Why PUFA is bad: how high membrane polyunsaturation decreases longevity

Hans

Member
Forum Supporter
Joined
Aug 24, 2017
Messages
5,856
Hi that was a very well formulated article. Everbody go read it.
Thanks man, appreciate it.

@Hans do you know anything about the studies claiming that a group beeing fed O6 only compared to the same amount of O6 + O3 having more inflamation. That seems to point to some contrary function to O6. Which also could be immunosuppression if O6 is less immunosuppressive the O3 (this is a seperate question to the analysiz of the percentage og O3s antiinflammatory effects being immunosuppressive )?
Omega 3 does lower inflammation if added on top of a high O6 diet, but that doesn't mean it's anti-inflammatory as the study mentioned. That's why a lot of studies find benefits with omega 3s. Also, people like to talk about resolvins, but sick people have dysregulated synthesis of resolvins. Peat also talked about resolvins in a recent podcast with Danny I think, but now I can't find it, or at least he didn't link it in the timestamps.
O3 is more immunosuppressive than O6, and that's why they give it to organ transplant patients and various other conditions as well. Haidut posted about it here: PUFA are potent immunosuppresive agents – To Extract Knowledge from Matter
The suppressive effect correlates with chain length and unsaturation.
 
OP
Mauritio

Mauritio

Member
Joined
Feb 26, 2018
Messages
5,669
Thanks!! That was a lot of info. Went through Tew's posts (unfortunatly he's article about birds was no longer up) . I think it also explains why some bodybuilders take Omega 6 and report better muscle gains. It's no surprise that things that produce increased growth is often not conducive to health - especially in adults. I think that's in line with Peat's ideas about HGH being a misnomer as it is not primerlty a growth hormone though it fills that role as well. And it also seems to fit with my idea that it is the within-speicies level that is most relevant (practically) as there are limits to how much we can (or should) manipulate fatty acid composition. It would seem that the enodogenous regulation of different spiecies (obviosly) fatty acid composition is indeed adjusted to the enviromental factors to which that species is confronted.
SInce humans seem quite susceptible to pufa exposure and its damaging side effects, it would seem to me to be only three logical explenations for that.

1: that we have developed in a very PUFA-low enviroment (I know Peat has suggested that we would have developed in warm climate on lots of fruit and low pufa - not sure about that thoug and would be interesting to compare human pufa-handling to that of other primates who has more of a diet like that to check it) ,

2: That we have developed in a very cold climate where it would be needed for mobility (peat has also hinted at this function as it is the explanation to why arctic and antarctic species have lots of PUFA to handle the cold), but I found that a bit weird.

3: That we have somehow lost our anti-oxidant capacity and that we once where more able to handle the pufa - That can be partly through as I belive that for various reasons modern humans are compromized physiologically but since the phenomenon of PUFA damage aslo occurs in other mammalians on land that has to a lesser degree had its habitat and habis disturbed (at least I think that's the case even though mainly Peats references to it is in supranatural amounts among caged/domesticated animals - but I think it is applicable)

I cant help but think all these three are a bit suspicious. If you look at archelogy and anthropology it is even if it is debated how much it has contributed quite obvious that high animals food diets have been predominant for at least 2 million years and the whole of the timeline of the species homo. DIsregarding the exact form of the trhee of the genus homo it is clear that homo-varieties have existed in northern eurasia for millions of years - meaning the fruit idea is sort of bunk. Even with honey taken into account. And most likely insects have been important and they are generally high pufa - especiall maggots and beatles which probably was the bulk of it.

I must also comment that Tew's opinion about not needing to think of pufa when low-fat is at least individual. I do eat fairly low fat but still adding just a teaspoon of oliveoil a day has delitrious effects - first noticalbe on my mucus membranes.

No idea where this goes except I think the inital answer from Peat about temp and glucose still gives sense to it a bit.

Thanks!! That was a lot of info. Went through Tew's posts (unfortunatly he's article about birds was no longer up) . I think it also explains why some bodybuilders take Omega 6 and report better muscle gains. It's no surprise that things that produce increased growth is often not conducive to health - especially in adults. I think that's in line with Peat's ideas about HGH being a misnomer as it is not primerlty a growth hormone though it fills that role as well. And it also seems to fit with my idea that it is the within-speicies level that is most relevant (practically) as there are limits to how much we can (or should) manipulate fatty acid composition. It would seem that the enodogenous regulation of different spiecies (obviosly) fatty acid composition is indeed adjusted to the enviromental factors to which that species is confronted.
SInce humans seem quite susceptible to pufa exposure and its damaging side effects, it would seem to me to be only three logical explenations for that.

