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Dana Carpendar at Hold the Toast blog recaps the results of an interesting study in the Archives of Internal Medicine:

47% of the low carb group had their blood pressure medication discontinued in the course of the study, as compared to 21% of the low fat group. Dr. William Yancy, who ran the study, said the difference in the two groups might have been even greater had subjects remained on their blood pressure medication, but they instead took people off medications as their readings normalized.

The study started the low carb group at the true low carb level promulgated by the Atkins diet, 20 grams per day. Far too often, studies comparing low carb diets to low fat diets use 100 or more grams per day of carbohydrate. The study lasted nearly a year, long enough for true differences in the diets to be seen. For the low fat diet group, the study added a common diet drug, orlistat, a drug that sequesters fat so it can be eliminated before being absorbed by the body.

Weight loss for the two groups is statistically insignificant, even though some low carbers have pointed to the results proudly. The small sample size and small difference in the number of pounds lost between the two groups just doesn’t lend itself to proclaiming any victory for the low carb diet. But the study does show the low carb diet is the equal of a low fat diet in nearly every respect. The study’s Abstract points this out.

No matter what you read, the main benefit of a low carb diet in this study was that it matched the low fat diet in nearly all areas, and was superior in controlling high blood pressure:

Conclusion: In a sample of medical outpatients, an LCKD [low carb ketogenic diet] led to similar improvements as O + LFD [orlistat plus low fat diet] for weight, serum lipid, and glycemic parameters and was more effective for lowering blood pressure.

It would be interesting to see how the participants felt about their low carb or low fat diet. My experience has been that the low carb diet is much easier to maintain, as I rarely struggle with hunger even while losing weight.

And, I love bacon.

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Dr. James Carlson is a board certified family physician with multiple degrees … biochemistry and molecular cellular biology from Cornell University, an MBA from Regis University, and a Juris Doctorate from Concord University. And that’s in addition to his medical education at the NY College of Osteopathic Medicine. Dr. Carlson is one of those smart guys I like, one that, like Dr. Eades, has actually had a medical practice with real patients and real mysteries to solve.

His blog post today covers a subject that many low carb dieters wonder about: for some reason, they stop losing weight, even though they have not increased their carb intake. In forums, these people are often told they are “cheating”, perhaps without knowing it. But I’m always struck with how much this kind of “advice” resembles the justifications for the failed low-fat diet: if you can’t stay on the diet, its your fault.

Dr. Carlson does a good job of describing a situation where protein can be made into glucose:

Ok, so back to protein. Yes, one can definitely over consume protein, allowing the glucogenic amino acids to be converted to glucose, this can cause a sugar rise, subsequent release of insulin and that is what is causing your weight loss stall or possibly weight gain.

There’s a lot more there about a topic most low carbers have heard, gluconeogenesis, and one they probably haven’t, glyceroneogenesis. Follow the link to read it all.

So why would a careful low carber, who has been losing steadily and eating all the right things, suddenly stop losing? Nothing has changed, right? Wrong.

No, the dieter isn’t necessarily cheating. The dieter has lost 20 or 30 pounds. I have lost 30 pounds, about 13% of my pre-diet body weight. And when I started the diet, I calculated my protein requirement based in large part upon … my weight. That’s what has changed.

So, for the low carb dieter who has lost weight, its back to the tables and charts to re-calculate what their protein requirement is; for most people, it will be less than before. While weight lifters may have more lean body mass, most of us will have less calculated lean body mass. I don’t think we are actually losing muscle. And while I’m not absolutely certain on this point, I think the charts and measurements we use have a built-in variation that gets more and more accurate as we reduce our body fat percentage.

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I noticed when I adopted the The Protein Power Lifeplan
way of eating that I was finally able to eat regularly spaced meals without getting hungry between them. Prior to that, I can’t remember a time in my life when I wasn’t fighting the urge to snack between meals.

In dietary circles, the ability of food to satisfy your hunger is referred to as the satiety factor. Some researchers claim satiety is tied to the feeling of fullness you get from bulkier foods, but my experience is that high fiber foods do not necessarily satisfy my hunger. They make me feel full, but still hungry. There’s always room for another slice of that fiber-rich pumpkin pie.

