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Membrane Unsaturation In Regards To Longevity

membrane fluidity polyunsaturated fat saturated fat free radicals oxidative stress lipid peroxidation delta 9 desaturase insulin diabetes monounsaturated fat

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#1 misterE

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Posted 02 December 2013 - 01:20 AM


Interesting research in animals has found that the amount of unsaturation in the cell membranes of animals determines their longevity [1]. Low levels of polyunsaturation are linked with increased longevity. Certain animals (and even animals within the same species) with greater longevity show that they have less polyunsaturated-fats incorporated in their cell membranes than other animals.


Bumble-bees are an interesting example. Worker-bees have a much reduced lifespan compared to the queen-bee. The reason scientists believe this to be true is due to the different diets of the bee’s and the different fatty-acid composition of the bee’s cells… with worker-bee’s containing more polyunsaturated-fats than the queen-bee’s which are much more monounsaturated.


Worker-bee’s eat pollen which contains a generous amount of polyunsaturated-fat, while the queen-bee is fed royal-jelly, which contains very little polyunsaturates. The queen-bee is then able to synthesize saturated-fat from the royal-jelly and from the saturated-fats synthesize monounsaturated-fats.


The scientists believe that more polyunsaturation leads to accelerated oxidation and free-radical production, inflammation and apoptosis.



Posted Image



Now what implications does this have for humans? Since humans cannot make polyunsaturated-fats, the amount we consume directly affects the composition of our cells. The American-diet has become more and more polyunsaturated since the early 1900’s [2] (mainly due to a huge increase in use of vegetables-oils and the use of corn and soybeans in animal-feedlots). Along with this novel dietary-change came the rampant increase of cancer and metabolic-syndrome. Since polyunsaturated-fats are unable to be synthesized by the human body… the total amount of polyunsaturation of our cell membranes depends entirely on the amount we consume.




Monounsaturated-fats (omega-9) seem to be the healthiest fat for the composition of the cells and supporting proper membrane fluidity. Saturated-fats are too stiff and tend to make the cell-membrane hard and inflexible; this impairs the flow of hormones (like insulin) into and out of the cells, while polyunsaturated-fats are too soft and pliable and tend to make the cell-membrane prone to oxidation.



Monounsaturated-fats are the perfect balance between the two extremes. Monounsaturated-fats are soft enough to allow insulin to enter the cell but hard enough to resist oxidation. This is why substituting monounsaturated-fats for saturated-fats improves insulin-sensitivity [3].



So how do we decrease the polyunsaturation of our cells and increase the amount of omega-9 concentration? The first step comes from removing overt sources of polyunsaturated-fats from the diet (like oils, nuts and animal-fats). This will decrease the overall polyunsaturation of our cell-membranes, leading to less lipid peroxidation within our body.



The next step is to synthesize more omega-9 fatty acids. Normally the body converts saturated-fats (which are harmful because an excessive accumulation of saturated-fatty acids leads to lipotoxicity and insulin-resistance) into the beneficial monounsaturated-fats thru an enzyme called delta-9-desaturase.



Delta-9-desaturase is activated by the hormone insulin [4]. So by eating insulinogenic-foods, you will accelerate the conversion of saturated-fats into monounsaturated-fats (which are beneficial). However delta-9-desaturase is deactivated in insulin-deficient or insulin-resistant states like diabetes [5].






[1] Age (Dordr). 2008 Sep;30(2-3):89-97. Explaining longevity of different animals: is membrane fatty acid composition the missing link? Hulbert AJ.

[2] Am J Clin Nutr. 1990 Sep;52(3):457-69. Trends in individual consumption of dietary fat in the United States, 1920-1984. Stephen AM, Wald NJ.

[3] Diabetologia. 2001 Mar;44(3):312-9. Substituting dietary saturated for monounsaturated fat impairs insulin sensitivity in healthy men and women: The KANWU Study. Vessby B, Uusitupa M, Hermansen K.

[4] Scand J Clin Lab Invest. 2011 Jul;71(4):330-9. Insulin induces fatty acid desaturase expression in human monocytes. Arbo I, Halle C, Malik D.

