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General : Signs of AA overload and release
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 Message 1 of 7 in Discussion 
From: MSN Nicknametaka00381  (Original Message)Sent: 9/24/2007 12:40 PM
Hans, I like your notion that the puffy look of many today's people in the developed nations consuming vegetable oils is caused by AA release. Indeed, I also notice that the truly healthy individuals don't have that look. But what do you think about the big belly of the undernourished and starved people - are they also releasing AA? This look puzzles me, it's unlikely to be a "beer belly" or VAT. An example picture is e.g. here:

http://en.wikipedia.org/wiki/Starvation


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 Message 2 of 7 in Discussion 
From: MSN NicknameHansSelyeWasCorrectSent: 9/25/2007 4:03 AM
I saw that one "expert" claimed that the stomach distension among some people who are starving to death is due to slowed metabolism, so my guess is that it may not be known. This does not occur in the West, however, such as in anorexics and cancer patients. Thus, I don't think this is related to AA or its metabolites. When I look at pictures of my great grandparents and look at my grandparents (who are still alive), I notice the big difference. My grandparents eat a lot of fried food (cooked with different oils, some highly polyunsaturated), unlike my great grandparents, who did not use the highly polyunsaturated oils.

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 Message 3 of 7 in Discussion 
From: MSN NicknameHansSelyeWasCorrectSent: 9/25/2007 4:08 AM
Here's another person's claim:

"The first is edema in the abdominal area [Moderator's note: edema represents a "puffiness" due to accumulation of fluid that has seeped from the bloodstream into surrounding tissues]. This edema is a result of a lack of proteins in the bloodstream. The proteins in the bloodstream cause water to remain in the bloodstream. As the concentration of proteins in the bloodstream decreases, the water moves out of the bloodstream and into the extracellular spaces. This causes edema. The edema is particularly evident in the abdomen--especially in children.

The second cuase of a protruding stomach is an enlarged liver which is a result of inflammation as well as an accumulation of fat. Fat accumulates in the liver because` there are not enough proteins to allow it to be transported in the bloodstream.

The third cause of the protruding stomach can be due to parasitic infections, which are very common in malnourished people and, of course, make their malnutrition worse."

Source: http://www2b.abc.net.au/science/k2/stn/archives/archive34/newposts/258/topic258451.shtm

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 Message 4 of 7 in Discussion 
From: MSN Nicknametaka00381Sent: 9/25/2007 7:06 AM
Thanks for the information Hans, so another reason to keep the dietary protein sufficient. Maybe giving the starving childrens the essential amino acids with some carbohydrates can safe them.

Now I am wondering what is the worst irritant that stimulates AA release and causes systemic inflammation. People talk about the AGEs (Maillard reaction products) lately but there are also the ALEs ...

Ann N Y Acad Sci. 2005 Jun;1043:482-91.

Renal effects of oral maillard reaction product load in the form of bread crusts in healthy and subtotally nephrectomized rats.

Sebeková K, Hofmann T, Boor P, Sebeková K Jr, Ulicná O, Erbersdobler HF, Baynes JW, Thorpe SR, Heidland A, Somoza V.
Slovak Medical University, Institute of Preventive and Clinical Medicine, Limbová 14, 833 03 Bratislava, Slovakia. [email protected]

The biological consequences of chronic consumption of Maillard reaction products (MRPs) on renal function in health and renal disease are still incompletely understood. We investigated the metabolic and renal effects of a diet with varying MRP content in healthy and subtotally nephrectomized rats. Male Wistar rats were subjected to sham operation (control, C, n = 12), or to 5/6 nephrectomy (5/6NX, n = 12). Both groups were randomized into subgroups and pair-fed with either a MRP-poor or -rich diet for six weeks. The diet was prepared by replacing 5% or 25% of wheat starch by bread crust (BC). In spite of pair-feeding, the rats on the 25% BC diet gained more body weight (C: 183 +/- 6 g; C + 5% BC: 197 +/- 7 g; C + 25% BC: 229 +/- 6 g [P < 0.05]; 5/6NX: 165 +/- 10 g; 5/6NX + 5% BC: 202 +/- 3 g; 5/6NX + 25% BC: 209 +/- 8 g [P < 0.05]) and had a higher organ weight (heart, liver, lung, kidney/remnant kidney). Bread crust-enriched diet induced proteinuria (C: 15 +/- 5 mg/24 h; C + 5% BC: 19 +/- 4; C + 25% BC: 26 +/- 3 [P < 0.05]; 5/6NX: 30 +/- 7 mg/24 h; 5/6NX + 5% BC: 47 +/- 9; 5/6NX + 25% BC: 87 +/- 19 [P < 0.01]) and a rise in urinary transforming growth factor beta(1) excretion (C: 0.4 +/- 0.1 ng/24 h; C + 5% BC: 0.6 +/- 0.1; C + 25% BC: 1.2 +/- 0.3; 5/6NX: 0.5 +/- 0.1 ng/24 h; 5/6NX + 5% BC: 0.9 +/- 0.1; 5/6NX + 25% BC: 1.6 +/- 0.2 [P < 0.01]). Plasma creatinine or creatinine clearance were not affected significantly. In conclusion, our data suggests that long-term consumption of a diet rich in MRPs may lead to damage of the kidneys.
PMID: 16037270


