Nonalcoholic fatty liver disease (NAFLD) is milder form of NASH, in which the liver becomes enlarged and accumulates fat. Ready for a shocker? The prevalence of NAFLD is thought to be between 20 and 30 percent in the Western world, and rising. It's typically associated with insulin resistance and often with the metabolic syndrome. This has lead some researchers to believe it's caused by insulin resistance. It's a chicken and egg question, but I believe it's the other way around if anything.
There are certain animal models of human disease that are so informative I keep coming back to them again and again. One of my favorites is the LIRKO mouse, or liver-specific insulin receptor knockout mouse. The LIRKO mouse is missing its insulin receptor in the liver only, so it is a model of severe insulin resistance of the liver. It accumulates a small amount of fat in its liver in old age, but nothing that resembles NAFLD. So liver insulin resistance doesn't lead to NAFLD or NASH, at least in this model.
What else happens to the LIRKO mouse? It develops severe whole-body insulin resistance, impaired glucose tolerance, high fasting blood glucose and hyperinsulinemia (chronically elevated insulin). So insulin resistance in the liver is sufficient to cause whole-body insulin resistance, hyperinsulinemia and certain other hallmarks of the metabolic syndrome, while liver and whole-body insulin resistance are not sufficient to cause NAFLD or NASH. This is consistent with the fact that nearly everyone with NAFLD is insulin resistant, while many who are insulin resistant do not have NAFLD.
In all fairness, there are reasons why NAFLD is believed to be caused by insulin resistance. For example, insulin-sensitizing drugs improve NAFLD. However, that doesn't mean the initial metabolic 'hit' wasn't in the liver. One could imagine a scenario in which liver insulin resistance leads to insulin resistance in other tissues, which creates a positive feedback that aggravates NAFLD. Or perhaps NAFLD requires two 'hits', one to peripheral insulin sensitivity and another directly to the liver.
In any case, I feel that the most plausible mechanism for NAFLD goes something like this: too much n-6 from polyunsaturated vegetable oil (along with insufficient n-3), plus too much fructose from sweeteners, combine to cause NAFLD. The liver becomes insulin resistant at this point, leading to whole-body insulin resistance, hyperinsulinemia, impaired glucose tolerance and general metabolic havoc.
Thursday, September 25, 2008
Wednesday, September 24, 2008
Refresher Course: 5 Day Pouch Test Soups
We get a lot of questions about the soups for the 5 Day Pouch Test. Here is an explanation directly from our forthcoming book: The 5 Day Pouch Test Owner's Manual. Many who have done the 5DPT and used the soups swear by them. Another question that I get frequently is, "Can I have the soups when I'm not doing the 5DPT?" The answer is a big resounding YES!Link to the Soup RecipesSoup
Tuesday, September 23, 2008
It's all happening in the Neighborhood
Autumn has arrived in the Northern Hemi and for me that means cool morning walks, beautiful colors as the leaves change and late-night tea in front of the fireplace. How are things in your neck of the woods? Our little calico, KeepHerKitty, is quite interested in the big round pumpkins just waiting to be carved.In the LivingAfterWLS Neighborhood the weather is always just right for over-the-fence
Agave Syrup
Anna brought up agave syrup in a comment on the last post, so I thought I'd put up a little mini-post so everyone can benefit from what she pointed out.
Agave syrup is made from the heart of the agave plant, which is pressed to release a juice rich in inulin. Inulin is a polymer made of fructose molecules. The inulin is then broken down either by heat or by enzymatic processing. The result is a sweet syrup that is rich in fructose.
Agave syrup is marketed as a healthy, alternative sweetener. In fact, it's probably as bad or worse than high-fructose corn syrup (HFCS). They are both a refined and processed plant extract. Both are high in fructose, with agave syrup leading HFCS (estimates of agave syrup range up to 92% fructose by calories). Finally, agave syrup is expensive and inefficient to produce.
The high fructose content gives agave syrup a low glycemic index, because fructose does not raise blood glucose. Unfortunately, as some diabetics learned the hard way, using fructose as a substitute for sucrose (cane sugar) has negative long-term effects on insulin sensitivity.
In my opinion, sweeteners come with risks and there is no free lunch. The only solution is moderation.
Agave syrup is made from the heart of the agave plant, which is pressed to release a juice rich in inulin. Inulin is a polymer made of fructose molecules. The inulin is then broken down either by heat or by enzymatic processing. The result is a sweet syrup that is rich in fructose.
Agave syrup is marketed as a healthy, alternative sweetener. In fact, it's probably as bad or worse than high-fructose corn syrup (HFCS). They are both a refined and processed plant extract. Both are high in fructose, with agave syrup leading HFCS (estimates of agave syrup range up to 92% fructose by calories). Finally, agave syrup is expensive and inefficient to produce.
The high fructose content gives agave syrup a low glycemic index, because fructose does not raise blood glucose. Unfortunately, as some diabetics learned the hard way, using fructose as a substitute for sucrose (cane sugar) has negative long-term effects on insulin sensitivity.
In my opinion, sweeteners come with risks and there is no free lunch. The only solution is moderation.
