Is Omega-3 Fish Oil Bad?

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So then If I read this right, it is better to keep more cholesterol in brain tissue than DHA.
Therefore, the idea that DHA must come from diet to increase uptake in the brain is foolish, and it does damage along the way.
The body can make it when needed, but as is evident from studies the DHA made from precursors like ALA or SDA or EPA do not let the DHA get in tissues for a good reason, coz DHA is disruptive.
 

Kartoffel

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The body can make it when needed, but as is evident from studies the DHA made from precursors like ALA or SDA or EPA do not let the DHA get in tissues for a good reason, coz DHA is disruptive.

I don't think it is ever needed. I think there is a reason our capacity to desaturase ALA and EPA to produce the longer, and less stable, DHA is severly limited. Our body doesn't seem to want to produce DHA because it's so agressive and detrimental to us. Cholesterol is the precursor to all the protective neurosteroids, and is by itself protective, so of course you want a lot of it in your brain. In fact, our brains contain 20% of total cholesterol in the body and about 20mg/g brain tissue.
 
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I don't think it is ever needed. I think there is a reason our capacity to desaturase ALA and EPA to produce the longer, and less stable, DHA is severly limited. Our body doesn't seem to want to produce DHA because it's so agressive and detrimental to us. Cholesterol is the precursor to all the protective neurosteroids, and is by itself protective, so of course you want a lot of it in your brain. In fact, our brains contain 20% of total cholesterol in the body and about 20mg/g brain tissue.
I agree, but still it could be useful in situations were brain damage or diseases has reduced the DHA content in the brain, but then via Curcumin + ALA in the diet. See my earlier post.

Curcumin increases DHA in the brain when consumed with the n-3 precursor ALA
"Animals were maintained on a diet supplemented with ALA (2.7% of total fatty acids) or ALA+CUR (250 or 500 ppm). ALA alone or CUR alone did not increase DHA content in the hippocampus compared to control group (p>0.05; Fig. 1A). However, when rats were fed ALA+CUR, DHA content was significantly higher (162 or 152% of CTL for 250 or 500 ppm curcumin-fed animals, respectively) in ALA+CUR than ALA alone group (p<0.05; Fig. 1A). These findings suggest that CUR may enhance the conversion of ALA to DHA in vivo and elevate DHA content in brain. We assessed the relevance of the dietary intervention on cognitive function using the elevated-plus maze, a measure of anxiety-like behavior. We found that the time spent in the open arm was significantly higher in ALA+CUR groups compared with ALA or CUR alone or CTL (p<0.05; Fig. 1B). We regressed DHA% of CTL measured in the hippocampus against elevated plus maze scores and found a significant positive correlation between brain DHA levels and time spent in the open arms, indicating that DHA in the brain is associated with reduced anxiety-like behavior (p<0.05; Fig. 1C)."
 

Kartoffel

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I agree, but still it could be useful in situations were brain damage or diseases has reduced the DHA content in the brain, but then via Curcumin + ALA in the diet. See my earlier post.

What kind of disease are you thinking about? In the disease that is most often said to be caused by a DHA deficiency (Zellweger's), DHA doesn't have any positive effect for the patients. I don't know of any disease that would be cured or alleviated by DHA in the long run. If DHA really "is essential for brain function and its deficiency is implicated in many types of neurological disorders." then it seems odd that the study Ray cited demonstrates that increased DHA seems to be an important factor in Parkinson's and other neurodegenerative diseases.
I'm always sceptical of these maze experiments, and what their results really mean. After all, there are dozens of them "showing" that sugar/fructose makes animals really anxious and stupid. Anyways, if it was in fact the increased DHA that caused any cognitive improvements, it shouldn't be hard to find a study where just supplementing DHA achieves the same results, even without such an odd study design. Can you provide one?
 
