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
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These studies aren't too convincing for me, as they are using a refined glucose, and not honey or potatoes. The problem might be calories, plus nutrients. If you eat too much, and deficient food at that, then you're in trouble whether your blood sugar is high or low. But if you eat just enough and lots of nutrients, there might not be any problem. Replacing refined sugars and PUFAs with SFAs, MUFAs, or proteins is good starting point. From there, potatoes and raw honey look good.
Fruit is risky as it's often picked under-ripe, and then shipped a long distance. Fresh local fruit that is ripe the first time you see it must be a priority. If that's not found, frozen, canned, or sun-dried fruits (without added sugars) are the next safest bet. Avoid food that is sent from thousands of miles away and is not naturally ripe or fresh. That's potentially a big problem. Somebody here commented on another forum how about eating a green (unripe) apple tore them up "something awful."
http://www.modernforager.com/blog/2008/03/11/book-review-in-defense-of-food/#comment-3734
So, just something to consider. And also the theory that it'st he mixed diet which causes a lot of problems today. Namely mixing starch, PUFAs, trans fat, protein, refined sugars, and maybe some alcohol too.
Try reading on the Hay Diet or Food Combining or Sequential Eating. The theory is similar to low-carb, with different conclusions. You can have carbs, but not sandwiches, burgers, pizzas, doughnuts, cookies, and the other modern abominations.
http://www.synergy-health.co.uk/healthnews/hay_diet19991130.html
These are test tube studies at the molecular level looking at the switches which control life or death on a cellular basis. There's obviously a lot more involved in real life. It is worth noting that the endotheial cells in this study were of bovine origin and the standard nutrient for most cells in tissue culture is foetal calf serum. Even an grain fed cow will be putting primarily saturated fats in to its physical structure and in to the serum of its calf. Which ever way we manage glucose on a macronutrient basis by diet, pushing pure glucose, the form it occurs in the plasma, above 22 mmol/l will flip switches that make for dead cells. However saturated my fat intake I'd still be loathe to crank my blood glucose up there in to acceptable ADA levels.
Personally I find this sort of study useful in context.
Peter
hey peter,
I think you should put up more examples of how you eat! I was wondering, after fat and protien, what order do your carbs come in....veggies, potatoes, fruit, grain, or something else? What carb source do you find most effecient? Thanks, and great blog again!!!!
I don't like test tube studies. Too many complexities in life. I prefer studies that look at mortality, and morbidity, pref over a long time. I often cite one study to show really how bad PUFAs are and how good SFAs are. You won't find a study of this sort nowadays. It's all short-term, indirect markers, cultured cells in test tubes, epidemiology, etc. This is not very reliable.
http://jn.nutrition.org/cgi/reprint/51/3/441.pdf
Animals were fed high-fat diets and each group got a different type of fat. They were injected with poison that caused diabetes and frequently death, but the animals fed coconut, MCTs, stearic, or palmitic acid had remarkable protection against death and disease. Even at more than 3.5x the dose, they had less mortality and morbidity than animals eating PUFA oils.
Another interesting result was that partially hydrogenated oil actually reduced mortality 37% and incidence of diabetes by 34% over the regular sunflower oil. This makes sense, as the partially hydrogenated oil had an iodine number 31% lower than the regular sunflower oil. 31-34-37. It suggests to me that the high iodine number was deadly. Meanwhile, those eating coconut oil and aturated fat had almost total immunity (71-95%) to the poison, even at a far higher
dose. It can't get much more clear.
The Scientific Debate Forum has all sorts of posts and articles arguing that glucose is beneficial and lack of it is harmful. He mentioned one study where adding more carbs to a person's diet reversed the problem of high triglycerides alleged to be caused by carbs by the carb-phobes. This is the other side of the issue that low-carbers ignore.
http://groups.msn.com/TheScientificDebateForum-/yourwebpage3.msnw
http://groups.msn.com/TheScientificDebateForum-/
http://raypeat.com/articles/articles/diabetes.shtml
Hi Bruce,
The diabetic rats are very interesting. Kwasnieski specifically states in Homo Optimus that the rats which had been fed on his Optimal Diet were remarkably difficult to euthanase at the end of the experimental period. He was using ether overdose. Control rats went a lot quicker than ON rats. No data supplied (as always). So I have no problem with the results.
I can see that the PUFA rats died rather more easily than sat fat rats in this paper. Is it possible to extract whether the high death rate in the PUFA rats was due to? I can't find this. No one was measuring insulin in those days.
What I mean is, were the rats protected from pancreatic beta cell failure by sat fats reducing the toxicity of alloxan or by sat fats protecting against hyperglycaemia?
If PUFA propagate free radicals to facilitate total beta cell failure under alloxan, the rats may well have died of acute insulin deficiency. They would obviously have had the highest glucose levels but glucose would not remotely have had the time to be causative in death. I'm not sure that this paper gives me the OK to accept hyperglycaemia under the protection of saturated fats. Is that what you meant?
Hopefully no one visiting here would ever purchase sunflower oil!
Peter
Hi Troy,
Lost the message in weekend work... I'm not sure I have any preferred carbs really. Neat fructose and combined fructose in sucrose are undoubtedly my least favourite. I don't think there is any real info on vegetables without fruit. They're probably neutral but are loaded with fiber, which I avoid as much as possible. This leaves things like potatoes and other root vegetables. It's a kind of default option, least harm to get your liver supplied with an oxaloacetate precursor in moderation... I certainly eat green leaf vegetables because I like them, but I don't hold out any great hope that they are nutritional panaceas!
Peter
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