This article was originally published in 2004 in the Chicago Tribune. It's still knocking around on the web in various places but the original seems to have disappeared. You can't have too much of a good thing. Obviously Stephan's recent posts on lard prompted me to put this one up. The imported nutritionist doesn't seem quite as dismissive as you might expect! But notice in the last paragraph that the big bogeyman is protein overload damaging the kidneys! On 60g/d of protein??? Sobor clearly knows nothing about high fat diets, certainly not the one he is commenting so authoritatively about in this case!
Peter
Praise the LARD
By Monica Eng
Chicago Tribune
CHICAGO -- Vinka Peschak starts each day by knocking back a full cup of heavy whipping cream.
That's at 8 a.m.
"At around 11 o'clock I take three or four egg yolks and make some kind of omelet with lard for breakfast," the Portage Park resident explains. Peschak, a native of Poland, eats her omelet with a cup of buttery boiled vegetables and a slender piece of almond toast slathered in more butter or lard.
Dinner is usually a fatty piece of pork or some kind of organ meat with lard-cooked french fries and more butter-soaked vegetables.
In the middle of the day she might have a cup of coffee, "but only with a lot of heavy whipping cream in it."
Peschak has been eating like this for more than five years. She is slim, energetic, and says, "I feel wonderful, never tired and never hungry."
She is not on Atkins. She is not on South Beach.
Peschak, along with an estimated 2 million folks worldwide is on the Optimal Diet, a Polish eating plan that requires the consumption of prodigious amounts of animal fat -- preferably lard.
The diet was hatched in Poland some 40 years ago by Dr. Jan Kwasniewski, who started developing it while working as a dietician for a military sanitarium in Ciechocinek, Poland. There he observed that many of his patients were sick, "not because of any pathogenic factors ... but the result of one underlying cause -- bad nutrition," according to his English language "Optimal Nutrition" book. After experimenting on his family and himself, Kwasniewski concluded that the ideal nutritional combo came from eating three grams of fat for every one gram of protein and half a gram of carbohydrates.
After a couple of decades of refining this theory, Kwasniewski published his first book in Poland in 1990. But it wasn't until converts came forward with their stories of weight loss and recovery from disease in the mid-'90s that the diet really took off it its native land and Kwasniewski's books went into wide circulation. Today there are at least two magazines devoted to the Optimal lifestyle and Kwasniewski writes a twice weekly column for the regional Polish newspaper Dziennik Zachodni.
It wasn't until 2001, though, that Chicago would become the North American capital for this eating plan. That's when Tomasz Zielinski bought a little storefront on Milwaukee Avenue and opened Calma Optimal Foods. The first and only one of its kind in the nation, it operates as a deli, meeting center and, as of this spring, a restaurant for those on the lard-laden plan. Peschak serves as its manager.
Sometimes called the Polish Atkins, the Optimal Diet severely restricts the intake of carbohydrates and sugars, but differs from Atkins by de-emphasizing protein and beefing up, or more accurately porking up, the fat to a level that would have even made the late Robert Atkins reach for his heart.
On average, the diet recommends a whopping 250 grams of fat per day, about four times what the FDA recommended for the average person to maintain his/her weight and about 10 times the amount of saturated fat allowed.
So despite its popularity in Poland -- Lech Walesa is reported to have lost 44 pounds and cured his diabetes on it recently -- the mainstream medical establishment there and here is skeptical.
"I am very against diets like this," says Jadwiga Roguska, a practicing internist at the Feinberg School of Medicine at Northwestern University. "All high-fat diets are unhealthy in the long term and there is absolutely no benefit to weight reduction of this sort because it is threatening to health. ... Of course, high-fat diets will give you the benefits of energy and weight loss, but they are just not good for you."
Roguska based her comments on a brief overview of its principles, but Chicago physician Mark Sobor has seen it up close and has watched an increasing number of his patients in the Polish community embrace it.
"Kwasniewski is pure fat," says Sobor who practices in Jefferson Park and is also a licensed acupuncturist. "Eat fat non-stop. Everything is pure fat. The more fat you can take in the better and these people are fanatics about it. But the thing is they're all skinny."
On a recent Sunday morning at the Optimal deli/center in Portage Park, Ill., about 30 mature, fairly slim followers of the Kwasniewski plan gathered for a weekly meeting and shared their stories.
There was the ginger-haired firecracker Irena Kozlowicz, 78, who went on the diet five years ago after Kwasniewski came to speak at the Copernicus Center in 1999. At the time she was suffering from chronic eye problems, asthma and pain in her knees.
"Now I can walk better than a young person," she chirps. "I can run up six floors of stairs and my grandson can't catch me. He's 17 years old. I meet young ladies and they are always tired and sweating, but I never am. I didn't need to lose weight, but I lost 8 pounds. I am 78, but I feel like I am 50. I thank God for the diet."
Then there is Jozef Michael Ostrowski, 71, who says he has been on a variation of the diet his whole life.
"Since the occupation of Poland my parents could only afford pork meat and liver and blood sausage and lard," Ostrowski says through an interpreter. "It is not like I was following this diet precisely but generally. At that time I didn't know this kind of natural food was good for me. I just knew that I could eat scrambled eggs with a thin piece of bread and lard and I would be full all day. I started eating regular food like McDonald's and I could not handle the pain and so I went back to the diet and have felt better and better every day."
Zofia Pawlik, 56, started the diet last year when she went on an Optimal vacation, a retreat to the Wisconsin Dells to learn about the program and eat its foods. Over the course of a year, she says she has lost 10 pounds while improving her energy and overall health.
IMPRESSIVE RESULTS
Chicago physician Christopher Kubik wasn't at the meeting, but in a phone interview he said that four and a half years ago he was overweight and suffering from fatigue and stones in the bladder. But within a couple of months of embarking on this high-fat journey he saw results.
"I was losing weigh gradually (he lost about 25 pounds in six weeks) but I felt fine. Since then, I didn't have any more problems with stones, my skin complexion improved and I am still feeling a lot of energy," says Kubik, 57, who reports that he breakfasts on fried eggs, bacon and string cheese seven days a week. "So I experienced myself significant detectable improvement even though I generally had good health to begin with. While I was losing the weight I could feel the ketones as a metallic tasted on the mouth, but after I reached my optimal weight, (the ketosis) stopped. Now my weight has remained steady at about 185, which is in the upper limit of normal for my height."
Kubik, who also has degrees in public health and health law, says he does not actively promote the diet, "because it is not considered a standard of care and the medical community still recommends low-fat diets and it is not something I could support if I were sued." But if patients ask, "I tell them that I am on it and have seen positive results."
Dr. Sobor has also seen a growing number of Kwasniewski converts who claim weight loss is only one of the benefits they've reaped.
Chester Matuszewski, 46, for instance says that four years ago he was diagnosed with rheumatoid arthritis and was told that there was no way he could be totally cured.
"Every single joint imaginable in my hips, elbows, knees and hands hurt," Matuszewski recalled. Remembering something he had read in a Polish newspaper about the Optimal diet, he decided to check it out even though it seemed unappetizing.
"For years I thought that pork is not good for you and I didn't like the smell, but I forced myself. ... After two months I started to feel better and I didn't want to attribute it to the diet. But my friends also saw a difference in me and I had so much energy. Today after four years, I have no pain and no swelling and I am totally cured."
Sobor hears these stories all the time, but still has his reservations.
"I'm sure you've heard their claims that their joint pain is gone and diabetes is gone," he says. "And they say it because it's true. You can apparently get a lot of benefits if you decrease your carbohydrate intake, and stop taking in all the white flour and stop taking in all the refined foods because you are not stressing your body out all the time with all of the insulin spikes and becoming hyperglycemic and hypoglycemic."
"But do I recommend the diet? I don't know," he says. "I don't think Kwasniewski is as good as Atkins or that it is something you should go on for a long time. Now the South Beach Diet that is a nice diet with more flexibility. But this Optimal diet is the most radical of the low-carb diets."
Despite the popularity of the diet in its country of origin, it remains controversial there among traditional Polish nutritionists who oppose its high cholesterol and fat recommendations.
"They don't like it because they see it endangers their own positions as nutritional authorities," says Peschak.
NO POSITION FROM THE AMA
In the U.S. the Optimal Diet hasn't yet caught the attention of the medical establishment. The American Medical Association doesn't have a position on Atkins, much less Optimal. And Lisa Dorfman, spokeswoman for the American Dietetic Association, had not heard of it either.
Still, based on a quick description of the diet, she didn't condemn it outright.
"I can see how this would be a very attractive program, certainly in the senior citizen community because these are nutrient dense foods and seniors don't need to eat a lot of food," says Dorfman, a licensed nutritionist.
"And some of the foods are very nutritious albeit very high in fat and cholesterol. Liver is very high in iron and B vitamins, which would be lovely for senior citizens because they need those vitamins and are usually on a budget in that time of life.
"But for the general public I see where there could be potential problems. We just know that long-term high-fat diets leave one with a heightened risk of heart disease, stroke and hypertension. This is certainly not for children, teenagers or pregnant women.
Most Americans are getting too much fat as it is and they are not getting enough activity and they have incredible risk for heart disease because of a whole multiple list of factors including genetics and stress. And so I can't imagine that adding fat and lard and cholesterol into the mix would be beneficial to that."
"But for this group of Polish seniors I think it's adorable, especially if it was developed by someone from the old country. As a psychotherapist, I can see where they must feel like you've got to be healthy eating this because there is a psychological connection to eating these foods. It's old country eating."
Going back to the basics. It is different from the commercial processing chemical laden foods. I certainly believe these people are benefiting in some way, but it may be more than one way and it may be for certain groups and not for others is my gut hunch. It might not be appropriate for three-quarters of the population but maybe they've hit the nail on the head and this is perfect for them."
WHAT WILL IT DO LONGTERM
Although there is general agreement in the health community that lots of refined flours and sugars and their accompanying insulin spikes are not healthful, most conventional nutritionists are still not ready to embrace low-carb, high-protein and high-fat diets because of their perceived effects on the organs.
But could wear and tear on the liver, kidneys and heart be worth it for an older person to be free of the health risks of obesity?
"That I don't know," Sobor says. "No one on Atkins has died of kidney failure yet, but you can probably find a nephrologist (kidney specialist) who says it's good, one who says its bad and one who is in between. Because the truth is no one really knows yet."
"The final question is who dies faster, the people who are obese or the people who go on these diets. You would have to take 2,000 people on the diet and then 2,000 controls to see what is going to kill them first, the extra pounds or the extra protein load on the kidneys or whatever this diet will do to you. The pounds are going to do it in the short and medium term. There's no question about that. But the jury is out on the long term. The final arbiter is death. If they live longer than you do, then they won."
Thursday, March 27, 2008
Wednesday, March 26, 2008
Back home
Got to paddle on Easter Sunday as soon as the wind dropped, four foot and clean. I kept most of the wet snow out of my dry suit, and the sun even came out when the snow stopped.
About the only Hyperlipidy aspect was that there doesn't appear to be a fall off in endurance ability with lack of practice. Paddled for about two and a half hours and could have carried on but the surf was dropping with the rising tide. The reflexes and muscles still work after what must be two years off of the surf...
What do you do with five days off line? Well, Nick Lane's "Power, Sex, Suicide" has been a very interesting read. Well over half way through it and it makes a great deal of sense.
Lots of catching up to do!
Peter
About the only Hyperlipidy aspect was that there doesn't appear to be a fall off in endurance ability with lack of practice. Paddled for about two and a half hours and could have carried on but the surf was dropping with the rising tide. The reflexes and muscles still work after what must be two years off of the surf...
What do you do with five days off line? Well, Nick Lane's "Power, Sex, Suicide" has been a very interesting read. Well over half way through it and it makes a great deal of sense.
Lots of catching up to do!
Peter
Thursday, March 20, 2008
Monday, March 17, 2008
Food; carnitas
Tonight was carnitas.
Buy some strips of belly pork. Be sure to pick over the selection for the fattiest if you're in a supermarket. Any time from lunch time onwards stick them in a large sauce pan and just cover with water. Add salt and pepper, a chopped onion and a whole root of garlic, cut in half horizontally. Two bay leaves are essential. Buy a bay tree if necessary. Dried might be okay, dunno, I've got the tree.
Cover tightly, bring to boil, turn heat very low and forget about for at least 3 hours. Five hours is fine. You can do this the night before, but the smell is so good I prefer to eat them on the day.
Pick out the strips (gently, they tend to break up) and cut up in to chunks about 2 inches long. I don't use the stock for anything. Transfer the meat pieces to a non stick heavy frying pan and cook them slowly in their own fat. Sprinkle with salt, pepper, chili powder, some cumin and some more chili powder. Flip the pieces once. You're aiming to have a crispy outside and the fat within fully softened. If you over-fry them all the fat runs out and you end up with hard meat in lard. Avoid!
That's it. We had them with sweet potatoes. They should absolutely melt in the mouth. They did.
Peter
Buy some strips of belly pork. Be sure to pick over the selection for the fattiest if you're in a supermarket. Any time from lunch time onwards stick them in a large sauce pan and just cover with water. Add salt and pepper, a chopped onion and a whole root of garlic, cut in half horizontally. Two bay leaves are essential. Buy a bay tree if necessary. Dried might be okay, dunno, I've got the tree.
Cover tightly, bring to boil, turn heat very low and forget about for at least 3 hours. Five hours is fine. You can do this the night before, but the smell is so good I prefer to eat them on the day.
Pick out the strips (gently, they tend to break up) and cut up in to chunks about 2 inches long. I don't use the stock for anything. Transfer the meat pieces to a non stick heavy frying pan and cook them slowly in their own fat. Sprinkle with salt, pepper, chili powder, some cumin and some more chili powder. Flip the pieces once. You're aiming to have a crispy outside and the fat within fully softened. If you over-fry them all the fat runs out and you end up with hard meat in lard. Avoid!
That's it. We had them with sweet potatoes. They should absolutely melt in the mouth. They did.
Peter
Sunday, March 16, 2008
Diabetes and hunger
I can vaguely remember being hungry, way back before LC eating. The sort of day when you would get home at 5.30 and you HAD to have to have two doorsteps of wholemeal bread, spread with peanut butter (to avoid the saturated fats) and filled with a sliced banana, because there was NO WAY you could wait the hour it was going to take you to get supper ready. In the door, slice the bread. I remember hopping on the scales at work once and thinking that skipping a meal here and there might drop that pound or two around my tummy. Then trying it!
At the time my need to eat didn't seem like greed.
We all know that if you are a type 2 diabetic you must have been greedy for years before getting your just comuppance (thinks your GP). It's self evident that fat people get fat by eating too much food and obviously it's the dietary fat which is the main factor. Obesity is clearly the cause of type 2 diabetes (except in skinny type 2s and those naughty extremely skinny people with lipodystrophy, duhh). It's also self evident that once you have a serious blood sugar regulation problem you should eat as much sugar as possible and avoid fat like the plague because otherwise you might get even fatter, which gives you more blood sugar problems (ADA advice).
So a type 2 diabetic should eat a diet which is as carbohydrate based as practical and make sure they loose weight, lots of it. I think it's reasonable to say that that's current diabetes advice.
One day I found this paper on diabetic rats. I'm not really sure how similar streptozotocin induced diabetes in lab rats is to type 2 diabetes in humans. Insulin production is blunted but not eliminated, so perhaps it is the equivalent to fairly late type 2, when the pancreas has finally started to give up under the strain of the ADA carbohydrate based diet. The paper was quite interesting from the point of view of hunger.
Lab rats don't generally get described as being lazy glutttons. Sitting in a cage all day limits your trips to the gym. You eat what the investigator gives you. It seems quite reasonable that rats eat to satiety and no more. Beyond that would be gluttony. But if you make a rat diabetic, then feed it a carbohydrate based diet, it exhibits "hyperphagia". It eats a LOT. And it becomes fat. Perhaps a little bit of streptozotocin and some lab chow equals gluttony.
Obviously no self respecting rat wants to be either diabetic or hyperphagic. Luckily rats are not stupid and, given a choice of macronutrients after its streptozotocin, a lab rat will automatically dump the carbs, eat the fat and keep both its waistline slim and its blood glucose within acceptable limits. Given the ADA diet they don't, or rather they can't. Why can't they?
Because they're hungry. Very, very hungry.
