Peat Wrong About Omega 3? DHA & EPA increase dopamine and lower serotonin

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Animal studies identify many effects of PUFAs in the dopamine system. Dietary deficiency of omega-3 PUFAs lowers levels of dopamine (de la Presa Owens and Innis, 1999), D2 receptors, D2 receptor mRNA and dopaminergic presynaptic vesicles (Zimmer et al., 2000a), and increases breakdown of dopamine (Zimmer et al., 1998), in the prefrontal cortex. Omega-3 PUFA deficiency also results in decreased tyrosine hydroxylase (Kuperstein et al., 2008), the rate-limiting enzyme in dopamine synthesis and the main target of prolactin feedback regulation of dopamine (Arbogast and Voogt, 1991), and fewer detectable dopaminergic neurons in the substantia nigra and ventral tegmentum (Ahmad et al., 2008), but higher dopamine levels, D2 receptor mRNA, D2 receptors, and less release and breakdown of dopamine in the nucleus accumbens (Zimmer et al., 2000b). Maternal omega-3 PUFA deficiency results in elevated post-natal expression of dopamine receptor genes in rat pups (Kuperstein et al., 2005). Dietary supplementation with omega-3 fatty acids increases dopamine levels and D2 receptor binding, and lowers monoamine oxidase B (MAO-B) activity in the prefrontal cortex and D2 receptor binding in the striatum (Chalon et al., 1998).


EPA levels within the brain are low in comparison to that of DHA, but this fatty acid also plays an important neuroactive role and may have benefits over DHA in treating Parkinson’s disease. Firstly, EPA is a natural precursor to the synthesis of DHA and also blocks the production of an enzyme called PLA2, which releases DHA from cell membranes. By blocking this enzyme, EPA therefore helps to maintain cell membrane integrity within the brain. EPA is also a potent anti-inflammatory, and, unlike DHA, can directly inhibit the production of inflammatory products from the omega-6 arachidonic acid, which themselves are known to contribute to the progression of Parkinson’s. EPA, again preferentially over DHA, is also involved in myelinogenesis by stimulating the production of several myelin proteins which are thought to be key to the inhibition of loss of myelin and therefore brain atrophy. More recently, EPA has been suggested to regulate dopamine turnover and down-regulate genes involved in neuronal cell death pathways, thus further supporting a beneficial role for ethyl-EPA supplementation as both a preventative and therapeutic tool in neurodegenerative diseases.
 
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DonLore

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But what kind of dosages are we talking about? If you eat eggs and shellfish we get DHA and EPA, is there any evidence we need multiple grams per day?
 

AnonE

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Bump for interest:) I don't seek out any "essential" foods but I do try and avoid all manner of PUFA.
 

Spartan300

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Interesting. I've noticed a decline in mood & what are likely serotonin/dopmine ratio issues since avoiding PUFA for the last 4 years
 

rei

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Omega-3 decreases D1 and D2 receptors expression in the prefrontal cortex​


You can arrive at any headline depending on how you design your study. Here they found omega3 to be so potent at demotivating you that it can be used to break amphetamine addiction.

Omega 3 deficiency (only) exists in a context of omega6 excess. This has been known and is fairly universally agreed on. What Peat says is that both are toxic, and omega3 should at most be considered as a medicine against omega6 toxicity, with it's own adverse effects.
 
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RenaissanceMan
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Omega-3 decreases D1 and D2 receptors expression in the prefrontal cortex​


You can arrive at any headline depending on how you design your study. Here they found omega3 to be so potent at demotivating you that it can be used to break amphetamine addiction.

Omega 3 deficiency (only) exists in a context of omega6 excess. This has been known and is fairly universally agreed on. What Peat says is that both are toxic, and omega3 should at most be considered as a medicine against omega6 toxicity, with it's own adverse effects.
That study used a crazy megadose (3g/kg). That would be the equivalent of 204 grams of fish oil for a 150 lb. human.

In typical doses we often see clearer outcomes that signify a therapeutic effect.

