Omega 3 Replaces Omega 6 And Lowers Prostaglandin Synthesis

Kartoffel

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Yes this might be true and might be the case. Same would go for iron. If you feed a rat with overdose of iron everyday it would end up with hemochromatosis and death. Does not mean low dose iron has its function. So whats your point?

My point was to ask haidut a question.

"...For example, if an animal contained 30% fat and it all hardened, it’s subcutaneous fat would become stiff, just the way a steak, when it's in the refrigerator, the fat is stiff; when it's in very warm conditions it becomes soft and flexible. So, in the tropics, even fish in the Amazon river for example, have fat as saturated as butter fat. "

I doubt that there is a fish with fat as saturated as butter, even in the amazon. In one interview he said "similar to olive oil". I don't think any fish can be this saturated.
 

haidut

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I doubt that there is a fish with fat as saturated as butter, even in the amazon. In one interview he said "similar to olive oil". I don't think any fish can be this saturated.

Yeah, I agree. But to his point, warm water fish does seem to spoil less easily than something like salmon, so the different fat composition is probably involved.
 
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Beefcake

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As one of the studies in my original list I sent you showed, the protein in seafood may be the protective factor, not the omega-3.
The Protein In Fish, Not Omega-3, May Be Protective Against Brain Disease
The Protein In Fish, Not Omega-3, May Be Protective Against Brain Disease

Seafood is also high in taurine, glycine, proline and some other anti-inflammatory amino acids. Selenium and zinc play huge roles too. Peat also spoke favorably of seafood, but one thing to keep in mind is that there is a BIG difference in fatty acid composition of fish depending on its region. The northern, cold-water fish are rich in omega-3 but the warm water fish contain mostly saturated fats. So, the regions like Vietnam you mention would be getting mostly good fats from fish and they also use a lot of coconut oil in their cooking.
Cholesterol, longevity, intelligence, and health.
"...Many antioxidant nutrients act like a thyroid supplement did in the 1934 rabbit experiments, preventing atherosclerosis even when extra toxic cholesterol is given to the animals. People who eat seafood get much more selenium in their diet than people who eat nothing from the sea, and selenium is one of the extremely protective nutrients that prevent atherosclerosis in animal experiments with excess cholesterol."
Cholesterol And Saturated Fats - East West Healing
"...For example, if an animal contained 30% fat and it all hardened, it’s subcutaneous fat would become stiff, just the way a steak, when it's in the refrigerator, the fat is stiff; when it's in very warm conditions it becomes soft and flexible. So, in the tropics, even fish in the Amazon river for example, have fat as saturated as butter fat. "

So, yeah, in case there is a misunderstanding - I don't think anybody here is against seafood. Quite to the contrary. Shrimp, oysters, warm-water fish, squid, etc are all great and have been discussed/recommended multiple times. The Peatarian argument is simply focused on avoiding exposure to too much omega-3.

Ok good that was my point aswell. Eat seafood but you see then seafood is protective and sure I can understand that minerals, proteins and vitamins in the fish can help abort some of the damaging effects of excess omega 3. But I’m still suspecting that low amounts of omega 3 has some biological role. And is not purely toxic. I also like to apologize. But I never started a post promoting fish oil supplements or anything. I said seafood once in awhile and the original study was an attempt to figure out that low doses of omega 3 seems to have some benefit on health parameters and it does in many studies. Sure many studies show its bad but they usually use more than 1 gram or even more. I don’t know actually and it’s all very confusing. Thats why I’m trying to have this debate. So we can try and educate each other and learn something new and not just spin the same old wheel.
 
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Fish usually isn't high in fish oil. It is often healthy. I did hear Dr. Peat recently as he said he avoids those predator fish high in the food chain due to industrial contamination and concentration of toxins. But he eats fish. I eat fish. It's good.

And there are many components in fish that may be protective. I've started investigating furan acid, for instance. These may actually help counteract some of the bad w-3 effects.
 
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Beefcake

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Yeah, I agree. But to his point, warm water fish does seem to spoil less easily than something like salmon, so the different fat composition is probably involved.