This looks to be what is happening, from the abstract:
"When maintained on a HC [high carbohydrate] diet, diabetic rats also exhibit increased gene expression of the orexigenic peptide neuropeptide Y (NPY) in the hypothalamic arcuate nucleus, and reduced expression of the anorectic peptide corticotropin-releasing hormone (CRH) in the paraventricular nucleus, and these changes are hypothesized to contribute to diabetic hyperphagia"
Orexigenic means hunger generating. Anorectic is the opposite.
Diabetic rats on the ADA diet are RAVENOUS. Oops, sorry, gluttenous. Diabetic rats on a genuine high fat diet are not. They're not very diabetic either.
Now take that to humans. I don't think humans are particularly different to rats. Telling a human diabetic to eat a carbohydrate based diet will bump up their neuropeptide Y levels and will drop their corticotropic releasing hormone levels. They'll be ravenous. Bit of a cruel trick really.
But here's the really funny bit.
You then tell them they MUST lose weight. When they fail to lose weight, you underline the bit in their case notes where it says glutton/failed to comply.
Don't laugh too much, it's not funny really.
Peter
At the time my need to eat didn't seem like greed.
We all know that if you are a type 2 diabetic you must have been greedy for years before getting your just comuppance (thinks your GP). It's self evident that fat people get fat by eating too much food and obviously it's the dietary fat which is the main factor. Obesity is clearly the cause of type 2 diabetes (except in skinny type 2s and those naughty extremely skinny people with lipodystrophy, duhh). It's also self evident that once you have a serious blood sugar regulation problem you should eat as much sugar as possible and avoid fat like the plague because otherwise you might get even fatter, which gives you more blood sugar problems (ADA advice).
So a type 2 diabetic should eat a diet which is as carbohydrate based as practical and make sure they loose weight, lots of it. I think it's reasonable to say that that's current diabetes advice.
One day I found this paper on diabetic rats. I'm not really sure how similar streptozotocin induced diabetes in lab rats is to type 2 diabetes in humans. Insulin production is blunted but not eliminated, so perhaps it is the equivalent to fairly late type 2, when the pancreas has finally started to give up under the strain of the ADA carbohydrate based diet. The paper was quite interesting from the point of view of hunger.
Lab rats don't generally get described as being lazy glutttons. Sitting in a cage all day limits your trips to the gym. You eat what the investigator gives you. It seems quite reasonable that rats eat to satiety and no more. Beyond that would be gluttony. But if you make a rat diabetic, then feed it a carbohydrate based diet, it exhibits "hyperphagia". It eats a LOT. And it becomes fat. Perhaps a little bit of streptozotocin and some lab chow equals gluttony.
Obviously no self respecting rat wants to be either diabetic or hyperphagic. Luckily rats are not stupid and, given a choice of macronutrients after its streptozotocin, a lab rat will automatically dump the carbs, eat the fat and keep both its waistline slim and its blood glucose within acceptable limits. Given the ADA diet they don't, or rather they can't. Why can't they?
Because they're hungry. Very, very hungry.
This looks to be what is happening, from the abstract:
"When maintained on a HC [high carbohydrate] diet, diabetic rats also exhibit increased gene expression of the orexigenic peptide neuropeptide Y (NPY) in the hypothalamic arcuate nucleus, and reduced expression of the anorectic peptide corticotropin-releasing hormone (CRH) in the paraventricular nucleus, and these changes are hypothesized to contribute to diabetic hyperphagia"
Orexigenic means hunger generating. Anorectic is the opposite.
Diabetic rats on the ADA diet are RAVENOUS. Oops, sorry, gluttenous. Diabetic rats on a genuine high fat diet are not. They're not very diabetic either.
Now take that to humans. I don't think humans are particularly different to rats. Telling a human diabetic to eat a carbohydrate based diet will bump up their neuropeptide Y levels and will drop their corticotropic releasing hormone levels. They'll be ravenous. Bit of a cruel trick really.
But here's the really funny bit.
You then tell them they MUST lose weight. When they fail to lose weight, you underline the bit in their case notes where it says glutton/failed to comply.
Don't laugh too much, it's not funny really.
Peter
Thursday, March 13, 2008
Food; chicken salsa
Tonight was chicken salsa. Melt lots of butter in a heavy wok. OK, a frying pan will do. We had a mix of cheap chicken drumsticks and thighs. Fry the chicken a bit to get it started but don't try to cook it through. When it's brown on the surface scoop it out and stick it in a bowl. The salsa sauce got a bit improvised. We used a red pepper, two cloves of garlic and an onion, all finely chopped. Add as much cumin as you like. We like lots. Some cayenne pepper was needed as we are out of chillies. Salt and pepper too. Ingredients got fried for a few minutes before pouring in a can of tomatoes. Once it's back to boiling put the chicken back in, turn the heat down, put a lid on and simmer for 20 minutes so the chicken cooks through. And takes up the flavour.
You can eat it just like that, but we like to lift the chicken out once it's had its time and let it cool a bit. We turn up the heat to reduce the sauce until it's really thick and tasty. Pour it over the chicken. There should be enough butter in the sauce that eating it with a spoon is still the only way to finish it. Use a bowl, not a plate!
If you have any fresh coriander chop some leaves over it as you dish up. We're out. It was great without.
Peter
I think we're a bit low on carbs as there was no time for added veg. Might have chips later.
You can eat it just like that, but we like to lift the chicken out once it's had its time and let it cool a bit. We turn up the heat to reduce the sauce until it's really thick and tasty. Pour it over the chicken. There should be enough butter in the sauce that eating it with a spoon is still the only way to finish it. Use a bowl, not a plate!
If you have any fresh coriander chop some leaves over it as you dish up. We're out. It was great without.
Peter
I think we're a bit low on carbs as there was no time for added veg. Might have chips later.
Food; steak and kidney casserole
My wife has already sorted tomorrow night's supper as I'm working a late shift and neither of us will get time to cook on the day. I'd pulled two containers of steak and kidney mix from the freezer earlier. She put a can of tomatoes in a casserole, put in the meat and kidneys, followed by a couple of small chopped onions, a chopped orange pepper and a small parsnip. Salt, pepper and a bouquet garni. Splash of red wine of course. Oh and butter. Lean meat equals lots of butter, add whatever you feel like. If it seems a bit random that's because it's made up of pretty well what was left in the fridge....
Oh, bring it to the boil, simmer for a couple of hours then take the lid off to let it reduce down to a thick stew. Stir occasionally.
Looking forward to my portion when I get home at 10 tomorrow night. Smells great already.
Peter
PS a day at work usually means nothing but cream and chocolate through the day. Might get my eggs before I go if I'm organised... It always seems to me that these are pretty ordinary meals, just no huge amount of added carbs when served and usually no carbs for the rest of the day. That's just how it seems to work out most days.
Oh, bring it to the boil, simmer for a couple of hours then take the lid off to let it reduce down to a thick stew. Stir occasionally.
Looking forward to my portion when I get home at 10 tomorrow night. Smells great already.
Peter
PS a day at work usually means nothing but cream and chocolate through the day. Might get my eggs before I go if I'm organised... It always seems to me that these are pretty ordinary meals, just no huge amount of added carbs when served and usually no carbs for the rest of the day. That's just how it seems to work out most days.
Glucose as a cure for hypertriglyceridaemia?
This is a very interesting paper, cited in one of Bruce's comments. It's interesting enough that it really had me thinking, so here are the thoughts. Eating 80% carbs continuously through the day cranks up your triglycerides, but they only go up overnight when you stop eating the carbs. Inhibiting overnight lipolysis with either a B3 infusion or by maintaining insulin levels at 30-50microIU/ml, by drinking 60g of sugar solution every two hours (gulp), sorts the rise in trigs out. Sort of. No, it does sort it out.
This is a cracker.
We know that B3 and insulin both inhibit hormone senstitive lipase in adipose tissue, so they limit FFA delivery to the plasma and so to the liver. The presumption, in this fascinating 1973 paper, is that this is what drops the triglycerides. But is this what is happening? In addition to inhibiting hormone sensitive lipase does insulin have a roll in inhibiting VLDL secretion? Can't be bothered chasing this at the moment, but I'll bet it does. After all, failure of the liver to listen to insulin is "associated" with massive elevations of triglycerides in some unlucky people. Niacin acts through the beta hydroxy butyrate receptor. Does activation of this receptor do anything in the liver? Like drop tryglycerides maybe?
There's a bit about B3 and trigs here.
"A second mechanism has been postulated. The second mechanism by which it’s postulated that there’s a decrease in triglyceride synthesis involves a pathway of triglyceride synthesis in which the last step in triglyceride synthesis is catalyzed by an enzyme called DGAT2. It is postulated that niacin may also act through inhibiting DGAT2".
If we look at the dutch study, comparing a group of type 2 diabetics who were crossed over between 89% carbohydrate calories and 89% fat calories we see that there was essentially no difference in fasting free fatty acids, yet the fasting triglycerides in the high fat period were half those of the high carb period. Not only that but the ability of insulin to suppress free fatty acids during a clamp (elevate plasma insulin and then give a glucose infusion to maintain a constant non fatal blood glucose level) was markedly reduced in the high fat group, yet still trigs were low during this phase. See table 2.
The whole premise of the 1973 paper, that FFAs induce hypertriglyceridaemia looks wrong to me, or at least simplistic. Insulin and B3 (which is a pharmacological mimic of beta hydroxybutyrate) suppress VLDL production (fasting trigs) from the liver. Never mind what they do to FFAs.
That all night oral glucose drinking dropped the morning trigs at the cost of an all night combined hyperglycaemia and hyperinsulinaemia. This isn't treating a problem, this is correcting a lab number at the cost of glucose poisoning. Fatty liver anyone?
Aside: The type IV hyperlipoproteinaemia patients spent 24 hours with blood glucose levels between 130 and 150mg/dl in the study, and insulin levels at over 100microIU/ml for most of that 24 hour period. And their cardiovascular problems will get blamed on the triglycerides!!!!!!
Enthralling paper, but I don't think I'd take it as an endorsement of drinking 60g of glucose every 2h through the night to lower my "fasting" triglycerides. If I had elevated triglycerides, which I don't!
Peter
This is a cracker.
We know that B3 and insulin both inhibit hormone senstitive lipase in adipose tissue, so they limit FFA delivery to the plasma and so to the liver. The presumption, in this fascinating 1973 paper, is that this is what drops the triglycerides. But is this what is happening? In addition to inhibiting hormone sensitive lipase does insulin have a roll in inhibiting VLDL secretion? Can't be bothered chasing this at the moment, but I'll bet it does. After all, failure of the liver to listen to insulin is "associated" with massive elevations of triglycerides in some unlucky people. Niacin acts through the beta hydroxy butyrate receptor. Does activation of this receptor do anything in the liver? Like drop tryglycerides maybe?
There's a bit about B3 and trigs here.
"A second mechanism has been postulated. The second mechanism by which it’s postulated that there’s a decrease in triglyceride synthesis involves a pathway of triglyceride synthesis in which the last step in triglyceride synthesis is catalyzed by an enzyme called DGAT2. It is postulated that niacin may also act through inhibiting DGAT2".
If we look at the dutch study, comparing a group of type 2 diabetics who were crossed over between 89% carbohydrate calories and 89% fat calories we see that there was essentially no difference in fasting free fatty acids, yet the fasting triglycerides in the high fat period were half those of the high carb period. Not only that but the ability of insulin to suppress free fatty acids during a clamp (elevate plasma insulin and then give a glucose infusion to maintain a constant non fatal blood glucose level) was markedly reduced in the high fat group, yet still trigs were low during this phase. See table 2.
The whole premise of the 1973 paper, that FFAs induce hypertriglyceridaemia looks wrong to me, or at least simplistic. Insulin and B3 (which is a pharmacological mimic of beta hydroxybutyrate) suppress VLDL production (fasting trigs) from the liver. Never mind what they do to FFAs.
That all night oral glucose drinking dropped the morning trigs at the cost of an all night combined hyperglycaemia and hyperinsulinaemia. This isn't treating a problem, this is correcting a lab number at the cost of glucose poisoning. Fatty liver anyone?
Aside: The type IV hyperlipoproteinaemia patients spent 24 hours with blood glucose levels between 130 and 150mg/dl in the study, and insulin levels at over 100microIU/ml for most of that 24 hour period. And their cardiovascular problems will get blamed on the triglycerides!!!!!!
Enthralling paper, but I don't think I'd take it as an endorsement of drinking 60g of glucose every 2h through the night to lower my "fasting" triglycerides. If I had elevated triglycerides, which I don't!
Peter
Tuesday, March 11, 2008
Diabetes; endothelial damage
Just in case anyone thought that it was only your myocardial cells which die as a result of hyperglycaemia, those lining your aorta are queueing up at the same time.
The people doing this research are extremely clever. The molecular mechanism looks complex and finding a drug to block the effect is certainly going to need people who are very bright to do it.
Of course you could cop out and do the simple thing, which is to avoid the hyperglycaemia in the first place. Unless you're a Kitavan that looks like LC eating to me. Where ever you live, the secret appears to be to live within the limits of carbohydrate intake dictated by your ability to maintain normoglycaemia. Of course eating less carbs than this shouldn't be a problem. More just might be.
Once the endothelial cells are dead they will leave a cell sized open wound on the lining of the aorta. This will be repaired by the endothelial cells adjoining the wound dividing or by endothelial progenitor cells from the blood stream settling down on the wound (or both). These cells need energy and cholesterol to grow or divide. Sugar caused the problem in the first place so I vote energy from lipid. Any sensible system would be set up to provide lipid and cholesterol. Perhaps the surrounding cells should up regulate their LDL receptor numbers? Note especially that a loss of glycosoaminoglycans from the endothelial surface also markedly up regulates LDL particle internalisation. These endothelial cells are not taking in LDL cholesterol particles to kill themselves. Glucose does that.
Peter
The people doing this research are extremely clever. The molecular mechanism looks complex and finding a drug to block the effect is certainly going to need people who are very bright to do it.
Of course you could cop out and do the simple thing, which is to avoid the hyperglycaemia in the first place. Unless you're a Kitavan that looks like LC eating to me. Where ever you live, the secret appears to be to live within the limits of carbohydrate intake dictated by your ability to maintain normoglycaemia. Of course eating less carbs than this shouldn't be a problem. More just might be.
Once the endothelial cells are dead they will leave a cell sized open wound on the lining of the aorta. This will be repaired by the endothelial cells adjoining the wound dividing or by endothelial progenitor cells from the blood stream settling down on the wound (or both). These cells need energy and cholesterol to grow or divide. Sugar caused the problem in the first place so I vote energy from lipid. Any sensible system would be set up to provide lipid and cholesterol. Perhaps the surrounding cells should up regulate their LDL receptor numbers? Note especially that a loss of glycosoaminoglycans from the endothelial surface also markedly up regulates LDL particle internalisation. These endothelial cells are not taking in LDL cholesterol particles to kill themselves. Glucose does that.
Peter
Diabetes and cardiac apotosis
There is nothing wrong with eating carbohydrate per se. What is completely unacceptable is the development of hyperglycaemia. There may well be people who can live on a diet of yams and sweet potatoes without cardiovascular problems. I would suspect that the pre requisite is that insulin sensitivity must be such that they avoid hyperglycaemia. If they don't you end up back in to the realms of apoptosis, with your myocardial cells deciding they've had so much sugar they'd rather die than have more. They then vote with their "cytochrome c-activated caspase-3 pathway" (whatever that is: EDIT, okay I've read PSS now and have more of a clue!) and take this to its logical conclusion. Blood glucose levels of 22 mmol/l and 33 mmol/l are well within the reach of any diabetic taking the ADA dietary advice.
One of the best quotes I've ever heard was very second hand. It came from a poster on Dr Bernstein's forum who had tried to convert another type 2 diabetic to LC eating. The quote was from the LC refusenik:
"I'd rather die than eat bacon and eggs without hash browns"
So be it.
Peter
One of the best quotes I've ever heard was very second hand. It came from a poster on Dr Bernstein's forum who had tried to convert another type 2 diabetic to LC eating. The quote was from the LC refusenik:
"I'd rather die than eat bacon and eggs without hash browns"
So be it.
