I don't want to leave you with those last two posts without giving you some practical ways to improve body composition. Body composition is the ratio of lean tissue to fat. The ideal ratio differs depending on gender and individual differences. In general, 10% and 20% bodyfat are good targets for men and women, respectively. There's no need to measure however, as the eye is a pretty good judge.
The most dangerous fat is visceral fat, or the "beer belly". Fortunately, it's also the most responsive to lifestyle changes.
The strategies I recommend all have one thing in common: they work to restore insulin sensitivity. This will not only improve body composition, it will normalize your metabolism on a fundamental level, reducing the risk of all the common chronic diseases. I may cover these topics again in more detail at another time.
1. Carbohydrate restriction. This is by far the most effective way to improve body composition. It will even benefit people who are already profoundly insulin resistant. Eliminating grains, legumes, potatoes and sugar is the simplest and best way to do this. That includes wheat, corn, rice, beans, oats, honorary grains like buckwheat and quinoa, and especially their derivatives. Carbohydrate is not the devil, but restricting intake to moderate amounts from vegetables and fruit is ideal for someone trying to lose weight. I think starchy root vegetables, soaked or sprouted legumes and soaked, sprouted or fermented non-gluten grains are OK for people who already have a healthy body composition.
2. Exercise. Our hunter-gatherer ancestors had a word for exercise: "life". Exercise helps improve insulin sensitivity by increasing the muscles' demand for fuel. It also builds muscle mass. Any exercise is great, but the best kind is brief and intense (anaerobic). This includes sprinting and brisk weight training. It's more effective than jogging at improving muscle mass, decreasing fat mass, decreasing insulin and improving other markers of metabolic health. Chris at Conditioning Research covers this topic regularly. Traditional sports like soccer and basketball are effective because they have anaerobic and aerobic components. Even walking up stairs or down the street have measurable health benefits, however.
3. Intermittent fasting. This is very effective at improving insulin sensitivity and body composition. IF isn't starvation; it simply postpones calorie intake. Nor is it unhealthy. In fact, it's probably closely in line with the variable energy intake to which we are fundamentally adapted. My method is one 24-hour, water-only fast per week. No juice; that defeats the purpose. If you have elevated insulin like most people, it's best to get into IF gradually. Try skipping breakfast first. If you can skip breakfast and lunch, you've completed a 23-hour fast.
4. Lose the soda! Soda and other sweet foods are the enemy of body composition and general health. Fructose, found abundantly in high-fructose corn syrup, table sugar and agave nectar, seems to have a particular talent for causing insulin resistance. It's rapidly converted to fat in the liver, which is partially stored on the spot, and partially exported into the bloodstream as triglycerides. Diet soda isn't much better. It's been associated with weight gain in humans, and actually causes weight gain in rats. Normalizing insulin through carbohydrate restriction and fasting reduces cravings for sweet foods. A moderate amount of fruit is probably fine.
Visceral Fat and Dementia
This study was released today, demonstrating in 6,583 patients that visceral fat mass in the 40s predicts the risk of dementia in old age. Patients in the highest quintile (20% with the most visceral fat mass) had an almost three-fold higher risk of dementia than patients in the lowest quintile. This is a greater effect than you see from "genetics". Overall fat mass was less strongly correlated with dementia. This study is so timely, they must have heard about my blog post.
They used a measure of visceral fat called the "sagittal abdominal diameter", basically the distance from the back to the belly button. In other words, the beer belly.
What we're looking at is another facet of the pervasive "disease of civilization" that rolls into town on the same truck as sugar and white flour. Weston Price described it in 14 different cultures throughout the world in Nutrition and Physical Degeneration. Diabetes, cardiovascular disease, obesity, cancer and dementia all seem to come hand-in-hand. It's hard to say exactly what the root cause is, but the chain of causality seems to pass through visceral fat and insulin signaling in many people.
They used a measure of visceral fat called the "sagittal abdominal diameter", basically the distance from the back to the belly button. In other words, the beer belly.