Yeah well that makes sense because in the amazon the temperature is higher and if the fish had higher pufa it would cause oxidative stress. If a fish had saturated coconut fatty acids in the cold depth of the sea that fat would be hard as hell inside the fish. Ever had coconut oil in the fridge and try to cut it. Impossible without a chain saw. That makes perfect sense. But you have to acknowledge that omega 3s are present in smaller amounts even in land animals even in hotter climates so then comes the standard question. Can we synthesis enough omega 3 if we actually do need them for some biological things? I don’t know but eating fish once in awhile would probably be enough. I just wanna study if there are health benefits on those low doses what are they? What is the biological function. I think comparing it to iron is a great comparison. Probably dangerous in excess but needed to a certain degree.
 
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Beefcake

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Role of docosahexaenoic acid in neuronal plasma membranes. - PubMed - NCBI

Also like to add this study in to the two dopamine studies I posted about omega 3 negativly correlates with prolactin. This means better omega 3 status equalls lower prolactin. The 2nd study was about abnormal/low omega 3 ratios in the brain of diseases with low dopamine thus suggesting that omega 3 might be the cause of the low dopamine and might have some involvement in neuronal membrane functions.
So this study highlights the importance of omega 3 in neuronal membrane structure and that the brain neurons prefers DHA to esterify it to phospholipids. Why does it prefer it? The human body is not some stupid machinery that would accept a poison without purpose. I know rays view on this that before birth the brain is mostly saturated and that with age we get more unsaturated. I buy that but still seems kinda off.
 

haidut

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But you have to acknowledge that omega 3s are present in smaller amounts even in land animals even in hotter climates so then comes the standard question. Can we synthesis enough omega 3 if we actually do need them for some biological things? I don’t know but eating fish once in awhile would probably be enough. I just wanna study if there are health benefits on those low doses what are they? What is the biological function. I think comparing it to iron is a great comparison. Probably dangerous in excess but needed to a certain degree.

Sure, they do exist in small amounts in our food supply. I think the argument has never been they are dangerous in any amounts. The liver has capacity to glucuronidate and (unfortunately for its own health, but in the name of protecting the rest of the organism) oxidize a decent amount of omega-3 found in diet. So, for people with decent liver function, eating trace amounts of omega-3 in it should not be a problem. Some people asked Peat something along the lines of "if PUFA is so pervasive in nature isn't is orthorexic to go to such great lengths to avoid it". His response was that it depended on the person's age, health status and fat stores. An older, obese, sickly person who probably has a ton of PUFA in his/her stores can probably benefit from great caution in avoiding most sources of PUFA, even if the amount is small. Same goes for a person with cancer, diabetes, or Alzheimer. When such pathology is already established and given how detrimental PUFA is then avoiding it all cost may be your best bet. But for most other people it is the SFA/PUFA ratio that matters most. If you eat mostly saturated fat and keep PUFA intake to say within 3g-4g daily and are not vitamin E deficient then you are probably OK. I don't remember off the top of my head what is the saturable capacity of the liver to oxidize/glucoronidate PUFA. I think it was something along the lines of a few grams per hour. So, if your liver is OK, you are not deficient in vitamin E, and you do not exceed this dietary influx per hour then it should be OK.
As far as their natural role in mammals, I don't think this is settled or known by anybody for sure. There is no real evidence for them being essential, at least for humans. Unlike omega-6 the omega-3 are not considered essential even by mainstream medicine as it has been shown conclusively that a person eating zero omega-3 (but some omega-6) is perfectly fine. Unfortunately, those studies did not check if these people on zero omega-3 diet were OK because there were able to synthesize omega-3 from omega-6 or if it was because omega-3 has no actual role in our health and we can do without it. The studies simply assumed that the people on zero omega-3 diet synthesized what they needed from the omega-6 as we are known to possess the enzymes for such synthesis. But short of doing extensive brain, fat, muscle, organ and tissue biopsies we don't really know if they actually synthesized enough (more?) omega-3 when deprived of it in diet, and of course such studies are considered unethical and would never be done. Peat mentioned a study on a person doing zero fat diet for months and he was doing fine, and his health apparently improved. But of course that does not prove anything conclusively since that person had non-zero fat stores, which almost certainly contained PUFA. So, the argument would always exist that he was synthesizing omega-3 as needed. However, rats on diets that make them fully EFA-deficient seem to do just fine and in fact are quite resilient to a variety of assaults such as lethal amounts of endotoxin, viral infections like rabies, lethal doses of ionizing radiation, etc.
We do know that PUFA have detrimental signalling mimicking estrogen, serotonin, cortisol, histamine, etc. Whether omega-3 survive long enough in unmetabolized state so that they can exert those effects is not very clear. Their hidden "benefit" may be precisely that they oxidize so easily, which prevents them from doing more (and longer term) damage like their omega-6 cousins (and some cases parents) do.
So, am afraid until some more definitive studies are done we will have to go with what we know so far biochemically - i.e. any amount of omega-3 that raises TBARS is likely bad for us and that is easily achieved by taking more than 2g of EPA or 1g of DHA in a single sitting. And if such amounts are consumed, I'd personally always take some vitamin E beforehand as that vitamin can sometimes directly deactivate PUFA and spare the liver the effort of processing it.
Just my 2c.
 