My Dad is really really really REALLY ill.
Dunno where to start, but I guess the beginning. Here goes.
Run down of stuff:
Wednesday 10th September - Reversal of illiostomy after cancer of the rectum (Bowel Cancer)
Sunday 14th September - He had his 1st turn out in 6 months, which apparently was great!
Monday 15th September - Released from Hospital.
Friday 19th September - In ICU -no change. Further surgery to wash out abdominal cavity and check for further localised infection. Anesthetic switched off at 6pm and put on heavy morphine. Wake up begins - or should do.
Saturday 20th September -In ICU - no change, still asleep. Very slight awareness to family voices. scrunching of eyebrows, especially to DS's voice and Mums.
Sunday 21st September - ICU - Nurses tried to wake him up by stopping morphine. Came around slightly but in obvious chronic discomfort, so morphine substitute re-introduced. Completely out of it, seemingly more asleep than before.
Monday 22nd September - ICU - STILL has raging temp, low BP, high pulse/heart rate and cannot breathe on his own - just small changes in awareness only. raising arms without particular control and raising eye lids a little although heavy towards family members. wriggling in bed, moving legs, but very obviously drugged movements like someone who is brain damaged.
Tuesday 23rd September - ICU - turn for the worse. Less movements, not absorbing food through the tube any more and excess building up in his stomach and going bad, having to be regularly pumped out. Food only being fed intravenously now. Still aware Mum there, but observations were not good. seems as if he does not get on with the morphine alternative, so put back on morphine. Possible lung infection, possible stomach infection. Tests
So I am a bit jiggered to be honest.
Also on Thursday, Felix (aka Dodgy) one of Mary's kittens she had back in May was savaged by the next door neighbours dog. He has broken ribs, broken pelvis, puncture wounds, pneumo-thorax and other associated shock problems, but is thankfully out of the woods.
Sue (our lodger) is £415 lighter and he has spent the last 2 nights in the Maternity cum Intensive Care caravan on the front drive. However, he had to move into the main quarters today as Mary gave birth this afternoon and evening to 6 lovely kittens. They are all yummy.
Here is a video of number 5's birth. They are a proper mixture. 2 are black and white tuxedo style and the rest are a tabby blend. One is a grey tabby and the others are varying degrees of tabby right down to black with grey go faster stripes down the side! 5 girls and 1 boy!
Run down of stuff:
Wednesday 10th September - Reversal of illiostomy after cancer of the rectum (Bowel Cancer)
Sunday 14th September - He had his 1st turn out in 6 months, which apparently was great!
Monday 15th September - Released from Hospital.
- Evening - pain in side and shoulder
- Night - could not sleep, excruciating pain
- Evening - A&E dept. given morphine to help pain. temperature, low BP, high pulse/heart rate obvious signs of infection as his body was in shock. Wound opened and blood & puss pour out and even spray my mother in the face!
- Night - wound stitches removed and scar opened up. A large amount of puss, blood and faeces removed from abdominal cavity through site of old stoma
- Night - Brought back from surgery straight to Intensive Care Unit (ICU) at approx 7pm. Completely our for the count on Life Support machine with respirator and 14 automatic drug administrators and untold monitors.
Friday 19th September - In ICU -no change. Further surgery to wash out abdominal cavity and check for further localised infection. Anesthetic switched off at 6pm and put on heavy morphine. Wake up begins - or should do.
Saturday 20th September -In ICU - no change, still asleep. Very slight awareness to family voices. scrunching of eyebrows, especially to DS's voice and Mums.
Sunday 21st September - ICU - Nurses tried to wake him up by stopping morphine. Came around slightly but in obvious chronic discomfort, so morphine substitute re-introduced. Completely out of it, seemingly more asleep than before.
Monday 22nd September - ICU - STILL has raging temp, low BP, high pulse/heart rate and cannot breathe on his own - just small changes in awareness only. raising arms without particular control and raising eye lids a little although heavy towards family members. wriggling in bed, moving legs, but very obviously drugged movements like someone who is brain damaged.
Tuesday 23rd September - ICU - turn for the worse. Less movements, not absorbing food through the tube any more and excess building up in his stomach and going bad, having to be regularly pumped out. Food only being fed intravenously now. Still aware Mum there, but observations were not good. seems as if he does not get on with the morphine alternative, so put back on morphine. Possible lung infection, possible stomach infection. Tests
So I am a bit jiggered to be honest.
Also on Thursday, Felix (aka Dodgy) one of Mary's kittens she had back in May was savaged by the next door neighbours dog. He has broken ribs, broken pelvis, puncture wounds, pneumo-thorax and other associated shock problems, but is thankfully out of the woods.
Sue (our lodger) is £415 lighter and he has spent the last 2 nights in the Maternity cum Intensive Care caravan on the front drive. However, he had to move into the main quarters today as Mary gave birth this afternoon and evening to 6 lovely kittens. They are all yummy.
Here is a video of number 5's birth. They are a proper mixture. 2 are black and white tuxedo style and the rest are a tabby blend. One is a grey tabby and the others are varying degrees of tabby right down to black with grey go faster stripes down the side! 5 girls and 1 boy!