1: that we have developed in a very PUFA-low enviroment (I know Peat has suggested that we would have developed in warm climate on lots of fruit and low pufa - not sure about that thoug and would be interesting to compare human pufa-handling to that of other primates who has more of a diet like that to check it) ,

2: That we have developed in a very cold climate where it would be needed for mobility (peat has also hinted at this function as it is the explanation to why arctic and antarctic species have lots of PUFA to handle the cold), but I found that a bit weird.

3: That we have somehow lost our anti-oxidant capacity and that we once where more able to handle the pufa - That can be partly through as I belive that for various reasons modern humans are compromized physiologically but since the phenomenon of PUFA damage aslo occurs in other mammalians on land that has to a lesser degree had its habitat and habis disturbed (at least I think that's the case even though mainly Peats references to it is in supranatural amounts among caged/domesticated animals - but I think it is applicable)

I cant help but think all these three are a bit suspicious. If you look at archelogy and anthropology it is even if it is debated how much it has contributed quite obvious that high animals food diets have been predominant for at least 2 million years and the whole of the timeline of the species homo. DIsregarding the exact form of the trhee of the genus homo it is clear that homo-varieties have existed in northern eurasia for millions of years - meaning the fruit idea is sort of bunk. Even with honey taken into account. And most likely insects have been important and they are generally high pufa - especiall maggots and beatles which probably was the bulk of it.

I must also comment that Tew's opinion about not needing to think of pufa when low-fat is at least individual. I do eat fairly low fat but still adding just a teaspoon of oliveoil a day has delitrious effects - first noticalbe on my mucus membranes.

No idea where this goes except I think the inital answer from Peat about temp and glucose still gives sense to it a bit.
You're welcome. I also think the most value can be found if you look at intraspecifc studies ,as the interspecifc differences are just too big
(Tyw mentioned some birds storing their PUFA in the wings for faster movement)
I think the review from the OP also cited some of those studies.

I tried to find tyw's article on the internet archive ,but it doesn't show up . Such a shame , would have really liked to read it .

I haven't gone through all of his posts on pufa, but he and the paper I posted both seem to imply that PUFA actually speeds up metabolism ...("Rats put what would be excessive amounts of PUFAs on their mitochondria in order to obtain faster metabolisms")
I'd really like to know through which mechanism pufa does that , because I cant see any scenario where that actually happens .
Only if it increases it in a kind of "wastefull" metabolism as seen in some cancer patients, who are literally wasting away .
 
Last edited:

Hans

Member
Forum Supporter
Joined
Aug 24, 2017
Messages
5,856
You're welcome. I also think the most value can be found if you look at intraspecifc studies ,as the interspecifc differences are just too big
(Tyw mentioned some birds storing their PUFA in the wings for faster movement)
I think the review from the OP also cited some of those studies.

I tried to find tyw's article on the internet archive ,but it doesn't show up . Such a shame , would have really liked to read it .

I haven't gone through all of his posts on pufa, but he and the paper I posted both seem to imply that PUFA actually speeds up metabolism ...("Rats put what would be excessive amounts of PUFAs on their mitochondria in order to obtain faster metabolisms")
I'd really like to know through which mechanism pufa does that , because I cant see any scenario where that actually happens .
Only if it increases it in a kind of "wastefull" metabolism as seen in some cancer patients, who are literally wasting away .
Peat mentioned that PUFAs can cause excess uncoupling. It activated the UCPs and also proton leak due to leaky membrane. Also too much inflammation is known to cause muscle catabolism, that's why aspirin is anabolic for older individuals.
 
OP
Mauritio

Mauritio

Member
Joined
Feb 26, 2018
Messages
5,669
Peat mentioned that PUFAs can cause excess uncoupling. It activated the UCPs and also proton leak due to leaky membrane. Also too much inflammation is known to cause muscle catabolism, that's why aspirin is anabolic for older individuals.
Okay thx . So I guess excessive uncoupling would be some kind of wasteful metabolism then.
 
OP
Mauritio

Mauritio

Member
Joined
Feb 26, 2018
Messages
5,669
Low body temperature increases membrane unsaturation:

"A reduction in temperature results in decreased membrane fluidity and as a consequence unsaturated fatty acid production through the fatty acid desaturation pathway is increased, thus maintaining the biological membrane in a fluid state."

