Poly-unsaturated fatty acids & Lipid peroxidation

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RRM
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Re: Poly-unsaturated fatty acids & Lipid peroxidation

Post by RRM »

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.
Are you claiming that elevated lipid oxidation is causing 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.
So shouldn't we prevent the formation of these compounds or are you all saying this is genetics at work?
You cannot prevent lipid oxidation.
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.
Also, why can't mead acid provide the autophagy and apoptosis task in your opinion?
Maybe it can, but obviously, the body prefers other PUFAs instead.
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.
And still, the higher suspectibility in lipid oxidation might also be a trigger itself for autophagy that is not needed.
Autophagy is associated with longevity.
If there is stress omega 6 will be released from the tissues and might induce cell destruction that is not needed.
Cellular stress results in enzymatic lipid oxidation.
If the cellular stress is too large, it will result in cell death.
What is not needed about that?
I still think a high saturated to high unsaturated fatty acid intake is beneficial.
Based on what epidemiological study?
overkees
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Re: Poly-unsaturated fatty acids & Lipid peroxidation

Post by overkees »

RRM wrote: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.
Elevated protein-bound levels of the lipid peroxidation product, 4-hydroxy-2-nonenal, in brain from persons with mild cognitive impairment.
Butterfield et al
We explored whether oxidation of docosahexaenoic acid (C22:6omega3), which is highly enriched in the brain, led to the formation of F2-isoprostane-like compounds, which we term F4-neuroprostanes. F4-neuroprostanes could be detected in normal human cerebrospinal fluid and levels in patients with Alzheimer’s disease (110 +/- 12 pg/ml) were significantly higher than age-matched controls (64 +/- 8 pg/ml) (p < 0.05). Roberts LJ 2nd et al
Lipoproteins and lipid peroxidation in Alzheimer's disease.
Taken together, the findings from in-vitro studies of lipid peroxidation induced by Abeta(1-42) and postmortem studies of lipid peroxidation (and its sequelae) in AD brain may help explain the APOE allele-related risk for AD, some of the functional and structural alterations in AD brain, and strongly support a causative role of Abeta(1-42)-induced oxidative stress in AD neurodegeneration. Butterfield et al
Acrolein, which is increased in AD brain, may be partially responsible for the dysfunction of mitochondria and loss of energy found in AD brain by inhibition of PDH and KGDH activities, potentially contributing to the neurodegeneration in this disorder.Pocernich and Butterfield
Collectively, these data demonstrate neurotoxicity mechanisms of arolein that might be important in the pathogenesis of neuron degeneration in AD.Acrolein, a product of lipid peroxidation, inhibits glucose and glutamate uptake in primary neuronal cultures.
These results suggest that lipid peroxidation occurs early in the pathogenesis of AD.Williams et al
And this goes on and on and on and on. If you want more I've got tons more.

RRM, it's about the antioxidant system not working properly due to genetics maybe. I don't know. But your response is that omega 3 will cause more AD. That's a different thing.
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Re: Lipid peroxidation & AD

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overkees wrote:RRM, it's about the antioxidant system not working properly due to genetics maybe.
Are you suggesting that lipid oxidation is the cause of AD, and the antioxidant system is not responding properly?
Your studies do not show that.
AD is a degenerative disease. Degeneration => cell death = lipid peroxidation.
As there is a lot of DHA in the brain, death of brain cells will come with a lot of lipid peroxidation in degenerative brain diseases.
Your studies show that lipid oxidation products are formed in AD.
But this is true for many diseases, particularly inflammatory diseases and degenerative diseases.
The reason: when cells get damaged, lipid oxidation occurs, as lipid oxidation is involved in cell death.
So, the lipid oxidation may very well be the RESULT of the damage involved in this disease,
and then of course, this lipid oxidation will also have damaging effects, including cell death.
If lipid oxidation would be the CAUSE of AD, then supplemental omega-3 would have shown to be bad for AD.
Since that is not the case, the lipid oxidation must be the result, and not the cause.
I don't know. But your response is that omega 3 will cause more AD. That's a different thing.
No, i said that if lipid oxidation would be the CAUSE of AD, made possible by a poor antioxidant defense,
then omega-3 supplementation would have to correlate with AD in epidemiological studies.
And that is not the case.
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Re: Poly-unsaturated fatty acids & Lipid peroxidation

Post by overkees »

Thanks for your reply, I must admit that I totally didn't look at it that way. Hmm, very interesting.
What might cause the stress done in AD?
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Re: Poly-unsaturated fatty acids & Lipid peroxidation

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overkees wrote:What might cause the stress done in AD?
The stress might just be a symptom.
What may be involved in the cause of AD, is the accumulation of Aβ peptide,
which may be the result of inefficient autophagy degradation of the Aβ peptide.
The accumulation of the peptide and peptide aggregates may be toxic to neurons. Billings et al
Dying neurons will result in lipid peroxidation.
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Poly-unsaturated fatty acids

Post by overkees »

I think my viewpoint has shifted 180 degrees by the last few posts.
We, however, still need to develop an optimal fatty acid composition. The fact that the synthesis of LCPUFAs are highly inhibited by fish oils shows that our body only needs only little of them. I definitely think they are medicinal in higher portions and it's against the wai way to consume such high amounts (10% for cardiovascular health for example). Also, interesting is how much an ideal saturation index is to promote autophagy, but not be too responsive to stress.
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