Low carb advocates often cite the satiety factor of their diet, as I have done in the first paragraph. Some point to the higher percentage of fat in the diet than the typical low-fat diet emphasized by most doctors, making the claim that you cannot gain weight if you eat a low carb diet with plenty of fat. But some people do gain weight that way, so something else may be at work.

When I started Protein Power, I calculated my daily minimum protein requirement, as the book recommends. I was surprised at how much food I could eat. With 25 – 30 grams of protein per meal as a minimum, that meant a hearty bacon and eggs breakfast of 3 eggs (18 grams) and 3 slices of bacon (9 grams). My usual breakfast routine was a toasted bagel, then a snack before lunch because by 10 AM I was very hungry. But after eating the eggs and bacon mentioned above … I was full, and remained so until lunch time.

As the title of the book suggests, Protein Power is about getting the right amount of protein as well as reducing carbohydrates. It works for me. And it may be the protein that satisfies, rather than just the increased fat.

Nutritional ecologist Professor David Raubenheimer of New Zealand’s Massay University, recently conducted a study on primate eating habits in collaboration with other experts. Studying the Bolivian rainforest spider monkey, Professor Raubenheimer found the monkey’s food intake increased when low protein food sources were the only ones available.

The findings, published in the latest issue of the journal Behavioural Ecology, reinforce the theory that humans and other primates are physiologically predisposed to maintain a constant level of protein in their diets. But when the range of foods available to them is low in protein (yet high in fats and carbohydrates) they are compelled to eat greater quantities in order to maintain correct protein levels.

I think this explains the satiety issue better, and gives an indication of why some people experience weight gain even on a low carb diet. If they aren’t meeting their body’s protein requirements, they will be hungry. And hungry people eat more.

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Gary Taubes, the nationally acclaimed science writer, explains why exercise and weight loss are not physiologically linked:

The one thing that might be said about exercise with certainty is that it tends to makes us hungry. Maybe not immediately, but eventually. Burn more calories and the odds are very good that we’ll consume more as well. And this simple fact alone might explain both the scientific evidence and a nation’s worth of sorely disappointing anecdotal experience.

The New York magazine article is a good read, and includes Taubes’ signature style of including historical perspective to frame the issue. And he gets to the underlying philosophy behind the “calories in / calories out” theory of weight loss: the idea that the body is a thermodynamic black box that has to respond to the balance of calories taken in and calories expended.

But we are not gasoline engines. Taubes explains that the thermodynamic black box theory (TBBT) fails to take into account the role of fat tissue in our metabolism. Studies showed fat people maintaining or gaining weight while eating less than thin counterparts. But the thin people were more active. The correlation seemed to support the TBBT theory. But studies of overweight people who increased activity substantially, including a controlled study where Finnish researchers trained overweight men and women to run a marathon, showed that they maintained their weight.

Overweight people who have tried the “diet and exercise” remedy can commiserate with their Finnish brothers and sisters.

Taubes relates that our bodies have been shown to try and maintain certain levels of blood sugar, hormones, etc. We have evolved to try and counteract the entropy of our environment and gradual breakdown of our bodies. Our survival depends on it:

The key is that among the many things regulated in this homeostatic system—along with blood pressure and blood sugar, body temperature, respiration, etc.—is the amount of fat we carry. From this biological or homeostatic perspective, lean people are not those who have the willpower to exercise more and eat less. They are people whose bodies are programmed to send the calories they consume to the muscles to be burned rather than to the fat tissue to be stored—the Lance Armstrongs of the world. The rest of us tend to go the other way, shunting off calories to fat tissue, where they accumulate to excess. This shunting of calories toward fat cells to be stored or toward the muscles to be burned is a phenomenon known as fuel partitioning.

What is the mechanism for storing calories as fat? Insulin, working in concert with an enzyme, lipoprotein lipase (LPL), determines if energy should be burned or stored as fat.

Low carb dieters know that one effect of eating a low carb diet is to even out the insulin response. Those of us with insulin resistance also know that as we even out the insulin response, our cells become less resistant to the insulin in the bloodstream, and more of the glucose in our blood is used for muscular energy rather than stored as fat.

A low carb diet is more than a weight loss diet; it is a lifestyle choice that leads to more stable weight for a lifetime. This is possible because, unlike exercise, eating lower carbohydrates in your daily diet aids in the feeling of being satisfied with the amount you have eaten. When you aren’t hungry, its easier to not reach for that snack.

