If lipid oxidation from dietary PUFAs were the central event in atherosclerosis, then there wouldn't be a consistent pattern of PUFA for SFA substitutions reducing CVD risk. Is lipid oxidation an issue? Perhaps, but it appears secondary to endothelial inflammation or high LDL.
The mechanistic studies on EPA/DHA support the idea that its the ratio to arachidonic acid that matters, more so than the absolute amounts. One can achieve this with fish oil megadoses, but its perhaps wiser just to take a smaller supplement while cutting out high arachidonic acid foods and high linoleic acid vegetable oils (safflower, corn, cottonseed, soybean, sunflower).
A budget fish oil is less likely to be refined to reduce persistant organic pollutant content, and this, as far as I can tell, is the major issue with knightly's fish oil megadose plan. POPs impair insulin sensitivity, and keeping insulin sensitivity high is a critical element of any longevity plan.
Turunen, A. W., Jula, A., Suominen, A. L., Männistö, S., Marniemi, J., Kiviranta, H., ... & Verkasalo, P. K. (2013).
Fish consumption, omega-3 fatty acids, and environmental contaminants in relation to low-grade inflammation and early atherosclerosis. Environmental research, 120, 43-54.
Serum triglyceride decreased across omega-3 PUFA tertiles in both sexes and studies. Insulin resistance, C-reactive protein, tumour necrosis factor a, and interleukin 6 decreased across omega-3 PUFA tertiles among the Health 2000 survey participants. Among the Fishermen study men, insulin resistance and arterial stiffness indicated by b-stiffness index tended to increase and the RR estimate for carotid artery plaque tended to decrease across tertiles of PCDD/FþPCB and MeHg. The hypothesised favourable effect on insulin sensitivity and arterial elasticity was suggested to be counteracted by high exposure to environmental contaminants but the effect on plaque prevalence appeared not to be harmful.
Ruzzin, J., Petersen, R., Meugnier, E., Madsen, L., Lock, E. J., Lillefosse, H., ... & Frøyland, L. (2010).
Persistent organic pollutant exposure leads to insulin resistance syndrome. Environmental health perspectives, 118(4), 465.
Adult male rats exposed to crude, but not refined, salmon oil developed insulin resistance, abdominal obesity, and hepatosteatosis. The contribution of persistant organic pollutants to insulin resistance was confirmed in cultured adipocytes where POPs, especially organochlorine pesticides, led to robust inhibition of insulin action. Moreover, POPs induced down-regulation of insulin-induced gene-1 (Insig-1) and Lpin1, two master regulators of lipid homeostasis.
Edited by Darryl, 30 May 2014 - 09:05 PM.