Paleo Diet and Paleolithic Diet Questions & Answers

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As I understand it, the membrane of LDL contains polyunsaturated fatty acids (PUFA), which are highly vulnerable to oxidation. This oxidation, due to poor LDL receptor activity, lack of antioxidants or otherwise, is what causes atherosclerotic plaque to form.

PUFAs are very delicate and prone to oxidation unlike saturated fats which are more stable.

So, by minimizing our intake of PUFAs, is that reducing possible oxidation of LDL? That would imply that the fatty acid profile of the LDL membrane would change?

or is it reducing oxidative damage only in other places and not really effecting oxidized LDL?

thanks

flag	asked Aug 2 2011 at 2:53 Jeff 16.5k●1●8●33

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the real problem is the length of the time the sdLDL remains in the blood because it is not taken up quickly enough in the peripheral tissues or in the liver to be repackaged to fat. So it is subjected to oxidation for two reasons.....length of time exposed to oxidants and poor receptor uptake due to poor gut/liver function. PUFA's chemically are subject to oxidants because of their double bonds. – The Quilt Aug 2 2011 at 3:02

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okay, so then is it fair to say that dietary PUFAs dont affect the buildup of atherosclerotic plaque? – Jeff Aug 2 2011 at 3:35

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is it fair.....no its not. It appears that dietary PUFA's are one of the causes off many neolithic disease. These fats get incorporated into our cells and they will eventually recycle many times over. They also compete directly with O3 for binding. Since the SAD has a 25-40 to 1 ratio of 6/3 they matter unless your ratio is solidly below 3/1 in my view. Testing becomes critical. And I look at all variables. I think if your VAP shows bad news and you have a high HS CRP you are in deep shit. – The Quilt Aug 2 2011 at 4:17

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and to throw some more controversy on this.....when your VAP is particle B and you have Apoe4 with a low vitamin D, high cortisol level, and a high HS CRP......taking fish oil may actually help kill you. Fish oil is not always a good thing. The reason is because supplementing elevates blood PUFA's and causes platelets to clump via PGI2 and it actually increase artery intima size. Not good for obstruction of vessels. Again.....context is key. In this same context eating fish would be a way smarter move. Real Fish and Fish oil are not handled the same way in this scenario. – The Quilt Aug 2 2011 at 4:28

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Take a look at the IOWA study.......its an eye opener. They found that LA/ALA ratios should be 2:1 for best health in CAD and cancer patients. Also insulin resistance got better with this ratio. It appears when the patient is far from optimal.....taking marine supplements may worsen them. After reading IOWA and other studies I no longer recommend to AD patients a high dose marine fish oil. I go hard to coconut oil. In fact I think we need more dietary coconut oil even for diabetics, CA and CAD patients. It maybe the missing piece to Otto Warberg's prediction about cancer and glucose. – The Quilt Aug 2 2011 at 4:31

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coprophagous · Answer 1 · 2011-12-17 03:31:36Z UTC

im surprised that this traditional dogma is on a paleo site. we have this wonderful mechanism to prevent death due to bleeding called atherosclerosis that was selected for when humans or some lessor creature lost the ability to form vitamin C and couldn't make collagen in its absence. its a stop gap mechanism. the topic of atherosclerosis is not even remotely related to cholesterol or oxidative processes or dietary fats. the human species is under chronic scurvey. i read just yesterday that 30 percent of americans have gingivitis. just look at the treatment for gingivitis just take vitamin c and it goes away.

Jerome Stans · Answer 2 · 2011-09-09 01:30:25Z UTC

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High CRP + Plaque = Bad News

http://chriskresser.com/episode-16-chris-masterjohn-on-cholesterol-heart-disease-part-2

edited Sep 9 2011 at 1:30

answered Sep 9 2011 at 1:08

Jerome Stans
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Hans · Answer 3 · 2011-11-12 20:19:56Z UTC

I don't think at this point we can be sure that there is a connection between PUFAs and oxLDL. Kismet over at Imminst addressed this issue in a post:http://www.longecity.org/forum/topic/48670-the-oxldlox-stress-pufa-connection-is-very-dubious-evidence/

The issue is that PUFAs could increase oxLDL in the serum because since it is lowering LDL oxLDL particles are being removed from the intimal space. However as I wrote about in my recent blog post (http://hanswuhealth.blogspot.com/2011/11/paleo-folk-beware-of-your-cholesterol.html) it is quite possible that oxLDL may be the instigator, however from then on there the process moves on at a pace determined by many factors (less cases like FH).

If we are arguing on the basis of PUFAs are less stable, thus they COULD cause oxidation in vivo, we don't really know that to be true. By that reasoning, SAFA would be the most stable, however studies comparing the two (albeit limited in number) show that SAFA leads to more oxLDL (possibly inflammatory? discussed here: http://hanswuhealth.blogspot.com/2011/11/lipid-profile-and-goals-part-ii-mufa-vs.html).

While there is lack of data showing the benefit of no PUFAs, there is also lack of data for increased PUFAs, for now I think we can settle down for 20g total a day. 2:1 ratio of w-6:w-3.

Adel · Answer 4 · 2011-11-27 18:14:42Z UTC

there is an interesting recent study on the o3 vs. o6 content of LDL and health - was released a few weeks ago... I will have to dig that up again. Its in the queue for next weeks SuppVersity news, anyways.

ok, I dug it up

Quantification of the major ω-3, ω-6 PUFAs using the Purdie assay and their ratios in different cholesterol types and the effects of gender and cholesterol on PUFA levels Mary Muriuki, Neil Purdie, Gerard Dumancas This study used the Purdie assay, a new assay, to quantify the levels of omega-3 (ω-3) and omega-6 (ω-6) polyunsaturated fatty acids (PUFAs) in mol/L and the ratio of ω-6:ω-3 in total cholesterol (TC), high-density lipoprotein cholesterol, (HDL-C) and low-density lipoprotein cholesterol (LDL-C) (referred to throughout as “non-HDL-C” in this study) fractions in 35 samples of human serum and also assessed the influence of gender and cholesterol types on levels of the analyzed PUFAs. Three principal components explained 89% of the total variance based on the variables measured. The ratio of ω-6:ω-3 PUFAs was significantly influenced by the type of cholesterol (F = 10.84, df = 2, 99, P = < 0.001) but not gender or interaction between gender and type of cholesterol, while the total PUFAs and the levels of ω-3 and ω-6 PUFAs were significantly influenced by gender, but age did not have a significant effect on the levels for total PUFAs. The findings of this study imply that, for males, more focus should be on the ratios of ω-6:ω-3 PUFAs in the non-HDL-C fraction and that the use of the ω-6:ω-3 ratio of PUFAs in serum is a better predictor of coronary heart disease than estimating LDL-C.

Oxidized LDL and PUFAs

4 Answers