For instance, this study shows that mice fed DHA/EPA abundant diets exert shorter immobility times in the forced swim test (FST) than mice fed a control diet, signifying lower serotonin levels than the control group.

This study on the role of omega-3s in dopaminergic pathways states that baseline prolactin is negatively correlated with omega-3 PUFAs. "The robust relationship of omega-3 PUFAs with dopaminergic but not serotonergic indices suggests that omega-6:eek:mega-3 balance may impact depression pathophysiology through effects on the dopaminergic system."

Still, breaking an addiction (in the study you linked) is a good sign, perhaps the body recognized an imbalance and utilized the omega-3 intake to adjust receptors accordingly.

Your study also said the fish oil "prevented AMPH-induced oxidative damages in the prefrontal cortex" which is another beneficial outcome.

If Peat is right about n-3 being toxic then why do the brain and retina utilize them for development and healing?

A low omega-3 diet also induces ADHD-like symptoms in rats and humans by decreasing dopamine.

1628525305308.png


Also this is slightly unrelated, but for anyone dealing with hair loss, omega-3s inhibit COX-2 and EPA specifically has been noted to suppress PGD2 (thought to be one of the drivers of baldness) in mast cells (immune cells) by competing with arachidonic acid at the COX enzymes and has been noted to suppress PGD2 elsewhere in macrophages.

I think if we all open our minds, we'll eventually accept that DHA and EPA are in fact Peaty (higher dopamine, lower serotonin, COX-2 inhibitor, better brain function).
 

Risingfire

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Do nuts have vitamin E? Just because a substance/food has something healthy in this doesn't mean it's overall healthy.
 
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RenaissanceMan
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This study shows that EPA and DHA are protective against harmful bacteria and endotoxin. Credit @rockarolla for posting this in his thread.

"Eicosapentaenoic (EPA) and docosahexaenoic acid (DHA) have antibacterial and inflammation-resolving effects in tuberculosis (TB). However, whether switching to a diet with optimum n-3 EFA intake after the infection has comparable benefits has not been investigated. We aimed to compare the effects of a diet with sufficient n-3 EFA content in an acceptable n-6/n-3 PUFA ratio for rodents ((n-3)eFAS group) with those on the same diet supplemented with EPA and DHA (EPA/DHA group) in Mycobacterium tuberculosis (Mtb)-infected C3HeB/FeJ mice with a low n-3 PUFA status.

These are the first findings that indicate that EPA/DHA supplementation provides benefits superior to a diet with sufficient n-3 EFAs concerning bacterial killing, weight gain and lung inflammation resolution in Mtb-infected mice with a low n-3 PUFA status.

Therefore, EPA and DHA may be worth considering as adjunct TB treatment."

 

Beastmode

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Interesting. I've noticed a decline in mood & what are likely serotonin/dopmine ratio issues since avoiding PUFA for the last 4 years

Our identities are shaped by early experiences in life and if much of that were driven by a stressful environment (inside our bodies and out,) the new "context" of how we might see the world, hence after getting our metabolic system right, I imagine there can be quite an adjustment.

Personally I got married and had a kid within the first year of "dialing in" my nutrition, lifeystyle, etc. It was a major shift away from my lifestyle before this. It definitely took some adjusting for sure.

Curious if the first part might align with your journey thus far?
 

rei

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That study used a crazy megadose (3g/kg). That would be the equivalent of 204 grams of fish oil for a 150 lb. human.

In typical doses we often see clearer outcomes that signify a therapeutic effect.

For instance, this study shows that mice fed DHA/EPA abundant diets exert shorter immobility times in the forced swim test (FST) than mice fed a control diet, signifying lower serotonin levels than the control group.

This study on the role of omega-3s in dopaminergic pathways states that baseline prolactin is negatively correlated with omega-3 PUFAs. "The robust relationship of omega-3 PUFAs with dopaminergic but not serotonergic indices suggests that omega-6:eek:mega-3 balance may impact depression pathophysiology through effects on the dopaminergic system."

Still, breaking an addiction (in the study you linked) is a good sign, perhaps the body recognized an imbalance and utilized the omega-3 intake to adjust receptors accordingly.

