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Previously having tried dietary tryptophan depletion combined with high dose BCAAs to inhibit LNAA dependent transport (used in Acute Tryptophan depletion), and having personally found this transient deprivation not to have any major detrimental effects, I decided to revisit this in light of Phair's hypotheisis, but with an incremental reintroduction of tryptophan intake, so not to re-saturate IDO1.
Initially TRP depletion was tried based on the notion that Indoleamine dioxygenase activity could by hyper-activated in ME secondary to Th1 cytokine elevation with an increased production of the neurotoxic NMDA-r ligand quinolinic acid. A prior beneficial response to NMDA-r antagonist memantine and neuroprotective drugs (pregabalin, Flupirtine) for CNS symptoms, but without any appreciable effect on physical endurance supported this notion.
Protocol consisted of the following, but is not based on any specific published protocol:
3 days of dietary tryptophan depletion through consumption of only:
1) dextrose
2) omega oils
3) All essential amino acids (except for Tryptophan)
4) multivitamin and minerals
14-10-18
2 days of tryptophan reintroduction (so far, as of 14-10-18), with TRP exposure on day 1 and 2 @ 25mg 3x daily. (NB. the approximate recommended daily TRP intake appears to be around 200-350 mgs for an approx. 80kg adult). I will update on changes/no changes in coming days.
DISCLAIMER: I do not endorse any one trying this themselves. Typtophan is a dietary essential amino acid and this will deplete serotonin and melatonin. I was only comfortable trying this as I had tried this before with no major adverse effects and it was important to ensure I had not missed a potential benefit.
15-10-18
Titrating TRP intake to 50mgs twice daily (100mgs/D) today.
Aiming to resume a normal (carbohydrates, fats) but relatively low protein diet soon after for some days after. Of course at this point TRP intake cannot further be carefully incremented.
Initially TRP depletion was tried based on the notion that Indoleamine dioxygenase activity could by hyper-activated in ME secondary to Th1 cytokine elevation with an increased production of the neurotoxic NMDA-r ligand quinolinic acid. A prior beneficial response to NMDA-r antagonist memantine and neuroprotective drugs (pregabalin, Flupirtine) for CNS symptoms, but without any appreciable effect on physical endurance supported this notion.
Protocol consisted of the following, but is not based on any specific published protocol:
3 days of dietary tryptophan depletion through consumption of only:
1) dextrose
2) omega oils
3) All essential amino acids (except for Tryptophan)
4) multivitamin and minerals
14-10-18
2 days of tryptophan reintroduction (so far, as of 14-10-18), with TRP exposure on day 1 and 2 @ 25mg 3x daily. (NB. the approximate recommended daily TRP intake appears to be around 200-350 mgs for an approx. 80kg adult). I will update on changes/no changes in coming days.
DISCLAIMER: I do not endorse any one trying this themselves. Typtophan is a dietary essential amino acid and this will deplete serotonin and melatonin. I was only comfortable trying this as I had tried this before with no major adverse effects and it was important to ensure I had not missed a potential benefit.
15-10-18
Titrating TRP intake to 50mgs twice daily (100mgs/D) today.
Aiming to resume a normal (carbohydrates, fats) but relatively low protein diet soon after for some days after. Of course at this point TRP intake cannot further be carefully incremented.
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