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. 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 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):

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.

• 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.
  

Okinawa and Lard

The inhabitants of Okinawa, an island prefecture of Japan, are one of the longest-lived populations in the world. Their diet and lifestyle have been thoroughly studied for this reason. Papers typically focus on their consumption of vegetables, fish, soy, sweet potatoes, exercise, and the fact that some of them may have been mildly calorie restricted for part of their lives.

The thing that often gets swept under the rug is that they eat lard. Traditionally, it was their primary cooking fat. Of course, they also eat the pork the lard came from.

I'm not saying lard will make you live to 100, but a moderate amount certainly won't stop you...

Real Food IV: Lard

Your great-grandmother would have told you that natural, homemade lard is an excellent cooking fat. It has a mild, savory flavor and a high smoke point. It's well suited for sauteing and frying foods, and it makes the flakiest savory crust. It's also cheap to buy and easy to render. Rendering lard is the process by which fat tissue is turned into pure fat. I buy the best quality lard available for $2/lb at my farmer's market, making it far cheaper than butter and olive oil of equivalent quality.

The best place to buy lard is at a local farmer's market. Look for pigs that have been "field-raised" or "pasture-raised", and are preferably organic. This ensures that they receive sunlight and have been treated humanely. The "organic" label by itself simply means they have been fed organic feed; the pigs will often not have had access to the outdoors. I recommend avoiding conventional (non-organic) pork at all costs, because it's profoundly inhumane and highly polluting. This is where I buy my lard.

If you don't have access to good quality local lard, there are a couple of sources on the Local Harvest website. Look for "leaf lard", which is the fat surrounding the kidneys. It's lowest in polyunsaturated oil and thus has the highest smoke point and the lowest omega-6 content. It's also practically pure fat. You will recover 90% of the pre-rendering volume from leaf lard. On to the recipe.


Ingredients and Equipment:

• Lard
• Cheesecloth
• Baking dish
• Jars
  

1. Preheat the oven to 225 F.

2. Cut off any pieces of meat clinging to the fat.

3. Cut fat into small (~1-inch) cubes.

4. Place them into a non-reactive baking dish and then into the oven.

5. Over the next 2-3 hours, periodically mash the fat with a potato ricer or the back of a large spoon. The fat will gradually separate from the residual protein as a clear liquid.

6. When you are satisfied that you've separated out most of the fat, remove the baking dish from the oven and allow it to stand until it's cool enough to be safe, but warm enough to be liquid.

7. Pour through a cheesecloth into jars. Save the "cracklins", these can be eaten.

8. If you plan on using the lard for crusts, cool it as quickly as possible by placing the jars in cold water. If the lard solidifies slowly, it will have a slightly grainy texture that works less well for crusts, but is irrelevant for other purposes.

Finished lard has a long shelf life but I like to keep it in the fridge or freezer to extend it even further.

Thoughts on Obesity, Part I

From the US Centers for Disease Control website:

Since the mid-seventies, the prevalence of overweight and obesity has increased sharply for both adults and children. Data from two NHANES surveys show that among adults aged 20–74 years the prevalence of obesity increased from 15.0% (in the 1976–1980 survey) to 32.9% (in the 2003–2004 survey).

In hunter-gatherer and some semi-agricultural societies, obesity is rare. In most, it's nonexistent. Wild animals typically do not accumulate enough fat to interfere with vigorous exercise, and when they do, it's because they're about to hibernate or migrate. Wild animals also tend to have similar amounts of body fat between individuals (at a given age and sex), unlike industrialized humans. This makes me think that obesity is an unnatural effect of our current lifestyle. Whatever the cause, it's getting progressively more common.

According to certain nutrition experts, we know exactly what causes overweight. It's a character flaw known as overeating. Calories in, calories out. And the cure is to eat less. The problem is, this treatment has a poor record of efficacy.

Restricting calories is also fraught with problems. Each person's metabolism has a preference for a specific body composition within the context of a particular lifestyle. If total calories are restricted without changing diet composition, the body reacts vigorously to maintain homeostasis. Energy expenditure is reduced; muscle and organ mass diminish. The psychological effects are particularly bad, as anyone can tell you who has been on a low-calorie diet. In 1944, Ancel Keys undertook a calorie restriction trial in conscientious objector "volunteers" in Minnesota. They remained on a 1,570-calorie diet that was low in fat and protein and high in carbohydrate, for 24 weeks. Hardly a draconian calorie count. Here's a quote from the study:

As starvation progressed, fewer and fewer things could stimulate the men to overt action. They described their increasing weakness, loss of ambition, narrowing of interests, depression, irritability, and loss of libido as a pattern characteristic of "growing old".

Some of the men ended up suffering from neurosis and borderline psychosis before the end of the study, one culminating in self-mutilation. This is what we're being prescribed for weight loss?

There are some diet trends that have associated with rising obesity in the US. Per capita calorie consumption has increased. This increase is due to a higher consumption of carbohydrate. Total protein and fat consumption have been almost identical for the past 30 years. This period also saw increases in the consumption of unsaturated vegetable oils, hydrogenated vegetable oils and high-fructose corn syrup. It's hard to say from this association which of these factors (if any) has caused us to gain weight in the last 30 years, but it certainly isn't total fat or protein. Fortunately, we have other clues.