Peter
Food: Liver and bacon
This is what we usually do with liver. Melt lots of butter in a fryingpan (You choose how much!). Finely chop an onion or two. Turn the heat down low and allow the onion to cook slowly until it's just brown around the edges and tastes of sugar. Chop up a piece of streaky bacon per person and fry this in the middle of the onion, usually I've scraped the onion to the edges of the fryingpan at this stage. Pull the cooked bacon in to a heap with the onions at the edge of the pan and fry the liver in the space they leave. I like lamb's liver. Turn it about twice so its nicely browned on the outside. We like it cooked through so I then mix the whole lot together, cover with it over with the lid from the stockpot and let it cook on a very low heat for about another 5 minutes. Dish it up and eat. Pepper is nice somewhere along the way but for me there is enough salt in the bacon.
I don't really do sophisticated cooking!
Peter
I don't really do sophisticated cooking!
Peter
Awful offal
Your kidneys convert about 5% of your cardiac output in to primitive urine. That's a lot urine per minute. They do it day in, day out until there is no cardiac output left, hopefully >100 years down the road. Then they stop. This is hard work. Primitive urine cannot be peed down the loo. It is absolutely loaded with stuff you need to stay alive. Water for a start. And sodium. You go on a zero salt diet and your kidneys will go in to overdrive to keep you alive despite your attentiveness to the AHA. You pour glucose in to this filtrate. You waste magnesium, potassium, bicarbonate, loads of stuff you can't do without. Then you claw it all back again. Back comes the glucose, back comes the sodium, back comes the water. Your kidneys pump 180 litres of water alone back in to your bloodstream every 24 hours. All of this is done against a concentration gradient. This takes energy. Lots of it.
While you are snoozing, your muscles are snoozing too. Same for a cow. Your kidneys are continuously working their cotton socks off, 24/7. So they must have the metabolic tools to generate serious amounts of ATP. Eating muscle tissue is a massive improvement on eating a Marsbar. Eating kidneys is the next level up. Liver (with the tubes) is the most phenomenally active organ for biochemical transformation you can imagine. You want a precursor molecule for something? Look in the liver. Or an egg yolk.
Aside: It's that age old question. Why is there so much cholesterol in an egg yolk? Because that's how much it takes to make a healthy chick. Anon (unless you know better).
Anyway, you want folate? Try some liver. B12? There too. Quite a lot of cholesterol too.
What about lung tissue? Lungs are special. Oxygen is amongst the most damaging and corrosive molecules that we all depend on to stay alive. The environment in the lung is harsh for alveolar epithelial cells. So alveolar cells know all about antioxidant defences. Staying alive in the lungs needs energy. You want useful metabolic molecules? You won't get them by eating tofu! I love haggis but can't eat the barley or oats it's made with. Now, gluten free haggis maybe. Add mashed neaps with tons of butter and just enough mashed potatoes, also with tons of butter, to stay within my carb limit. And a wee dram if I'm willing to damage my joints for the pleasure. Anyway...
I won't mention brain as it's essentially unavailable in the UK. But guess where you find a number of interesting lipids in addition to cholesterol?
I could go on. I'll shut up now. I like offal.
Peter
While you are snoozing, your muscles are snoozing too. Same for a cow. Your kidneys are continuously working their cotton socks off, 24/7. So they must have the metabolic tools to generate serious amounts of ATP. Eating muscle tissue is a massive improvement on eating a Marsbar. Eating kidneys is the next level up. Liver (with the tubes) is the most phenomenally active organ for biochemical transformation you can imagine. You want a precursor molecule for something? Look in the liver. Or an egg yolk.
Aside: It's that age old question. Why is there so much cholesterol in an egg yolk? Because that's how much it takes to make a healthy chick. Anon (unless you know better).
Anyway, you want folate? Try some liver. B12? There too. Quite a lot of cholesterol too.
What about lung tissue? Lungs are special. Oxygen is amongst the most damaging and corrosive molecules that we all depend on to stay alive. The environment in the lung is harsh for alveolar epithelial cells. So alveolar cells know all about antioxidant defences. Staying alive in the lungs needs energy. You want useful metabolic molecules? You won't get them by eating tofu! I love haggis but can't eat the barley or oats it's made with. Now, gluten free haggis maybe. Add mashed neaps with tons of butter and just enough mashed potatoes, also with tons of butter, to stay within my carb limit. And a wee dram if I'm willing to damage my joints for the pleasure. Anyway...
I won't mention brain as it's essentially unavailable in the UK. But guess where you find a number of interesting lipids in addition to cholesterol?
I could go on. I'll shut up now. I like offal.
Peter
Monday, March 10, 2008
Brain on a statin
Apoptosis is an essential component of the maintenance process of our bodies. It is a highly controlled and organised technique for removing unwanted cells from any organ by the process of induced metabolic suicide.
Tinkering with this process is a potentially catastrophic game, that good old law of unintended consequences could have a field day here.
Statins promote apoptosis. They do it in diseased tissues, including cancer cells; hooray for Lipitor. Unfortunately they also do it in normal tissues too; boo for Lipitor.
Statins promote apoptosis in heart muscle. You just have to imagine what having heart muscle cells commit suicide does for your pumping ability. Most of the work on statins and myopathy focuses on coenzyme Q10 depletion. This looks to be an additional problem.
Statins promote apoptosis in the vascular epithelium. Again you just have to wonder what the death of vascular lining cells does for your circulation. Brings to mind those folks in Japan who were highly susceptible to simvastatin. This is the effect on mortality from cardiac causes when you really respond to a statin.
Statins also promote apoptosis in brain cells, or at least do so in a lab prep designed to mimic brain cells. This is your brain on a statin. Last sentence of the paper:
"These findings could contribute to elucidate the molecular mechanisms by which statins induce growth suppression and/or apoptosis in neuronal cells, and may also help to explain the CNS side effects associated with statin therapy."
Just going back to that J-Litt paper, the death rate from accidents/suicides were increased just under three fold in the TC <160mg/dl group. Seems like low cholesterol causes you to throw punches at a well armed wide boy in a down town bar.
However all is not doom and gloom. Here is your brain on chocolate!
OK, that's a complete cheat. I've absolutely no idea how much of the stearic acid in the topping of a dessert cheesecake ever gets remotely near a human brain neurone in real life. Much less activate PPAR gamma there. But I'd prefer (real) chocolate to a statin any day if I was looking to avoid Alzheimer's (or anything else for that matter).
Peter
Tinkering with this process is a potentially catastrophic game, that good old law of unintended consequences could have a field day here.
Statins promote apoptosis. They do it in diseased tissues, including cancer cells; hooray for Lipitor. Unfortunately they also do it in normal tissues too; boo for Lipitor.
Statins promote apoptosis in heart muscle. You just have to imagine what having heart muscle cells commit suicide does for your pumping ability. Most of the work on statins and myopathy focuses on coenzyme Q10 depletion. This looks to be an additional problem.
Statins promote apoptosis in the vascular epithelium. Again you just have to wonder what the death of vascular lining cells does for your circulation. Brings to mind those folks in Japan who were highly susceptible to simvastatin. This is the effect on mortality from cardiac causes when you really respond to a statin.
Statins also promote apoptosis in brain cells, or at least do so in a lab prep designed to mimic brain cells. This is your brain on a statin. Last sentence of the paper:
"These findings could contribute to elucidate the molecular mechanisms by which statins induce growth suppression and/or apoptosis in neuronal cells, and may also help to explain the CNS side effects associated with statin therapy."
Just going back to that J-Litt paper, the death rate from accidents/suicides were increased just under three fold in the TC <160mg/dl group. Seems like low cholesterol causes you to throw punches at a well armed wide boy in a down town bar.
However all is not doom and gloom. Here is your brain on chocolate!
OK, that's a complete cheat. I've absolutely no idea how much of the stearic acid in the topping of a dessert cheesecake ever gets remotely near a human brain neurone in real life. Much less activate PPAR gamma there. But I'd prefer (real) chocolate to a statin any day if I was looking to avoid Alzheimer's (or anything else for that matter).
Peter
Food; Mutton or lamb in orange sauce
This is the plan for the left over mutton tonight:
Spicy Orange Lamb adapted from Ken Hom.
You can use fresh lamb, briefly stir fried, if you have it to hand. I've got cold mutton!
Melt lots of butter in a wok. Throw in as much garlic as you like (say four cloves, finely sliced), about a cubic inch of fresh root ginger, peeled and finely chopped and the thinly peeled rind of an orange (no pith), also finely chopped. And some pepper, plenty of salt will come from the soy sauce.
After a few seconds of stir frying throw in the cubed lamb/mutton and cook until the fat is soft. Add two tablespoons of fresh orange juice from the orange that provided the peel and as much soy sauce (gluten free, we use Tamari) as you feel is safe on an excitotoxin basis. I have been known to throw in a little cooking sherry or white wine. Cook it a bit longer, maybe 5 mins. Add a little sesame oil just before serving.
It will probably go with chips tonight, might use sweet potatoes, but any other carb source would do. You know how you need something to soak up the butter sauce...
Spicy Orange Lamb adapted from Ken Hom.
You can use fresh lamb, briefly stir fried, if you have it to hand. I've got cold mutton!
Melt lots of butter in a wok. Throw in as much garlic as you like (say four cloves, finely sliced), about a cubic inch of fresh root ginger, peeled and finely chopped and the thinly peeled rind of an orange (no pith), also finely chopped. And some pepper, plenty of salt will come from the soy sauce.
After a few seconds of stir frying throw in the cubed lamb/mutton and cook until the fat is soft. Add two tablespoons of fresh orange juice from the orange that provided the peel and as much soy sauce (gluten free, we use Tamari) as you feel is safe on an excitotoxin basis. I have been known to throw in a little cooking sherry or white wine. Cook it a bit longer, maybe 5 mins. Add a little sesame oil just before serving.
It will probably go with chips tonight, might use sweet potatoes, but any other carb source would do. You know how you need something to soak up the butter sauce...
Ah well, another night without raw cabbage.
Peter
Peter
Food; Mutton followed by cheesecake
Last weekend we happened on the Farmer's Market in Newbury, completely by chance. Some serious meat and free bones. Happy!
Yesterday's supper, a 1.3kg breast of mutton. I just stuck it in the Chicken Brick with two small potatoes and two small parsnips (chopped and posted in to the space around the meat). I added some beef dripping to get the veggies started before enough fat melted out of the mutton to start them roasting properly. Sprinkled salt over the lot. Stuck the whole thing in to a fan assisted oven at 150 deg C for 2 and a quarter hours. It was good. The junkfood was the cauliflower we ate with it.
The Chicken Brick.
For afters we had cheesecake. The cake base was 200g nuts chopped in a blender, solidified with 50g butter and sweetened with 25g honey. Junk food; a layer of blueberries. Cheese part was a 50:50 mix of Mascarpone and creme fraiche, a capful of vanilla and 25g honey. Topping was a 100g bar of 70% cocoa chocolate melted. Boil 100ml of cream, mix with the chocolate and throw in 25g butter. Stir until even, allow to cool slightly and pour on while still liquid enough to be self leveling. Stick it in the fridge and wait while the mutton digests enough to leave some room, then eat.
It's quite nice. You can always adjust sweetness to taste/carb limits. I didn't count anything with this!
Peter
Yesterday's supper, a 1.3kg breast of mutton. I just stuck it in the Chicken Brick with two small potatoes and two small parsnips (chopped and posted in to the space around the meat). I added some beef dripping to get the veggies started before enough fat melted out of the mutton to start them roasting properly. Sprinkled salt over the lot. Stuck the whole thing in to a fan assisted oven at 150 deg C for 2 and a quarter hours. It was good. The junkfood was the cauliflower we ate with it.
The Chicken Brick.
For afters we had cheesecake. The cake base was 200g nuts chopped in a blender, solidified with 50g butter and sweetened with 25g honey. Junk food; a layer of blueberries. Cheese part was a 50:50 mix of Mascarpone and creme fraiche, a capful of vanilla and 25g honey. Topping was a 100g bar of 70% cocoa chocolate melted. Boil 100ml of cream, mix with the chocolate and throw in 25g butter. Stir until even, allow to cool slightly and pour on while still liquid enough to be self leveling. Stick it in the fridge and wait while the mutton digests enough to leave some room, then eat.
It's quite nice. You can always adjust sweetness to taste/carb limits. I didn't count anything with this!
Peter
Saturday, March 08, 2008
Gluten and rheumatoid arthritis
The quote below comes from Dr Freed, written in an editorial for the British Medical Journal, to commemorate the public sacrifice of Dr Arpad Pusztai on the altar of GM agribusiness (see the last line of the editorial). Dr Freed:
"Lectins stimulate class II HLA antigens on cells that do not normally display them"
Wheat germ agglutinin is a lectin and sections of gliadin (in gluten) are "lectin like". If you have an auto immune disease the quote is quite important. What is a class II HLA antigen?
If you really really want to know you can have a look here, which explains what MHC class I and class II molecules are. It's the simplified version, including the sausage in a hot dog metaphor which made my wife laugh. Sort of. EDIT: You probably need to know she's an immunologist to understand that last comment.
Here's a rough translation.
Class II molecules sit on the surface of cells, holding out a fragment of foreign protein (in this case a short fragment of gluten). Only certain sub families of immune cells should do this, certainly it should never be done by tissue cells of organs like the pancreas or thyroid as cited by Freed. I would add joint cells in the case of rheumatoid arthritis.
Class II expression is different from MIC expression but just as bad, if not worse.
Waving around a class II molecule on your cell surface is a direct invitation to a subset of white blood cells (in particular a sub group of lymphocytes, ie those with a certain molecule called the CD4 molecule on their surface) to come and interact with the cell displaying the Class II marker. CD4 molecules generally "talk to" class II molecules.
The class II marker molecule has to be holding out a gluten fragment and the CD4+ cell has to be able to recognise that fragment for them to interact. Given this situation, things happen. The CD4 positive cell does several things, one of which is that it starts producing lymphokines. That is it causes inflammation. Note that antibody production is not needed for this to occur.
Of course once the CD4+ cell has seen gluten it may well trot off to get antibodies produced. Or it may not. The immune system is frighteningly complex. If the CD4+ cell does interact with an antibody producing lymphocyte you get this.
Avoiding gluten helps. Forget the vegan bit, it's a failure to control variables in the study and not remotely needed. The gluten avoidance is essential.
LC is very helpful too. I'll post the refs some time but basic premise is that the inflammatory soup production in response to class II/CD4 interaction is controlled to a large extent by NF kappa B, which is controlled by insulin which is controlled by carbohydrate in the diet. Insulin per se is anti inflammatory, chronic hyperinsulinaemia is pro inflammatory.
There are also non specific effects of PUFA in propagating the free radicals generated by the inflammatory response. Suet and dripping contain far more stable fats than vegetable oil does and these highly saturated fatty acids are almost immune to free radical attack in an inflammatory soup.
Vitamin D modulates the irritablity of most cells in the immune system so supplementation or serious sun bathing, without sun burn, probably has an effect to diminish all auto immune problems.
If you read the whole vegan paper you will see there was no radiographic improvement, though patients felt better. Too much carbohyrate, too many PUFA and there are several other plant sources of lectins beyond gluten. Anecdotally nightshade lectins (also mentioned by Freed) can be a potent trigger for rheumatoid arthritis in much the same way as gluten.
That's without going on to Ebringer's work on bacterial proteins and rheumatoid disease....
This aspect is probably also amenable to LC eating. Anyone with a degree of insulin resistance may well be transiently glucosuric on occasions while eating a normal diet. Bacteria love glucose. LC eating should starve any Proteus in the urinary tract because it stops any glycosuria. Proteus also lives in our gut and starving it here too, this time by fiber avoidance, would probably help.
So there are a few factors involved in rheumatoid arthritis. A serious LC, high saturated fat and minimal lectin diet should help.
As would an all over tan.
Peter
"Lectins stimulate class II HLA antigens on cells that do not normally display them"
Wheat germ agglutinin is a lectin and sections of gliadin (in gluten) are "lectin like". If you have an auto immune disease the quote is quite important. What is a class II HLA antigen?
If you really really want to know you can have a look here, which explains what MHC class I and class II molecules are. It's the simplified version, including the sausage in a hot dog metaphor which made my wife laugh. Sort of. EDIT: You probably need to know she's an immunologist to understand that last comment.
Here's a rough translation.
Class II molecules sit on the surface of cells, holding out a fragment of foreign protein (in this case a short fragment of gluten). Only certain sub families of immune cells should do this, certainly it should never be done by tissue cells of organs like the pancreas or thyroid as cited by Freed. I would add joint cells in the case of rheumatoid arthritis.
Class II expression is different from MIC expression but just as bad, if not worse.
