewer aches and pains
  
• No heartburn
  
• No acid reflux
  
• Fewer colds
  
• No more sleepy feeling in the afternoon
  
• Better sleep at night
  
• Better stamina

Are these results guaranteed for everybody? No. But there are definitely more benefits to the low-carb lifestyle than simple weight loss.

More on Tim Russert

Since Tim Russert's untimely death on June 13, 2008, more information about his medical history has come to light.

According to Tim's physician, Dr. Michael Newman, we know that Tim had these findings:

Fasting blood glucose=104 (Normal is 70-100)
Hemoglobin A1c=5.7 (Normal is 4-6)
HDL (the "good cholesterol")=37 (Normal is greater than 40)
LDL (the "bad cholesterol)=68 (Normal is less than 130)
Elevated triglycerides
Increased waist circumference
High blood pressure, controlled by medication
Heart scan=210 in 1998 (The score should be zero)

Tim did not have diabetes, but his fasting blood sugar was elevated. His HDL was low and his triglycerides were high. This indicates that he ate a relatively high percentage of carbohydrates in his diet. He was overweight and had high blood pressure. Taken together, these findings suggest that Tim Russert was starting to experience metabolic syndrome, a condition which includes elevated fasting blood glucose and insulin resistance.


The picture above illustrates some of the damage discussed in the previous post, describing what elevated blood glucose and insulin do to the interior of our arteries. They produce fat and cholesterol deposits, promote smooth muscle thickening, cause oxidative damage and make the arteries stiffer because of AGE (Advanced Glycation Endproduct)-related damage. If the carbohydrate hypothesis of heart disease is correct, Tim Russert was a prime candidate for a heart attack, not a person whose sudden death from cardiac arrest should have come as a surprise to his physician.

----------------------
In case you're interested, several other bloggers have written about the issues raised by Tim Russert's untimely death:
Jackie Eberstein, R.N.
Jimmy Moore
William Davis, M.D.

What Causes Coronary Artery Disease?

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

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

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

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

Tim Russert and Sudden Cardiac Arrest

Tim Russert, for many years the host of NBC's Meet the Press Sunday morning show, died suddenly on June 13, 2008. Michael Newman, Tim Russert's physician, said in an interview that the 58 year old newsman had died of coronary artery disease. This was surprising because his blood pressure was well controlled and his cholesterol fractions were optimal. Dr. Newman said that Tim had shown a high level of stamina on his stress test on April 29th, worked out regularly, and had done so on the morning of his death.

According to Dr. Newman, the postmortem on Tim Russert showed that, although Tim had been asymptomatic, he had significant heart disease, particularly in the left anterior descending coronary artery. Tim had a sudden rupture of a cholesterol plaque in the wall of that coronary artery. This produced a large clot which lodged in his heart, caused ventricular arrhythmia and took his life.

Could this have been avoided? Tim Russert had the best of medical care and tried to follow good health practices. The American medical community recommends regular exercise and keeping blood cholesterol low by eating sparingly of fat- and cholesterol-containing foods and by taking cholesterol-lowering medications if dietary measures are not sufficient. Americans have, in fact, been following these recommendations, and there has not been a large decline in the incidence of heart disease. There has actually been a slight increase in the incidence of heart disease, despite the fact that more and more Americans are also giving up smoking.

We cannot know if Tim Russert's health choices were the proper ones for him. Indeed, they might have enabled him to live longer than he would have lived without them. However, it is important to consider that there is an alternative to the cholesterol-lipid hypothesis for the incidence of heart disease. We'll look at that in the next post.

Glycosylation and Glycation

Two more big words.

When proteins are assembled in our cells, sometimes specific sugar molecules are attached to them in carefully-defined ways. This is called "glycosylation." Enzymes add the sugar molecules to help proteins fold properly and to route proteins to various places inside and outside the cell. Glycosylation patterns also help our bodies to distinguish proteins that are "self" versus "not-self" and are useful in immune responses. Glycosylation results from controlled reactions and is important for our biochemical wellbeing.

When we have glucose in our blood (and if we're alive, we do), sugar molecules are also added to proteins in a random fashion. The random addition of sugar molecules to proteins is called "glycation." If only single glucose molecules have been added to a protein, when the blood sugar level drops, the glucose can detach and the protein will again be normal. But if blood glucose remains high, more sugars will be added. These will rearrange and crosslink, eventually producing something called an Advanced Glycation Endproduct or AGE. One example of an AGE is hemoglobin A1c, the form of hemoglobin found elevated amounts in the red blood cells of poorly-controlled diabetics. Evidence suggests that many other proteins in our bodies are also converted into Advanced Glycation Endproducts by elevated blood sugar. Glucose and fructose in the blood interact with and crosslink these other proteins in our bodies, forming AGEs that accumulate in our eyes, kidneys, arteries, nerve endings, joints and skin.

Although our bodies have mechanisms to cope with the identification and disposal of AGEs, the AGEs gradually accumulate and stiffen our tissues. The elasticity of youth is slowly replaced by the physical degeneration of old age. In other words, crosslinked AGE proteins produce in us the symptoms we associate with old age. This happens in all people, but the process is made worse and happens more quickly in the presence of high blood sugar.