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nwo2012

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Yeah nothing new, omega 3s not as poisonous as 6s or 9s but still more poisonous than none.
 

Mito

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Can we synthesis enough omega 3 if we actually do need them for some biological things? I don’t know but eating fish once in awhile would probably be enough.
I really miss @Travis posts...here is one of his gems on this subject.

“I think it's practically unavoidable, and the bigger danger is ω−6 fatty acids displacing the small yet ubiquitous amounts of α-linolenic acid (18∶3ω−3) found naturally in leaves and grass-fed dairy. Practically all the DHA found in non-fish-eating mammals had initially been elongated and desaturated from α-linolenic acid. Omega−6 fatty acids such as linoleic (18∶2ω−6) and γ-linolenic (18∶3ω−6) acids compete with α-linolenic acid (18∶3ω−3) at the elongation/desaturation stage, the former two intending to become arachidonic (20∶4ω−6) and osbond (22∶5ω−6) acids while the latter vies to become eicosapentaenoic (20∶5ω−3) or docosahexanenoic (22∶6ω−3).

linoleic γ-linolenic ⟶ dihomo-γ-linolenicarachidonic ⟶ osbond

α-linolenic ⟶ eicosatetraenoic eicosapentaenoic ⟶ docosapentaenoic docosahexanenoic

The first step of elongation/desaturation outlined above yields the eicosanoids, shown in red. The omega−6 dihomo-γ-linolenic and arachidonic acids are directly analogous to omega−3 eicosapentaenoic acid and displace it from similar locations. These are the only three lipid precursors of prostaglandins:

dihomo-γ-linolenic ⟶ prostaglandin E₁

arachidonic ⟶ prostaglandin E₂

eicosapentaenoic ⟶ prostaglandin E₃
All three prostaglandin types have variable activity. Since humans had evolved equitorally, it could be fair to consider the 3-series prostaglandins the more natural ones. Studies indicate that prostaglandin E₃ has about ¹⁄₄ the potency of prostaglandin E₂, and the leukotrienes differ even more in potency: Neutrophils are attracted to leukotriene B₄ at concentrations 5000 × lower than leukotriene B₅. Leukotriene B₃, synthesized from Mead acid (20∶3ω−9), is about five times less potent.

Mead acid ⟶ leukotriene B₃

arachidonic ⟶ leukotriene B₄

eicosapentaenoic ⟶ leukotriene B₅
Mead acid is the omega−9 eicosanoid created during omega−6 restriction. Mead acid can form a leukotriene yet it cannot form a prostaglandin; cyclooxygenase will hydroxylate this lipid yet will not cyclize it. Unfortunately, the longer 22-carbon lipids do not seem to have a functional omega−9 analogue so we cannot make them ourselves. The docosanoids don't appear to have a hormonal function are are strictly functional membrane lipids.

linoleic γ-linolenic ⟶ dihomo-γ-linolenicarachidonic ⟶ osbond

α-linolenic ⟶ eicosatetraenoic eicosapentaenoic ⟶ docosapentaenoic docosahexanenoic
The sum of osbond + DHA in the brain appears to be a constant, always falling within the range of 14–17% in the grey matter. It appears as though we must choose one type or the other, and since omega−6 fatty acids are invariably associated with pathology I think we should choose 'the other.' Omega−6 fatty acids compete with omega−3 fatty acids during multiple stages during the four-carbon elongation/desaturation phase, making their dietary ratio of critical importance.

Despite its name, osbond acid will not make you feel like a secret agent. This lipid cannot exclude cholesterol from the cell membrane as well as DHA and its' presence there yields less glucose-permeable membranes. The substitution of DHA with osbond acid has implications in both insulin resistance and cardiovascular disease.

