Arachidonic acid

[dime]

Can someone explain why are egg yolks more needed by women? All articles/studies point that egg yolks may increase menstrual cramps due to the higher contents of arachidonic acid.

[RRM]

All articles/studies point that egg yolks may increase menstrual cramps due to the higher contents of arachidonic acid.

What studies do so?
Yes, arachidonic acid (AA) is the precursor for PGF2α, a prostaglandin which induces cramping of the smooth muscles in the uterus through the FP receptors.
But through that same pathway it also leads to bronchoconstriction (leading to coughing, wheezing and shortness of breath) and modulates the fluid pressure in the eye.
And thats just one prostaglandin and one receptor.
Prostaglandins are also responsible for smooth muscle relaxation (not just contraction).
And in virtually all cells that have a nucleus, AA is converted (by COX enzymes as required) into many prostaglandins, prostacyclins, thromboxanes and leukotrienes (all eicosanoids).
So that if there would be an increase of AA, there is no way this would selectively lead to uterus cramping.
If any, to a general status of inflammation, as the eicosanoids derived from AA generally promote inflammation.

Also, egg yolks are high in fat, containing relatively little AA (relative to other fats).

veal 6.5% (AA in % of total fat)
horse meat 4.5%
chicken 2.8%
salmon 2.2%
tuna 1.8%
mackerel 1.4%
beef 0.79%
egg yolks 0.66%
lamb meat 0.27%
herring 0.2%

So, if eating of a lot of egg yolks would have to lead to elevated AA levels,
this would have to lead to overal increased levels of AA and other fatty acids and triglycerides first.
And such elevated levels would be stored as adipose fat, or converted into available energy.
There is no way this could selectively lead to elevated AA levels.

Yes, diet does influence serum fatty acid profiles, but even an over 3 fold higher relative AA intake does not cut it.
Helmersson-Karlqvist J.¨Oily fish (salmon) intervention altered fatty acid concentrations but did not affect urinary 15-keto-dihydro-PGF(2α) concentrations in pregnant women. PGF(2α) being the prostaglandin that induces uterus contraction.

Influence of menstrual factors and dietary habits on menstrual pain in adolescence age. Primary dysmenorrhea is very common in young women. The risk factors for this pathology are early menarche, long and heavy menstrual flow, and lower consumption of fish, eggs, and fruit.

[dime]

I must have misread something..

So that if there would be an increase of AA, there is no way this would selectively lead to uterus cramping.
If any, to a general status of inflammation, as the eicosanoids derived from AA generally promote inflammation.

According to wikipedia, AA is not associated with inflammation:

Under normal metabolic conditions, the increased consumption of arachidonic acid is unlikely to increase inflammation. ARA is metabolized to both proinflammatory and anti-inflammatory molecules.[20] Studies giving between 840 mg and 2,000 mg per day to healthy individuals for up to 50 days have shown no increases in inflammation or related metabolic activities.[20][21][22][23] Increased arachidonic acid levels are actually associated with reduced pro-inflammatory IL-6 and IL-1 levels, and increased anti-inflammatory tumor necrosis factor-beta.[24] This may result in a reduction in systemic inflammation.

Arachidonic acid does still play a central role in inflammation related to injury and many diseased states. How it is metabolized in the body dictates its inflammatory or anti-inflammatory activity. Individuals suffering from joint pains or active inflammatory disease may find that increased arachidonic acid consumption exacerbates symptoms, presumably because it is being more readily converted to inflammatory compounds. Likewise, high arachidonic acid consumption is not advised for individuals with a history of inflammatory disease, or who are in compromised health. Of note, while ARA supplementation does not appear to have proinflammatory effects in healthy individuals, it may counter the anti-inflammatory effects of omega-3 fatty acid supplementation.[25]

One egg yolk contains about 75mg AA, so it would be hard to ingest more than the tested 2000mg.

[RRM]

One egg yolk contains about 75mg AA, so it would be hard to ingest more than the tested 2000mg.

But even then, what matters is whether the serum fatty acid profile can be changed towards high in AA.
Besides AA supplementation, this can only happen if the consumed fat has a 'high-AA profile', and egg yolks have a 'low-AA profile' (only 0.66% of total fat)
So, its not possible.

According to wikipedia, AA is not associated with inflammation

So, if the collective characteristic of AA-derived eicosanoids is inflammatory, whereas AA is not associated with inflammation,
then the selective display of a characteristic (uterus cramping) of just one of the AA-derived eicosanoids is even more unlikely to be associated with AA.

[Kasper]

From wikpedia:
"Under normal metabolic conditions, the increased consumption of arachidonic acid is unlikely to increase inflammation. ARA is metabolized to both proinflammatory and anti-inflammatory molecules.[20] Studies giving between 840 mg and 2,000 mg per day to healthy individuals for up to 50 days have shown no increases in inflammation or related metabolic activities.[20][21][22][23] Increased arachidonic acid levels are actually associated with reduced pro-inflammatory IL-6 and IL-1 levels, and increased anti-inflammatory tumor necrosis factor-beta.[24] This may result in a reduction in systemic inflammation.
Arachidonic acid does still play a central role in inflammation related to injury and many diseased states. How it is metabolized in the body dictates its inflammatory or anti-inflammatory activity. Individuals suffering from joint pains or active inflammatory disease may find that increased arachidonic acid consumption exacerbates symptoms, presumably because it is being more readily converted to inflammatory compounds. Likewise, high arachidonic acid consumption is not advised for individuals with a history of inflammatory disease, or who are in compromised health. Of note, while ARA supplementation does not appear to have proinflammatory effects in healthy individuals, it may counter the anti-inflammatory effects of omega-3 fatty acid supplementation.[25]"

Alot of pathogens seem to ride on the AA release flow. And this is indeed the problem. More on this later. If there is nothing to activate it, there will be no problems. However, it might be easier to prevent the heavy inflammation reaction caused by too much AA.

Two hypothesis I've read:

Inflammation is not bad if it is acute, but only chronic inflammation causes health problems

Inflamation stimuli --> Phospholipase A --> AA released --> acute inflammation --> no anti-inflammation message --> chronic inflammation
versus
Inflamation stimuli --> Phospholipase A --> AA released --> acute inflammation --> cortisol stimulates lipocortin and vasocortin --> inflammation stops

I doubt that omega-6 consumption causes problems because it is directly converted to those pro-inflammatory prostaglandins.
I do that think that omega-6 consumption can cause problems, but I think this because of factors such as:
1. lipid peroxidation
2. omega3/omega6 ratio
etc.

AA causes no problems, it is about a (too) high AA/EPA blood ratio

Depression scale:


Interesting is that AA/EPA ratio is already much higher than normal in the beginning.
Is this because all depressed people eat very much omega 6 and very little omega 3 ?
I actually doubt that this is the only factor, I think that other factors signal the body to make (too much) AA.

[overkees]

Dietary LCPUFAs highly inhibit delta 6 desaturase (in mice) and therefore inhibit AA generation Raz M, et al.
Pro inflammatory reduction might be important, as the body is attacking itself when AA eicosanoids are too high.

[RRM]

The response of the body with AA eicosanoids is not the problem. Thats part of our defense.
Its not like these eicosanoids are out of control; they are subject to feedback mechanisms.