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.
Thursday, March 27, 2008
Wednesday, March 26, 2008
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.
Monday, March 24, 2008
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, exercise, and the fact that some of them may have been mildly calorically 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, and they use it liberally. Of course, they also eat the pork the lard came from.
I'm not saying lard will make you live to 100, but it certainly won't stop you...
The thing that often gets swept under the rug is that they eat lard. Traditionally, it was their primary cooking fat, and they use it liberally. Of course, they also eat the pork the lard came from.
I'm not saying lard will make you live to 100, but it certainly won't stop you...
Health Benefits of Vegetarianism
Diana gave up meat many years ago. She said it made her feel sluggish and mentally slow. Diana is 55 years old and teaches yoga classes. She says eating meat affected her yoga practice.
See an interesting article about the health benefits of vegetarianism. They say people who cut meat from their diet have about half the cancer risk and are 50 percent less likely to develop heart disease. Vegetarians are less likely to be obese. They have lower cholesterol, blood pressure, rates of hypertension, type 2 diabetes and prostate and colon cancer.
See an interesting article about the health benefits of vegetarianism. They say people who cut meat from their diet have about half the cancer risk and are 50 percent less likely to develop heart disease. Vegetarians are less likely to be obese. They have lower cholesterol, blood pressure, rates of hypertension, type 2 diabetes and prostate and colon cancer.
Sunday, March 23, 2008
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:
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.
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
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.
"I'm... Dreaming... of a white... Easter...!"
Yes, a snowman penguin built on Easter Sunday. DS was busy building this large beast before we were even out of bed - this is worked out according to the simple equation of
kids + snow = lie in for Mum and Dad
Yes. That's right. The whole village is covered in the white stuff. Wish I had put a couple of quid on that one! I consider the most impressive thing about this snowman's construction to be the fact that it is so particularly well clothed. As you can see, DS wasted no time in making sure it didn't catch 'warm' and gave it his £90 North Face coat. Ahhh Bless.
*Insert blank, furious face, of a mother who works fingers to the bone for
said child to have nice clothes*
Also, thankfully DS pays attention to his science lessons, because he told me he found out the best thing to save a snowman from melting was to clothe it for insulation. "Yeah, they said so on Mythbusters" he chirped.
Oh Goody.
Happily, after calming myself down by looking at my husband having hysterics at how cute our son is... I was able to pleasure myself with the fact that snow at the end of March usually means that within about 4 weeks it will be roasting hot sunshine. Every time we have had a strange tumble of snow this late in the year, it has been followed by a really great summer. I hope that's the case this year.
Today I am going to be mostly doing nothing. I am currently trying to eat some pomegranate and raspberry wheats with milk from Tesco. I have eaten about 20g of the 50g serving I gave myself. Monsieur Bandino, however, seems a little pissed off today for some reason, so I am giving up. Just so you can see how wonderfully little I am eating here is a funky little picture of the remains!
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