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What kind of disease are you thinking about? In the disease that is most often said to be caused by a DHA deficiency (Zellweger's), DHA doesn't have any positive effect for the patients. I don't know of any disease that would be cured or alleviated by DHA in the long run. If DHA really "is essential for brain function and its deficiency is implicated in many types of neurological disorders." then it seems odd that the study Ray cited demonstrates that increased DHA seems to be an important factor in Parkinson's and other neurodegenerative diseases.
I'm always sceptical of these maze experiments, and what their results really mean. After all, there are dozens of them "showing" that sugar/fructose makes animals really anxious and stupid. Anyways, if it was in fact the increased DHA that caused any cognitive improvements, it shouldn't be hard to find a study where just supplementing DHA achieves the same results, even without such an odd study design. Can you provide one?
- I assumed that the developed brain should have the necessary structured DHA incorporated in a delicate balance, and so with "diseases" I mean anything that deviates from that balance, especially during embryo development.
Examples from that article: neurocognitive disorders such as anxiety-like behavior [1, Exposure to a maternal n-3 fatty acid-deficient diet during brain development provokes excessive hypothalamic-pituitary-adrenal axis responses to stress and behavioral indices of depression and anxiety in male rat offspring later in life. 2, Omega-3 fatty acid deficiency during brain maturation reduces neuronal and behavioral plasticity in adulthood.], and impaired attention [7, Maternal DHA and the development of attention in infancy and toddlerhood. 8, Maternal DHA levels and toddler free-play attention.].
 

MrSmart

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I don't think it is ever needed. I think there is a reason our capacity to desaturase ALA and EPA to produce the longer, and less stable, DHA is severly limited. Our body doesn't seem to want to produce DHA because it's so agressive and detrimental to us. Cholesterol is the precursor to all the protective neurosteroids, and is by itself protective, so of course you want a lot of it in your brain. In fact, our brains contain 20% of total cholesterol in the body and about 20mg/g brain tissue.

That's actually a counter-argument to yours. The body only needs to produce a very small amount, or it would not have evolved with the enzyme at all. Especially since ALA intake was much higher during our evolution.
 
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...additionally,
The Discussion part about Curcumin + ALA for DHA is very interesting...
"While DHA can be obtained through animal sources in the diet, vegetarians and vegans may face challenges getting adequate dietary DHA [35]. Increasingly, vegetarianism and veganism is being adopted in the Western world [65]. Circulating omega 3 fatty acids are lower in vegetarians and non-fish eaters than in people who consume fish [66]. Furthermore, changes in farming practices and food consumption have taken place over the last century such that the dietary n-3 fatty content may be declining [67]....
Other dietary sources of DHA, such as beef [75] and eggs [76] have reduced DHA content when using the most prevalent farming practices of grain corn feeding vs pasture-feeding. Thus, even for omnivores, obtaining DHA through the diet may be increasingly difficult in the current modern food climate.