Waving around a class II molecule on your cell surface is a direct invitation to a subset of white blood cells (in particular a sub group of lymphocytes, ie those with a certain molecule called the CD4 molecule on their surface) to come and interact with the cell displaying the Class II marker. CD4 molecules generally "talk to" class II molecules.
The class II marker molecule has to be holding out a gluten fragment and the CD4+ cell has to be able to recognise that fragment for them to interact. Given this situation, things happen. The CD4 positive cell does several things, one of which is that it starts producing lymphokines. That is it causes inflammation. Note that antibody production is not needed for this to occur.
Of course once the CD4+ cell has seen gluten it may well trot off to get antibodies produced. Or it may not. The immune system is frighteningly complex. If the CD4+ cell does interact with an antibody producing lymphocyte you get this.
Avoiding gluten helps. Forget the vegan bit, it's a failure to control variables in the study and not remotely needed. The gluten avoidance is essential.
LC is very helpful too. I'll post the refs some time but basic premise is that the inflammatory soup production in response to class II/CD4 interaction is controlled to a large extent by NF kappa B, which is controlled by insulin which is controlled by carbohydrate in the diet. Insulin per se is anti inflammatory, chronic hyperinsulinaemia is pro inflammatory.
There are also non specific effects of PUFA in propagating the free radicals generated by the inflammatory response. Suet and dripping contain far more stable fats than vegetable oil does and these highly saturated fatty acids are almost immune to free radical attack in an inflammatory soup.
Vitamin D modulates the irritablity of most cells in the immune system so supplementation or serious sun bathing, without sun burn, probably has an effect to diminish all auto immune problems.
If you read the whole vegan paper you will see there was no radiographic improvement, though patients felt better. Too much carbohyrate, too many PUFA and there are several other plant sources of lectins beyond gluten. Anecdotally nightshade lectins (also mentioned by Freed) can be a potent trigger for rheumatoid arthritis in much the same way as gluten.
That's without going on to Ebringer's work on bacterial proteins and rheumatoid disease....
This aspect is probably also amenable to LC eating. Anyone with a degree of insulin resistance may well be transiently glucosuric on occasions while eating a normal diet. Bacteria love glucose. LC eating should starve any Proteus in the urinary tract because it stops any glycosuria. Proteus also lives in our gut and starving it here too, this time by fiber avoidance, would probably help.
So there are a few factors involved in rheumatoid arthritis. A serious LC, high saturated fat and minimal lectin diet should help.
As would an all over tan.
Peter
Wednesday, March 05, 2008
Familial Hypercholesterolaemia and porcelain
What IS an LDL particle? There is a very neat picture here. Perhaps the most striking thing about it is that there is only one single protein molecule embedded in the particle surface, the apo-B100 protein molecule. It wraps neatly around the sphere of lipid to give support and identity. Identity is very important.
Of course the LDL particle has to come from somewhere. It is derived from IDL (Intermediate Density Lipoprotein) and before that from VLDL (Very Low Density Lipoprotein), which was secreted by the liver. All of these precursors also have the apo-B100 protein molecule, plus a whole load of other proteins too, apo-C1, apo-C2, apo-C3, and apo E. VLDLs are big (relatively), they need to be to fit all those proteins on to their surface! Most of these proteins are there to either turn on or turn of lipoprotein lipase, in order to get fatty acids from the lipid particle in to cells. That's how lipids get bulk transported. Apo-E gets the particle back in to the liver, should the liver want it back.
Quite where all of these proteins disappear to as LDL is formed is a bit of a mystery to me. Certainly it looks like LDL, derived from IDL/VLDL, has only apo-B100 and none of the other surface proteins of VLDL/IDL particles. Probably they hop on to HDL particles. Some of them came from there in the first place, rather than the liver directly, so that would be appropriate.
So there is this bag of lipid with just one identification tag on its surface, looking for a home. There is a receptor which exactly fits the apo-B100 id tag. The LDL cholesterol receptor. This is the archetypal, best studied endocytosis receptor of all time. LDL attaches to this receptor and the whole lipoprotein is engulfed by the cell sporting the receptor. The particle gets stripped of the engulfing apparatus, eventually fused with a lysosome and the cell is in clover with a supply of both lipid and cholesterol. It recycles the LDL receptor to the cell surface and does it all again. Cells appear to need both lipid and cholesterol.
But here's the interesting bit. The LDL receptor is a statin as in:
"Consistent with this hypothesis, they found that addition of LDL to the culture medium of normal human fibroblasts inhibits the activity of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMG-CoA reductase), the rate-limiting enzyme in the cholesterol biosynthetic pathway
EDIT: When you go to the original authors it becomes obvious that it is the cholesterol itself which inhibits HMG-CoA, a classic negative feed back mechanism. Have to do some more thinking about xanthomata. End edit.
The LDL receptor inhibits the intracellular synthesis of cholesterol, at the HMG-CoA step, when activated by an LDL particle. There is impeccable logic to this. Cholesterol is a complex molecule, synthesised in a stupendously intricate and energy demanding process. Usually the liver does this for cells of the body, shipping it out in lipoprotein particles. After all the liver is a biosynthetic powerhouse with lots of energy to play with. It's not some poor smooth muscle cell or fibroblast struggling to make metabolic ends meet in the arterial media. If, as a cell, you have just swallowed a big ball of cholesterol you can afford to switch off the production apparatus. It would be wasteful not to.
Cells need cholesterol. Homozygous familial hypercholesterolaemia means that a patient's cells have zero functional LDL receptors. If they can't get cholesterol by swallowing whole LDL particles they really do have to make it themselves. But the other feature of a non functional LDL receptor (remember, it's a statin) is that it doesn't give the ability to limit local cholesterol synthesis, so there might be quite a lot of cholesterol made. Enough to generate tendon xanthomas. These xanthomas should be composed of cholesterol synthesised from acetate in local cells, not from sticky LDL particles. I don't suppose anyone has checked this.
The synthesis of one molecule of cholesterol requires 14 NADPH molecules and 18 ATPs. It yields 6 phosphate (Pi) molecules and 4 pyrophosphate (PPi) molecules. While PPi appears to be an inhibitor of soft tissue calcification Pi is a promoter. Alkaline phosphatase, an enzyme whose production is upregulated by hyperglycaemia, converts PPi (calcification inhibitor) to Pi (calcification promoter). Hyperglycaemia is a feature of refined carbohydrate diets. Did I say low fat?
So there is the potential for an awful lot of inorganic phosphate ions, possibly 14 per molecule, being produced as a spin off from cholesterol synthesis on low fat diets. One LDL particle provides about 2000 molecules of cholesterol.
We know that insulin converts smooth muscle cells to bone secreting cells. Local cholesterol synthesis provides a supply of inorganic phosphate. A low fat (high sugar) diet raises insulin.
Perhaps it should come as no surprise that there is the phenomenon of "porcelain aorta", seen in patients with homozygous familial hyprecholesterolaemia. Aortic cells manufacturing cholesterol, which they can't get from LDL, produce inorganic phosphate and pyrophosphate as a spin off from the synthesis. A modern low fat diet, based on sugar, elevates blood glucose which increases alkaline phosphatase production and so the conversion of pyrophosphate to inorganic phosphate. A modern low fat diet elevates insulin too, which makes smooth muscle cells secrete bone matrix proteins.
Add calcium to phosphate in soft tissues and you have bone.
How good is the evidence base for current dietary recommendations in Familial Hypercholesterolaemia, particularly in children, who don't seem to get put on a pharmaceutical statin (yet)?
The Cochrane Review seems to think they are completely unsubstantiated.
Should all homozygous FH people be on a pharmaceutical statin? Another post there.
Peter
NB I didn't see any calcium or phosphate in that picture of the LDL particle. Soddy: "Rutherford, this is transmutation!" Rutherford snapped back, "For Christ's sake, Soddy, don't call it transmutation. They'll have our heads off as alchemists." Or cardiologists.
Of course the LDL particle has to come from somewhere. It is derived from IDL (Intermediate Density Lipoprotein) and before that from VLDL (Very Low Density Lipoprotein), which was secreted by the liver. All of these precursors also have the apo-B100 protein molecule, plus a whole load of other proteins too, apo-C1, apo-C2, apo-C3, and apo E. VLDLs are big (relatively), they need to be to fit all those proteins on to their surface! Most of these proteins are there to either turn on or turn of lipoprotein lipase, in order to get fatty acids from the lipid particle in to cells. That's how lipids get bulk transported. Apo-E gets the particle back in to the liver, should the liver want it back.
Quite where all of these proteins disappear to as LDL is formed is a bit of a mystery to me. Certainly it looks like LDL, derived from IDL/VLDL, has only apo-B100 and none of the other surface proteins of VLDL/IDL particles. Probably they hop on to HDL particles. Some of them came from there in the first place, rather than the liver directly, so that would be appropriate.
So there is this bag of lipid with just one identification tag on its surface, looking for a home. There is a receptor which exactly fits the apo-B100 id tag. The LDL cholesterol receptor. This is the archetypal, best studied endocytosis receptor of all time. LDL attaches to this receptor and the whole lipoprotein is engulfed by the cell sporting the receptor. The particle gets stripped of the engulfing apparatus, eventually fused with a lysosome and the cell is in clover with a supply of both lipid and cholesterol. It recycles the LDL receptor to the cell surface and does it all again. Cells appear to need both lipid and cholesterol.
But here's the interesting bit. The LDL receptor is a statin as in:
"Consistent with this hypothesis, they found that addition of LDL to the culture medium of normal human fibroblasts inhibits the activity of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMG-CoA reductase), the rate-limiting enzyme in the cholesterol biosynthetic pathway
EDIT: When you go to the original authors it becomes obvious that it is the cholesterol itself which inhibits HMG-CoA, a classic negative feed back mechanism. Have to do some more thinking about xanthomata. End edit.
The LDL receptor inhibits the intracellular synthesis of cholesterol, at the HMG-CoA step, when activated by an LDL particle. There is impeccable logic to this. Cholesterol is a complex molecule, synthesised in a stupendously intricate and energy demanding process. Usually the liver does this for cells of the body, shipping it out in lipoprotein particles. After all the liver is a biosynthetic powerhouse with lots of energy to play with. It's not some poor smooth muscle cell or fibroblast struggling to make metabolic ends meet in the arterial media. If, as a cell, you have just swallowed a big ball of cholesterol you can afford to switch off the production apparatus. It would be wasteful not to.
Cells need cholesterol. Homozygous familial hypercholesterolaemia means that a patient's cells have zero functional LDL receptors. If they can't get cholesterol by swallowing whole LDL particles they really do have to make it themselves. But the other feature of a non functional LDL receptor (remember, it's a statin) is that it doesn't give the ability to limit local cholesterol synthesis, so there might be quite a lot of cholesterol made. Enough to generate tendon xanthomas. These xanthomas should be composed of cholesterol synthesised from acetate in local cells, not from sticky LDL particles. I don't suppose anyone has checked this.
The synthesis of one molecule of cholesterol requires 14 NADPH molecules and 18 ATPs. It yields 6 phosphate (Pi) molecules and 4 pyrophosphate (PPi) molecules. While PPi appears to be an inhibitor of soft tissue calcification Pi is a promoter. Alkaline phosphatase, an enzyme whose production is upregulated by hyperglycaemia, converts PPi (calcification inhibitor) to Pi (calcification promoter). Hyperglycaemia is a feature of refined carbohydrate diets. Did I say low fat?
So there is the potential for an awful lot of inorganic phosphate ions, possibly 14 per molecule, being produced as a spin off from cholesterol synthesis on low fat diets. One LDL particle provides about 2000 molecules of cholesterol.
We know that insulin converts smooth muscle cells to bone secreting cells. Local cholesterol synthesis provides a supply of inorganic phosphate. A low fat (high sugar) diet raises insulin.
Perhaps it should come as no surprise that there is the phenomenon of "porcelain aorta", seen in patients with homozygous familial hyprecholesterolaemia. Aortic cells manufacturing cholesterol, which they can't get from LDL, produce inorganic phosphate and pyrophosphate as a spin off from the synthesis. A modern low fat diet, based on sugar, elevates blood glucose which increases alkaline phosphatase production and so the conversion of pyrophosphate to inorganic phosphate. A modern low fat diet elevates insulin too, which makes smooth muscle cells secrete bone matrix proteins.
Add calcium to phosphate in soft tissues and you have bone.
How good is the evidence base for current dietary recommendations in Familial Hypercholesterolaemia, particularly in children, who don't seem to get put on a pharmaceutical statin (yet)?
The Cochrane Review seems to think they are completely unsubstantiated.
Should all homozygous FH people be on a pharmaceutical statin? Another post there.
Peter
NB I didn't see any calcium or phosphate in that picture of the LDL particle. Soddy: "Rutherford, this is transmutation!" Rutherford snapped back, "For Christ's sake, Soddy, don't call it transmutation. They'll have our heads off as alchemists." Or cardiologists.
Thursday, February 28, 2008
Cholesterol (the HDL sort) kills?
This article was picked up by GinnyL, a prolific reader of diabetes news and a poster on Dr Bernstein's site. There are no links to anywhere from the article, so I pubmeded the guy who got a mention by name, Dr Genest, for 2008, and came up with this ref, which I can get at the full text of.
BTW there are some interesting papers of FH he's published, maybe another day.
There's a lot of waffle but you do get the fact he is talking about EPIC-Norfolk and IDEAL. This appears to be a reasonable summary of their findings:
The more HDL particles you have the better, the less cholesterol in the particles the better. ie you want to have a high HDL-C particle count with not too much cholesterol in each particle.
Your lab work merely picks out any HDL it can find, measures the total cholesterol in this fraction and gives you that number. Compare this to the accepted wisdom re LDL-C, typically from Dr Davis:
Your lab work just picks out the LDL, measures the cholesterol and guesses (sorry, calculates) an approximate number. Actually that's completely wrong. The lab measures the TC, subtracts a few numbers, adds VAT, subtracts the first number you thought of and that's the best guess of your LDL-C concentration. Maybe.
Anyway, if your really do measure particle sizes/numbers, the fewer LDL particles you have better, the more cholesterol in each particle the better.
Are you seeing a pattern here? It all comes down to particle numbers, sizes, contents. What controls all of these? Not statin deficiencies, as in IDEAL.
Forget your cholesterol. What marker predicts heart attacks and total mortality without all of the paradoxes?
Follow EPIC and HbA1c (yes, same that same EPIC study as this one) to get some sort of clue. Control what you are doing wrong diet/lifestyle-wise to glycosylate your haemoglobin and your liver will sort out whatever cholesterol particles sizes/numbers it needs for health.
The EPIC/IDEAL paper is quite amusing for the shock horror throughout the discussion that high HDL could be killing people via heart attacks, but you get used this sort of rhetoric from cardiologists. It sort of gets summed up by Dr Genest's comments about torcetrapib:
"The second such compound, torcetrapib, proved toxic despite causing a large increase in HDL-C levels and was withdrawn from clinical use"
No, Dr Genest, think again. Perhaps it's not "despite", perhaps it's "because". Perhaps it is the artificial packing of cholesterol in to HDL particles which was toxic, not the drug per se. Treating a lab number is all torcetrapib did, it's for idiots. Sort out your diet so as to live within the limits of your own personal level of insulin resistance and leave your lipids alone. On Kitava and for the fishing Bantu this can involve 70% of calories from carbohydrate producing an HDL <1.0mmol/l with excellent cardiovascular health. For an insulin resistant Norfolk diabetic it might mean 5% of calories from carbs and the rest from saturated fat giving an HDL of 2.0mmol/l.
It's not the labels on the lipids that do the damage.
Peter
PS Also from Dr Genest
"Mutations that impair the function of cholesteryl ester transfer protein (CETP) are associated with marked elevations in HDL-C levels but not necessarily with protection against coronary heart disease (8)"
Ref (8) does not quite say that the mutation (the one which torectrapib mimicked) was neutral, it said it was bad. Naughty mis-citation. He must be a cardiologist. And people are surprised at torcetrapib killing people, using heart attacks? Torcetrapib was a success, it did exactly what it should do! The Zhong et al paper was published in 1996. It was the basis for the development of torcetrapib. You can't say Pfizer didn't know what they were doing. You can't understand why they did it either.
BTW there are some interesting papers of FH he's published, maybe another day.
There's a lot of waffle but you do get the fact he is talking about EPIC-Norfolk and IDEAL. This appears to be a reasonable summary of their findings:
The more HDL particles you have the better, the less cholesterol in the particles the better. ie you want to have a high HDL-C particle count with not too much cholesterol in each particle.