[5] Diabetes. 1979 May;28(5):479-85. Fatty acid desaturation in experimental diabetes mellitus. Eck MG, Wynn JO, Carter WJ.

Edited by misterE, 02 December 2013 - 01:32 AM.

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#2 theconomist

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Posted 02 December 2013 - 08:17 PM

The more you dig the more obvious the dietary choices become. From a macro point of view; not a single person has been able to point out a long lived people that based their diets on meats and fats. From a micro point of view; wether it's methionine restriction, casein promoting cancer or research showing pufa as something to avoid, the evidence keeps on pointing towards the superiority of a plant based diet.
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#3 JohnD60

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Posted 03 December 2013 - 12:54 AM

From a macro point of view; not a single person has been able to point out a long lived people that based their diets on meats and fats.

This is an interesting point. It would be nice if we had some good data on this, but of course we don't. It does seem that anecdotal reports of old vegans exist, and that similar reports of old carnivores do not exist, but I attribute this primarily to Vegan Bias, where the ideological vegans seek out such old vegans to brag about them, but that there is no such counter ideological group seeking out old carnivores to brag about them.

I am not quite sure what you mean by "based their diet on meats and fats". I would say that even ardent carnivores obtain less than 70% of their calories from meat (including fish and eggs) and fats. Surely not everyone that consumes some meat in their diet is classified as having a meat based diet.

Olive oil may be plant based, but it is still a fat. Do you just mean animal fats?

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#4 niner

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Posted 03 December 2013 - 01:13 AM

The more you dig the more obvious the dietary choices become. From a macro point of view; not a single person has been able to point out a long lived people that based their diets on meats and fats. From a micro point of view; wether it's methionine restriction, casein promoting cancer or research showing pufa as something to avoid, the evidence keeps on pointing towards the superiority of a plant based diet.

Well, it's pretty obvious that PUFAs are bad, but the vast majority of the PUFA excess in the modern bad diet comes from plants, not animals. Like John said above, I'm not sure what you mean by "based their diets on meats and fats"... I think that the majority of us eat more like Michael Pollan suggests: "Eat food, mostly plants, not too much." There's plenty of evidence that people who eat like that are long lived. (e.g. The Mediterranean Diet)

#5 misterE

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Posted 03 December 2013 - 02:10 AM





the vast majority of the PUFA excess in the modern bad diet comes from plants, not animals





Animals contain PUFA’s because they are fed corn and soybeans and the small amount of PUFA’s in the corn and soybean bioaccumulate in animal-flesh. The PUFA’s in the animal-flesh are also different from the PUFA’s in plants. Plants contain linoleic-acid which is less harmful compared to its metabolite; arachidonic-acid which is found in high concentrations in muscle-meat and egg-yolks.
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#6 Brett Black

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Posted 03 December 2013 - 02:38 AM

MisterE and niner, you both already duscussed this ove here:
http://www.longecity...ing-hypothesis/

Did you forget, misunderstand or disagree with the point(s) that Michael Rae made: total polyunsaturate fraction in membranes is not altered by dietary polyunsaturated fat intake, only sub-types of polyunsaturated fats can be altered, and of the sub-types, only DHA is correlated with lifespan.

In other words, lowering polyunsaturated fat in the diet won't lower polyunsaturated fat in membranes.

Edited by Brett Black, 03 December 2013 - 02:49 AM.

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#7 niner

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Posted 03 December 2013 - 02:42 AM

the vast majority of the PUFA excess in the modern bad diet comes from plants, not animals


Animals contain PUFA’s because they are fed corn and soybeans and the small amount of PUFA’s in the corn and soybean bioaccumulate in animal-flesh. The PUFA’s in the animal-flesh are also different from the PUFA’s in plants. Plants contain linoleic-acid which is less harmful compared to its metabolite; arachidonic-acid which is found in high concentrations in muscle-meat and egg-yolks.

I don't think so.

Beef fat is 2% linoleic, 2% "other", Butter is 2% linoleic, 6% "other" The rest is SAFA and MUFA.