Paradoxically, in Asia, vegetarianism has been practiced for centuries without high incidence of cognitive impairment. No ill effects were reported in pregnancy outcomes of South Asian vegetarians vs North London omnivores [77] and Seventh Day Adventists residing in the Southwestern United States reported significantly less negative emotion compared with omnivores, despite reduced levels of DHA [78].
Due to the apparent discrepancy between animal studies showing clear cognitive impairment associated with reduced DHA in the brain and human data showing improved mental health in vegetarians, we sought to investigate whether other components commonly consumed in traditional vegetarian diets could enhance DHA content in the brain and the synthesis of DHA from vegetarian sources.
...
We recently reported that curcumin supplementation promoted increased DHA content in the brain following TBI, and that this effect was associated with elevated levels of enzymes involved in DHA synthesis [22]. We therefore investigated whether curcumin enhances DHA synthesis from vegetarian precursors. Here we report that, when combined with dietary ALA, curcumin increases the DHA content in both liver and brain tissues. Furthermore, we found that the elevated DHA content was associated with elevated levels of the enzymes FADS2 and elongase 2, which are important for DHA synthesis.
...
It has been reported that in order to achieve similar amounts of long chain omega 3 fatty acids in the brain on an ALA enriched, vs a preformed EPA + DHA enriched diet, ALA needed to be consumed at 33.5 times the amount [96]. The action of FADS2 and Elov2 are important control points (enzymatic reaction-limitation) during the synthesis of DHA. Excessive ALA consumption may inhibit the activity of enzymes involved in DHA synthesis. In particular FADS2 is subject to competitive inhibition between substrates. For example, administration of ALA to HepG2 cells results in increased accumulation of EPA, but not DHA, consistent with competitive inhibition of FADS2 by DPA [52]. We found that, when combined with the vegetarian precursor ALA, dietary curcumin increased levels of FADS2 and elongase 2 in both liver and brain tissues. Accordingly, our results showed that curcumin produced greater hepatic and central DHA increases compared to animals fed ALA alone. Thus, our data support that by increasing the level of these key enzymes curcumin may enhance the conversion of ALA to DHA, even when ALA levels are increased in the diet. Accordingly, our in vitro data suggest that the effects of curcumin to enhance DHA synthesis are dependent on the effective functioning of FASD2 enzyme, suggesting that curcumin effects are partially at the level of DHA synthesis.
...
Curcumin has been reported to cross the blood brain barrier [97, 98], and to be neuroprotective [99][41, 100, 101]. It is known that DHA is an essential component of nerve cell "membranes" [102, 103], but the synthesis of DHA is very limited in the brain [29].
...
Our current study provides new evidence indicating that curcumin increases levels of enzymes FADS2 and elongase 2, which are involved in DHA synthesis, in brain tissue. Additionally, we found that brain levels of DHA and DHA synthesis enzymes were enriched in animals fed curcumin and ALA together, but were unchanged when rats were fed the ALA-enriched diet without curcumin. Though the rate of synthesis is low, the brain seems to have the capacity to synthesis DHA from ALA [29]. Thus it is possible that curcumin elevates DHA in the brain, in part, through de novo synthesis in brain tissue. This possibility warrants further investigation, though liver synthesis seems the more likely contributor to increased brain pools of DHA, since curcumin is highly metabolized in the liver [108]. From our current dataset, we cannot exclude the possibility that observed elevations in brain DHA comes from the liver, since curcumin also promotes the DHA synthesis in the liver.

Curcumin has known antioxidant, anti-inflammatory and antiapoptotic properties (for review see [109]), thus we cannot exclude the possibility that elevated levels of DHA measured in brain and liver are the indirect result of reduced oxidative stress or anti-inflammatory properties of curcumin. For example, oxidative stress is inversely related to liver FASD2 and Δ5 desaturase activities and it has been hypothesized that reduction in plasma antioxidant activity may promote the direct inactivation or reduced expression of liver FASD2 [110]. Thus, the effect of curcumin on levels of FASD2 may be indirectly related to its antioxidant properties. During oxidative stress free radicals generate lipid degradation products, such as 4-HNE. We measured levels of 4-HNE in brain and liver tissues as a biomarker of oxidative stress. Surprisingly, curcumin alone did not reduce 4-HNE in brain or liver, suggesting that curcumin alone in the diet did not reduce lipid peroxidation under homeostatic conditions. In these terms, it is likely that the antioxidant action of curcumin may be more prevalent under challenging conditions such as brain injury. Treatment with ALA either alone or in combination with curcumin significantly reduced levels of 4-HNE. In brain tissue, the combined treatment with ALA and curcumin further reduced lipid peroxidation, whereas in liver it did not. ..."

So, what is also interesting in the last part quoted above, the fact that the antioxidant and reduced lipid peroxidation and neuroprotective effects of a substance like curcumin can be as important as its effects on the enzymes to stimulate conversion of DHA that's supposed to be good for brain health.

"it is likely that the antioxidant action of curcumin may be more prevalent under challenging conditions such as brain injury."
- But how is this possible? because of the electric nature of the oxidation and peroxidation process with ions and neuron-signaling?
Does the body "sense" reactive pathways to follow upon via underlying electric principles?
 
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Kartoffel

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Especially since ALA intake was much higher during our evolution.

How do you know that?

That's actually a counter-argument to yours. The body only needs to produce a very small amount, or it would not have evolved with the enzyme at all.

Just because we have the enzyme for something doesn't mean we need it, or that a substance is essential. Otherwise I could say the same thing about Mead Acid. Since you want to make an evolutionary argument about the enzyme and the historical importance of ALA to DHA conversion, then tell me this: If DHA is so vital, and we have always relied on getting enough from it via the conversion of ALA, why has our ability to use the desaturase enzymes become weaker, as our supply of ALA has decreased? The whole PUFA community keeps telling us that everybody, especialy newborns, are terribly DHA deficient, and need to reive supplements. Seems our evolution has been pretty misguided...
 