Mol Nutr Food Res. 2007 Sep 13;51(9):1102-1106

Dietary ALEs are a risk to human health - NOT!

Baynes JW.

Advanced lipoxidation end-products (ALEs) are formed by reaction of protein with lipid-derived reactive peroxyl and carbonyl compounds produced during food processing and cooking. There is concern that ALEs may induce damage in the gastrointestinal tract, affecting gut health, or enter the body and promote vascular inflammation and tissue damage. However, there is no direct evidence that ALE-proteins are a source of damage in the intestines or that they are transported into the circulation and cause pathology. Modification of proteins by ALEs impedes their digestion, and reactive ALEs released by gastrointestinal proteases would react with proteins or peptides in the gut, limiting their absorption. There are also potent enzymatic mechanisms for detoxifying ALEs or their precursors prior to their entry into the circulation. If ALEs gain access to the circulation, a battery of protective enzymes in tissue provides a second level of defense. These enzymes may be induced in intestinal epithelia and liver by low doses of ALEs, and adaptive responses would provide enhanced protection against future exposure to ALEs. Overall, except in persons with compromised organ function, e. g., vascular, hepatic, or renal diseases, there is little evidence that food ALEs will have any significant pathological effects.Introduction: http://dx.doi.org/10.1002/mnfr.200700030Pro arguments: http://dx.doi.org/10.1002/mnfr.200600303.
PMID: 17854007

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 Message 5 of 7 in Discussion 
From: MSN NicknameHansSelyeWasCorrectSent: 9/25/2007 11:44 PM
Nobody knows all the details on this subject, but again, why not eliminate the AA from your cells, and then not worry about this?

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 Message 6 of 7 in Discussion 
From: MSN Nicknametaka00381Sent: 10/2/2007 4:23 PM
Eliminating AA from the cells may be indeed a very good strategy in the space exploration. There is very high radiation exposure in the space causing mostly apoptosis, cataracts and sometimes cancer. The Bush administration is funding lot of scientific research trying to develop strategies to make humans less sensitive to space radiation when going back to the Moon and to the Mars in the future. I have been personally familiarized with some of these projects which are exploring antioxidants and certain drugs to minimize DNA damage during the long haul space flights. But a simple 2 year PUFA-less diet course may be perhaps the best preparation for such a space mission ...

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 Message 7 of 7 in Discussion 
From: MSN Nicknametaka00381Sent: 10/2/2007 4:33 PM
Speaking of AGEs here is one interesting article about their effects on LDL - does it mean that we should not be eating the bread crust?

SOURCE: http://tinyurl.com/2pcwwq

QUOTE: Increased consumption of dietary AGEs can alter LDL (the “bad�?cholesterol) in a way that increases its negative effects. In a study of 24 diabetic subjects, LDL from subjects consuming a high-AGE diet experienced more free radical damage (oxidation) and was more susceptible to glycation compared to subjects on the low-AGE diet. When this oxidized, glycated LDL was added to human endothelial cells from vein walls it promoted inflammation, an effect not seen with the LDL not exposed to AGEs. The LDL from the subjects consuming the high-AGE diet also significantly increased vascular cell adhesion molecule-1, a molecule that encourages blood cells to stick to the artery walls and block the arteries, providing further evidence to support the possibility that AGEs are the reason why diabetics have an increased risk of heart disease.8 The study authors concluded that exposure to dietary AGEs increased LDL-induced vascular toxicity and that “this can be prevented by dietary AGE restriction.”UNQUOTE.

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