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@haidut regarding the study you posted, and the high intake of methionine,
I recently emailed Ray to discuss the inflammatory amino acids. One thing I asked him was if being in a hypermetabolic state makes the inflammatory amino acids less harmful or more likely to take their alternate conversation pathway.
For example under stress tryptophan converts into serotonin, but as Ray has mentioned calcium (due to its pro-metabolic effects) helps skew the tryptophan in favor of the niacin pathway for better glucose oxidation and metabolism.
Cysteine and methionine are also needed to make taurine which you have posted many studies showing the benefits on.
I believe methionine and cysteine also can be converted into other things like glutathione and a couple others but I can't quite remember.
Do you believe that the low intake of PUFA and iron / heavy metals for example offered protection from what would have been very harmful doses of methionine or inflammatory amino acids? Due to their hypermetabolic state? I know the study was rodents but still it would be interesting to know your take on this,
It sounds as though the inflammatory amino acids may only be an issue for hypometabolic individuals?
This was Ray's response and he also linked studies showing that estrogen is likely to skew amino acid metabolism either in favor of stress adaptation pathway, or beneficial hypermetabolic pathway.
Re: Discussions on inflammatory amino acids and protein intake
Ray: I think of taurine as the result of the protective decomposition of cysteine, analogous to the conversion of glutamate to GABA.
I think that good functioning of the metabolism protects against cysteine and tryptophan; for example, a vitamin B6 deficiency or estrogen excess increases their toxicity, causing lower niacinamide and taurine, higher serotonin. I regularly eat eggs, including yolks which are rich in essential nutrients, though they don’t have taurine.
Am J Physiol Gastrointest Liver Physiol. 2015 Feb 15;308(4):G277-86.
Estradiol decreases taurine level by reducing cysteine sulfinic acid
decarboxylase via the estrogen receptor-α in female mice liver.
Ma Q(1), Zhao J(1), Cao W(1), Liu J(1), Cui S(2).
(1)State Key Laboratory of Agrobiotechnology, College of Biological Sciences,
China Agricultural University, Beijing, People's Republic of China.
(2)State Key Laboratory of Agrobiotechnology, College of Biological Sciences,
China Agricultural University, Beijing, People's Republic of China
[email protected].
Cysteine sulfinic acid decarboxylase (CSAD) and cysteine dioxygenase (CDO) are
two rate-limiting enzymes in taurine de novo synthesis, and their expressions are
associated with estrogen concentration. The present study was designed to
determine the relationship between 17β-estradiol (E₂) and taurine in female mice
liver. We initially observed the mice had lower levels of CSAD, CDO, and taurine
during estrus than diestrus. We then, respectively, treated the ovariectomized
mice, the cultured hepatocytes, and Hep G2 cells with different doses of E₂, and
the CSAD and CDO expressions and taurine levels were analyzed. The results showed
that E₂ decreased taurine level in the serum and the cultured cells by inhibiting
CSAD and CDO expressions. Furthermore, we identified the molecular receptor types
through which E₂plays its role in regulating taurine synthesis, and our results
showed that estrogen receptor-α (ERα) expression was much higher than estrogen
receptor-β (ERβ) in the liver and hepatocytes, and the inhibiting effects of E₂
on CSAD, CDO, and taurine level were partially abrogated in the
ICI-182,780-pretreated liver and hepatocytes, and in ERα knockout mice. These
results indicate that estradiol decreases taurine content by reducing taurine
biosynthetic enzyme expression in mice liver.
J Biomed Sci. 2010; 17(Suppl 1): S1.
Role of taurine in the central nervous system
Jang-Yen Wu1 and Howard Prentice1