Are you claiming that elevated lipid oxidation is causing AD?overkees wrote:alzheimers disease is clearly the result of an antioxidant system that wasn't enough to inhibit the formation of excessive acrolein that is found in AD.
If lipid oxidation was a major contributor to AD, and as n-3 PUFAs are most susceptible to lipid oxidation,
epidemiological studies would consistently suggest a deleterious effect of n-3 PUFA on AD.
Epidemiological studies (inconsistently) suggest a protective role of n-3 PUFA against Alzheimer's disease (AD). Lopez LB et al
"In humans, fish consumption or administration of DHA has been associated with cognitive improvement in many, but not all, studies.
In contrast, administration of triglycerides to mice decreases learning and memory and impairs long-term potential." Morley JE et al
"Based on epidemiological data, fish including oily fish could be advised ... although the evidence for better cognition is only fairly consistent." Cederholm T et al
"Epidemiologically, low fish intake and low blood levels of the omega-3 polyunsaturated fatty acid docosahexaenoic acid (DHA) have been related to an increased risk of AD." Pauwels EK et al
"There is substantial epidemiological evidence from a number of recent studies that demonstrate a protective role of omega-3 fatty acids" Morris MC
"A dietary pattern strongly associated with lower AD risk was characterized by higher intakes of ... nuts, fish ... and a lower intake of high-fat dairy products ... and butter" Gu Y et al
"...omega-3 fatty acids deficieny may exacerbate pathological processes in the brain" Kamphuis BJ et al
"Results to-date suggest that DHA may be more effective if it is begun early or used in conjunction with antioxidants." Cole GM et al
etc etc etc
There are also several studies that show no correlation at all between dietary / supplemental omega-3 intake and dementia or AD.
You cannot prevent lipid oxidation.So shouldn't we prevent the formation of these compounds or are you all saying this is genetics at work?
Even if you drastically decrease your PUFA intake, lipid oxidation will still be there significantly.
Also, both enzymatic lipid oxidation (in autophagy) and non-enzymatic lipoxidation (apoptosis) have biological functions.
In my view, the only thing you need to do, is not take fish oil / PUFA supplements, and not eat cooked foods.
Maybe it can, but obviously, the body prefers other PUFAs instead.Also, why can't mead acid provide the autophagy and apoptosis task in your opinion?
Mead acid is associated with essential fatty acid deficiency.
When these fatty acids are not deficient, mead acid is drastically lowered by the body.
If the human body does not use this back up for many generations, the body even stops producing it all together.
Autophagy is associated with longevity.And still, the higher suspectibility in lipid oxidation might also be a trigger itself for autophagy that is not needed.
Cellular stress results in enzymatic lipid oxidation.If there is stress omega 6 will be released from the tissues and might induce cell destruction that is not needed.
If the cellular stress is too large, it will result in cell death.
What is not needed about that?
Based on what epidemiological study?I still think a high saturated to high unsaturated fatty acid intake is beneficial.