Overkees's research topic

[overkees]

Since I don't want to open a topic for everything I find, I will post my undeveloped thoughts and researches in my own topic, just like Kasper does.

As I am not claiming to know everything I am very open for discussion. If you have been reading this forum for a longer time, you must have noted that I tend to attack the wai diet. This is not due to the fact that I don't like the wai diet, otherwise I wouldn't follow a wai inspired like diet. But the reason why I do it is that my goal is to develop an ultimate variant of the wai diet combined with other optional super foods
(I see butter, for example, as a very useful addition the wai diet. Or stuff like very good quality bee pollen. And even carrots). I think you should always try to filter out possible flaws in a system. The more attacks a system withstands, the more credible it gets.

Central themes: breathing, CO2 and its protective effects, high metabolism and heat generation, thyroid, sugars like fructose and sucrose, fasting and caloric restriction, cholesterol, free radicals, stress, PUFAs, genetics and calcium.

[overkees]

Cholesterol and desaturases:
The major effect of cholesterol supplementation was to decrease the rate of desaturation (delta 6 desaturase) of LA, when fed in combination with the beef-tallow diet, whereas delta 6-desaturation was unaffected when cholesterol was fed along with diets high in omega 3 fatty acids (linseed oil or fish oil)....
Inclusion of cholesterol into the beef-tallow or linseed-oil diets resulted in decreased membrane AA content with concomitant increase in LA content. However, addition of cholesterol to the fish-oil diet did not alter the microsomal membrane content of AA Garg ML et al

The addition of 1% dietary cholesterol to a low-EFA diet induced, as in animals fed a high-EFA diet, a marked increase in liver stearoyl-CoA desaturase-1 mRNA and enzyme activity. This increased activity apparently evoked a similar enhancement of palmitoleic and oleic acids in total and microsomal liver lipids...Taken together, these results indicate that through its modulating effect on the desaturases, dietary cholesterol may lead an animal or human fed low-EFA diet to a true deficiency by the decreased synthesis of the highly polyunsaturated acids derived from linoleic and alpha-linolenic acids.Brenner RR et al

LA -> AA decreases with dietary cholesterol only in the case of low LCPUFAs

But LCPUFAs decrease AA formation (by comptetition) without cholesterol.

So AA is normally reduced by fish oil, but when fed extra cholesterol it stays the same. I can't figure this one out completely. Cholesterol also seems to increase oleic acid and palmitoleic acid production, which are both inhibitors (not sure of palmitoleic) of the AGEs/ALEs.

Now sugar is a potential cholesterol increaser, sugar should have similar effects? Hmm..

[overkees]

Carbs result in the highest CO2 production.

Carbohydrate metabolism results in a marked increase in CO2 production.Askanazi J, et al., Robin AB, et al.

“It is well established that the combustion of one calorie of carbohydrate, fat and protein produces 0.2, 0.15 and 0.191 of CO2 respectively.” al-Saady NM, et al.

So that one calorie of carbohydrate results in 30% more CO2 than one calorie of fat!

This is indeed what is seen in patients receiving a high fat feeding, their CO2 production drops:

During the feeding period, PaCO2 just prior to weaning fell by 16% in the high fat group but increased by 4% in the standard feed group (p = 0.003) in patients with acute respiratory failure requiring artificial ventilation. al-Saady NM, et al.

Another study using feeds identical to al-Saady of patients with acute respiratory failure showed that CO2 production was 24% lower on the high fat feed.Garfinkel F, et al.

[dime]

overkees what do you think about this?

Dietary Fructose Causes Liver Damage in Animal Model

What I find especially interesting is

In the high-fructose group, the researchers found that the type of intestinal bacteria hadn't changed, but that they were migrating to the liver more rapidly and causing damage there. It appears that something about the high fructose levels was causing the intestines to be less protective than normal, and consequently allowing the bacteria to leak out at a 30 percent higher rate
...
"We studied fructose because it is the most commonly added sugar in the American diet, but based on our study findings, we can't say conclusively that fructose caused the liver damage," Kavanagh said. "What we can say is that high added sugars caused bacteria to exit the intestines, go into the blood stream and damage the liver.

The biggest problem I find with this study is that the diets were quite different, instead of being different just in the fructose amount.. so I'm not sure how could they say that exactly fructose was causing what they observed.

Both diets had the same amount of fat, carbohydrate and protein, but the sources were different, Kavanagh said. The high-fructose group's diet was made from flour, butter, pork fat, eggs and fructose (the main ingredient in corn syrup), similar to what many people eat, while the control group's diet was made from healthy complex carbohydrates and soy protein.

Anyway, the most important thing I learned from this is that gut bacteria can enter the blood and just go to the liver or wherever, and the scale on which this happens depends somewhat on your diet.