Canola: 36% PUFA
Safflower: 75% PUFA
Olive: 8% PUFA

Source: web.pdx.edu/~wamserc/C336S06/fat.pdf

#8 misterE

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Posted 03 December 2013 - 03:04 AM

In other words, lowering polyunsaturated fat in the diet won't lower polyunsaturated fat in membranes.





That’s not true because feeding animals polyunsaturated-fats DOES alter their fatty-acid composition. That’s why grass-fed animals have less total PUFA in their flesh compared to feedlot animals.

I don't think so.

Beef fat is 2% linoleic, 2% "other", Butter is 2% linoleic, 6% "other" The rest is SAFA and MUFA.





What about pork, poultry and eggs? Beef and dairy are low in PUFA... but high in saturated-fats, which are just as harmful.

Edited by misterE, 03 December 2013 - 03:08 AM.

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#9 niner

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Posted 03 December 2013 - 03:38 AM

I don't think so.

Beef fat is 2% linoleic, 2% "other", Butter is 2% linoleic, 6% "other" The rest is SAFA and MUFA.


What about pork, poultry and eggs? Beef and dairy are low in PUFA... but high in saturated-fats, which are just as harmful.

They're all lower in PUFA than the seed oils. As for SAFA, I thought that the premise of this thread was that a high degree of unsaturation in membranes was bad from a longevity perspective. That should be a plus for SAFA, although I appreciate the significance of MUFA that you detailed above.
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#10 Brett Black

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Posted 03 December 2013 - 03:46 AM

MisterE and niner, you both already duscussed this ove here:
http://www.longecity...ing-hypothesis/

Did you forget, misunderstand or disagree with the point(s) that Michael Rae made: total polyunsaturate fraction in membranes is not altered by dietary polyunsaturated fat intake, only sub-types of polyunsaturated fats can be altered, and of the sub-types, only DHA is correlated with lifespan.

In other words, lowering polyunsaturated fat in the diet won't lower polyunsaturated fat in membranes.


I reread the thread I linked to above and it seems Michael said it was the total fraction of membrane "unsaturated" fatty acids in membranes NOT "polyunsaturated" fatty acids that is not amenable to alteration by modifying dietary fat intake.
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#11 misterE

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Posted 03 December 2013 - 05:17 AM

They're all lower in PUFA than the seed oils.



As for SAFA, I thought that the premise of this thread was that a high degree of unsaturation in membranes was bad from a longevity perspective. That should be a plus for SAFA







Yes, they are lower in total PUFA. But the type of PUFA in oils is not as harmful as the type of PUFA in meat and egg-yolks called archidonic-acid. Linoleic-acid converts into Archidonic-acid as needed in the body, however if you eat premade archidonic-acid that the animal made, you bypass the regulatory process of archidonic-acid synthesis and you overload the system when it is not necessary, which causes problems no? The same could be said with alpha-linolenic-acid and DHA.



Yes, the premise of the thread is that a high degree of unsaturation of membranes is harmful to longevity… but like most things in life there has to be a perfect balance. Too much saturation and the cell becomes way too hard, too much polyunsaturation and it becomes way too soft. Neither one of those situations is ideal because when cells are too hard; the hormones that interact with that cell have a difficult time sending their signal. On the other extreme, when cells are too soft, they are less stable (leaky) and more prone to damage. That is why I believe that monounsaturated-fat is the optimal fat for cell-membrane structure. Obviously countries that eat more monounsaturated-fats (like the Mediterranean countries) and have higher levels of monounsaturated-fat composed of in their membranes, have better insulin-sensitivity, than the nations who eat more saturated-fats ( like western-Europe and USA).
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#12 rwac

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Posted 03 December 2013 - 10:42 AM

Yes, the premise of the thread is that a high degree of unsaturation of membranes is harmful to longevity… but like most things in life there has to be a perfect balance. Too much saturation and the cell becomes way too hard, too much polyunsaturation and it becomes way too soft. Neither one of those situations is ideal because when cells are too hard; the hormones that interact with that cell have a difficult time sending their signal. On the other extreme, when cells are too soft, they are less stable (leaky) and more prone to damage. That is why I believe that monounsaturated-fat is the optimal fat for cell-membrane structure. Obviously countries that eat more monounsaturated-fats (like the Mediterranean countries) and have higher levels of monounsaturated-fat composed of in their membranes, have better insulin-sensitivity, than the nations who eat more saturated-fats ( like western-Europe and USA).