Unstable docosahexaenoic acid needs never to be consumed because its precursor α-linolenic acid is found in leaves and grass-fed dairy/beef. I am aware of the idea that 'all DHA is initially synthesized in the liver before it travels to the brain,' yet I somewhat doubt this because 18-carbon endogenous lipids are freely found there—i.e. linoleic acid. Radiolabeled oleic acid has also been shown to cross the blood brain barrier, so it could be wise to consume the more stable α-linolenic acid because its direct brain transport seems certain. Since we all eat this already, it makes more sense to simply avoid omega−6 with increased diligence. This way, we can ensure a proper DHA∶osbond ratio while keeping lipofuscin to a minimum. Lipofuscin increases with age in non-mitotic neurons, slowly lowering their metabolism until death. Postmortem analysis of centenarians reveal that lipofuscin can account for up to 75% of the internal volume in motor neurons.”

Deep Fried Food, What Is Your Opinion?
 

CLASH

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This is a great thread. Debate and argument can sometimes bring out the best solutions and understandings. Emotional investment seems to be neccesary to provide adequate stimulus in the form of neccesity to drive human action. In its absence I think were all resigned to relaxation lol.

Check these out:

I read the full text before and posted about it on another thread, this is an exercept from the abstract because I dont want to go back through the whole study....
Fatty acid composition of membrane bilayers: Importance of diet polyunsaturated fat balance - ScienceDirect
“Extensive changes in diet SFA, MUFA and PUFA had minimal effect on membranes (average slopes 0.01, 0.07, 0.07 respectively), but considerable influence on adipose tissue and plasma triglycerides (average slopes 0.27, 0.53, 0.47 respectively). Diet balance between n−3 and n−6 PUFA had a biphasic influence on membrane composition. When n−3 PUFA < 10% of total PUFA, membrane composition completely conformed to diet (average slope 0.95), while diet PUFA balance > 10% had little influence (average slope 0.19). The modern human diet has an average PUFA balance ~ 10% and this will likely have significant health implications.”
 
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CLASH

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This was the study @olive posted, I read the full text :)
http://m.jlr.org/content/36/10/2164.long?view=long&pmid=8576642

DF1EC1B8-C8B7-4515-979B-A631220C5D92.png

This is an analysis of rats retroperitineal fatty acid composition.
The control diet is the rats not fed fish oil and EPA (they used herring oil). The other day 1, day 7, and day 10 are analysis of the fatty stores of the rats initially fed fish oil and then fasted for a 10 days. As you can see the fish oil fats do seem to make it to the fatty tissue for storage.
There seems to be selective mobilization of specific fatty acids.

“As expected, compared to the control group, Rp (retroperitoneal) TAG of fish oil-fed rats contained higher amounts of some very long chain (20-22 carbon atoms) monounsaturated fatty acids and of n-3 polyun- saturated fatty acids with 4-6 double bonds. During
fasting, the weight % of all but five fatty acids changed significantly. The weight % of highly unsaturated (4-5 double bonds) fatty acids with 16-20 carbon atoms, and of 18:3n-3 and 16:ln-7 decreased by 2- to 18-fold(P< 0.001or less),the weight %of 20:5n-3 showing the most dramatic decrease. In contrast, the weight % of very long chain (20-24 carbon atoms)saturatedand monounsatu- rated fatty acids increased by 3- to 5-fold (P< 0.001 or less). Very similar changes were observed in subcutane- ous, epididymal, and mesenteric adipose tissues (data not shown).”

“The molecular structure of fatty acids influenced their in vivo mobilization. For a given chain length the in vivo relative mobilization increased with the number of doublebonds (Fig.2,leftpanel) whereas for a given number of double bonds it decreased as the chain length in- creased (Fig. 2, right panel). For fatty acids with 18 or 20 carbon atoms, the relative mobilization increased exponentially with unsaturation (Table4), two of the three parameters of the equation of the line of best fit differing significantly.Notably, the exponent was higher for the shorter chain length, indicating that the shorter the fatty acids were, the greater was the effect of unsatu- ration. The relative mobilization of fatty acids with 16 or 22 carbon atoms also increased significantly with increasing unsaturation, but the limited number of dou- ble bonds precludes a detailed analysis of the relation- ships.”