 

Hans

Member
Forum Supporter
Joined
Aug 24, 2017
Messages
5,856
Low body temperature increases membrane unsaturation:

"A reduction in temperature results in decreased membrane fluidity and as a consequence unsaturated fatty acid production through the fatty acid desaturation pathway is increased, thus maintaining the biological membrane in a fluid state."

On a similar note, during hypothyroidism, unsaturated fats (O3 and O6) accumulate in the brain and there is also an increase in ROS production, oxidative stress and lipid peroxidation. There is also a positive correlation between hypothyroidism and oxidized LDL. Being hypo is pretty bad, I don't understand why some people think a slow metabolism and being hypothyroid is better for longevity.
 
OP
Mauritio

Mauritio

Member
Joined
Feb 26, 2018
Messages
5,669
On a similar note, during hypothyroidism, unsaturated fats (O3 and O6) accumulate in the brain and there is also an increase in ROS production, oxidative stress and lipid peroxidation. There is also a positive correlation between hypothyroidism and oxidized LDL. Being hypo is pretty bad, I don't understand why some people think a slow metabolism and being hypothyroid is better for longevity.
Yes , what I'm wondering is if the body tries to keep the membrane in a more fluid state via increasing UFAs when we increase temperature ,wouldn't it do the same when we increase SFAs in the diet (is this where mead acid comes into play?)
And if that's true ,doesnt that reflect a physical need of the membrane to be somewhat fluid /unsaturated, as the body is always trying to keep homeostasis?


The problem is there is some evidence for rate of living theory or caloric restriction, which makes it less black and white and harder to understand for the normal people . It would be easier to explain if caloric restriction studies showed disastrous results ,but they do show some benefits .
The question is: is that a way one wants to live their life :cold, slow, and bored? Plus there's plenty of more convincing evidence for increasing metabolism .
 

PolishSun

Member
Joined
May 25, 2020
Messages
447
If someone is hypothyroid, he does not have enough energy, and losing the energy means losing the structure.
 

Hans

Member
Forum Supporter
Joined
Aug 24, 2017
Messages
5,856
Yes , what I'm wondering is if the body tries to keep the membrane in a more fluid state via increasing UFAs when we increase temperature ,wouldn't it do the same when we increase SFAs in the diet (is this where mead acid comes into play?)
Unsaturated accumulate during hypothyroid and when temps drop. The inverse is true when thyroid and temps increase. I do think that the increase in unsaturation is a compensation, but it predisposes to a lot of issues.
And if that's true ,doesnt that reflect a physical need of the membrane to be somewhat fluid /unsaturated, as the body is always trying to keep homeostasis?
Yes, we do need a certain amount of unsaturation, that's why the body creates Mead acid. But it's much more stable than O6 and especially O3.
The problem is there is some evidence for rate of living theory or caloric restriction, which makes it less black and white and harder to understand for the normal people . It would be easier to explain if caloric restriction studies showed disastrous results ,but they do show some benefits .
The question is: is that a way one wants to live their life :cold, slow, and bored? Plus there's plenty of more convincing evidence for increasing metabolism .
Well, calorie restriction's benefits are due to less methionine, cysteine, tryptophan, iron, endotoxin, PUFA, etc. So it's a general reduction in the consumption of toxins that reduces longevity.
 

S-VV

Member
Joined
Jul 23, 2018
Messages
599
This is basically my understanding as well. The "accepted" hypothesis posits channels and individual pumps for each electrolyte, etc. Ling proved the alleged pumps would require far more energy than ATP could provide, even accepting that the phosphate bond provides the energy and is as high an energy bond as supposed. The far simpler and more elegant alternative is that water, electrically structured by proteins, i.e., the gel-like "protoplasm", provides the cellular electrolyte gradient and all other functions distinguishing the living cell from its environment, and that the "membrane" is an artifact of the observaton process.

Removing the membrane hypothesis from this argument, it should still be possible to demostrate the deleterious effect of PUFAs under the Association Induction thoery. Maybe someone better informed than myself would like to take a stab at it?
Well, the lipids are there. The question is where. That organelles and the cells are surrounded by a lipid bilayer is a fact. That they are responsible for maintaining electrochemical gradients, probably not.