Eh, I only see speculation about saturated fat.

Even study #3 (Substituting dietary saturated... ) doesn't seem to specify details about exactly what the source of saturated fat in the diet was. Or at least I can't seem to find it.

The Saturated fat was mostly butter. Apparently Stephan Guyenet finds it unconvincing, and there's another study that finds that SFA has no effect on Insulin sensitivity.

http://wholehealthso...ensitivity.html

Effects of dietary fat modification on insulin sensitivity and on other risk factors of the metabolic syndrome--LIPGENE: a European randomized dietary intervention study. http://www.ncbi.nlm....pubmed/20938439
"In weight-stable subjects, reducing dietary SFA intake had no effect on SI..."
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#13 misterE

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Posted 03 December 2013 - 10:49 PM

The evidence condemning saturated-fat for causing insulin-resistance is quite strong and well established.
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#14 kismet

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Posted 05 December 2013 - 11:05 PM

Interestingly, there are no meta-analyses on the topic of SAFA and insulin resistance that I could find. The issue may be unresolved to this day.

And again, the best argument against saturated fat is that it is simply inferior to olive oil or nut-derived monounsaturates (or MUFA in general [1], but it's not an entirely convincing study), whether this is due to polyphenolic compounds or the fatty acids per se is irrelevant in this case, because you can only eat so much fat per day. And after the PREDIMED study most of it should be MUFA from olive oil and nuts.

[1]
Ann Nutr Metab. 2011 Oct;58(4):290-6. doi: 10.1159/000331214. Epub 2011 Sep 9.
Effects of monounsaturated fatty acids on glycaemic control in patients with abnormal glucose metabolism: a systematic review and meta-analysis.
Schwingshackl L, Strasser B, Hoffmann G.
NB: It's an analysis from our university, unfortunately not in the healthy. :)

Edited by kismet, 05 December 2013 - 11:06 PM.


#15 misterE

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Posted 10 February 2014 - 07:27 AM

Coming back to this topic; Saturated-fats cause insulin-resistance (in my opinion and according to my research) by overstuffing your fat-cell and causing them to enlarge and become insulin-resistant themselves, this is actually the very beginning stages of metabolic-syndrome. When the fat-cell (adipocyte) becomes resistant to the anti-lipolytic effect of insulin, it release a contanst stream of FFA’s into the circulation. This constant outpour of FFA’s then goes on to induce insulin-resistance within virtually every organ in the body, leading to increased metabolic dysfunction and apoptosis (wasting).

Saturated-fats are highly attracted to adipocytes, while polyunsaturated-fats aren’t. The degree of saturation and the chain length of each given saturation determines how easily mobilized these fats are as fuel. For instance saturated-fats are less likely to be used for fuel as either monounsaturates or polyunsaturates: the less saturation, the easier they come out of adipocytes and the higher degree of oxidation (for fuel).

Insulin stimulates a process in fatty-acids called desaturation; insulin promotes the desaturation of fatty-acids, for instance it converts saturated-fats into monounsaturated-fats, and it converts linoleic-acid into arachidonic-acid, etc. High intakes of saturated-fat are easily stored within the adipocytes, and only when insulin is secreted can it convert into monounsaturated-fats to be readily used as fuel. This process ensures that the adipocytes will not enlarge and become overstuffed. But if a person eats a high saturated-fat diet and simultaneously reduces their starch intake, they will increase their saturation, and decrease the rate at which that saturation can be desaturated. I also believe this happens on a high saturated-fat diet combined with sugar as the main carbohydrate source as with the rich American-diet.

