The further a society drifts from the truth, the more it will hate those who speak it. ... In a time of deceit, telling the truth is a revolutionary act. George Orwell

Sunday, August 31, 2008

Diabetes, liver, fructose and omega-3

[under construction]

Peter's post:

http://high-fat-nutrition.blogspot.com/2008/08/age-rage-and-ale-vldl-degradation-and_25.html

made me think about the whole issue.

Omega-3 fats destroy or block the nascent VLDL particles inside the liver causing fat retention. The liver is probably protecting itself against fat accumulation by reducing fat synthesis out of glucose, which is probably causing a surplus glucose to remain in circulation. Without omega-3 liver would probaly convert excessive glucose into VLDL/triglycerides which then would be used up by the body as a fuel.

The whole point of Peter's article, as I understood, was I think to point out that omega-3 given in excess to diabetics may improve their numbers but not necessary their health.

If one eats excessive sugar and omega-3 fats together then the liver has a choice of either processing excess glucose into fatty acids and accumulating it, since it cannot release it into the bloodstream, or it has a choice NOT to convert glucose but instead let it remain in the bloodstream. I think the liver does the latter, to protect itself against fatty liver and cirrhosis. It's no wonder that omega-3 lowers triglycerides but increases blood glucose (when one consumes too much sugar).

How about fructose? Can liver choose not to convert fructose to triglycerides? I don't think so unless body was designed to kill off it's own neural system (thrugh fructose induced retinopathy, neuropathy) to protect it's liver. More likely, the liver would continue to manufacture fat out of fructose to get rid of fructose as quickly as it can, and suffer! What is the most lethal combination in this picture? Fructose plus omega-3 polyunsaturated oil! How about fructose with omega-6 PUFA? Peter?

Makes one wonder why no cooking in the world ever incorporated fruit or honey and fish in a single dish? Why did we not think about that before?

Monday, August 25, 2008

Very-Low-Fat Diets: What Are the Benefits?

JC from the WebMD Diet Debate forum posted the following slide - see beside and the reference below (thanks!). The author's conclusions do not surprize me. MI ("heart attack") events depend on the quality (type) of plaque more than on the quantity of plaque. Excess polyunsaturated fats (e.g. popular vegetable oils) lead probably to abnormalities in the composition of cellular structures that use fats, such as cellular membranes. This probably affects mostly the newly grown tissue such as scar tissue and the plaque tissue (plaque is a scar tissue!). The bulk of the plaque on the other hand, according to Dr. Jan Kwasniewski ("Homo Optimus"), results from excessive pentose cycle that synthesizes fats (and NADP, RNA etc) in-situ inside the arterial walls. Pentose cycle is on the other hand driven by excessive carbohydrates (plus a few other conditions such as reduced availability of oxygen, lack of magnesium etc).

If that hypothesis is true then one could perhaps draw the following general guidelines:

- To reduce the overall plaque buildup - consume less carbohydrates!

- To reduce the risk of MI events (once the plaque exists) - reduce consumption of vegetable oils and artificial baking fats (polyunsaturated fats, transfats)

Please notice that low fat vegan diets also reduce vegetable fats by discouraging all fats. They also may reduce the total glycemic load. Interestingly, when you stop eating fat, liver will manufacture some of the necessary fats internally - mostly saturated fat! Did anyone notice that this theory is the only one that explain why both types of diets: low fat vegan (sometimes) and high animal fat low carb (always) may reduce the risk of MI?!

------

Reference:

Very-Low-Fat Diets: What Are the Benefits?

Effects of Lifestyle and Dietary Modification on HDL-C Levels (Margo A. Denke, MD)


Friday, August 15, 2008

Snacking and glucose/ketogenic cycling

This is a theory, very speculative. I came to think about it, inspired after reading the latest articles by Peter (Hyperlipid blog, see also his Kitava articles). I am thinking about the effect of frequent snacking in between the meals on a high carb diet, may be more damaging than we thought. Under a healthy metabolism, even on a high carb diet, one's body goes back to ketogenic state some time after every meal, when most body tissues revert back to using lipids and ketone bodies as fuel. This should happen in between the meals providing that the body is given enough time to burn glucose off and to switch. On the other hand, any time one eats something sugary or starchy in between the meals, insulin inrush causes the body to switch back to glucose processing state, turning off production of ketone bodies and turns off the release of adipose fat into bloodstream. It takes about 1-2 hours to work out all that insulin peak. Probably longer for older people.