Same thing with membrane proteins. They have been cloned, mutated and inserted into giant frog eggs for study. They exist. They have hydrophobic and hydrophilic regions exactly where it makes sense for them to be in order to be inserted. The peripheral membrane proteins are prenylated in order to be attached. No prenyl chain, no localisation to the cells periphery.

The membrane channels kinda look like channels and are indeed selective for certain ions, the pumps do have ATPase activity and so on. However, they do not maintain the ionic steady state. Instead the probably give the “spark” that triggers the cytoplasmic reorganisation, based on the selective ion adsorption Ling-Gyorgy secret mechanism.

Sometimes Ray goes too far in his holism and generality, and we end up with membraneless cells, and phantom proteins. I think he does it on purpose in order to get the reader interested in the subject.
 
OP
Mauritio

Mauritio

Member
Joined
Feb 26, 2018
Messages
5,669
Well, calorie restriction's benefits are due to less methionine, cysteine, tryptophan, iron, endotoxin, PUFA, etc. So it's a general reduction in the consumption of toxins that reduces longevity.
Yes I know. I was replying to your question why people think a slow metabolism is good .
There is evidence for it, it's not convincing to me but its apparently enough to convince others.
 

Doc Sandoz

Member
Joined
Jun 21, 2020
Messages
821
Well, the lipids are there. The question is where. That organelles and the cells are surrounded by a lipid bilayer is a fact. That they are responsible for maintaining electrochemical gradients, probably not.

Same thing with membrane proteins. They have been cloned, mutated and inserted into giant frog eggs for study. They exist. They have hydrophobic and hydrophilic regions exactly where it makes sense for them to be in order to be inserted. The peripheral membrane proteins are prenylated in order to be attached. No prenyl chain, no localisation to the cells periphery.

The membrane channels kinda look like channels and are indeed selective for certain ions, the pumps do have ATPase activity and so on. However, they do not maintain the ionic steady state. Instead the probably give the “spark” that triggers the cytoplasmic reorganisation, based on the selective ion adsorption Ling-Gyorgy secret mechanism.

Sometimes Ray goes too far in his holism and generality, and we end up with membraneless cells, and phantom proteins. I think he does it on purpose in order to get the reader interested in the subject.
So, let me see if I've got you right. Certain lipids and proteins aggregate at the edge of the cell where they form a sort of boundary, but not a membrane in the sense typically meant: a lipid bilayer balloon or bag that separates structureless water on the outside of the cell from structureless water on the inside, and which alone maintains the integrity of the cell. Thus, this boundary is not an artifact as claimed by some, but is real, just not a "membrane" in the sense normally attributed.
 

Eberhardt

Member
Joined
Apr 28, 2019
Messages
607
Not sure if this clearifies but about the membrane being "proven" I am not so sure about that. I know they have been photographted but I don't remember if it was Peat or @haidut or both who listed the ridiculuous amount of manipulation it took to produce it. I don't remember it at all but it was like. wash the whole thing in chloroform, freezedry it, boil it in oil, dehydrate it again, chlorinate it and encase it ian polymer solution freeze it againg and lo and behold look theres the membrane. Something along those lines... not saying that the description above is necessarily wrong just that the "proofs" are so heavily massaged its not suppricing you end up with a happy ending... :P

on the question of hydrophilic and hydrophobic proteins, I am not trusting it completly, Not necessarily that they have not been able to integrate the proteins in the whatever kind of membrane that DO exist, but the possibility that the hydrophobic/philic thing is a result of the bioelectrical charge instead is definatly there. If you look at some of Gerrard Pollacks work on the 4th state of water it's pretty heavily integrated - f.ex structured water with exclusion zones gather around hydrophobic surfaces so maybe it is more actually a proof of Lings view of the cell?? I also saw something from Pollacks earlier work on muscles suggesting that the shortening of a muscle might not be due to the common myofibrin chains moving but simply proteins folding and unfolding due to electrical charge (that is by the cells structured water). So maybe its just an inside out view of seeing that indeed the lipid and proteins on the outer side of the cell indeed are held together by the charge in the cell creating structured water thus affecting the proteins. It would also fit with the theroies on how the blood moves in the circulator system where blood viscosity as well as movement seems to be partly regulated by the structured water in the blood reacting with the sulphur / arthery walls. (sorry for the very crude description for sake of brevity)
 

S-VV

Member
Joined
Jul 23, 2018
Messages
599
So, let me see if I've got you right. Certain lipids and proteins aggregate at the edge of the cell where they form a sort of boundary, but not a membrane in the sense typically meant: a lipid bilayer balloon or bag that separates structureless water on the outside of the cell from structureless water on the inside, and which alone maintains the integrity of the cell. Thus, this boundary is not an artifact as claimed by some, but is real, just not a "membrane" in the sense normally attributed.
Yes! There is no need for the membrane to perform the heroic tasks of maintaining homeostasis all of itself. Its simply is a specialised organelle in the cell withe certain functions and distinct morphology, governed by basic physical principles, like the rest of the cell. The channels, receptors and pumps certainly exist, but they probably do not work like "mainstream" cell biology describes.