What we're looking at is another facet of the pervasive "disease of civilization" that rolls into town on the same truck as sugar and white flour. Weston Price described it in 14 different cultures throughout the world in Nutrition and Physical Degeneration. Diabetes, cardiovascular disease, obesity, cancer and dementia all seem to come hand-in-hand. It's hard to say exactly what the root cause is, but the chain of causality seems to pass through visceral fat and insulin signaling in many people.
Visceral Fat
This week, I stumbled upon a very interesting series of articles from the lab of Dr. Nir Barzilai.
The first article I came across showed that surgical removal of the visceral fat deposit of rats increased their lifespan. Visceral fat (VF) is the "beer belly", and consists of the perinephratic fat around the kidneys and the omental fat in front of the intestines. It doesn't include subcutaneous fat, the fat layer under the skin.
VF is tightly associated with the metabolic syndrome, the quintessential "disease of civilization" that affects 24% of Americans (NHANES III). It's defined by three or more of the following criteria: high blood pressure, large waist circumference, low HDL cholesterol, high triglycerides, and high fasting glucose. The metabolic syndrome is associated with a 3-4-fold increase in the risk of death from cardiovascular disease, and a 6-fold increase in the risk of developing type II diabetes. From a review on the metabolic syndrome (parentheses mine):
This is all well and good, but who cares? What's to say VF plays any role other than as a simple marker for overweight?
The longevity paper led me to Dr. Barzilai's previous papers, which answered this question rather thoroughly. Rats raised on standard rat chow, which is a sad little compressed pellet made of grains and added nutrients, develop elevated insulin and insulin resistance with age, just like humans. Unless they don't have VF. Rats that had their VF surgically removed did not develop insulin resistance or elevated insulin with age, despite rebounding to their original total fat mass rather quickly (VF accounts for ~18% of total fat in these rats). These parameters are unaffected by removing an equal amount of subcutaneous fat, which has been shown in human liposuction patients as well.
Removing VF also improved diabetes-prone Zucker rats, which are profoundly insulin-resistant (leptin receptor loss-of-function). It kept wild-type rats just as insulin-sensitive as calorically restricted controls, which had a small amount of VF. This shows that VF isn't just a passive player; it's essential for the development of insulin resistance. It also shows, along with human studies, that insulin resistance is not an inevitable consequence of aging.
Adipose (fat) tissue is being increasingly recognized as an important endocrine (hormone-secreting) organ. It produces many different hormones that affect insulin sensitivity and appetite regulation, among other things. These hormones are collectively known as fat-derived peptides (FDPs). At least one of these FDPs, TNF-alpha, promotes insulin resistance.
Dr. Barzilai's group went on to explore the mechanism of VF contributing to insulin resistance. They increased the rate of glucose flux into the fat tissue of rats by infusing either glucose or insulin into the bloodstream. These treatments both cause increased glucose uptake by fat cells. What they saw when they dissected the rats was striking. The VF had ramped up its production of FDPs from 2- to 15-fold, while the subcutaneous fat had barely changed. Incidentally, insulin increased glucose uptake by VF twice as much as subcutaneous fat.
I'll say this again, because it's important. They forced glucose into VF cells, and those cells dramatically upregulated FDP production. And again, no visceral fat, no FDPs.
In earlier papers, he also showed that the removal of VF dramatically reduces the expression of TNF-alpha and leptin (two FDPs) in subcutaneous fat on a longer timescale, showing that VF and subcutaneous fat communicate to alter the metabolism. Again, TNF-alpha promotes insulin resistance, making it a possible link between the fat tissue and peripheral effects. VF removal had no effect on triglycerides, suggesting that they're only a marker of insulin dysfunction rather than a cause.
Now to take this research to its logical conclusion. Here's a plausible sequence of events leading up to the metabolic syndrome:
The first article I came across showed that surgical removal of the visceral fat deposit of rats increased their lifespan. Visceral fat (VF) is the "beer belly", and consists of the perinephratic fat around the kidneys and the omental fat in front of the intestines. It doesn't include subcutaneous fat, the fat layer under the skin.