“The same selectivity of fatty acid release from adipo- cytes in vitro and net loss from adipose tissue in vivo was demonstrated under conditions of intense lipolysis,i.e., when the net efflux and loss of fatty acids, respectively, massively reflects the hydrolysis of adipocyte TAG (35). This observation supports the suggestion that the selec- tivity of the release of fatty acids originates from a selective hydrolysis of TAG by HSL (hormone sensitive lipase), as previously ob- served in vitro for several polyunsaturated fatty acids (15). Among putative mechanisms, a preferential loca- tion and thus accessibility to HSL of TAG with the highest polarity at the lipid-water interface (TAG d r o p let-cytoplasm) has been proposed (16).In consequence, during prolonged lipolysis, the least polar fatty acids would be released at a progressively increasing rate in proportion to the “peelingoff of the most polar ones by HSL. This would explain that the mobilizationof fatty acids is selective but not as stringent as it would be in the classical sense of enzyme specificity.The observation during fasting of a progressive decrease in the weight % (Table 2) and in the relative rate of mobilization (Table 3) of the most polar fatty acids (e.g., 184n-3, 20:4n-6, and 20:5n-3 in the present context) and of the reverse changes for those with the lowest polarity (e.g., very long chain saturated and monounsaturated fatty acids) is consistent with this hypothesis.“


*The TLDR for people who dont give a sh*t:

Fish oil puts long chain unsaturated fats in your fat stores.

During fasting the more double bonds a fat has the easier it is liberated from fat stores. The longer the chain length of the fat, the more difficult it is to liberate it. Thus long chain monounsaturated and saturated fats are much more difficult to liberate from fat stores by hormone sensitive lipas.

The reason this occurs according to the authors is due to the polarity of the fat (meaning ability of the fatty molecule to interact with water... i think... lol). The more double bonds with the shorter chain length, the higher the polarity of the fat, thus the easier it is for hormone sensitive lipase to liberate the fat from the tissues. As there are less and less polyunsaturated fats in the tissues to liberate more and more monounsaturated and saturated fats are liberated.

*practical applications in my mind:

1) avoid all PUFA, even fish oil

2) maintain a high muscle mass to burn off the PUFA that you do ingest

3) post argumentative anti-peat stances on the ray peat forum in moderation so that we can stimulate these discussions so I can read interesting articles :)
 
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lampofred

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This is a great thread. Debate and argument can sometimes bring out the best solutions and understandings. Emotional investment seems to be neccesary to provide adequate stimulus in the form of neccesity to drive human action. In its absence I think were all resigned to relaxation lol.

lol what is great about this thread? it's not a real discussion, it's just some people who haven't actually read Peat's articles posting studies they found via a 1-minute Google search that have the headlines they are looking for. but all of the points they are bringing up have already been covered in Peat's articles and interviews as to why O3 oils can have beneficial effects in the short-run.

i was reading some threads from a few years ago, and in general, the quality of discussion on this site has drastically gone down. recently there has been a large number of threads with people bringing in mainstream ideas as if these ideas were something new without actually refuting Peat's articles which have already explained the issues with those ideas.
 

CLASH

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@lampofred
I think its good to keep reassessing and reaffirming your beliefs. I also think its good to see oppositional beleifs and the info supporting them. Theres alot of garbage to wade through to find the gold. Peat may be right, I generally think he is, but I would rather read the info myself then take his word for it. I like to see my perspective confirmed continuously. I want the truth above all. I need my paradigm gut chucked consistently to see its resiliency. There may be ego and bull**** over all of it, with arguments and posturing, thats all filler and surface bs, but sometimes little gems come out and I learn something new or my position strengthens.
 

mujuro

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Japan consumes loads of salmon. Its like the most fatty fish. Besides now you saying fish is ok to eat? Hello thats what I said from mu first post!!! Never did i say to consume large amounts or taking fish oil. My point is omega 3 has some biological function. Besides lots of fish has fat soulable antioxidants. Not the purified oil thats rancid that i also said. And i never touted eating fish everyday i said max once a week should be enough. Focus on the larger stores of fatty acids in the body like saturated fat. But once in awhile you might need a small dose of omega for some biological purpose

I get what you mean, and PUFA do have biological roles, but your OP implied that we here think that anything more than zero PUFA is not good enough. I didn't read it but it says in the abstract w-3 PUFA. Are they talking about ALA or EPA/DHA? It's ridiculously hard to get <2g of PUFA in a daily diet (I believe Peat says <4g is a good goal). Some on here have tried but it is tough and restrictive and no way to live. You're always going to be ingesting w-3 and w-6. Peat's entire message is to reduce them as much as you can, don't go out of your way to eat them, and certainly never supplement them. I don't mind a bit of fish every now and then. Is it damaging? I suppose you'd need observational studies to figure out how much fish per week is enough to be damaging. A Japanese observational study might work, but you'd need a control group of Japanese who never consume fish to draw any meaning from it.