For example, the receptor proteins are exquisitely sensitive to their cognate ligands, but so are many other proteins not traditionally labelled as receptors. And so the traditional receptors are part of a larger system of integrated cellular response. In the end it all forms a coherent structure. I believe that the traditionally described second messenger systems cAMP, protein kinases etc... work in tandem with the basic principle of water structuring/de-structuring and selective adsorption, not in opposition, exclusion or contradiction. That is, mainstream cell biology is wrong not in that it describes things that don't exists, rather they misattribute or underestimate their functions.
 

S-VV

Member
Joined
Jul 23, 2018
Messages
599
Not sure if this clearifies but about the membrane being "proven" I am not so sure about that. I know they have been photographted but I don't remember if it was Peat or @haidut or both who listed the ridiculuous amount of manipulation it took to produce it. I don't remember it at all but it was like. wash the whole thing in chloroform, freezedry it, boil it in oil, dehydrate it again, chlorinate it and encase it ian polymer solution freeze it againg and lo and behold look theres the membrane. Something along those lines... not saying that the description above is necessarily wrong just that the "proofs" are so heavily massaged its not suppricing you end up with a happy ending... :P

on the question of hydrophilic and hydrophobic proteins, I am not trusting it completly, Not necessarily that they have not been able to integrate the proteins in the whatever kind of membrane that DO exist, but the possibility that the hydrophobic/philic thing is a result of the bioelectrical charge instead is definatly there. If you look at some of Gerrard Pollacks work on the 4th state of water it's pretty heavily integrated - f.ex structured water with exclusion zones gather around hydrophobic surfaces so maybe it is more actually a proof of Lings view of the cell?? I also saw something from Pollacks earlier work on muscles suggesting that the shortening of a muscle might not be due to the common myofibrin chains moving but simply proteins folding and unfolding due to electrical charge (that is by the cells structured water). So maybe its just an inside out view of seeing that indeed the lipid and proteins on the outer side of the cell indeed are held together by the charge in the cell creating structured water thus affecting the proteins. It would also fit with the theroies on how the blood moves in the circulator system where blood viscosity as well as movement seems to be partly regulated by the structured water in the blood reacting with the sulphur / arthery walls. (sorry for the very crude description for sake of brevity)
The levels of manipulation are necessary to prepare a histological sample for microscopic observation. Its is very difficult to get tiny slices of cells if they are not pre-treated with a lot of different aggressive chemicals first. Once the slices are obtained, further treatment is necessary in order to reveal the elements of the cell: dyes, counter-dyes etc..This is not malice, but necessity.( Newer methods are being developed that use less chemicals, so hopefully well get a definitive picture soon enough) If electron microscopy wants to be used, then it gets even harder and very electronegative agents like Osmium need to be introduced in order to see anything.

There are some nice experiments that powerfully hint to the membrane existing, or at leats something with similar 2D-diffusion behaviour:

 

Eberhardt

Member
Joined
Apr 28, 2019
Messages
607
The levels of manipulation are necessary to prepare a histological sample for microscopic observation. Its is very difficult to get tiny slices of cells if they are not pre-treated with a lot of different aggressive chemicals first. Once the slices are obtained, further treatment is necessary in order to reveal the elements of the cell: dyes, counter-dyes etc..This is not malice, but necessity.( Newer methods are being developed that use less chemicals, so hopefully well get a definitive picture soon enough) If electron microscopy wants to be used, then it gets even harder and very electronegative agents like Osmium need to be introduced in order to see anything.