Monday, September 22, 2008
How to Fatten Your Liver
Steatohepatitis is a condition in which the liver becomes inflamed and accumulates fat. It was formerly found almost exclusively in alcoholics. In the 1980s, a new condition was described called nonalcoholic steatohepatitis (NASH), basically steatohepatitis without the alcoholism. Today, NASH is thought to affect more than 2% of the adult American population. The liver has many important functions. It's not an organ you want to break.
This week, I've been reading about how to fatten your liver. First up: industrial vegetable oil. The study that initially sent me on this nerd safari was recently published in the Journal of Nutrition. It's titled "Increased Apoptosis in High-Fat Diet–Induced Nonalcoholic Steatohepatitis in Rats Is Associated with c-Jun NH2-Terminal Kinase Activation and Elevated Proapoptotic Bax". Quite a mouthful. The important thing for the purpose of this post is that the investigators fed rats a high-fat diet, which induced NASH.
Anytime a study mentions a "high-fat diet", I immediately look to see what they were actually feeding the animals. To my utter amazement, there was no information on the composition of the high-fat diet in the methods section, only a reference to another paper. Apparently fat composition is irrelevant. Despite the fact that a high-fat diet from coconut oil or butter does not produce NASH in rats. Fortunately, I was able to track down the reference. The only difference between the standard diet and the high-fat diet was the addition of a large amount of corn oil and the subtraction of carbohydrate (dextrin maltose).
Corn oil is one of the worst vegetable oils. You've eaten corn so you know it's not an oily seed. To concentrate the oil and make it palatable, manufacturers use organic solvents, high heat, and several rounds of chemical treatment. It's also extremely rich in n-6 linoleic acid. The consumption of corn oil and other n-6 rich oils has risen dramatically in the US in the last 30 years, making them prime suspects in NASH. They have replaced the natural (more saturated) fats we once got from meat and milk.
Next up: fructose. Feeding rats an extreme amount of fructose (60% of calories) gives them nonalcoholic fatty liver disease (NAFLD), NASH's younger sibling, even when the fat in their chow is lard. Given the upward trend of US fructose consumption (mostly from high-fructose corn syrup), and the refined sugar consumed everywhere else (50% fructose), it's also high on my list of suspects.
Here's my prescription for homemade foie gras: take one serving of soybean oil fried french fries, a basket of corn oil fried chicken nuggets, a healthy salad drenched in cottonseed oil ranch dressing, and wash it all down with a tall cup of soda. It's worked for millions of Americans!
This week, I've been reading about how to fatten your liver. First up: industrial vegetable oil. The study that initially sent me on this nerd safari was recently published in the Journal of Nutrition. It's titled "Increased Apoptosis in High-Fat Diet–Induced Nonalcoholic Steatohepatitis in Rats Is Associated with c-Jun NH2-Terminal Kinase Activation and Elevated Proapoptotic Bax". Quite a mouthful. The important thing for the purpose of this post is that the investigators fed rats a high-fat diet, which induced NASH.
Anytime a study mentions a "high-fat diet", I immediately look to see what they were actually feeding the animals. To my utter amazement, there was no information on the composition of the high-fat diet in the methods section, only a reference to another paper. Apparently fat composition is irrelevant. Despite the fact that a high-fat diet from coconut oil or butter does not produce NASH in rats. Fortunately, I was able to track down the reference. The only difference between the standard diet and the high-fat diet was the addition of a large amount of corn oil and the subtraction of carbohydrate (dextrin maltose).
Corn oil is one of the worst vegetable oils. You've eaten corn so you know it's not an oily seed. To concentrate the oil and make it palatable, manufacturers use organic solvents, high heat, and several rounds of chemical treatment. It's also extremely rich in n-6 linoleic acid. The consumption of corn oil and other n-6 rich oils has risen dramatically in the US in the last 30 years, making them prime suspects in NASH. They have replaced the natural (more saturated) fats we once got from meat and milk.
Next up: fructose. Feeding rats an extreme amount of fructose (60% of calories) gives them nonalcoholic fatty liver disease (NAFLD), NASH's younger sibling, even when the fat in their chow is lard. Given the upward trend of US fructose consumption (mostly from high-fructose corn syrup), and the refined sugar consumed everywhere else (50% fructose), it's also high on my list of suspects.
Here's my prescription for homemade foie gras: take one serving of soybean oil fried french fries, a basket of corn oil fried chicken nuggets, a healthy salad drenched in cottonseed oil ranch dressing, and wash it all down with a tall cup of soda. It's worked for millions of Americans!
Friday, September 19, 2008
20gram Protein Drink! Refreshing!
Hello Neighbors!Will we ever get tired of talking about protein drinks?I have a new cocktail that is really tasty! And it is non-dairy. One reason I don't care much for most protein drinks is the texture of dairy and the digestive upset I get from dairy based food. Yesterday I came across Kellogg's "SpecialK2O Protein Water" that promises to take the edge off hunger. I purchased a 4-pack of
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