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The American Heart Association is now recommending a lower carb diet for prevention of cardiovascular heart disease, heralding the beginning of the Low Carb Age!

A new study, recently presented at the American Heart Association annual meeting in Orlando, FL, tested the effect of a low fat verses moderate fat diet. The low fat diet contained 20 percent of calories from fat, 65 percent from carbs and 15 percent from protein (this is the standard low fat diet that has been recommended for years). The “moderate fat diet” increases fat, and to keep the calories consistent, lowers the carbohydrate contribution. The moderate fat diet in the study has 40 percent of the calories from fat, 45 percent from carbohydrate and 15 percent protein. HealthDay, from the National Institutes of Health, quotes the AHA:

“This is a good study that essentially confirms that the current recommendations are appropriate,” said Alice Lichtenstein, a spokeswoman for the American Heart Association (AHA). “Since 2000, the AHA has been recommending not a low-fat diet, but one that is low in saturated fats and trans fatty acids.”

People with metabolic syndrome are glucose-intolerant, meaning they can’t process blood sugar well. Low-fat, high-carbohydrate diets exacerbate this condition, Lichtenstein explained.

The study is explained in more detail on our Diabetes and Metabolic Syndrome research page. The conclusion of the study gives the bottom line:

Conclusions: This is the first study to examine the effects of low fat vs. moderate fat diet in MetS. MF compared to LF diet improves the atherogenic dyslipidemia of MetS. MF diet is a preferable dietary intervention in people with MetS to improve CVD risk.

Whew. What the heck does that mean? Here’s a layman’s plain English translation:

This is the first study to examine the effects of low fat vs. a moderate fat diet with lower carbohydrates in patients with metabolic syndrome. The moderate fat diet compared to the low fat diet improves the heart disease related risks of various blood fats (VLDL, LDL, triglycerides, etc.) in people with metabolic syndrome. The moderate fat diet is therefore a better diet for people with metabolic syndrome.

Health Day goes on to quote other experts:

Experts familiar with the study aren’t surprised by the findings. “This sort of falls within the boundaries of what we used to call the Atkins diet, which was a high-lipid and low-carb diet. Normally this kind of diet suppresses appetite, improves diabetes,” said Dr. Alfred Bove, president of the American College of Cardiology. “This diet looks like it does a good job of altering the negative metabolic effects of early diabetes or high carbohydrate stimulation,” he said.

“Much of this we’ve known before, but the idea is that a moderate-fat diet is something most people can tolerate,” Bove said. “It probably affects the way insulin is released because if you have a lot of carbohydrates in the diet, you tend to generate a lot of insulin, and insulin is the hormone that lowers blood sugar,” Bove explained. “In addition to lowering blood sugar, it also increases appetite so a lot of people on high-carb diets are restimulated to eat more.”

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Stunning statistics from a study published in the December issue of Diabetes Care, as reported by Health Day News:

The number of people with diabetes in the United States is expected to double over the next 25 years, a new study predicts.

That would bring the total by 2034 to about 44.1 million people with the disease, up from 23.7 million today.

At the same time, the cost of treating people with diabetes will triple, the study also warns, rising from an estimated $113 billion in 2009 to $336 billion in 2034.

The increase is from adult onset, or type II diabetes. Health Day attributes the increase to obesity:

Factors driving the increase in diabetes cases include the aging population and continued high rates of obesity, both of which are risk factors for type 2 diabetes, in which the body does not produce enough insulin or the cells don’t use it correctly. In the study, the researchers assumed that the obesity rate would remain relatively stable, topping out at about 30 percent in the next decade and then declining slightly to about 27 percent in 2033.

The problem is that the official stance towards this problem has little hope of solving the underlying issue: our addiction to carbohydrates. While the general consensus is that people would not be diabetic if they lost weight, telling people to lose weight has proven to be a dismal failure. The reason is that very few people will starve themselves voluntarily.

The standard American diet is one rich in refined, processed foods (i.e., carbs). The “optimum” diet recommended by nutritionists is one that is low in dietary fat and eschews refined, processed foods in favor of “complex carbohydrates, such as whole grains, cereal, rice, pasta, potatoes, dry beans, carrots and corn”, with calorie reduction necessary to lose weight. It doesn’t work because you are always hungry on that diet.

Hungry people eat. And if they eat “complex carbs” that are “low in fat” they never feel sated, and will never stop eating.