Your lab work merely picks out any HDL it can find, measures the total cholesterol in this fraction and gives you that number. Compare this to the accepted wisdom re LDL-C, typically from Dr Davis:
Your lab work just picks out the LDL, measures the cholesterol and guesses (sorry, calculates) an approximate number. Actually that's completely wrong. The lab measures the TC, subtracts a few numbers, adds VAT, subtracts the first number you thought of and that's the best guess of your LDL-C concentration. Maybe.
Anyway, if your really do measure particle sizes/numbers, the fewer LDL particles you have better, the more cholesterol in each particle the better.
Are you seeing a pattern here? It all comes down to particle numbers, sizes, contents. What controls all of these? Not statin deficiencies, as in IDEAL.
Forget your cholesterol. What marker predicts heart attacks and total mortality without all of the paradoxes?
Follow EPIC and HbA1c (yes, same that same EPIC study as this one) to get some sort of clue. Control what you are doing wrong diet/lifestyle-wise to glycosylate your haemoglobin and your liver will sort out whatever cholesterol particles sizes/numbers it needs for health.
The EPIC/IDEAL paper is quite amusing for the shock horror throughout the discussion that high HDL could be killing people via heart attacks, but you get used this sort of rhetoric from cardiologists. It sort of gets summed up by Dr Genest's comments about torcetrapib:
"The second such compound, torcetrapib, proved toxic despite causing a large increase in HDL-C levels and was withdrawn from clinical use"
No, Dr Genest, think again. Perhaps it's not "despite", perhaps it's "because". Perhaps it is the artificial packing of cholesterol in to HDL particles which was toxic, not the drug per se. Treating a lab number is all torcetrapib did, it's for idiots. Sort out your diet so as to live within the limits of your own personal level of insulin resistance and leave your lipids alone. On Kitava and for the fishing Bantu this can involve 70% of calories from carbohydrate producing an HDL <1.0mmol/l with excellent cardiovascular health. For an insulin resistant Norfolk diabetic it might mean 5% of calories from carbs and the rest from saturated fat giving an HDL of 2.0mmol/l.
It's not the labels on the lipids that do the damage.
Peter
PS Also from Dr Genest
"Mutations that impair the function of cholesteryl ester transfer protein (CETP) are associated with marked elevations in HDL-C levels but not necessarily with protection against coronary heart disease (8)"
Ref (8) does not quite say that the mutation (the one which torectrapib mimicked) was neutral, it said it was bad. Naughty mis-citation. He must be a cardiologist. And people are surprised at torcetrapib killing people, using heart attacks? Torcetrapib was a success, it did exactly what it should do! The Zhong et al paper was published in 1996. It was the basis for the development of torcetrapib. You can't say Pfizer didn't know what they were doing. You can't understand why they did it either.
Wednesday, February 27, 2008
Gluten and NK cells (forget the antibodies)
I just thought I'd stick this down as it's minor and it will get forgotten if I don't say something. There are grades/types of inflammatory bowel disease. The really easy one to treat is coeliac disease, where gluten avoidance is all that is required. There are also a host of problems which are responsive to gluten avoidance which do not come up positive on antibody test or have "typical" coeliac gut biopsy results.
I stumbled across this paper which grabbed me because my wife works with Natural Killer (NK) cells and has pointed out their relevance to surviving diseases before antibodies kick in. I was lucky to get the full text.
This is from the introduction, before it discusses coeliac disease, which is the second disease it covers (rheumatoid arthritis is the first):
"MIC A/B are stress-induced molecules acting as danger signals to alert NK cells and CD8 T lymphocytes through engagement of the NKG2D activating receptor [2]. At variance with classical MHC class I molecules, MIC are specialized for reporting stress without the requirement for peptide (or other ligand) binding and can direct NK and T cells to kill transformed or infected cells."
This translates as:
Gluten stresses your gut cells. They scream on the molecular level. NK cells cells get in there and put them out of their misery. This is (auto) immunity. It does NOT REQUIRE antibody production.
Background
Antibody production appears to be an add on to the immune system, a memory storage facility for preventing future re infection with a previous encountered bug. The acute survival of an infection, like influenza, relies on the innate immune system, based around NK cells. If you had to wait 10 days for your lymphocytes to get around to antibody production before you recovered, all viruses would be lethal. NK cells are non specific and use molecules like MIC as markers that something is seriously wrong with a cell and it's time to get killin'. MIC is a like a large target sign painted on a cell and NK cells are equipped an AK47 looking for that target. Usually a cell expressing MIC is infected, but gluten appears to do as much "stressing" as a viral infection.
Relevance:
Gluten reactions do not need antibody production. It is perfectly possible to have serious on going gut damage without a positive antibody test. Statistically it is quite probable that you WILL get a positve antibody test. There is so much damage going in that battlefield which is your gut under the influence of gluten that there is a trauma "soup". All you need is for an "antigen presenting cell" (APC) to collect some gluten from this soup, give it to your lymphocytes and tell them "we want this stuff recognised by an antibody, get producing". Of course the APC may pick up tissue transaminase, endomysial protein or any of a host of other proteins to push at the lymphocytes (which make the antibodies). But there is a chance you may not get either gluten or transaminase etc presented (ie no antibodies in our current lab tests), so you continue with "psychosomatic" gut problems or get labeled as inflammatory bowel disease, which is not regarded as gluten responsive. Severe IBD requires more than gluten avoidance but this basic step is probably essential.
Antibodies are a consequence, and an amplifier, of gluten toxicity, not a cause. That's intrinsic to gluten, MIC and NK cells. What brought this on?
Speculation time.
Did I have psoriasis or Dermatitis Herpetiformis (essentially coeliac disease of the skin)?
Answer: Maybe it's the same parallel as gut problems. WGA certainly gets in to the systemic circulation. I think it's a reasonable assumption gluten does too. It will be landing on vascular and/or dermal cells in the skin. Gluten induced stress here results in MIC expression. NK cells have that AK47, an itchy trigger finger and are seriously looking for MIC. Sometimes there is antibody production, sometimes there isn't. This could easily be the result of receptor subtypes (genetic) on your antigen presenting cells. Different labels, different lab results (if it ever gets that far) but a similar approach is needed. Perhaps there are a host of immune mediated problems triggered by gluten that are not antibody producing.
Peter
I stumbled across this paper which grabbed me because my wife works with Natural Killer (NK) cells and has pointed out their relevance to surviving diseases before antibodies kick in. I was lucky to get the full text.
This is from the introduction, before it discusses coeliac disease, which is the second disease it covers (rheumatoid arthritis is the first):
"MIC A/B are stress-induced molecules acting as danger signals to alert NK cells and CD8 T lymphocytes through engagement of the NKG2D activating receptor [2]. At variance with classical MHC class I molecules, MIC are specialized for reporting stress without the requirement for peptide (or other ligand) binding and can direct NK and T cells to kill transformed or infected cells."
This translates as:
Gluten stresses your gut cells. They scream on the molecular level. NK cells cells get in there and put them out of their misery. This is (auto) immunity. It does NOT REQUIRE antibody production.
Background
Antibody production appears to be an add on to the immune system, a memory storage facility for preventing future re infection with a previous encountered bug. The acute survival of an infection, like influenza, relies on the innate immune system, based around NK cells. If you had to wait 10 days for your lymphocytes to get around to antibody production before you recovered, all viruses would be lethal. NK cells are non specific and use molecules like MIC as markers that something is seriously wrong with a cell and it's time to get killin'. MIC is a like a large target sign painted on a cell and NK cells are equipped an AK47 looking for that target. Usually a cell expressing MIC is infected, but gluten appears to do as much "stressing" as a viral infection.
Relevance:
Gluten reactions do not need antibody production. It is perfectly possible to have serious on going gut damage without a positive antibody test. Statistically it is quite probable that you WILL get a positve antibody test. There is so much damage going in that battlefield which is your gut under the influence of gluten that there is a trauma "soup". All you need is for an "antigen presenting cell" (APC) to collect some gluten from this soup, give it to your lymphocytes and tell them "we want this stuff recognised by an antibody, get producing". Of course the APC may pick up tissue transaminase, endomysial protein or any of a host of other proteins to push at the lymphocytes (which make the antibodies). But there is a chance you may not get either gluten or transaminase etc presented (ie no antibodies in our current lab tests), so you continue with "psychosomatic" gut problems or get labeled as inflammatory bowel disease, which is not regarded as gluten responsive. Severe IBD requires more than gluten avoidance but this basic step is probably essential.
Antibodies are a consequence, and an amplifier, of gluten toxicity, not a cause. That's intrinsic to gluten, MIC and NK cells. What brought this on?
Speculation time.
Did I have psoriasis or Dermatitis Herpetiformis (essentially coeliac disease of the skin)?
Answer: Maybe it's the same parallel as gut problems. WGA certainly gets in to the systemic circulation. I think it's a reasonable assumption gluten does too. It will be landing on vascular and/or dermal cells in the skin. Gluten induced stress here results in MIC expression. NK cells have that AK47, an itchy trigger finger and are seriously looking for MIC. Sometimes there is antibody production, sometimes there isn't. This could easily be the result of receptor subtypes (genetic) on your antigen presenting cells. Different labels, different lab results (if it ever gets that far) but a similar approach is needed. Perhaps there are a host of immune mediated problems triggered by gluten that are not antibody producing.
Peter
Saturday, February 23, 2008
What, Sweden again?
I've had this paper kicking around since it was published. There are a few things which grabbed me about it. I was initially a bit dubious; a diet containing 20% of calories as carbohydrate didn't really seem low enough to be seriously useful for a diabetic. But then I twigged that these people were using a calorie restricted diet, so the absolute amounts of carbs were actually down at 80-90g/d. That's just above Dr Lutz's suggestion of 72g/d and not hugely above Kwasniewski's recommendations. Of course it's WAY above Dr Bernstein's recommendations (30g/d), but he really is a perfectionist, a good one too. The 50% of calories from dietary fat under weight loss conditions was obviously being supplemented from stored adipose tissue (quite highly saturated I believe), hence the weight loss.
These are some of the sections of text I particularly enjoyed.
From the introduction:
"The objective of the present study, therefore, was to determine to what degree the changes among the 16 patients in the low-carbohydrate diet group at 6-months were preserved or changed 22 months after start, even without close follow-up. In addition, we report that, after the 6 month observation period, two thirds of the patients in the high-carbohydrate changed their diet. This group also showed improvement in bodyweight and glycemic control."
OK, it's a short study. A couple of years is way too quick to see changes in heart attack rate from eating all that fat. Isn't it? You know, fatty streaks to soft plaque to... (yawn)
The other feature here was the comment about "changed their diet" applied to the control group (low fat, ADA style diet). It's made clearer in the methods:
"Seven of the controls switched to a 20 % carbohydrate diet immediately after the follow-up period. For those we have data 12–14 months after the change. Three more have later sought information and have changed diet. We have no long-term data for those. Five of the original controls have not changed diet."
This was an open study by the look of it. You can't spend hours sitting in a diabetes clinic chatting to someone who is loosing weight, dropping HbA1c and binning their insulin without realising that the LC intervention diet works. Only an ADA diabetologist is stupid enough to miss this. Given the option to change, you change. Unless you really are as stupid as...
But of course, all of that fat will have the LC diet group dropping like flies from heart attacks. We all know that. We've been told.
So, from the discussion:
"We have examined the medical charts for both the original high-carbohydrate group and the low-carbohydrate group from 3 months after the initiation of the diet therapy – when an effect might be detected – and forward for episodes of cardiovascular disease. Three episodes of cardiovascular disease have occurred among the 5 patients that never changed diet. The 16 patients in the low-carbohydrate diet group (19 months observation time) and the 7 from the high-carbohydrate diet group that changed diet (10 months observation time) – totalling 23 patients – have been free of cardiovascular disease during the follow-up period (p < 0.03. Fischer Exact)."
So we have three out of five people with episodes of CV disease during about a year of ADA style low fat diet and zero out of 23 patients on Lutz style high fat.
Must be a paradox. Ha! (now think of the Queen launching a new ship) I name this paradox "The Swedish Paradox".
What, again? Ok, there are only a limited number of countries in the world and so many paradoxes looking for names...
Peter
These are some of the sections of text I particularly enjoyed.
From the introduction:
"The objective of the present study, therefore, was to determine to what degree the changes among the 16 patients in the low-carbohydrate diet group at 6-months were preserved or changed 22 months after start, even without close follow-up. In addition, we report that, after the 6 month observation period, two thirds of the patients in the high-carbohydrate changed their diet. This group also showed improvement in bodyweight and glycemic control."
OK, it's a short study. A couple of years is way too quick to see changes in heart attack rate from eating all that fat. Isn't it? You know, fatty streaks to soft plaque to... (yawn)
The other feature here was the comment about "changed their diet" applied to the control group (low fat, ADA style diet). It's made clearer in the methods:
"Seven of the controls switched to a 20 % carbohydrate diet immediately after the follow-up period. For those we have data 12–14 months after the change. Three more have later sought information and have changed diet. We have no long-term data for those. Five of the original controls have not changed diet."
This was an open study by the look of it. You can't spend hours sitting in a diabetes clinic chatting to someone who is loosing weight, dropping HbA1c and binning their insulin without realising that the LC intervention diet works. Only an ADA diabetologist is stupid enough to miss this. Given the option to change, you change. Unless you really are as stupid as...
But of course, all of that fat will have the LC diet group dropping like flies from heart attacks. We all know that. We've been told.
So, from the discussion:
"We have examined the medical charts for both the original high-carbohydrate group and the low-carbohydrate group from 3 months after the initiation of the diet therapy – when an effect might be detected – and forward for episodes of cardiovascular disease. Three episodes of cardiovascular disease have occurred among the 5 patients that never changed diet. The 16 patients in the low-carbohydrate diet group (19 months observation time) and the 7 from the high-carbohydrate diet group that changed diet (10 months observation time) – totalling 23 patients – have been free of cardiovascular disease during the follow-up period (p < 0.03. Fischer Exact)."
So we have three out of five people with episodes of CV disease during about a year of ADA style low fat diet and zero out of 23 patients on Lutz style high fat.
Must be a paradox. Ha! (now think of the Queen launching a new ship) I name this paradox "The Swedish Paradox".
What, again? Ok, there are only a limited number of countries in the world and so many paradoxes looking for names...
Peter
Wednesday, February 20, 2008
Bantu Lp(a) and Swedish Lp(a)
Lipoprotein (a) is interesting enough that I might put up some more thoughts about it, but this post is based on the Bantu cross sectional study cited, as all the best cardiac studies are, by Dr Davis of Track Your Plaque.
The initial link is to this paper which explains quite a lot about Lp(a) and its genetics.
I wanted to compare values of the Bantu with an intervention trial in some Swedes, and to think about eating fish and taking fish oil, to reduce that "risk factor" for heart disease. And yes, Lp(a) is a "risk factor" for all forms of vascular disease; ischaemic heart disease, peripheral vascular disease, cerebrovascular disease and abdominal aortic aneurism.
First the Bantu. That first paper covered the Bantu genetics, apoprotein (a) sizes and Lp(a) blood levels. Basically, if you match individual gene types, the fish eating Bantu always have lower Lp(a) than their matched apo(a) size vegetarian Bantu equivalents. You get nothing about diet in this initial paper, for that you need to go to a previous publication from the same group.
Fish eaters and vegetarians were pretty well matched for calorie intake at around 2100kcal/d. The fish eaters ate 18% of calories from protein, 12% from fat and 70% from complex carbohydrate. The values for the vegetarians were 11% from protein, 7% from fat and 82% from complex carbohydrate. Dean "Mcdonalds" Ornish would be proud of the vegetarians. BTW, both groups ate 4g/day of salt, worth remembering that.
On a fully vegetarian, completely home grown, ultra low fat, low salt, complex carbohydrate diet these Bantu natives show exactly the same rise in blood pressure with age as Westeners do. Their systolic pressure approximates quite closely to that "age plus 100" rule of thumb which used to be considered normal in the UK and diastolic pressure followed systolic as you would expect. Fish eaters stuck with a systolic around 120-130mmHg and a diastolic around 70mmHg, life long. Remember both groups only ate 4g/d of salt. Now what does that tell you about salt and hypertension? Anyway, the politically correctest Bantu had significant markers of CV deterioration with age, not so the fish eaters.