Strangely enough, since saturated-fats are so easily stored within the adipocytes however, I believe this would actually benefit blood-sugar metabolism, considering fatty-acids and glucose compete for the same oxidation pathways. Polyunsaturated-fats, since they are less likely to be stored-within the adipocyte, are less likely to cause them to enlarge and become insulin-resistant, however since they are so easily oxidized, their oxidation interferes with the oxidation of glucose. Polyunsaturated-fats also inhibit the delta-9-desaturase enzyme, which means that high intakes of polyunsaturated-fats also decrease the rate in which ingested saturated-fats can be converted into harmless monounsaturated-fats. The reason for this is because insulin preferably desaturates polyunsaturated-fats over saturated-fats. Evolutionarily, this made sense because why would the body go thru the trouble of desaturating saturated-fats into monounsaturates to begin their mobilization and oxidation, when there is a nice supply of polyunsaturated-fats readily available to be desaturated and easily oxidized.


So saturated-fats cause adipocyte insulin-resistance by causing them to enlarge and altering their adipocytokine expression, while polyunsaturated-fats suspend glucose-oxidation and alter the rate in which saturated-fats are desaturated. I also believe the reason why saturated-fat is so closely linked to diabetes and insulin-resistance is due to the fact that diabetics have an inability to desaturate saturated-fats, because in insulin-resistant states, all functions stimulated by insulin (like delta-9-desaturase) are disabled.

Edited by misterE, 10 February 2014 - 07:37 AM.

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#16 Kevnzworld

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Posted 06 March 2014 - 12:46 AM

Here is a recent article on the subject
" It is possible that the extent of fatty acid unsaturation of the mitochondrial membrane determines susceptibility to lipid oxidative damage and downstream protein and genome toxicity, thereby acting as a determinant of aging and lifespan. Reviewing the vast number of comparative studies on mitochondrial membrane composition, metabolism and lifespan reveals some evidence that lipid unsaturation ratios may correlate with lifespan. "
http://www.longevity...46-2395-3-3.pdf
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#17 InquilineKea

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Posted 01 April 2014 - 07:36 PM

I'm actually curious: could this be a reason why eating too many omega-3s could possibly decrease lifespan? (despite its benefits to healthspan)?

Since most fish are cold-blooded, they probably don't face the same risk of lipid peroxidation that warm-blooded animals do.

==

Anyways my preliminary conclusion is that MUFAs are ideal.
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#18 addx

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Posted 01 April 2014 - 08:32 PM

What about medium length saturated like coconut oil, that seems most beneficial. Infact a ketogenic diet with lots of coconut oil is used to cure epilepsy(by increasing mitochondrial function which stabilises the neurones, I think it works in about 50% of epilepsy cases.

#19 misterE

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Posted 02 April 2014 - 12:03 AM

I'm actually curious: could this be a reason why eating too many omega-3s could possibly decrease lifespan? (despite its benefits to healthspan)?

Since most fish are cold-blooded, they probably don't face the same risk of lipid peroxidation that warm-blooded animals do.







I believe this is exactly the case. Animals and plants in colder regions and especially the arctic-regions have high levels of polyunsaturation to protect against cold. Polyunsaturates are Mother-Nature’s anti-freeze for both seeds and animals living in cold regions. Saturated-fats are resistant to heat and light, and where are saturated-fats mostly found? The tropical-regions… go figure! Even the fish that live in tropical regions are more saturated than fish living near the poles.

#20 misterE

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Posted 02 April 2014 - 12:08 AM

What about medium length saturated like coconut oil, that seems most beneficial.





Personally I believe that the type of fat you synthesize yourself from simple-sugar is probably the most beneficial metabolically. The essential-fatty-acids should be taken in trace amounts.

#21 MachineGhostX

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Posted 19 August 2014 - 09:19 PM

Yes, the premise of the thread is that a high degree of unsaturation of membranes is harmful to longevity… but like most things in life there has to be a perfect balance. Too much saturation and the cell becomes way too hard, too much polyunsaturation and it becomes way too soft. Neither one of those situations is ideal because when cells are too hard; the hormones that interact with that cell have a difficult time sending their signal. On the other extreme, when cells are too soft, they are less stable (leaky) and more prone to damage. That is why I believe that monounsaturated-fat is the optimal fat for cell-membrane structure. Obviously countries that eat more monounsaturated-fats (like the Mediterranean countries) and have higher levels of monounsaturated-fat composed of in their membranes, have better insulin-sensitivity, than the nations who eat more saturated-fats ( like western-Europe and USA).