Try this experiment … go to the sugar bowl and spoon out a scoop of sugar onto the counter. Then another. And another. Keep going, and when you have 22 spoonfuls of sugar on the counter, you have the average American’s intake of sugar. But what if you cut out all the added sugar found in soft drinks, cookies, candy and other snacks (even low fat ones)?

If you follow the various guidelines by the USDA, American Heart Association, et. al., you’ll limit fat to 20% of your dietary intake, and get adequate protein, making up the rest of your diet with those complex carbohydrates. Let’s take an example of a 2,000 calorie diet, and see how that works out in grams of each micro nutrient:

• Fat, 44g at 9 calories each = 20% of calories
• Protein, 100g at 4 calories each = 20% of calories
• Carbohydrates, 300g at 4 calories each = 60% of calories

Carbohydrates turn to sugar (glucose) in your gut in a very short time, within 2 to 4 hours. Even “complex carbs” turn to sugar.

Spoon out another 75 teaspoons of sugar onto your counter. That is the amount you are asking your body to metabolize when you eat 300g of carbohydrates per day.

Here’s a layman’s explanation of what is happening: The body needs sugar to run, but if it can’t use it in a very short time, it is stored as fat. Blood sugar spikes in 2 to 4 hours after eating carbs, and the body reacts by releasing insulin to drive the sugar into the cells so they can use it for energy. If the cells have enough, they refuse insulin’s prompting, and the sugar is stored as fat. As you abuse this system by overloading it with sugar, the cells become more and more resistant to insulin, and the body sends out more and more. When the sugar is pushed into fat cells, your blood sugar level drops, and hunger returns even though you ate only a few hours ago. So you eat again, and start the process all over again (if you eat a diet “rich in complex carbohydrates”). Sound familiar?

The emphasis on low fat, high carbohydrate diets has caused our expanding waistlines, and emphasizing that people should continue to eat this way but reduce calorie intake is counter intuitive. Survival depends on getting enough to eat, and your body will betray you if it thinks it is starving.

A better approach is to limit carbohydrates to about 1/3 of all calories if you are at your goal weight and otherwise healthy. For a 2,000 calorie diet, that’s about 167 grams of carbs. The rest of your calories can come from fat and protein. It is best to calculate your minimum protein requirement, usually calculated at about a half gram per pound of lean body weight. “Lean body weight” is your weight minus your fat (take your body fat percentage times your weight, and deduct that from your total weight to get your “lean body weight”). The book The Protein Power Lifeplan has this approach as a “maintenance diet”, and people can tolerate it for life … because you don’t get hungry.

And if you need to get to your goal weight, the first phase of the diet can help you do that without getting hungry. You can short-circuit the vicious cycle of carb intake, insulin response, fat storage and premature hunger by eating a diet that is tuned to your needs.

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Tom Naughton deconstructs the “obesity epidemic” at his blog Fat Head:

But what I found most interesting was the data on who’s “overweight” and by how much. Here are the numbers:

• More than 50 pounds overweight: 6%
• 21-50 pounds overweight: 17%
• 11-20 pounds overweight: 15%
• 1-10 pounds overweight: 24%
• At ideal weight: 18%
• 1-10 pounds underweight: 7%
• 11-20 pounds underweight: 3%
• More than 20 pounds underweight: 1%
• Undesignated: 9%

As we noted in our post Does Being Overweight Harm Your Health, all-cause mortality studies show that you have a 17% less chance of dying if you are in the “overweight” BMI (as compared to being “normal weight”). Even being “obese” was statistically even with being “normal weight” in these studies. The absolute worse thing you can do is be “underweight”, with a stunning 73% greater risk of dying than a “normal” weight person.

We have also noted our belief that individuals have to assess their own health needs and identify their individual risk factors, rather than focusing on a “society wide goal”. If your risk factors lean more towards developing diabetes II, then controlling blood sugar levels may be more important than being within 10 pounds of some goal weight. And as McNaughton notes, adult onset diabetes is at epidemic levels:

A different Gallup poll underscores another point I made in the film: there is a genuine epidemic out there, and it’s called diabetes. More than 11% percent of Americans adults have diabetes now, and more than 90% of those have type 2 diabetes, which is mostly preventable. The rate has more than doubled in the last decade alone. Among senior citizens, the numbers are even more harrowing: nearly one-quarter have diabetes. Just think of all the physical damage that’s causing. And even those numbers don’t count the pre-diabetics.