BTW, as an aside, HDL figures were abysmal with both groups at under 1.0mmol/l, exactly as you'd expect on a low fat diet. They were slightly higher in the vegetarian group, presumable because they drank more alcohol. Triglycerides were higher in the veggie group, again pretty much as you'd expect from their carb intake.
The theory was/is that it was the omega three fats which were saving the fish eaters from hypertension and Lp(a) elevation. They undoubtedly did eat more omega three fats, and less omega six fats, and we know from the Lyon Heart Study that this is probably a Good Thing.
The Bantu fishermen were getting roughly 5% of calories from fish derived fat, that's 105kcal, equivalent of about 12ml of fish oil per day, as fish. This intake of fish oil is associated with a Lp(a) concentration of 201mg/dl as opposed to 321mg/dl in the vegetarians.
So what happens if we take a group of Swedes and give them more than twice that dose of fish derived lipid, as 30ml of fish oil per day, then track their Lp(a) level? Initially the subjects were on a typical Swedish diet (no information given) and were advised not to change it throughout the study. The fish oil was added at 30ml plus some vitamin E per day for three weeks, then there were two weeks off of fish oil, then three more weeks on fish oil, but without the vitamin E (for Bruce; yes, lipid peroxides rocketed on the later protocol).
Lp(a) before fish oil plus vit E: 128mg/dl, after three weeks supplemented: 125mg/dl. Back on Swedish diet for 2 weeks: 124mg/dl, after fish oil without E for three weeks: 128mg/dl.
All of these figures are essentially identical. Fish oil at 30ml per day does nothing to Lp(a) levels on a Swedish diet. It's also worth noting that, although we don't know the Swedish geneotypes for apoprotein (a) size, these values are all much lower than either of the Bantu groups. Maybe 35% of calories from fat in Sweden?
So is it really the fish oil which is saving the carnivorous Bantu from the hypertension and elevated Lp(a) which are prevalent in their vegetarian cousins?
Somehow I doubt it, based on the Swedish data and the behaviour of Lp(a).
Intervention studies show us that low fat diets increase Lp(a) and high fat diets decrease it, I put the studies here.
The fish eating Bantu got through more than half a kilo of fish on a good day. If your average calorie in take stays unchanged, that's an awful lot of complex carbohydrate you didn't eat. If I assume causality, not eating complex carbohydrate appears to be extremely good for your cardiovascular system. And your Lp(a) levels.
You don't need any "magic" fats to drop Lp(a), unless those magic fats are saturated fats, which seem to do the job best (just turn the DELTA study on its head).
Peter
BTW: No, I don't believe our liver manufactures Lp(a) to kill us. Again, more thoughts on Lp(a) to come. I might even talk hedgehogs if I can get my head around what they were doing with their lipids!
Another BTW, the Kitava studies showed these islanders ran at 70% calories from carbs but with Swedish levels of Lp(a). Kitava was lowish in fat at 20% of calories, but their dietary fats were almost all saturated (from coconut), with just a little omega 3s from fish. So it looks to be arguable whether you need to consume saturated fats to keep you Lp(a) levels down or keep carbs below the vegetarian Bantu levels. Ignoring genetics. Open to discussion on that one.
EDIT 28th Feb: Just been back to the Kitava papers for something else and noticed Lipoprotein(a) was around 300mg/dl, ie Bantu levels, bad Bantu levels. No heart disease. Bear in mind Lp(a) is notoriously variable from lab to lab. But still needs slotting in to Lp(a) and heart disease.
The initial link is to this paper which explains quite a lot about Lp(a) and its genetics.
I wanted to compare values of the Bantu with an intervention trial in some Swedes, and to think about eating fish and taking fish oil, to reduce that "risk factor" for heart disease. And yes, Lp(a) is a "risk factor" for all forms of vascular disease; ischaemic heart disease, peripheral vascular disease, cerebrovascular disease and abdominal aortic aneurism.
First the Bantu. That first paper covered the Bantu genetics, apoprotein (a) sizes and Lp(a) blood levels. Basically, if you match individual gene types, the fish eating Bantu always have lower Lp(a) than their matched apo(a) size vegetarian Bantu equivalents. You get nothing about diet in this initial paper, for that you need to go to a previous publication from the same group.
Fish eaters and vegetarians were pretty well matched for calorie intake at around 2100kcal/d. The fish eaters ate 18% of calories from protein, 12% from fat and 70% from complex carbohydrate. The values for the vegetarians were 11% from protein, 7% from fat and 82% from complex carbohydrate. Dean "Mcdonalds" Ornish would be proud of the vegetarians. BTW, both groups ate 4g/day of salt, worth remembering that.
On a fully vegetarian, completely home grown, ultra low fat, low salt, complex carbohydrate diet these Bantu natives show exactly the same rise in blood pressure with age as Westeners do. Their systolic pressure approximates quite closely to that "age plus 100" rule of thumb which used to be considered normal in the UK and diastolic pressure followed systolic as you would expect. Fish eaters stuck with a systolic around 120-130mmHg and a diastolic around 70mmHg, life long. Remember both groups only ate 4g/d of salt. Now what does that tell you about salt and hypertension? Anyway, the politically correctest Bantu had significant markers of CV deterioration with age, not so the fish eaters.
BTW, as an aside, HDL figures were abysmal with both groups at under 1.0mmol/l, exactly as you'd expect on a low fat diet. They were slightly higher in the vegetarian group, presumable because they drank more alcohol. Triglycerides were higher in the veggie group, again pretty much as you'd expect from their carb intake.
The theory was/is that it was the omega three fats which were saving the fish eaters from hypertension and Lp(a) elevation. They undoubtedly did eat more omega three fats, and less omega six fats, and we know from the Lyon Heart Study that this is probably a Good Thing.
The Bantu fishermen were getting roughly 5% of calories from fish derived fat, that's 105kcal, equivalent of about 12ml of fish oil per day, as fish. This intake of fish oil is associated with a Lp(a) concentration of 201mg/dl as opposed to 321mg/dl in the vegetarians.
So what happens if we take a group of Swedes and give them more than twice that dose of fish derived lipid, as 30ml of fish oil per day, then track their Lp(a) level? Initially the subjects were on a typical Swedish diet (no information given) and were advised not to change it throughout the study. The fish oil was added at 30ml plus some vitamin E per day for three weeks, then there were two weeks off of fish oil, then three more weeks on fish oil, but without the vitamin E (for Bruce; yes, lipid peroxides rocketed on the later protocol).
Lp(a) before fish oil plus vit E: 128mg/dl, after three weeks supplemented: 125mg/dl. Back on Swedish diet for 2 weeks: 124mg/dl, after fish oil without E for three weeks: 128mg/dl.
All of these figures are essentially identical. Fish oil at 30ml per day does nothing to Lp(a) levels on a Swedish diet. It's also worth noting that, although we don't know the Swedish geneotypes for apoprotein (a) size, these values are all much lower than either of the Bantu groups. Maybe 35% of calories from fat in Sweden?
So is it really the fish oil which is saving the carnivorous Bantu from the hypertension and elevated Lp(a) which are prevalent in their vegetarian cousins?
Somehow I doubt it, based on the Swedish data and the behaviour of Lp(a).
Intervention studies show us that low fat diets increase Lp(a) and high fat diets decrease it, I put the studies here.
The fish eating Bantu got through more than half a kilo of fish on a good day. If your average calorie in take stays unchanged, that's an awful lot of complex carbohydrate you didn't eat. If I assume causality, not eating complex carbohydrate appears to be extremely good for your cardiovascular system. And your Lp(a) levels.
You don't need any "magic" fats to drop Lp(a), unless those magic fats are saturated fats, which seem to do the job best (just turn the DELTA study on its head).
Peter
BTW: No, I don't believe our liver manufactures Lp(a) to kill us. Again, more thoughts on Lp(a) to come. I might even talk hedgehogs if I can get my head around what they were doing with their lipids!
Another BTW, the Kitava studies showed these islanders ran at 70% calories from carbs but with Swedish levels of Lp(a). Kitava was lowish in fat at 20% of calories, but their dietary fats were almost all saturated (from coconut), with just a little omega 3s from fish. So it looks to be arguable whether you need to consume saturated fats to keep you Lp(a) levels down or keep carbs below the vegetarian Bantu levels. Ignoring genetics. Open to discussion on that one.
EDIT 28th Feb: Just been back to the Kitava papers for something else and noticed Lipoprotein(a) was around 300mg/dl, ie Bantu levels, bad Bantu levels. No heart disease. Bear in mind Lp(a) is notoriously variable from lab to lab. But still needs slotting in to Lp(a) and heart disease.
Fiber, inulin and cancer
Just a quickie,
It has come up off blog on a number of occasions that inulin, a fructose polymer completely indigestible to humans but edible by bacteria, is a potential carcinogen. Couple of refs here and here. I was a bit dubious of this model as it showed beef to be carcinogenic too. That upsets my biases!!!! And slightly odd as this different model showed bacon, yes you read that correctly as bacon, to be protective. Beef and chicken were neutral in this chemical carcinogen based model. I decided that playing with mice, especially bowel cancer prone mice like ApcMin/+ engineered mice, might say relatively little about humans. Still not sure.
Now this dropped out of Pubcrawler today. If you are a ApcMin/+ mouse you can choose you carcinogen from wheat bran or apple pulp (that's the healthy fiber from healthy fruit, apples):
"In conclusion, both types of resistant carbohydrates increased polyp number and tumour burden and this was associated with elevated epithelial cell proliferation and crypt fission."
Because my access account doesn't allow me the full text I can't see what the fiber did to the wild type control mice. Always the most interesting bit and not in the abstract.
Crypt fission is bad, it's what wheat germ agglutinin and insulin do. Looks like all sorts of fiber do too. Just an extreme mouse model, but next time someone extolls their belief in the benefits of resistant starches or fiber, maybe they should read and think!
Peter
It has come up off blog on a number of occasions that inulin, a fructose polymer completely indigestible to humans but edible by bacteria, is a potential carcinogen. Couple of refs here and here. I was a bit dubious of this model as it showed beef to be carcinogenic too. That upsets my biases!!!! And slightly odd as this different model showed bacon, yes you read that correctly as bacon, to be protective. Beef and chicken were neutral in this chemical carcinogen based model. I decided that playing with mice, especially bowel cancer prone mice like ApcMin/+ engineered mice, might say relatively little about humans. Still not sure.
Now this dropped out of Pubcrawler today. If you are a ApcMin/+ mouse you can choose you carcinogen from wheat bran or apple pulp (that's the healthy fiber from healthy fruit, apples):
"In conclusion, both types of resistant carbohydrates increased polyp number and tumour burden and this was associated with elevated epithelial cell proliferation and crypt fission."
Because my access account doesn't allow me the full text I can't see what the fiber did to the wild type control mice. Always the most interesting bit and not in the abstract.
Crypt fission is bad, it's what wheat germ agglutinin and insulin do. Looks like all sorts of fiber do too. Just an extreme mouse model, but next time someone extolls their belief in the benefits of resistant starches or fiber, maybe they should read and think!
Peter
Tuesday, February 19, 2008
Cat rawfeeding; scroll down the comments
Just like to say thanks to everyone who posted comments on the last blog entry.
Thanks, they're appreciated.
Peter
Thanks, they're appreciated.
Peter
Best ever statin study comment?
Hi All and possibly Brian,
I'd just like to direct anyone who is remotely interested in a diametrically opposite view to my own to the comment down on this post.
This is an essential read. I think we all have to realise that there MUST be two sides to a given controversy and, while I wouldn't want to make a habit of it, both sides of the argument need an airing.
For Brian's benefit,
Yes, my diet is exactly as described, no joking.
You ask:
"Are all these experts wrong, as well as the expert advisory panels on cardiovascular disease?"
Yes!
A much better question:
Which hormone converts a vascular smooth muscle cell to an osteogenic cell (calcium phosphate secreting) in the vascular media?
Answer: Insulin
The NCEP answer: It's a statin deficiency! (what was the question? Oh never mind)
Thanks for the list of references, but I already feel there is far too much cholesterol hypothesis bashing on my blog. To go through them one at a time would be tedious and far better commentators than I have done so many times.
I note in passing that you cite the PROSPER study. Which particular cancer would you prefer to trade for your heart attack? Or perhaps you'd like to choose one for a grandparent?
Your concerns for my well being are touching, but I'll stick as I am thanks.
Peter
I'd just like to direct anyone who is remotely interested in a diametrically opposite view to my own to the comment down on this post.
This is an essential read. I think we all have to realise that there MUST be two sides to a given controversy and, while I wouldn't want to make a habit of it, both sides of the argument need an airing.
For Brian's benefit,
Yes, my diet is exactly as described, no joking.
You ask:
"Are all these experts wrong, as well as the expert advisory panels on cardiovascular disease?"
Yes!
A much better question:
Which hormone converts a vascular smooth muscle cell to an osteogenic cell (calcium phosphate secreting) in the vascular media?
Answer: Insulin
The NCEP answer: It's a statin deficiency! (what was the question? Oh never mind)
Thanks for the list of references, but I already feel there is far too much cholesterol hypothesis bashing on my blog. To go through them one at a time would be tedious and far better commentators than I have done so many times.
I note in passing that you cite the PROSPER study. Which particular cancer would you prefer to trade for your heart attack? Or perhaps you'd like to choose one for a grandparent?
Your concerns for my well being are touching, but I'll stick as I am thanks.
Peter
Thursday, February 14, 2008
French paradox in Sweden
This press release came out today, can't see anything on pubmed, but the findings are what you'd expect. Nice, whatever you think of Spurlock (not alot). Quote from Nystrom and his press release:
That signs of liver damage were linked to carbohydrates was another key finding, he said.
"It was not the fat in the hamburgers, it was rather the sugar in the coke," he said.
But the most startling result implies that an intensive fast food diet might have some health benefits too, apparently from fat.
"We found that healthy HDL cholesterol actually increased over the four-week period -- this was very counter-intuitive," said.
HDL, sometimes called "good cholesterol," seems to clean the walls of blood vessels, removing excess "bad cholesterol" that can cause coronary artery disease and transporting it to the liver for processing [in the fairyland of the lipid hypothesis that is, Peter].
Nystrom has yet to publish the cholesterol findings, but said they were consistent with the so-called "French Paradox." For nearly two decades, scientists have wrestled to explain how the French can consume a diet rich in fats -- from abundant butter, cream, cheese and meat -- yet have generally low levels of heart disease and hypertension.
Quick summary of the findings:
Sugar mangles your liver (a ten fold increase is ALT is VERY scary), saturated fat improves your lipids (and lots of other things), there is no French Paradox.
I love the French "Paradox", it makes me think of reality kicking hard at a very heavily barred door.
Peter
That signs of liver damage were linked to carbohydrates was another key finding, he said.
"It was not the fat in the hamburgers, it was rather the sugar in the coke," he said.
But the most startling result implies that an intensive fast food diet might have some health benefits too, apparently from fat.
"We found that healthy HDL cholesterol actually increased over the four-week period -- this was very counter-intuitive," said.
HDL, sometimes called "good cholesterol," seems to clean the walls of blood vessels, removing excess "bad cholesterol" that can cause coronary artery disease and transporting it to the liver for processing [in the fairyland of the lipid hypothesis that is, Peter].
Nystrom has yet to publish the cholesterol findings, but said they were consistent with the so-called "French Paradox." For nearly two decades, scientists have wrestled to explain how the French can consume a diet rich in fats -- from abundant butter, cream, cheese and meat -- yet have generally low levels of heart disease and hypertension.
Quick summary of the findings:
Sugar mangles your liver (a ten fold increase is ALT is VERY scary), saturated fat improves your lipids (and lots of other things), there is no French Paradox.
I love the French "Paradox", it makes me think of reality kicking hard at a very heavily barred door.
Peter
Wednesday, February 13, 2008
Vitamin D supplementation: Bad?
There's a new discussion paper out on vitamin D which deserves serious reading:
Vitamin D discovery outpaces FDA decision making
Some of it is very interesting if you want an opinion that suggests vitamin D supplementation, at any level, is bad and that low levels of 25 OH D3 are a product of disease, not a contributor. And as such are a marker of good things happening in the immune system. He includes the changes in gut flora as a source of obesity as being triggered by D2 supplementation (not had time to read all of this in detail) and I'm not sure I agree with him on what's happening (anywhere!), but there's plenty there to think about here. You have to look at both sides of a decision making process.