Your study also said the fish oil "prevented AMPH-induced oxidative damages in the prefrontal cortex" which is another beneficial outcome.

If Peat is right about n-3 being toxic then why do the brain and retina utilize them for development and healing?

A low omega-3 diet also induces ADHD-like symptoms in rats and humans by decreasing dopamine.

View attachment 26378

Also this is slightly unrelated, but for anyone dealing with hair loss, omega-3s inhibit COX-2 and EPA specifically has been noted to suppress PGD2 (thought to be one of the drivers of baldness) in mast cells (immune cells) by competing with arachidonic acid at the COX enzymes and has been noted to suppress PGD2 elsewhere in macrophages.

I think if we all open our minds, we'll eventually accept that DHA and EPA are in fact Peaty (higher dopamine, lower serotonin, COX-2 inhibitor, better brain function).
In the same way as ethanol is known to be an antidote to methanol poisoning. Perhaps the better alternative is to limit methanol intake so that continuous ethanol is not needed...
 

cedric

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According to recent mitochondrial congress omega-3 is needed to introduce thyroid hormone to the brain. If somene has low antioxidants level brain thyroid doesn't work. First improve antioxidant status then thyroid hormones plus omega -3 will work.
If you are iron-toxic don/t exegerate with omega-3 or thyroid hormones. That way Peaty and anti-Peaty could meet halfway.
 
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RenaissanceMan
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Um, no, it wouldn't. It would be more like 37g of Fish Oil. You need to learn about Human Equivalent Doses.
That's still a ***t ton of fish oil regardless. Practically no one is taking such a high amount on a daily basis.
 

Missenger

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Wouldn't it be safer just to skip on the fish oil and limit omega 6 spikes with a balanced pufa protein source like cheese or raw-ish dairy or something and supplement with non-overcooked fish accordingly? Fish oil makes amyloid-beta precursor protein which just builds up to the development of amyloid plaque.

 
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Kvothe

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Wouldn't it be safer just to skip on the fish oil and limit omega 6 spikes with a balanced pufa protein source like cheese or raw-ish dairy or something and supplement with non-overcooked fish accordingly? Fish oil makes amyloid-beta precursor protein which just builds up to the development of amyloid plaque.


I just love how these reductionist junk studies are dug up again and again. The simple and elegant experiments are clear - feed animals a lot of omega-3 and they die earlier than everyone else. Omega-3 fats are much more toxic than omega-6. I'd rather fry my potatoes in corn oil than fish oil.
It seems like someone has been reading too much of the late Travis' stupid arguments on omega-3. Next it will be claimed that omega-3 deficiency is the cause for Zellweger's disease :banghead:
 
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Angel45

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Interesting. I've noticed a decline in mood & what are likely serotonin/dopmine ratio issues since avoiding PUFA for the last 4 years
Do you eat eggs and fish. I stay away from the seed oils and keep my eggs and fish in.
 

PaRa

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this study on RATS found that omega 3 are pro thyroid and pro thermogenesis

 

yourke

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this study on RATS found that omega 3 are pro thyroid and pro thermogenesis

Hi, some additional studies that show that fish oils are not that great (other than stopping the omega 6.

When DHA is incorporated into the mitochondria, it decreases enzymatic activities compared to 18:2, omega-6https://raypeatforum.com/community/#_edn1. This feature of reduced function of mitochondria is often observed when there is an accumulation of unsaturated fats in the mitochondria[ii].


Compared to olive oil (monounsaturated), fish oils will reduce Co2 production and thermogenesis[iii][iv]. Mitochondria enzymes are reduced with fish oil compared to safflower[v]. Compared to soy oil, fish oil decreases metabolic heat in organisms[vi].

Compared to the omega-6 rich corn oil, fish oil oxygen consumption is reduced via reduced cytochrome C[vii], and compared to coconut oil, the TTC mitochondrial tricarboxylate carrier is reduced on fish oils[viii], as is seen in hypothyroidism[ix] and starvation[x].