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Any how, you continue arguing about this, i dont care, I am going for closure:

hey I see a few posts of people saying PUFA (Polyunsaturated fatty acids) is bad? so this includes omega-3 also? if yes that is weird because it goes against everything I have read about it.

-When should you to take fish oil?
From my practical orthomolecular point of view:

1. You are starting with "Peating" by slowly reducing your monthly PUFA intake, and want to keep the n-6:n-3 ratio in balance to prevent inflammation via prostaglandin inhibition.
2. When you are genetically evolved with fish oils in the diet and come from cold environments.
3. You have experienced brain damage or neurocognitive disease and want to repair your health.

Note: take it with coconut oil so the ratio of SFA:PUFA is 2:1.
and combining the fish oil with bioavailability boosted Curcumin supplement is highly recommended in all situations: to minimize oxidative stress and increase the effectiveness of DHA convertion and it's delivery.
 
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Kartoffel

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and combining the fish oil with bioavailability boosted Curcumin supplement is highly recommended in all situations

I'm sure Ray will completely agree on this ;) If there are two things that he loves it's DHA and allergenic spices
 

MrSmart

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How do you know that?

Untitled.png


Just because we have the enzyme for something doesn't mean we need it, or that a substance is essential. Otherwise I could say the same thing about Mead Acid. Since you want to make an evolutionary argument about the enzyme and the historical importance of ALA to DHA conversion, then tell me this: If DHA is so vital, and we have always relied on getting enough from it via the conversion of ALA, why has our ability to use the desaturase enzymes become weaker, as our supply of ALA has decreased? The whole PUFA community keeps telling us that everybody, especialy newborns, are terribly DHA deficient, and need to reive supplements. Seems our evolution has been pretty misguided...

We can pass on genes that are inert, but virtually unheard of to my knowledge that we pass on such an important gene as a lipase enzyme used in the assimilation of daily food and be detrimental to our survival.

Do you have a source for this?

The whole PUFA community keeps telling us that everybody, especialy newborns, are terribly DHA deficient

Newborns get their supply from breastfeeding. Which is most likely the main reason women are more efficient converters of DHA, primarily due to their estrogen status, especially maternally when it is quite high.
 
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I'm sure Ray will completely agree on this ;) If there are two things that he loves it's DHA and allergenic spices
Whatever, I don't care if he does not like it, he is not clear about this DHA semi-essential issue, only responds about some stupid membrane theory not being correct, but avoiding the real practical orthomolecular applications of DHA.
So I gave my own suggestion to it's application.
 
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I'm sure Ray will completely agree on this ;) If there are two things that he loves it's DHA and allergenic spices
By the way "curcumin" is not a spice -> Kurkuma is the spice. Curcumin is the isolated substance from the root Curcuma longa. I think Ray would not mind it at all if it can reduce the bad side effects of DHA :)
 

MrSmart

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You cannot mean that our paleolithic ancestors eat these vegetables, coz veggies are domesticated / cultivated for food that did not exist in ancient times...

You're thinking of grains, and even then they existed but in lower production.

Assuming you're right about paleolithic humans, the animals did eat them. Grass has roughly 1% of ALA by mass, and it's even higher than that in milk, which Ray recommends. Not to mention the many who lived near open water sources who fed on fish.
 
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...If DHA really "is essential for brain function and its deficiency is implicated in many types of neurological disorders." then it seems odd that the study Ray cited demonstrates that increased DHA seems to be an important factor in Parkinson's and other neurodegenerative diseases.

I'm always sceptical of these maze experiments, and what their results really mean. After all, there are dozens of them "showing" that sugar/fructose makes animals really anxious and stupid.