Nutritionists tend to focus on the weight end of the scale (so to speak), but they are missing the point. You can’t push a string. People are overweight because of their blood sugar levels (i.e., hyperinsulinemia, insulin resistance and related disorders leading to diabetes). They are not suffering from high blood sugar levels because of their weight. As Naughton sums it up:

The constant drumbeat about the obesity epidemic and the emphasis on losing weight is sending the wrong message. We need to tell people to get their blood sugar checked and keep it under control with the proper diet. If we do that, the 10 pounds will take care of itself. And if it doesn’t, well … so what? A bit of belly won’t kill you if it’s not the result of high blood sugar.

If your blood sugar is elevated, the way to get it under control is by adopting a low carb eating lifestyle. You will lose weight, but the most important thing is that you will live longer. And living longer is the goal.

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Statins are a class of drugs that lower cholesterol levels, and, the reasoning goes, should reduce the risk of heart attack. But the reality has been less illuminating than the promise. This morning word of another study showing that the popular statins containing ezetemibe, Vytorin and Zetia, do not lower the risk of heart disease. As the LA Times reports:

For the second time in as many years, a large clinical trial has found that the key ingredient in the heavily advertised drug Vytorin provides little or no benefit in preventing heart disease compared to a competing product. The ingredient is ezetemibe, which blocks the absorption of cholesterol in the intestines. It is sold alone under the brand name Zetia or in combination with the cholesterol-lowering drug simvastatin under the brand name Vytorin. The combination of drugs has been shown to reduce cholesterol more than simvastatin alone, but that apparently does not translate into a lower risk of heart disease.

Statins are often credited with a number of unpleasant side effects, including uncomfortable muscle aches. And evidence is mounting that while they may lower LDL cholesterol numbers, they aren’t providing the reduction in heart attacks that “should” result.

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You can find several variations on the low carb pumpkin pie recipe, most often without a crust. One recipe uses crushed pecans, but they are expensive now. I found an old recipe for “Nut Brown Crust” in the American Home All Purpose Cookbook, published in 1966.

Nut Brown Crust

1 1/2 Cup finely ground almonds, walnuts, Brazil nuts or pecans
3 Tbls Sugar (or sugar substitute, like Splenda)
2 Tbls soft butter

Blend finely ground nuts, butter and sweetener together with fingers. Press firmly into a lightly buttered 9-inch pie plate. Bake at 400°F for 6 – 8 minutes. Cool before filling.

Using almond meal (sometimes called almond “flour”), I found I could make a very good crust that acts a bit like a graham cracker crust. This crust works well with pumpkin pie filling.

The almond meal has a total of 30 grams of carbohydrates, with 18 of them fiber. The net carb count is therefore 12 grams for the entire pie. Many of the low carb pumpkin pie fillings come in at about 12 grams for the entire pie also. Slice that pie into 8 slices and each is only 3 grams of carbs.

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Diabetics and many people diagnosed as “pre-diabetics” may be helped by vitamin D supplementation, according to a new study previewed in our Diabetes Research Page.

Unlike studies that look at populations and try to determine the underlying factors for a certain health aspect, this study is a true randomized, double-blind study. One group of 42 insulin-resistant women were given 4000 IU of vitamin D3 and another group of 39 were given a placebo. As is standard in this type of study, neither the women or their doctors knew if they were getting the vitamin or the placebo. To further refine the study, all of the women were south Asian, to try and account for any racial or ethnic differences in the way the vitamin might be metabolized. The trial lasted 6 months, with direct testing of insulin levels.

The study will be published soon; the link above is to the synopsis and “preview” of the study’s results. The conclusion of the researchers is that supplementing vitamin D levels improved insulin resistance and made the cells more sensitive to insulin without affecting the pancreas’ insulin secretion (that’s a good thing). In addition, they didn’t note any change in overall lipid profile (cholesterol, triglycerides, etc.) or high sensitivity C-reactive protein, a measure of inflammation associated by some researchers with increased risk of coronary heart disease. Another good thing!

Diabetics should consult with their physician to see if supplementing with vitamin D can be a part of their treatment. If the vitamin D response is the same as found in this study, it may be possible to reduce of the amount of insulin needed daily.