No time to read it in detail today, arghhhh
Peter
EDIT later in the day
By the time you've been through enough of the easily available references to realise that they don't actually say what the author claims they say, you tend to bin the review. There's the bin, dump goes the review. Gimme the D3.
Vitamin D discovery outpaces FDA decision making
Some of it is very interesting if you want an opinion that suggests vitamin D supplementation, at any level, is bad and that low levels of 25 OH D3 are a product of disease, not a contributor. And as such are a marker of good things happening in the immune system. He includes the changes in gut flora as a source of obesity as being triggered by D2 supplementation (not had time to read all of this in detail) and I'm not sure I agree with him on what's happening (anywhere!), but there's plenty there to think about here. You have to look at both sides of a decision making process.
No time to read it in detail today, arghhhh
Peter
EDIT later in the day
By the time you've been through enough of the easily available references to realise that they don't actually say what the author claims they say, you tend to bin the review. There's the bin, dump goes the review. Gimme the D3.
Tuesday, February 12, 2008
Single vessel disease
Once again, thanks have to go to Dr Davis of Track Your Plaque for a nice introduction to an interesting subject.
Have a read through this blog post, just the comments are enough. The second comment is from a man with all of his coronary calcium score localised in to one single coronary artery. His bemused query is:
"Doesen't the same blood with the same small particle, low HDL and everything else travel through ALL the arteries? How come it only harms me in 1 artery? This doesen't make any sense to me."
Absolutely. I cannot see how the lipid hypothesis could remotely explain this phenomenon. If our liver merely makes LDL-C as a never ending supply of arterial suicide bombs, surely that evil LDL would attack ALL blood vessels? Sometimes it does, sometimes it doesn't. Often the attack is very specifically localised.
Another comment from a further anonymous poster is equally telling:
"When nurse called with results her explaination was that I must be a non smoker, which i am, because in smokers the plaque tends to spread more evenly in the coronary arteries and in non smokers they tend to show up in 1 or 2 arteries."
So another confirmation that, in non smokers at least, plaque is often localised to one or two out of four arteries. This localisation phenomenon is real. You just have to ask a lipid believer why this should occur.
Basically it was pretty well sorted out back in 1954. Well maybe not the smoking bit. My assumption for that is that smoking just damages everything, vascular linings included. Anyway, have a read here.
I really like this paper. It's solid, basic, core hydraulic physics. It could almost have been written by an anaesthetist. Page 2 of the pdf has a neat diagram, complete with algebra, explaining how the tension in the wall of a curved artery has to be highest on the inside of the curve. If you are going to get wall damage, that's where it will show first. He goes through Laplace's general law relating vessel wall tension to hydrostatic pressure (in excess of that of the surrounding tissue), the radius of curvature of the vessel along its course and the radius of the vessel itself.
He then settles down to predict where arteriosclerosis is likely and unlikely to occur under various circumstances and backs it up with histology slides. The article is over 8 pages long and does deserve careful reading, but here is his suggestion as to why some coronary arteries are more prone to arteriosclerosis than others. He suggests it may be surrounding tissue pressure that reduces wall damage in some sections of some coronary arteries. Probably also curved arteries are more prone, tortuous arteries most prone. Wide diameter arteries are more prone. Lapalce's Law predicts this.
"Geringer has pointed out that in the instances where a portion of the anterior descending coronary artery lies buried in the myocardium, the buried segment is spared from atherosclerosis. Branches of the same artery lying in the epicardial fat, and therefore not surrounded by appreciable tissue pressure, are affected by atherosclerosis."
This ref to Geringer is from 1951 and seems to have fallen off of the bottom of pubmed! It's Geringer, E.: Am. Heart J., 41: 359, 1951 for anyone with access to a well established library and a duster.
Completely independently Wexler made this observation in a detailed analysis of spontaneous arteriosclerosis in aged breeding rats, back in 1964:
"One wonders if the physical pressure of the surrounding myocardium may decrease the need for maintaining the structural rigidity of these medium sized arteries by calcification. In the case of the larger epicardial branches, however, the presence of calcium could promote increased polymerization of mucopolysaccharides. The increased polymerization would provide the turgor or rigidity required by the exposed epicardial arteries."
What would be very interesting to see is is how protected or exposed individual calcified vs non calcified arteries are on EBCT scans...
It was obvious, at least as recently as 1964, that arteriosclerosis was a repair process. Possibly a repair process gone wrong, but a repair process never the less.
In 2008, lost in the lipid hypothesis, these oddities are inexplicable.
Arteriosclerosis today is merely our liver trying to kill us with sticky Lp(a).
Peter
Have a read through this blog post, just the comments are enough. The second comment is from a man with all of his coronary calcium score localised in to one single coronary artery. His bemused query is:
"Doesen't the same blood with the same small particle, low HDL and everything else travel through ALL the arteries? How come it only harms me in 1 artery? This doesen't make any sense to me."
Absolutely. I cannot see how the lipid hypothesis could remotely explain this phenomenon. If our liver merely makes LDL-C as a never ending supply of arterial suicide bombs, surely that evil LDL would attack ALL blood vessels? Sometimes it does, sometimes it doesn't. Often the attack is very specifically localised.
Another comment from a further anonymous poster is equally telling:
"When nurse called with results her explaination was that I must be a non smoker, which i am, because in smokers the plaque tends to spread more evenly in the coronary arteries and in non smokers they tend to show up in 1 or 2 arteries."
So another confirmation that, in non smokers at least, plaque is often localised to one or two out of four arteries. This localisation phenomenon is real. You just have to ask a lipid believer why this should occur.
Basically it was pretty well sorted out back in 1954. Well maybe not the smoking bit. My assumption for that is that smoking just damages everything, vascular linings included. Anyway, have a read here.
I really like this paper. It's solid, basic, core hydraulic physics. It could almost have been written by an anaesthetist. Page 2 of the pdf has a neat diagram, complete with algebra, explaining how the tension in the wall of a curved artery has to be highest on the inside of the curve. If you are going to get wall damage, that's where it will show first. He goes through Laplace's general law relating vessel wall tension to hydrostatic pressure (in excess of that of the surrounding tissue), the radius of curvature of the vessel along its course and the radius of the vessel itself.
He then settles down to predict where arteriosclerosis is likely and unlikely to occur under various circumstances and backs it up with histology slides. The article is over 8 pages long and does deserve careful reading, but here is his suggestion as to why some coronary arteries are more prone to arteriosclerosis than others. He suggests it may be surrounding tissue pressure that reduces wall damage in some sections of some coronary arteries. Probably also curved arteries are more prone, tortuous arteries most prone. Wide diameter arteries are more prone. Lapalce's Law predicts this.
"Geringer has pointed out that in the instances where a portion of the anterior descending coronary artery lies buried in the myocardium, the buried segment is spared from atherosclerosis. Branches of the same artery lying in the epicardial fat, and therefore not surrounded by appreciable tissue pressure, are affected by atherosclerosis."
This ref to Geringer is from 1951 and seems to have fallen off of the bottom of pubmed! It's Geringer, E.: Am. Heart J., 41: 359, 1951 for anyone with access to a well established library and a duster.
Completely independently Wexler made this observation in a detailed analysis of spontaneous arteriosclerosis in aged breeding rats, back in 1964:
"One wonders if the physical pressure of the surrounding myocardium may decrease the need for maintaining the structural rigidity of these medium sized arteries by calcification. In the case of the larger epicardial branches, however, the presence of calcium could promote increased polymerization of mucopolysaccharides. The increased polymerization would provide the turgor or rigidity required by the exposed epicardial arteries."
What would be very interesting to see is is how protected or exposed individual calcified vs non calcified arteries are on EBCT scans...
It was obvious, at least as recently as 1964, that arteriosclerosis was a repair process. Possibly a repair process gone wrong, but a repair process never the less.
In 2008, lost in the lipid hypothesis, these oddities are inexplicable.
Arteriosclerosis today is merely our liver trying to kill us with sticky Lp(a).
Peter
Monday, February 11, 2008
High fat Dutch style
Thanks to erik for the link to the project outline for the dutch study looking at the influence of a high fat meal on cholecystokinin release. This looks to be part of the lead up to using high fat feeding to ameliorate the liver failure, loss of gut wall integrity and what looks like systemic inflammatory response syndrome in major trauma human patients.
A quick pubmed on the group leader gave this paper from when Greve was visiting Edinburgh. High fat syringe feeding by mouth before major blood loss in rats was the project. It improved all sorts of parameters, as any high fat eater would expect. But you have to be careful with these models of bled-out rats as it is hard to get a project license which allows the rats to live or die. Fair enough, I don't like rats suffering either. I'm very fond of rats. They make good pets. But ultimately improved survival is what is needed for human trauma patients and this cannot always be predicted by acute amelioration of lab findings in the first 24 hours.
But the fat will deliver! I believe... (sounding like a statinator here).
A quick look at the full text of one of the group's related papers gives an idea of what they mean by high fat feeding. It's about 50% of calories from olive oil. I feel 85% from beef dripping would be even better, but just try and get that through the nozzle of a 5ml syringe at room temperature!
Usually when the Dutch talk high fat they mean HIGH fat, just look at this paper on diabetes. Human clinical type 2 diabetics on 89% of calories from fat. They improve. Mind you, if you've eaten as much Utrecht cheese cake as I have, you'd realise why the Dutch are not afraid of fat.
It was a crossover study so you can see what the same patients were like on 89% of calories from carbohydrate. Just look at the basal figures on the left hand side of table 2. As a diabetic which would you prefer to be? Check the fasting glucose, look at the lipids if you care about them.
Just compare this to the Philadelphia approach to diabetes. I hit on this paper as it's the first related link to the Dutch one. It grabbed my attention as the high protein diet did badly! Luckily I have access to the full text and in Philly they essentially starved two groups of diabetics on 1300kcal/d (for people with BMI well over 30). Both groups were low fat (45g/d) and they were either high carb (138g/d) or very high carb (HC,170g/d). The merely high carb (138g/d) group was describes as a high protein diet (HP). Whatever. The high protein group did worse on an HbA1c basis, slightly surprisingly. This looks to have been because both groups ended up with similar final values (final HbA1c for HC of 6.9%, HP gave 6.6%). The higher protein group had a non significant drop from baseline as their starting value was lower (Initial HbA1c for HP 7.6%, for HC 8.2%). Would you have guessed that from the abstract?
BTW the HDL-C deteriorated in both groups, as you would expect on 45g of fat per day. No surprise there. Only the HC group had a fall which reached statistical significance. Bet you didn't see that in the abstract either.
What both Philadelphia groups needed was a Dutch 89% fat milkshake six times a day, with enough calories for weight stability. Of course, at that level of fat intake they wouldn't be hungry, so skipping the occasional shake would allow weight loss if so desired. Even without weight loss they'd still really get their HbA1c down.
And actually improve their lipids.
Peter
A quick pubmed on the group leader gave this paper from when Greve was visiting Edinburgh. High fat syringe feeding by mouth before major blood loss in rats was the project. It improved all sorts of parameters, as any high fat eater would expect. But you have to be careful with these models of bled-out rats as it is hard to get a project license which allows the rats to live or die. Fair enough, I don't like rats suffering either. I'm very fond of rats. They make good pets. But ultimately improved survival is what is needed for human trauma patients and this cannot always be predicted by acute amelioration of lab findings in the first 24 hours.
But the fat will deliver! I believe... (sounding like a statinator here).
A quick look at the full text of one of the group's related papers gives an idea of what they mean by high fat feeding. It's about 50% of calories from olive oil. I feel 85% from beef dripping would be even better, but just try and get that through the nozzle of a 5ml syringe at room temperature!
Usually when the Dutch talk high fat they mean HIGH fat, just look at this paper on diabetes. Human clinical type 2 diabetics on 89% of calories from fat. They improve. Mind you, if you've eaten as much Utrecht cheese cake as I have, you'd realise why the Dutch are not afraid of fat.
It was a crossover study so you can see what the same patients were like on 89% of calories from carbohydrate. Just look at the basal figures on the left hand side of table 2. As a diabetic which would you prefer to be? Check the fasting glucose, look at the lipids if you care about them.
Just compare this to the Philadelphia approach to diabetes. I hit on this paper as it's the first related link to the Dutch one. It grabbed my attention as the high protein diet did badly! Luckily I have access to the full text and in Philly they essentially starved two groups of diabetics on 1300kcal/d (for people with BMI well over 30). Both groups were low fat (45g/d) and they were either high carb (138g/d) or very high carb (HC,170g/d). The merely high carb (138g/d) group was describes as a high protein diet (HP). Whatever. The high protein group did worse on an HbA1c basis, slightly surprisingly. This looks to have been because both groups ended up with similar final values (final HbA1c for HC of 6.9%, HP gave 6.6%). The higher protein group had a non significant drop from baseline as their starting value was lower (Initial HbA1c for HP 7.6%, for HC 8.2%). Would you have guessed that from the abstract?
BTW the HDL-C deteriorated in both groups, as you would expect on 45g of fat per day. No surprise there. Only the HC group had a fall which reached statistical significance. Bet you didn't see that in the abstract either.
What both Philadelphia groups needed was a Dutch 89% fat milkshake six times a day, with enough calories for weight stability. Of course, at that level of fat intake they wouldn't be hungry, so skipping the occasional shake would allow weight loss if so desired. Even without weight loss they'd still really get their HbA1c down.
And actually improve their lipids.
Peter
Tracking plaque 1950s style
Before EBCT scanners arrived on the scene, this is how you assessed plaque in peripheral arteries. Certainly back in the 1950s this was cutting edge. Coronary arteries are a non starter using this technique!
"With both needles securely in place [one in each femoral artery, no local block, ouch! My comment], 20 c.c. of 35%, Diodrast [an old fashioned type of iodine contrast, very irritant, again my comment] was injected simultaneously into both arteries from 50 c.c. syringes equipped with stopcocks, polyethylene tubing and Luer locks. The injection lasted about 7 seconds and was accompanied by fairly severe but transient pain followed by a burning sensation passing down into the legs and feet and lasting 20 to 30 seconds. This was followed by visible flushing of the skin of the legs in some cases. Meanwhile 5 to 7 x-ray films 14" x 17" (35 x 42.5 cm.) were exposed with a cassette changer at 1.5 second intervals, starting when about 10 c.c. of the dye had been injected."
No one died from reaction to the dye and all of them came back for a repeat arteriogram using the same technique. Some even came back twice!
Assessing the radiographs in the paper is quite difficult. Getting X rays in to journals while trying to maintain diagnostic quality is never easy, even today. When it's a pdf of a scan of a print of an X ray in a journal published in 1954 which you have in front of you, you need the eye of faith to see what the authors saw. However, with it being a three author paper this probably increases the likelihood of plaque regression cited as being real.
Yes, it seems they had plaque regression in 1954. It was a very small series (reading through the technique, I'm not surprised!) and the changes are not particularly convincing when viewed from 53 years later. But they do claim some degree of reversal over about a 3 month period. The radiologist scoring the radiographs for plaque changes was blinded as to treatment vs control when he assessed the arteriograms.
Apart from Professor Yudkin's throw away comment about ascobate and heart failure, I don't think I've seen a lot of information on ascorbate for atherosclerosis in the literature. Obviously the Vitamin C Foundation makes lots of claims nowadays, but I don't think I've seen anything serious in print. Dr Davis has only commented once on the Pauling/Rath therapy (ascorbate/lysine/proline) for IHD, and that was to say it doesn't drop Lp(a). Fair enough, but Lp(a) is another story. Obviously if anyone is eating modest fat, lots of fruit and vegetables and avoiding saturated fat there is no way they will drop their Lp(a), whatever vitamins they take!
The group doing the arteriograms were giving ascorbate at 500mg three times a day as their treatment, without change in diet. This strikes me as a miniscule dose. I just wonder how much ascorbate Prof Yudkin's elderly heart failure patients were taking in the 1970s. Oh, and whether Dr Willis' patients (it's a Canadian study) were getting more sunshine during those two to six months of his study period........ Vitamin D again? The paper was published in December 1954, it all depends on how long it took them to gather and publish their data. A modern day research scientist can get a paper from results to e-pub in about six weeks. Modern clinicians can take >2 years!
But however it is achieved, I don't think it's arguable; atherosclerosis is reversible.