Anyways, if it was in fact the increased DHA that caused any cognitive improvements, it shouldn't be hard to find a study where just supplementing DHA achieves the same results, even without such an odd study design. Can you provide one?
- DHA is semi-essential for brain function, coz it can be synthesized. But the "deficiency" dogma is from the wrong idea that is must come from the diet coz the synthesis in our body is not sufficient.
-The odd thing about fatty acids that have highly reactive electrons is that the underlying system of electric nature in neuron signaling as a system is not understood by biomolecular science, coz they are stuck with dogma of isolated globular things like "atoms" and "electrons" particles, while they knew some time ago from Tesla and Faraday etc that aether and vibrational frequency is what governs physics not particles colliding.

-The maze experiments are pretty solid way of testing behavior. But the problem is with isolated substances that are studied that give skewed results, but that does not mean mazes are no good way of testing.
-No, no need to look for DHA only studies, coz you need in vivo whole diets to compare like the diets used in the examples I gave you of the CUR + ALA studies are sufficient, coz they use the same diets like this:
edit: see previous post

Ingredient Amount (g/100 g diet)

Alacid 710, acid casein 20 20
Cornstarch 15 15
Sucrose 10 10
Dextrose 19 19.9
Maltose-dextrin 15 15
Cellulose 5 5
Salt-mineral mix 3.5 3.5
Vitamin mix 1 1
L-cystine 0.3 0.3
Choline bitartrate 0.25 0.25
TBHQ 0.002 0.002

Fat sources: n-3 adq n-3 def
Hydrogenated coconut oil 7.45 8.1
Safflower oil 1.77 1.9
Flaxseed oil 0.48 none
DHA 1.2 none
 
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You're thinking of grains, and even then they existed but in lower production.

Assuming you're right about paleolithic humans, the animals did eat them. Grass has roughly 1% of ALA by mass, and it's even higher than that in milk, which Ray recommends. Not to mention the many who lived near open water sources who fed on fish.
No, I am not "thinking" about grains. Take broccoli, it is cultivated from a tiny bud plant. You cannot speak of paleolithic vegetables the same as veggies that we have now. And pak choi is related to the family Brassicaceae, to which vegetables such as cabbage, mustard greens, cauliflower, broccoli, water cress and radish belong. They were grown by humans. Records of the cultivation of pak choi in south China date as far back as the 5th century AD. But did not exist before that in the form we have now.
 
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MrSmart

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No, I am not "thinking" about grains. Take broccoli, it is cultivated from a tiny bud plant. You cannot speak of paleolithic vegetables the same as veggies that we have now. And pak choi is related to the family Brassicaceae, to which vegetables such as cabbage, mustard greens, cauliflower, broccoli, water cress and radish belong. They were grown by humans. Records of the cultivation of pak choi in south China date as far back as the 5th century AD. But did not exist before that in the form we have now.

The table was representative of vegetable food, not this in particular. Maybe you need to read Melamed, Yoel, et al. "The plant component of an Acheulian diet at Gesher Benot Ya ‘aqov, Israel." Proceedings of the National Academy of Sciences113.51 (2016): 14674-14679.

You don't need to argue it though, my second point about eating exclusively meat also stands.
 
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The table was representative of vegetable food, not this in particular. Maybe you need to read Melamed, Yoel, et al. "The plant component of an Acheulian diet at Gesher Benot Ya ‘aqov, Israel." Proceedings of the National Academy of Sciences113.51 (2016): 14674-14679.

You don't need to argue it though, my second point about eating exclusively meat also stands.
OK well, I only see circumstantial evidence of plants in rock layers. No smoking guns, no evidence of plants in hominid's stomach or gut. I think this kind of archaeology is bad science. Also I do not believe carbon dating fossils to be correct, I believe more in the controversial Mud Fossil research.
 

Travis

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Ok and I did get a good laugh at some of this:

Me to RP...
Is Ray Peat aware that a decrease of DHA (22∶6ω−3) without a corresponding increase of osbond acid (22∶5ω−6) has ostensibly never been observed in a mammalian brain? The sum of these two long-chained polyunsaturated fatty acids—one being ω−3 and the other omega minus six—always adds up to between ~13–16%. If anyone doesn't believe me, just try to prove me wrong.

If you accept this as an incontrovertible fact of life, or even a hypothetical one, which would you rather have in your brain?
 
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