 

Except that the composition of body fat in nature is not dominant mono-unsaturated.  It's primarily saturated, secondarily mono-unsaturated and minorly polyunsaturated.  That should be the optimal intake.



#22 MachineGhostX

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Posted 19 August 2014 - 09:21 PM

The evidence condemning saturated-fat for causing insulin-resistance is quite strong and well established.

 

If that is so, how was Atkins able to reverse diabetes in his patients?  He was the original low-carb "Bacon 'n Butter" whackjob.


Edited by MachineGhostX, 19 August 2014 - 09:45 PM.

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#23 MachineGhostX

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Posted 19 August 2014 - 09:32 PM

Coming back to this topic; Saturated-fats cause insulin-resistance (in my opinion and according to my research) by overstuffing your

 

I thought your hypothesis sounded familiar:
 

Increase in cell membrane permeability

The third effect that insulin has on cancer cells is to activate enzyme activity in the cell membrane making them more permeable.

Cell membranes are largely made up of triglycerides, which are built of fatty acids. The more saturated that a fatty acid is, the higher the melting point (example: butter [a saturated fat with a higher melting point] is solid at room temperature, whereas olive oil [an unsaturated fat with a lower melting point] is a liquid). The enzyme that insulin activates is called delta-9 desaturase and the action of this enzyme is to de-saturate - to make a saturated fat into an unsaturated fat. Delta-9 desaturase - once it has been activated by insulin - de-saturates the fatty acids that make up the cell membrane of cancer cells. This fatty acid – saturated stearic acid– has a melting point of 65 °C. Stearic acid once it has been de-saturated, becomes mono-unsaturated oleic acid, which has a melting point of 5 °C. At physiologic temperatures (the temperature of the body, about 37.5 °C) tristearin – triglyceride with three stearic acids attached that composes the cancer cell membrane - is going to be more "waxy" than "oily" because of its higher melting point. This makes for a less permeable cell membrane. On the other hand, once the insulin has activated the enzyme delta-9 desaturase, the cell membrane of cancer cells is composed of triolein – the triglyceride with three oleic acids attached – with a melting point of 5 °C. This cell membrane will be more permeable at physiologic temperatures. The chemotherapy drugs are thus able to enter the cancer cells more easily because of the increased cell membrane permeability, providing the required intracellular dose intensity to kill the cancer.

Insulin is used in IPT to enhance anticancer drug cytoxicity and safety, via 1) an effect of biological differentiation based on insulin receptor concentration, 2) an effect of metabolic modification to increase the S-phase fraction in cancer cells, enhancing their susceptibility to cell-cycle phase-specific agents, and 3) a membrane permeability effect to increase the intracellular dose intensity of the drugs. Significantly less drug can thus be targeted more specifically and more effectively to cancer cells, all this occurring with a virtual elimination of the dose-related side effects.[24][25]

 

http://www.thefullwi...tiation_therapy


Edited by MachineGhostX, 19 August 2014 - 09:48 PM.


#24 MachineGhostX

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Posted 19 August 2014 - 09:39 PM

I believe this is exactly the case. Animals and plants in colder regions and especially the arctic-regions have high levels of polyunsaturation to protect against cold. Polyunsaturates are Mother-Nature’s anti-freeze for both seeds and animals living in cold regions. Saturated-fats are resistant to heat and light, and where are saturated-fats mostly found? The tropical-regions… go figure! Even the fish that live in tropical regions are more saturated than fish living near the poles.

 

 

But on the other hand, Eskimos living in the far north eating massive amounts of polyunsaturated fats from seafood die of hemorrhaging bleeding/strokes at alarming rates (those on the traditional diet anyway).  So I don't think anything but land animals have the proper ratios of fats for a human being to ingest.