Fish oil is known to reduce heart rate[xi][xii] and is associated with lower body temperature[xiii].



https://raypeatforum.com/community/#_ednref1 Sullivan EM, Pennington ER, Sparagna GC, et al. Docosahexaenoic acid lowers cardiac mitochondrial enzyme activity by replacing linoleic acid in the phospholipidome. J Biol Chem. 2018;293(2):466–483. doi:10.1074/jbc.M117.812834
[ii]Figueroa-García MdC, Espinosa-García MT, Martinez-Montes F, Palomar-Morales M, Mejía-Zepeda R (2015) Even a Chronic Mild Hyperglycemia Affects Membrane Fluidity and Lipoperoxidation in Placental Mitochondria in Wistar Rats. PLoS ONE 10(12): e0143778. https://doi.org/10.1371/journal.pone.0143778
[iii]Müller HL, Kirchgessner M. Thermogenese und Energieverwertung bei Verabreichung von Olivenöl und Fischöl im Modellversuch an Sauen [Thermogenesis and energy utilization of olive oil and fish oil in a model study with sows]. Z Ernahrungswiss. 1995;34(2):143–150. doi:10.1007/bf01636948
[iv] Kirchgessner M, Müller HL. Thermogenese im Bereich der Uberernährung bei Verabreichung von Olivenöl und Fischöl im Modellversuch an Sauen [Thermogenesis in overfeeding with administration of olive oil and fish oil in a swine model study]. Z Ernahrungswiss. 1995;34(3):206–213. doi:10.1007/bf01623159
[v]Mohan PF, Phillips FC, Cleary MP. Metabolic effects of coconut, safflower, or menhaden oil feeding in lean and obese Zucker rats. Br J Nutr. 1991;66(2):285–299. doi:10.1079/bjn19910032
[vi] Kargar S, Ghorbani GR, Fievez V, Schingoethe DJ. Performance, bioenergetic status, and indicators of oxidative stress of environmentally heat-loaded Holstein cows in response to diets inducing milk fat depression. J Dairy Sci. 2015;98(7):4772–4784. doi:10.3168/jds.2014-9100
[vii] Yamaoka S, Urade R, Kito M. Mitochondrial function in rats is affected by modification of membrane phospholipids with dietary sardine oil. J Nutr. 1988;118(3):290–296. doi:10.1093/jn/118.3.290
[viii] Giudetti AM, Sabetta S, di Summa R, et al. Differential effects of coconut oil- and fish oil-enriched diets on tricarboxylate carrier in rat liver mitochondria. J Lipid Res. 2003;44(11):2135–2141. doi:10.1194/jlr.M300237-JLR200
[ix]Siculella L, Sabetta S, Giudetti AM, Gnoni GV. Hypothyroidism reduces tricarboxylate carrier activity and expression in rat liver mitochondria by reducing nuclear transcription rate and splicing efficiency. J Biol Chem. 2006;281(28):19072–19080. doi:10.1074/jbc.M507237200
[x]Zara V, Gnoni GV. Effect of starvation on the activity of the mitochondrial tricarboxylate carrier. Biochim Biophys Acta. 1995;1239(1):33–38. doi:10.1016/0005-2736(95)00125-m
[xi] Peoples, Gregory & Mclennan, Peter & Howe, Peter & Groeller, Herbert. (2008). Fish Oil Reduces Heart Rate and Oxygen Consumption During Exercise. Journal of cardiovascular pharmacology. 52. 540-7. 10.1097/FJC.0b013e3181911913
[xii] Kang JX. Reduction of heart rate by omega-3 fatty acids and the potential underlying mechanisms. Front Physiol. 2012;3:416. Published 2012 Oct 30. doi:10.3389/fphys.2012.00416
[xiii]Berger MM, Tappy L, Revelly JP, et al. Fish oil after abdominal aorta aneurysm surgery [published correction appears in Eur J Clin Nutr. 2009 Feb;63(2):302]. Eur J Clin Nutr. 2008;62(9):1116–1122. doi:10.1038/sj.ejcn.1602817
 
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