(The illustration is taken from the cover of the journal Science, March 23, 2001.)

Glycemic Index

What happens if a large percentage of your diet consists of bread, potatoes, gravy, corn, sugary soft drinks and desserts? How could that contribute to obesity and type II diabetes?

The key to this question comes from understanding the Glycemic Index or GI.

The glycemic index of a food is measured by having a person eat a certain amount of that food and measuring how much of the carbohydrate in the food is converted into glucose in the blood within two hours. If a food has a high glycemic index, it will raise blood glucose very rapidly. If it has a low glycemic index, it will raise it slowly. In general, the higher the glycemic index, the more insulin your pancreas will have to secrete in order to bring your blood glucose reading back into the safe and normal range.

If pure glucose has a glycemic index of 100, a baked potato has a glycemic index of 111. Kellogg's Corn Flakes have a glycemic index of 92. Wonder Bread has a glycemic index of 73. Coca Cola has a glycemic index of 58. Beef, chicken and fish have a glycemic index close to zero.

It used to be thought that simple carbohydrates (like the high fructose corn syrup in Coca Cola) raised blood sugar quickly and complex carbohydrates (like the starch in potatoes) raised it slowly. From studying the glycemic index of various foods, we now know this isn't true. If you want to raise your blood sugar rapidly and release a large amount of insulin in response, eating significant quantities of any carbohydrate will do it for you. That's fine as long as your muscles and liver remain insulin responsive. But when they start to become insulin resistant, your blood sugar will go higher than it should and will stay elevated for longer than it should. Your pancreas will have to secrete more insulin to keep your blood sugar levels under good control. As we have seen, hyperinsulinemia is hard on our bodies. Hyperglycemia is hard on our bodies, too. Unfortunately, it's a Catch-22.

Obesity Can Fool You

When you look at a fat person, what do you see? Somebody who eats too much? Somebody who exercises too little? Do you ever think that you might be looking at a person who is suffering from internal starvation?

We live in a society where the tastiest, cheapest, easiest-to-obtain calories come from carbohydrates. If you look around, the poorest among us are also the fattest. They eat breaded meats, casseroles, potatoes, gravy, rolls, corn, sugary soft drinks and desserts. Because they are poor, they often work jobs that require manual labor, but the extra exercise does not seem to keep them from becoming obese. They suffer from increased rates of heart disease, high blood pressure and Type II diabetes. Is it possible that it is not their lifestyle, nor the amount of food they are eating, but the type of food they are eating that is putting them at risk? Is it possible that they are giving their bodies empty calories (delicious calories, but empty calories nonetheless) and in exchange are becoming both obese and unhealthy?

(The illustration is made of screen captures from http://www.youtube.com/watch?v=Cs3ZNLQhe40 by Svegen.)

Internal Starvation

We've learned in the previous two posts that insulin is necessary to maintain life. Insulin is your friend. We've also learned that some of us develop a condition called insulin resistance. In insulin resistance, the food we eat is not stored properly. Our pancreas responds by producing more insulin, and the food does get stored. In the case of fat, there is a complication. The food is stored properly, but the additional insulin makes it very difficult to get the fat back out of storage. Our bodies are not able to use all of the calories in the food we eat. As insulin levels rise, a percentage of what we eat is stored in our fat cells and stays there. Calories in no longer equal calories out and we begin to put on weight. Insulin is becoming our enemy. We are starting to experience internal starvation.

Imagine that a penny equals a calorie. Imagine that the only grocery store in town is your body. If you took $20.00 (2000 calories) to the grocery store every day to buy food, you would expect to receive $20.00 (2000 calories) worth of groceries. But what if the stockers in the store became "resistant" to managment and decided to change the rules? What if they decided that you would only get $18.00 (1800 calories) worth of food to use for yourself? The stockers would keep the other $2.00 (200 calories) worth of groceries stacked in the corner, but they wouldn't let you get to it. Eventually you would grow angry because you would see all that unavailable food stacked in the corner.

You might decide to cut back your budget and spend $10.00 (1000 calories) a day on groceries instead. The store would keep $1.00 (100 calories) worth of groceries and would allow you to have $9.00 worth of food. Groceries would still stack up in the corner, but at a slower rate, and you would find that you're getting hungry. Say you get tired of that and decide to spend $25.00 (2500 calories) a day on groceries for a while. You aren't hungry any more, but now the store keeps $2.50 (250 calories) worth of your groceries and the stack in the corner grows even faster.


You have figured out by now that the stack of food in the corner represents fat deposits. If you are experiencing insulin resistance, you can eat a little or eat a lot, and the fat deposits grow slowly or they grow quickly, but in the long run they always grow. With insulin resistance, even if you have iron willpower and eat exactly as many calories as you should for your height, weight and metabolic level, you will experience internal starvation. You end up looking fat on the outside, but at the same time your cells are starving for proper nutrition on the inside. You are experiencing internal starvation.