VF is tightly associated with the metabolic syndrome, the quintessential "disease of civilization" that affects 24% of Americans (NHANES III). It's defined by three or more of the following criteria: high blood pressure, large waist circumference, low HDL cholesterol, high triglycerides, and high fasting glucose. The metabolic syndrome is associated with a 3-4-fold increase in the risk of death from cardiovascular disease, and a 6-fold increase in the risk of developing type II diabetes. From a review on the metabolic syndrome (parentheses mine):
The most common alteration related to the impaired glucose metabolism with aging is the progressively increased fasting and postprandial [post-meal] plasma insulin levels, suggesting an insulin-resistant state.
This is all well and good, but who cares? What's to say VF plays any role other than as a simple marker for overweight?
The longevity paper led me to Dr. Barzilai's previous papers, which answered this question rather thoroughly. Rats raised on standard rat chow, which is a sad little compressed pellet made of grains and added nutrients, develop elevated insulin and insulin resistance with age, just like humans. Unless they don't have VF. Rats that had their VF surgically removed did not develop insulin resistance or elevated insulin with age, despite rebounding to their original total fat mass rather quickly (VF accounts for ~18% of total fat in these rats). These parameters are unaffected by removing an equal amount of subcutaneous fat, which has been shown in human liposuction patients as well.
Removing VF also improved diabetes-prone Zucker rats, which are profoundly insulin-resistant (leptin receptor loss-of-function). It kept wild-type rats just as insulin-sensitive as calorically restricted controls, which had a small amount of VF. This shows that VF isn't just a passive player; it's essential for the development of insulin resistance. It also shows, along with human studies, that insulin resistance is not an inevitable consequence of aging.
Adipose (fat) tissue is being increasingly recognized as an important endocrine (hormone-secreting) organ. It produces many different hormones that affect insulin sensitivity and appetite regulation, among other things. These hormones are collectively known as fat-derived peptides (FDPs). At least one of these FDPs, TNF-alpha, promotes insulin resistance.
Dr. Barzilai's group went on to explore the mechanism of VF contributing to insulin resistance. They increased the rate of glucose flux into the fat tissue of rats by infusing either glucose or insulin into the bloodstream. These treatments both cause increased glucose uptake by fat cells. What they saw when they dissected the rats was striking. The VF had ramped up its production of FDPs from 2- to 15-fold, while the subcutaneous fat had barely changed. Incidentally, insulin increased glucose uptake by VF twice as much as subcutaneous fat.
I'll say this again, because it's important. They forced glucose into VF cells, and those cells dramatically upregulated FDP production. And again, no visceral fat, no FDPs.
In earlier papers, he also showed that the removal of VF dramatically reduces the expression of TNF-alpha and leptin (two FDPs) in subcutaneous fat on a longer timescale, showing that VF and subcutaneous fat communicate to alter the metabolism. Again, TNF-alpha promotes insulin resistance, making it a possible link between the fat tissue and peripheral effects. VF removal had no effect on triglycerides, suggesting that they're only a marker of insulin dysfunction rather than a cause.
Now to take this research to its logical conclusion. Here's a plausible sequence of events leading up to the metabolic syndrome:
- A meal high in quickly digested carbohydrate elevates blood glucose. OR, excessive fructose causes insulin resistance in the liver which leads to high fasting glucose.
- Visceral fat responds by increasing production of FDPs.
- FDPs, directly and/or indirectly, cause insulin resistance in the liver, muscle and other tissue. Liver insulin resistance causes alterations in lipoprotein ("cholesterol") profile (more on this in another post). Fat tissue remains insulin-sensitive.
- Fat tissue (including VF) grows in size, because due to its insulin sensitivity it's taking up more than its share of glucose.
- The vicious cycle continues, with increased visceral fat size and glucose uptake increasing FDP production, which makes the liver more insulin resistant, which increases glucose production by the liver, etc.
- In the absence of lifestyle changes, the cycle only stops when the fat tissue becomes insulin-resistant, at which point you lose control over blood sugar and become diabetic.
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