I think the argument has never been they are dangerous in any amounts.

+1
 
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CLASH

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I think peat’s quote is 4g/2000kcal

If your going to eat 4000kcal a day, 4g is just as difficult to hit as less than 2g on 2000kcal. I know this personally, thats why I bring it up.

I think the goal is less than 2% of calories from pufa.
 

tara

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My point is sort of more like @olive said and as @Travis also believes. Fresh fish once in awhile. Just because something is beneficial in small amount does not mean you have to go get super natural doses everyday.
I think there are a number of people, possibly Travis among them, saying that there may be a good use/need for tiny amounts of some particular omega 3s (ALA?). But that it's a bit academic, because if you are eating foods (especially some greens, as opposed to just refined sucrose etc), it's almost impossible to avoid getting enough. No need to deliberately eat oily fish.

Having said that, I enjoy the occasional small portion of oily fish like salmon or sardines as part of a varied diet and because it sometimes tastes good. :) And more other sea food -shell fish, white fish like cod etc.

I've always wondered if fish oil is so bad how comes nearly all athletes take fish oil and are healther than most people? When I read weight lifting forums nearly everyone is taking fish oil and they are in better health and shape than most people on this forum? .
My guess is people who are healthy are more likely to get into athletics and weightlifting, regardless of whether they eat fish oil.

I don't think anybody here is against seafood. Quite to the contrary. Shrimp, oysters, warm-water fish, squid, etc are all great and have been discussed/recommended multiple times. The Peatarian argument is simply focused on avoiding exposure to too much omega-3.
+1
 

yerrag

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I am not scaremongering at all. It is just an illustration of what happens when there is sufficient elevation of FFA. While extreme as an example, it is actually a VERY good example of what elevated FFA does to your organs, because during a marathon you will be burning predominantly fat. So, less extreme stress such as say running 5-6 miles may be less damaging but how much evidence do we actually have on safety of such shorter runs? Long story short - there is strong evidence that even brief elevation of FFA damages organs. How much damage occurs is largely determined by length of exposure to elevated FFA. If you don't like it, so be it. But evidence is evidence.
https://raypeatforum.com/community/threads/increased-fat-oxidation-is-the-cause-of-kidney-damage.27087/

Glycogen-bound running is probably OK. As soon as FFA start to rise, you are already in danger zone. Weight lifting and sprinting are two of the few safe intense sports.
You just gave me an answer to something I've long wondered about: why long-distance runners have low heart rates. I think it's because of all the PUFA metabolites that comes out of metabolizing PUFA free fatty acids when glycogen/glucose supply is in short supply or exhausted. Would these metabolites accumulate eventually in the blood vessels, as well as cholesteryl esters from oxidized LDL, which are linked to PUFAs but not to saturated fats? Wouldn't these plaques form and eventually restrict tissue oxygenation? And with less oxygen being available, the mitochondria would have to downregulate energy production. And with the lowered metabolism, heart rate would also be lower. Being that it is so hard for runners (as well as people with low heart rates) to increase their heart rates, it makes the case that it is a permanent handicapping of our metabolic throughput. And plaques, being difficult to remove (and risky as well) is what I can think of that causes this permanent handicapping.

It would be interesting though to find out how long distance runners on a PUFA-free diet would compare to those on a PUFA-full diet. Wonder if such a study has even been attempted.
 
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Beefcake

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My point is why does studies show omega 3 increase testosterone in rats. Increase sperm in humans (isnt the production of sperm dependent on androgen receptors? If now omega 3 ”degrade AR”). Lower prolactin and increase dopamine signaling? This means it has to have some biological role in smaller amounts. Maybe ALA is good enough. And that the cold water fish is not needed and might be harmful. But eating tropical fish with some degree of other seafood likely has benefits that outweigh the negative and possibly even the smaller amounts of omega 3s in these foods actually have som degree of biological function.
Besides most high source ALA foods seem to have other negative properties which would make eating fresh fish likely better than trying to get high ALA food like seed oils.
 

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