Why PUFA is bad: how high membrane polyunsaturation decreases longevity

cremes

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I infer from this that a human who is Essential Fatty Acid Deficient(EFAD) may live longer.

Im putting a post together on 4 approaches to achieving EFAD. I’ll try and get that out in next few days. And then im going to attempt one of them.
 
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Mauritio

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I infer from this that a human who is Essential Fatty Acid Deficient(EFAD) may live longer.

Im putting a post together on 4 approaches to achieving EFAD. I’ll try and get that out in next few days. And then im going to attempt one of them.
Ok, cool.
From what I read though . Mice and rats are more easily affected by their diet when it comes to the fatty acid membrane composition , so I'm not sure how much that's applicable to humans.
Interspecific differences are important to keep in mind IMO

Although this study makes me question that somewhat :

- Consumption of virgin olive oil influences membrane lipid composition and regulates intracellular signaling in elderly adults with type 2 diabetes mellitus - PubMed
 
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Mauritio

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"The saturation index (SI) of cell membrane is the ratio of stearic acid to oleic acid and it is considered an indicator of membrane rigidity [7]. Low levels of SI have been associated to the cell malignant phenotype [3]. Analysis of fatty acid extracted from leukemic cells and solid tumor tissue showed a significant increase in the oleic acid content respect to stearic acid [10, 11].In erythrocytes membranes, low levels of SI have been demonstrated to be predictors of postmenopausal breast cancer [12].

The subjects with severe NAFLD showed a significant decrease of the ratio of stearic acid to oleic acid (saturation index, SI) compared to controls..."
 
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@Mauritio Does the ratio increase strictly with the increase in saturated fats?
 
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Mauritio

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Whales can live hundreds of years. Yet their diet mainly consists of PUFA , a lot of omega 3 fatty acids actually . Yet their fat and cell membranes contain a lot more MUFA than they should.
The authors of "human longevity" suppose that they have gut bacteria that can convert PUFA into MUFA making their diet a lot safer. They also eat a lot of chitin which they can convert into glucose . That might explain their remarkable longevity despite their diet high in PUFA .
I'd be interested in the data on sharks since they live even longer and don't develop any cancers.

Also if we could take a probiotic that would hydrogenate PUFA into MUFA or SFA that would be fantastic.

I can really recommend the book "human longevity" by valentine and valentine . A lot of what I post here is from this book. I'll continue to post interesting excerpts and stories as I get further along in the book.
 
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Mauritio

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Mauritio

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PUFA contributes to artherosclerosis:

"When rabbits were fed oxidized fatty acids [=PUFA] or oxidized cholesterol, the fatty streak lesions in the aorta were increased by 100%. Moreover, dietary oxidized cholesterol significantly increased aortic lesions in apo-E and LDL receptor-deficient mice. A typical Western diet is rich in oxidized fats and therefore could contribute to the increased arterial atherosclerosis in our population."

- The role of dietary oxidized cholesterol and oxidized fatty acids in the development of atherosclerosis - PubMed
 
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Mauritio

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In this human study they showed that the level of the major lipid peroxidation product malonaldehyde (MA) was 3,6 times higher in human that ate a diet rich in PUFA compared to humans that ate a MUFA-rich diet .

"The average adduct level in the SO diet group was 7.4 +/- 8.7 adducts/10(7) nucleotides (n = 23). This level was 3.6-fold higher than that found in individuals in the RO diet group (P < 0.001). Our results, in conjunction with the mutagenic and carcinogenic properties of MA, thus suggest the interaction of lipid peroxidation products such as MA with DNA as one plausible mechanism explaining the involvement of dietary fat in carcinogenesis."

I just read that again and find it interesting that even the switch from PUFA to MUFA lowers MDA by 3.6 times . Imagine the difference to a SFA diet.
 

Eberhardt

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PUFA contributes to artherosclerosis:

"When rabbits were fed oxidized fatty acids [=PUFA] or oxidized cholesterol, the fatty streak lesions in the aorta were increased by 100%. Moreover, dietary oxidized cholesterol significantly increased aortic lesions in apo-E and LDL receptor-deficient mice. A typical Western diet is rich in oxidized fats and therefore could contribute to the increased arterial atherosclerosis in our population."

- The role of dietary oxidized cholesterol and oxidized fatty acids in the development of atherosclerosis - PubMed
I think its important to remember that rabbits are notorious in these studies. It has been rampant to use rabbits since the time of early cholesteral research around WWI (or maybe a bit earlier) as rabbits are unike in the animal kingdom due to their total inhability to handle any dietary cholesterol. This is an unike feature of rabbits probably due to their unusual diet - there are very few animals living on such a purely vegan diet as rabbits in nature. Initially it was possible to feign obliviousness to this fact, but this would be at best highly incompetent at worst pure fraud.
 
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Mauritio

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I think its important to remember that rabbits are notorious in these studies. It has been rampant to use rabbits since the time of early cholesteral research around WWI (or maybe a bit earlier) as rabbits are unike in the animal kingdom due to their total inhability to handle any dietary cholesterol. This is an unike feature of rabbits probably due to their unusual diet - there are very few animals living on such a purely vegan diet as rabbits in nature. Initially it was possible to feign obliviousness to this fact, but this would be at best highly incompetent at worst pure fraud.
Thanks for sharing I didnt know that.
 

Sitaruîm

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PUFA contributes to artherosclerosis:

"When rabbits were fed oxidized fatty acids [=PUFA] or oxidized cholesterol, the fatty streak lesions in the aorta were increased by 100%. Moreover, dietary oxidized cholesterol significantly increased aortic lesions in apo-E and LDL receptor-deficient mice. A typical Western diet is rich in oxidized fats and therefore could contribute to the increased arterial atherosclerosis in our population."

- The role of dietary oxidized cholesterol and oxidized fatty acids in the development of atherosclerosis - PubMed
How does the cholesterol in food oxidize? Will boiling an egg for eight minutes and frying it for two lead to different outcomes?
Is it better to let our bodies synthesize cholesterol from sugar and minimize cholesterol intake, so as to minimize oxidized cholesterol intake?
 

Eberhardt

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How does the cholesterol in food oxidize? Will boiling an egg for eight minutes and frying it for two lead to different outcomes?
Is it better to let our bodies synthesize cholesterol from sugar and minimize cholesterol intake, so as to minimize oxidized cholesterol intake?
It differs quite much. My understanding is that it's a bit like with AGE-products. It's better to have some heavily oxidized instead of lot of partly oxidized which would favour flash cooking. I tend to like the idea of rather synthesizing it from sugar though Im not absolute in my conviction. I think the degree to which we are able to do so is largely inherited according to studies investigating the endogenous cholesterol production. Though Im not sure how important that is as I tend to think we are more mallable then genetics suggest. Maybe some will need lower fat/more time to trigger it/better metabolism. But I have no proof of this. I attach a paper showing why you should at least avoid cooled cooked food if you want to keep it low: Cooking, storage, and reheating effect on the formation of cholesterol oxidation products in processed meat products - Lipids in Health and Disease
 
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