For some reason, our bodies probably require this alternating between glucose-burning/ketogenic cycles to be done throughout the day to work properly. This is based upon the assumption that ketogenic mode is essential for the body and must take place at least some of the time throughout the day, every day. I suspect that frequent snacking on a high carbohydrate diet derails that cycling and may be one of main triggering factors behind the development of the metabolic syndrome.

From my personal observation, one can notice that people who are used to snack frequently are often obese and often have metabolic syndrome. Perhaps there is a causual connection? Perhaps it is not just what and how much one eats but how often and when?

Diets based on natural whole food like our vegetarian friends recommend, usually discourage sugary or starchy snacks, or discourage consumption of the processed food that forms the typical fast food snacks. It makes snacking more difficult, especially that preparation of meals out of natural unprocessed whole food is time consuming and labor intensive. Perhaps that may be one of the reason why such whole food natural diets are often helpful?

Of course, the high fat low carb diets make that issue irrelevent since a high fat snack would not cause the glucose+insulin spike thus would not break the ketogenic mode. This could be another reason why the high fat low carb diets work so well!

Just some thought,
Stan (Heretic)

Wednesday, August 13, 2008

Carbohydrates and Diabetes

Response for TG (on McDougall forum)

http://www.drmcdougall.com/forums/viewtopic.php?t=8095&postdays=0&postorder=asc&start=0

I know you have studied this issue and you did notice that your glucose response is dependent on the carbohydrate load (primarily) while other factors such as the presence of fat may only modulate the insulin sensitivity somewhat but it is not the main factor. The main factor is the total glycemic load ( GL = GI * mass of carbs ).

Typically, our insulin response is equal to about 10 insulin units per every 100g of carbohydrate (GL). It is as simple as that and no amount of wiggling or waving by vegan followers with their refined versus natural theories; potatoes versus rice versus sweet potateoes etc., is going to change this.

Your blood glucose post-prandial peaks at 140mg/dl are on the higher limit of the normal (on a high carbohydrate diet) and probably indicate that your insulin secretion may be insufficient (as I wrote before check against dm t1) or that your tissue became insulin resistant (metabolic syndrome).

Insulin resistance depends on the amount of fat you consume with the carbohydrates but important is also that you allow a time of metabolic rest in between the meals. This is the period when the body wants to switch from burning glucose to burning lipids (from body fat) and ketone bodies.

Preventing the appearance of such a cycle of rest in-between the meals, through frequent snacking may be one of the culprit behind the metabolic syndrome.


There are two ways of preventing metabolic syndrome:

1) Eat low fat high carbohydrate natural low glycemic food (vegetarianism is not necessary and probably not even relevant) and make long breaks between the meals to allow for the ketogenic cycle in between the meals

2) Eat a low carbohydrate high ANIMAL fat meals. Avoid polyunsaturated oils and transfats! In this case snacking in between the meals is not harmful as long as it is with fat only, not with carbohydrates (the reason is that fatty snacks do not break the ketogenic "resting" cycle).

Both styles of eating 1 or 2 will result in low average insulin level in between the meals, and will protect you against the chronic diseases associated with the metabolic syndrome such as CHD, cancer and autoimmune. Such disease are associated with the elevated insulin level rather than with the glucose itself. Kidney failure however, is related to glucose peaks since every time it exceeds 160mg/dl, it forces kidneys to excrete glucose. Other risk factors have different causes. For example diabetic neuropathy (and retinal damage) is probably more associated with fructose leakage to the bloodstream than with glucose.

If you decide to follow (2) then do not try to avoid fat. The more fat (animal, saturated and monounsaturated) the better it works. There is absolutely no need to worry about the heart disease since it is the insulin, not fat, in particular not animal fat, that seems to be the main growth promoter for arterial plaque and arteriosclerosis. For example, see R.W. Stout http://www.ptbo.igs.net/~stanb/Lancet_Stout_pg_702.pdf and http://www.ptbo.igs.net/~stanb/Lancet_Stout_pg_467.pdf

Besides if what I am saying were wrong and McDougall's crowd were right, I wouldn't be typing it. I would be dead. Over in the last 9 years I have been consuming about 150g (to 200g) of butter, cream or pork lard every day. If you read this message it means it's true! :)

Stan (Heretic)