There are some nice experiments that powerfully hint to the membrane existing, or at leats something with similar 2D-diffusion behaviour:

I am agreeing there is no malice, and I maybe you are right or maybe even this is a difference of only of degree. I dont habe a sufficient understading of biochemics to fullybevaluate this so I cant really comment the details. I just dont find any very conclusive procedures, and certenately nothing that implies that the indeed well intended procedures doesnt produce what they're looking for. It's a bit like the search for dark matter. It looks well researched and impressive but not really any proofs. (Of course there is a difference as there are at least some material sightings when it comes to the membranes, while dark matter is purely speculative).

I do agree there is something around the cell and it doesnt really matter if there are pumps as long as the way in wich they operate are in agreement with bioenergitics but I still think its very thin evidence.

Maybe someone should get an update from Ray on his views on the matter as he is more able (I presume) to interpret the science.
 
OP
Mauritio

Mauritio

Member
Joined
Feb 26, 2018
Messages
5,669
Naked mole rat has only 2-6% DHA containing membranes leading to lower lipid peroxidation :

Mitchell TW, Buffenstein R, Hulbert AJ.
Phospholipids containing highly polyunsaturated fatty acids are particularly prone to peroxidation and membrane composition may therefore influence longevity. Phospholipid molecules, in particular those containing docosahexaenoic acid (DHA), from the skeletal muscle, heart, liver and liver mitochondria were identified and quantified using mass-spectrometry shotgun lipidomics in two similar-sized rodents that show an approximately 9-fold difference in maximum lifespan. The naked mole rat is the longest-living rodent known with a maximum lifespan of >28 years. Total phospholipid distribution is similar in tissues of both species; DHA is only found in phosphatidylcholines (PC), phosphatidylethanolamines (PE) and phosphatidylserines (PS), and DHA is relatively more concentrated in PE than PC. Naked mole-rats have fewer molecular species of both PC and PE than do mice. DHA-containing phospholipids represent 27-57% of all phospholipids in mice but only 2-6% in naked mole-rats. Furthermore, while mice have small amounts of di-polyunsaturated PC and PE, these are lacking in naked mole-rats. Vinyl ether-linked phospholipids (plasmalogens) are higher in naked mole-rat tissues than in mice. The lower level of DHA-containing phospholipids suggests a lower susceptibility to peroxidative damage in membranes of naked mole-rats compared to mice. Whereas the high level of plasmalogens might enhance membrane antioxidant protection in naked mole-rats compared to mice. Both characteristics possibly contribute to the exceptional longevity of naked mole-rats and may indicate a special role for peroxisomes in this extended longevity.

 
OP
Mauritio

Mauritio

Member
Joined
Feb 26, 2018
Messages
5,669
Naked mole rat has only 2-6% DHA containing membranes leading to lower lipid peroxidation :

Mitchell TW, Buffenstein R, Hulbert AJ.
Phospholipids containing highly polyunsaturated fatty acids are particularly prone to peroxidation and membrane composition may therefore influence longevity. Phospholipid molecules, in particular those containing docosahexaenoic acid (DHA), from the skeletal muscle, heart, liver and liver mitochondria were identified and quantified using mass-spectrometry shotgun lipidomics in two similar-sized rodents that show an approximately 9-fold difference in maximum lifespan. The naked mole rat is the longest-living rodent known with a maximum lifespan of >28 years. Total phospholipid distribution is similar in tissues of both species; DHA is only found in phosphatidylcholines (PC), phosphatidylethanolamines (PE) and phosphatidylserines (PS), and DHA is relatively more concentrated in PE than PC. Naked mole-rats have fewer molecular species of both PC and PE than do mice. DHA-containing phospholipids represent 27-57% of all phospholipids in mice but only 2-6% in naked mole-rats. Furthermore, while mice have small amounts of di-polyunsaturated PC and PE, these are lacking in naked mole-rats. Vinyl ether-linked phospholipids (plasmalogens) are higher in naked mole-rat tissues than in mice. The lower level of DHA-containing phospholipids suggests a lower susceptibility to peroxidative damage in membranes of naked mole-rats compared to mice. Whereas the high level of plasmalogens might enhance membrane antioxidant protection in naked mole-rats compared to mice. Both characteristics possibly contribute to the exceptional longevity of naked mole-rats and may indicate a special role for peroxisomes in this extended longevity.

As its been said the high levels of plasmalogen of naked mole Rats compared to mice has additional benefits.
It functions as anantioxdisnt . So species might get away with a higher membrane unsaturation, if they have a higher plasmalogen membrane level.
Makes me wonder what plasmalogen level birds have ...

 

Similar threads

Back
Top Bottom