But okay, it sounds fair enough. No fatty fish for me until we find out how and when exactly the mead acids begins to form.
I would go for a diet sufficient high in EPA. But I'm also very interested in what your experiment will lead to.
Here is what I think will happen if you are going to lower EPA drastically (note this is speculation):
After some time, your body is going to signal that your body is low in EPA.
Then you're body is going to increase delta-5 saturase activity (so it can produce EPA).
Delta-5 saturase prefers n-3 above n-6 above n-9. In the beginning the body will try to convert n-3 to EPA.
If you limit n-3 in your diet, D5D will fail to convert n-3 to EPA. Instead it will convert DGLA to AA.
So, an
increase in AA and a
decrease in DLGA.
As we've seen in one study, if there is much n-9 available, not only n-6 will be converted, but also some n-9.
D5D prefers n-6 above n-9, so this will only be a little bit n-9.
This process will go on, until most of your n-6 are converted to AA.
If you are able to drastically lower your omega-6, after a while there is almost no n-6 left for D5D.
Then, while your body is very low DGLA and EPA, there will be some bright side.
D5D will produce mead acid in very high amounts, and AA will slowly get removed from your membranes.
If you really want to have high mead acid in your membranes, I think you should do close the same thing they did in those experiments.
Really cut down your omega 3 and omega 6 to close to 0% of your calories.
You will get low AA, very low DGLA, very low EPA, and high mead acid in your membranes.
I very much doubt how healthy this is.
I agree that low AA is something desirable. But I think it is better to go for another strategy, inhibit D5D activity (naturally) by eating sufficient EPA (and maybe other stategies).
This will make sure AA will slowly get replaced by DGLA and EPA.
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But I've a little bit AA overdose at this moment. I'm studying how uric acid can cause inflammation at the moment:
"Purine metabolism is an aspect of intrigue in biology. Lower species, such as microbes, process it to the end product of ammonia. Through evolution, its metabolism becomes less and less complete. In mammals, uric acid is processed to become allantoin and uricase expression is confined to peroxisomes in hepatocytes. However, in primates, a silent mutation has eliminated the uricase function, and gout ensues. It has been an interesting discussion as to why such a loss of function was necessary at the expense of a major disease and possibly cardiovascular complications. Two hypotheses have been put forward. One proposal is that loss of uric acid degradation sustains serum salt levels and sufficiently high blood pressure in low salt environments (18). The other, more blithe, idea is that uric acid targets purine receptors in the cerebral cortex in ways similar to caffeine, rendering primates more mentally alert and intellectuals more prone to gouty arthritis (the disease of distinction) (19, 20). In light of the work of Kono et al. (5), we have gained experimental evidence that evolution may have had an additional incentive for eliminating the ability to degrade uric acid. In conjunction with a urate anion exchange regulator in the kidney (21), elevated uric acid levels push to the edge of precipitation. As such, any cell death or tissue insult can immediately raise levels above those required for precipitation (70 μg/ml), thereby bringing into the picture a powerful trigger of inflammation, MSU crystals. By lacking the ability to degrade uric acid, the primate host therefore becomes more efficient at monitoring cellular stress. In large-scale injury and trauma, as well as other situations where inflammation is collectively beneficial to the host, high uric acid could have been a substantial survival advantage (22). If future research supports such reasoning, it is expected that uric acid will be found to participate in sterile inflammation in additional contexts and that it will present the promise of a therapeutic target."
In short, the uric acid balance seems like this:
Low uric acid (MS) << Normal uric acid << High uric acid (Gout)
"One clinical observation that may speak to uric acid’s antioxidative effect is the near absence of multiple sclerosis (MS) in gout patients [5]."
'Another theory, first proposed in the 1950s, suggests that uric acid is structural homolog of caffeine (which in turn is a structural homolog of adenosine), and that high uric acid levels promoted mental alertness for primates and contributed to the development of human intelligence [8]. This hypothesis has been increasingly supported by experimental observations, although its role in evolution remains to be confirmed."
). I think we all want to look for what is optimal, right?