Peter
"With both needles securely in place [one in each femoral artery, no local block, ouch! My comment], 20 c.c. of 35%, Diodrast [an old fashioned type of iodine contrast, very irritant, again my comment] was injected simultaneously into both arteries from 50 c.c. syringes equipped with stopcocks, polyethylene tubing and Luer locks. The injection lasted about 7 seconds and was accompanied by fairly severe but transient pain followed by a burning sensation passing down into the legs and feet and lasting 20 to 30 seconds. This was followed by visible flushing of the skin of the legs in some cases. Meanwhile 5 to 7 x-ray films 14" x 17" (35 x 42.5 cm.) were exposed with a cassette changer at 1.5 second intervals, starting when about 10 c.c. of the dye had been injected."
No one died from reaction to the dye and all of them came back for a repeat arteriogram using the same technique. Some even came back twice!
Assessing the radiographs in the paper is quite difficult. Getting X rays in to journals while trying to maintain diagnostic quality is never easy, even today. When it's a pdf of a scan of a print of an X ray in a journal published in 1954 which you have in front of you, you need the eye of faith to see what the authors saw. However, with it being a three author paper this probably increases the likelihood of plaque regression cited as being real.
Yes, it seems they had plaque regression in 1954. It was a very small series (reading through the technique, I'm not surprised!) and the changes are not particularly convincing when viewed from 53 years later. But they do claim some degree of reversal over about a 3 month period. The radiologist scoring the radiographs for plaque changes was blinded as to treatment vs control when he assessed the arteriograms.
Apart from Professor Yudkin's throw away comment about ascobate and heart failure, I don't think I've seen a lot of information on ascorbate for atherosclerosis in the literature. Obviously the Vitamin C Foundation makes lots of claims nowadays, but I don't think I've seen anything serious in print. Dr Davis has only commented once on the Pauling/Rath therapy (ascorbate/lysine/proline) for IHD, and that was to say it doesn't drop Lp(a). Fair enough, but Lp(a) is another story. Obviously if anyone is eating modest fat, lots of fruit and vegetables and avoiding saturated fat there is no way they will drop their Lp(a), whatever vitamins they take!
The group doing the arteriograms were giving ascorbate at 500mg three times a day as their treatment, without change in diet. This strikes me as a miniscule dose. I just wonder how much ascorbate Prof Yudkin's elderly heart failure patients were taking in the 1970s. Oh, and whether Dr Willis' patients (it's a Canadian study) were getting more sunshine during those two to six months of his study period........ Vitamin D again? The paper was published in December 1954, it all depends on how long it took them to gather and publish their data. A modern day research scientist can get a paper from results to e-pub in about six weeks. Modern clinicians can take >2 years!
But however it is achieved, I don't think it's arguable; atherosclerosis is reversible.
Peter
Sunday, February 10, 2008
Lipoprotein(a) and DELTA
This has got to be one of the strangest abstracts I've read. Because it's only an abstract most of the really interesting information, like insulin levels, lies hidden in the American Journal of Clinical Nutrition.
It's a crossover design so all people acted as their own control group. The study participants were chosen as having low HDL cholesterol and/or elevated triglycerides, two classic markers of insulin resistance. The purpose of the study was to see which of two interventions decreased the participants "risk factors" for heart disease (ie it was a short study with no body count). Both interventions reduced some of the dreaded saturated fat from the of 35% of total fat in the Average American Diet (usually termed the Standard American Diet or SAD, but...). Excellent move to improve lipids wouldn't you think? Except replacing the saturated fat with carbohydrate decreased HDL by 7.2% and using monounsaturated fat decreased HDL by a mere 4.3%.
How about triglycerides? Well the MUFA substitution did nothing to triglycerides (the phrase used is "tended to be lower", meaning no change unless viewed through rose tinted spectacles. I hope their statistician resigned over this phrase, or has since been sacked). The use of carbohydrate cranked up triglycerides, but by how much it doesn't say, just "significantly".
But the best results were lipoprotein(a). You know, that BAD lipoprotein with the genetically pre programmed blood level. It got un-genetically reprogramed upward by 20% in the increased carbohydrate period. The MUFA feeding did far better on this front, MUFA replacing saturated fat only increased lipoprotein(a) by 11%.
In the murky world of lipid belief these changes are, I understand, considered to be BAD. All of them, except perhaps that non-changed triglyceride value in the MUFA feeding period.
Luckily the calculated LDL-C went down, although goodness knows what happened to lipid particle size and numbers (actually you can pretty well assume they got worse, especially the small dense LDL during the carbohydrate period). The abstract certainly makes no suggestion the researchers considered anything other than calculated LDL. It was enough that this reduced a little to allow the DELTA researchers to claim improved CV risk for both interventions.
Actually they claim that MUFA "improved" cardiac "risk" more than carbs. Even if you believe their LDL stupidity, can anyone really believe that a 6.3% reduction is either statistically or biologically "better" than a 7.0% reduction? In your dreams, cardiologist.
What came out rather well was the Average American Diet, SAD or not.
Peter
It's a crossover design so all people acted as their own control group. The study participants were chosen as having low HDL cholesterol and/or elevated triglycerides, two classic markers of insulin resistance. The purpose of the study was to see which of two interventions decreased the participants "risk factors" for heart disease (ie it was a short study with no body count). Both interventions reduced some of the dreaded saturated fat from the of 35% of total fat in the Average American Diet (usually termed the Standard American Diet or SAD, but...). Excellent move to improve lipids wouldn't you think? Except replacing the saturated fat with carbohydrate decreased HDL by 7.2% and using monounsaturated fat decreased HDL by a mere 4.3%.
How about triglycerides? Well the MUFA substitution did nothing to triglycerides (the phrase used is "tended to be lower", meaning no change unless viewed through rose tinted spectacles. I hope their statistician resigned over this phrase, or has since been sacked). The use of carbohydrate cranked up triglycerides, but by how much it doesn't say, just "significantly".
But the best results were lipoprotein(a). You know, that BAD lipoprotein with the genetically pre programmed blood level. It got un-genetically reprogramed upward by 20% in the increased carbohydrate period. The MUFA feeding did far better on this front, MUFA replacing saturated fat only increased lipoprotein(a) by 11%.
In the murky world of lipid belief these changes are, I understand, considered to be BAD. All of them, except perhaps that non-changed triglyceride value in the MUFA feeding period.
Luckily the calculated LDL-C went down, although goodness knows what happened to lipid particle size and numbers (actually you can pretty well assume they got worse, especially the small dense LDL during the carbohydrate period). The abstract certainly makes no suggestion the researchers considered anything other than calculated LDL. It was enough that this reduced a little to allow the DELTA researchers to claim improved CV risk for both interventions.
Actually they claim that MUFA "improved" cardiac "risk" more than carbs. Even if you believe their LDL stupidity, can anyone really believe that a 6.3% reduction is either statistically or biologically "better" than a 7.0% reduction? In your dreams, cardiologist.
What came out rather well was the Average American Diet, SAD or not.
Peter
Saturday, February 09, 2008
What do I eat (2) recipes
I mentioned a few posts ago that I had some typical recipes on my hard drive, well here they are. I've tidied them up a bit and put a rough analysis on the end of each one. Salt and pepper can be added as preferred, It strikes me that none of them are special, this is just the sort of meals I've always cooked, but now we eat the meat portion, often with enough veg to keep carb intake reasonable and no bulk carbs. Obviously anyone needing bulk calories can simply add more butter to any recipe. Muscle building might need a little extra protein. You can improve the flavour by browning the onions and meat first if you like. I also cook a fair few Ken Hom wok recipes too, replace conservative vegetable oil with bulk butter or coconut oil and be careful to keep the fat...
So here are some typical main meal recipes. Some we eat with a vegetable, some not. Depends on the rest of the day...
Bolognese sauce.
1 lb 21% fat beef.
1 rasher bacon, chopped.
1 small can Sainsbury's chopped black olives (about 0.5 cupful), drained.
Butter 50g
Olive oil 1 tablespoon (20ml)
Tin tomatoes.
1 medium onion chopped.
1 sweet green pepper de seeded and chopped.
30 ml Pesto sauce (olive oil, not sunflower based).
2 cloves garlic crushed.
Splash red wine.
Place all ingredients in a saucepan, boil, stir, simmer for an hour, reduce to a thick sauce. Cheddar or parmesan grated on top to serve. You need a spoon for the fat.
This probably serves three. Eating half is a challenge. More than half is a fat overload. I've tried, don't go there.
Total estimated food in the pan: 2300kcal, Fat 193g, carbs 38g, protein 99g.
African beef stew, serves 2, maybe 3...
1 lb diced beef
Tin tomatoes.
Medium carrot, sliced.
Medium onion, chopped.
50-75g butter, depends on how fatty the meat is.
50g peanut butter.
Bayleaf.
About 200ml water, to just cover meat.
Salt and pepper to taste.
Fresh root ginger, however much you like.
3 cloves garlic, crushed
Pinch Cayenne pepper
Pinch ground cloves
Tablespoon vinegar or lemon juice.
Place all ingredients in a casserole, bring to boil, stir well, cover, place in oven at gas mark four for 2-3 hours until meat melts in the mouth. Stir every half hour.
Can be cooked very slowly on top of the cooker.
Total estimated casserole: 1600-2000kcal (extra butter), fat >125g, carbs 33g, protein 100g
Goulash. Serves 2.
1 lb diced pork or beef.
medium onion, chopped
sweet red pepper, deseeded and chopped.
Butter 70g
Tin tomatoes.
Full packet (20g?) paprika.
5fl oz soured cream.
Place all ingredients except soured cream in a casserole. Bring to boil, stir well, place in oven around gas mark 4 for 2-3 hours until meat melts in the mouth. Just before serving add soured cream.
Total in casserole 2100kcal, fat 170g, carbs 35g, protein 100g
Chili Mix - serves 2
450g economy mince. Can use pork mince.
1 medium onion, chopped.
1 red pepper, de seeded and chopped.
2 cloves of garlic, crushed.
400g tin tomatoes.
Splash red wine.
50g butter, more if your economy beef is now reduced fat.
1 fresh red chili pepper, finely chopped or 1/2 teaspoon chili powder or both.
1 tablespoon ground cumin
cayenne pepper to taste (not essential)
Preparation:
Prepare ingredients and place all in saucepan. Bring to boil, simmer for 40 mintues, stirring occasionally. Reduce to a thick sauce. Serve with grated cheese on top.
Very aprox per casserole : 1600kcal, 130g fat, 30g carbs, 90g protein
Any cook book will provide a host of recipes. Nourishing Traditions is good too, I just avoid grains and increase fat.
Oh, never forget the ice cream!
Six egg yolks, 1 pint double cream, 20g glucose (can use sucrose), 10g honey, capful of vanilla extract. Blend and freeze.
Enjoy.
Peter
So here are some typical main meal recipes. Some we eat with a vegetable, some not. Depends on the rest of the day...
Bolognese sauce.
1 lb 21% fat beef.
1 rasher bacon, chopped.
1 small can Sainsbury's chopped black olives (about 0.5 cupful), drained.
Butter 50g
Olive oil 1 tablespoon (20ml)
Tin tomatoes.
1 medium onion chopped.
1 sweet green pepper de seeded and chopped.
30 ml Pesto sauce (olive oil, not sunflower based).
2 cloves garlic crushed.
Splash red wine.
Place all ingredients in a saucepan, boil, stir, simmer for an hour, reduce to a thick sauce. Cheddar or parmesan grated on top to serve. You need a spoon for the fat.
This probably serves three. Eating half is a challenge. More than half is a fat overload. I've tried, don't go there.
Total estimated food in the pan: 2300kcal, Fat 193g, carbs 38g, protein 99g.
African beef stew, serves 2, maybe 3...
1 lb diced beef
Tin tomatoes.
Medium carrot, sliced.
Medium onion, chopped.
50-75g butter, depends on how fatty the meat is.
50g peanut butter.
Bayleaf.
About 200ml water, to just cover meat.
Salt and pepper to taste.
Fresh root ginger, however much you like.
3 cloves garlic, crushed
Pinch Cayenne pepper
Pinch ground cloves
Tablespoon vinegar or lemon juice.
Place all ingredients in a casserole, bring to boil, stir well, cover, place in oven at gas mark four for 2-3 hours until meat melts in the mouth. Stir every half hour.
Can be cooked very slowly on top of the cooker.
Total estimated casserole: 1600-2000kcal (extra butter), fat >125g, carbs 33g, protein 100g
Goulash. Serves 2.
1 lb diced pork or beef.
medium onion, chopped
sweet red pepper, deseeded and chopped.
Butter 70g
Tin tomatoes.
Full packet (20g?) paprika.
5fl oz soured cream.
Place all ingredients except soured cream in a casserole. Bring to boil, stir well, place in oven around gas mark 4 for 2-3 hours until meat melts in the mouth. Just before serving add soured cream.
Total in casserole 2100kcal, fat 170g, carbs 35g, protein 100g
Chili Mix - serves 2
450g economy mince. Can use pork mince.
1 medium onion, chopped.
1 red pepper, de seeded and chopped.
2 cloves of garlic, crushed.
400g tin tomatoes.
Splash red wine.
50g butter, more if your economy beef is now reduced fat.
1 fresh red chili pepper, finely chopped or 1/2 teaspoon chili powder or both.
1 tablespoon ground cumin
cayenne pepper to taste (not essential)
Preparation:
Prepare ingredients and place all in saucepan. Bring to boil, simmer for 40 mintues, stirring occasionally. Reduce to a thick sauce. Serve with grated cheese on top.
Very aprox per casserole : 1600kcal, 130g fat, 30g carbs, 90g protein
Any cook book will provide a host of recipes. Nourishing Traditions is good too, I just avoid grains and increase fat.
Oh, never forget the ice cream!
Six egg yolks, 1 pint double cream, 20g glucose (can use sucrose), 10g honey, capful of vanilla extract. Blend and freeze.
Enjoy.
Peter
Tuesday, February 05, 2008
Fructose and Gout
Many thanks to Stan for pointing me to this BBC article and the study it relates to.
Obviously anyone making a habit of soft drink consumption, be that sucrose or HFCS sweetened, is in trouble metabolically. The joy of this report is the association between not only orange juice and gout, but also with apples and oranges as whole fruit. Observational perhaps, but the biochemistry is all there to support causality.
Ultimately fructose is fructose is fructose. Eat an orange and your liver will immediately set about defending you as best it can. When it fails or goes wrong, you get gout.
I like the BBC's picture. The chap with metabolic syndrome and gout is probably wealthy enough in the 1700s to buy sugar and to drink port, possibly the sweetest bulk consumption form of alcohol. Obesity and gout.
A few choice fruity quotes:
"I can think of some situations, for example in severe treatment failure gout, where reducing sweet fruits, such as oranges and apples could help," he added.
Translation, take drugs, more drugs and even more drugs. In absolutely dire straits, dump fruit. Why not just dump the fruit in the first place? Gout drugs do not look to be much fun.
"But this finding needs to be balanced against the benefit of fruit and vegetables in preventing other chronic disorders like heart disease and stroke."
Show me the data!
"...and fructose rich fruits (apples and oranges) were associated with a higher risk, the researchers said."
Quite a lot of fructose in grapes and plums and and kiwis and peaches and bananas and and and...
The nice thing about science is that eventually the truth will out.
Eventually.
Peter
Obviously anyone making a habit of soft drink consumption, be that sucrose or HFCS sweetened, is in trouble metabolically. The joy of this report is the association between not only orange juice and gout, but also with apples and oranges as whole fruit. Observational perhaps, but the biochemistry is all there to support causality.
Ultimately fructose is fructose is fructose. Eat an orange and your liver will immediately set about defending you as best it can. When it fails or goes wrong, you get gout.
I like the BBC's picture. The chap with metabolic syndrome and gout is probably wealthy enough in the 1700s to buy sugar and to drink port, possibly the sweetest bulk consumption form of alcohol. Obesity and gout.
A few choice fruity quotes:
"I can think of some situations, for example in severe treatment failure gout, where reducing sweet fruits, such as oranges and apples could help," he added.
Translation, take drugs, more drugs and even more drugs. In absolutely dire straits, dump fruit. Why not just dump the fruit in the first place? Gout drugs do not look to be much fun.
"But this finding needs to be balanced against the benefit of fruit and vegetables in preventing other chronic disorders like heart disease and stroke."
Show me the data!
"...and fructose rich fruits (apples and oranges) were associated with a higher risk, the researchers said."
Quite a lot of fructose in grapes and plums and and kiwis and peaches and bananas and and and...
The nice thing about science is that eventually the truth will out.
Eventually.
Peter
Subscribe to:
Posts (Atom)