#25 MachineGhostX

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Posted 19 August 2014 - 09:43 PM


Personally I believe that the type of fat you synthesize yourself from simple-sugar is probably the most beneficial metabolically. The essential-fatty-acids should be taken in trace amounts.

 

 

Homeostasis: Omega-6 4% max of calories, Omega-3 1.50% max of calories.  And that means AA and DHA which are the true EFA's.  So you can't help but fill the rest with saturated and mono-unsaturated.  However, far too many conflate excess AA with saturated fat since they tend to occur in the same foods.



#26 treonsverdery

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Posted 20 August 2014 - 06:46 PM

There is a study noting that Royal Jelly increases mammal longevity about a quarter http://www.ncbi.nlm....pubmed/12954483. It is possible this is linked to the protein royalactin, which I think I remember causes drosophila to live about a third longer; view Nature image at http://www.nature.co...ature10093.html

 

Using a mRNA profiling chip researchers could find out which particular royal jelly physioprocess responses cause the longevity improvement.  Enzymes or cytokines that effect different lipid structuralizations could be a part of that. There is a mRNA royal jelly study about improved neurofunction  published http://www.ncbi.nlm....pubmed/15849420

 

Mammals as well as bugs living more than a quarter longer from a protein is beneficial.  I think genetically engineering yeast to make large amounts or Royalactin or other longevity cytokines would make this material available at human longevity dosages

 

Also, you may like this video.  It does not say how much cocoa butter to replace with DHA though, although apparently numerous grams or more of DHA are beneficial

 

 

 



#27 misterE

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Posted 22 August 2014 - 05:26 AM

 

 


 

If that is so, how was Atkins able to reverse diabetes in his patients?  He was the original low-carb "Bacon 'n Butter" whackjob.

 

 

Fatkins is dead. When he was autopsied it was proven he had heart-disease, while his long time adversary Nathan Pritikin did not. Wackjob is an appropriate title for him.


Edited by misterE, 22 August 2014 - 05:27 AM.

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#28 misterE

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Posted 22 August 2014 - 05:32 AM

 So I don't think anything but land animals have the proper ratios of fats for a human being to ingest.

 

 

But not all land mammals are the same. Ruminant animals have very low levels of polyunsaturated-fat, while non-ruminant have higher levels.



#29 misterE

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Posted 22 August 2014 - 05:35 AM

 

 However, far too many conflate excess AA with saturated fat since they tend to occur in the same foods.


 

 

 

 

 

I agree here. The reason why animal-fat is so unhealthy isn't because of the saturated-fat per say, but rather from the AA. A good example of this is with eggs. Eggs are considered a high saturated-fat food, but it is also one of the richest sources of AA. However a high saturated-fat diet is extremely fattening and leads to diabetes.


Edited by misterE, 22 August 2014 - 05:39 AM.


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#30 MachineGhostX

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Posted 23 August 2014 - 02:48 AM

 

Fatkins is dead. When he was autopsied it was proven he had heart-disease, while his long time adversary Nathan Pritikin did not. Wackjob is an appropriate title for him.

 

You need to dig deeper.  Atkins had infectious cardiomyopathy and gained over 50 lbs on his 6' frame after admittance while in the coma (not uncommon with the drugs used).  Neither was caused by his dietary habits, nor was his death.  The most that can be said is that an extreme zero or low-carb diet doesn't protect against infectious cardiomyopathy and it doing the ultimate deed of a heart attack (or even that maybe you don't get enough calcium and K2 to protect your head from cracking!).  This is theoretically possible since mucus is needed for membrane protection/integrity and extreme low-carb diets inhbit mucus generation for the intestines and the mucus membranes at the very minimum.


Edited by MachineGhostX, 23 August 2014 - 02:54 AM.

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Also tagged with one or more of these keywords: membrane fluidity, polyunsaturated fat, saturated fat, free radicals, oxidative stress, lipid peroxidation, delta 9 desaturase, insulin, diabetes, monounsaturated fat

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