4 replies to this topic

[brosci]

Is there an ideal approach to timing glycine for minimizing the negatives associated with methionine / homocysteine and maximize the benefits (like glutathione synthesis) ?

 

I found this chart:

 

It looks like methionine peaks about 4 hours after dinner and glycine peaks about 30 minutes after ingestion.  If there's an ideal place for consuming glycine in the day, would it be with meals, 2-3 hours after a meal, or before bed?  (Or, maybe it doesn't make much of a difference?)

 

[platypus]

Before bed since it is a good sleep-aid. Everyone needs deep restful sleep. 

[Darryl]

I personally take ~6 g before bed, as sweetener in herbal tea.

 

While the sleep benefit figures, I'm also avoiding coingesting glycine with the niacin and salicyate I take 2x daily, which I hope are having synergistic effects in the NAD+, Sirt1, TRPV1, and AMPK pathways. Both are excreted via glycine conjugation, and in fact one can reduce niacin flushing and increase half-life with coingestion.

[brosci]

Would taurine synergistically pair well with glycine, or do they compete?  I've read taurine is a sleep aid as well.

 

I'm currently taking 2g of beta-alanine in the mornings, where I've read that it depletes taurine and competes with taurine for absorption (raising free taurine which might increase angiogenesis, which might have negative effects?)  Does it make sense to do ~1.5g beta-alanine in the morning, 0.5g taurine with dinner, and 4g glycine before bed?  (Long term, could this negatively affect GABA?)

[zorba990]

Taurine bbb transport mechanism is not yet classified
http://www.ncbi.nlm....pubmed/12437590
bstractSend to:
J Neurochem. 2002 Dec;83(5):1188-95.
Regulation of taurine transport at the blood-brain barrier by tumor necrosis factor-alpha, taurine and hypertonicity.
Kang YS1, Ohtsuki S, Takanaga H, Tomi M, Hosoya K, Terasaki T.
Author information
Abstract
Taurine is the abundant sulfur-containing beta-amino acid in brain where it exerts a neuroprotective effect. Although it is known that the blood-brain barrier (BBB) mediates taurine transport, the regulation of taurine transport have not been clarified yet. A conditionally immortalized rat brain capillary endothelial cells (TR-BBB13), an in vitro model of the BBB, exhibited [3H]taurine uptake, which was dependent on both Na+ and Cl-, and inhibited by beta-alanine. Taurine transporter (TAUT) mRNA was detected in TR-BBB13 cells, and TAUT protein was also expressed at 70 kDa. TR-BBB13 cells exposed to 20 ng/mL TNF-alpha and under hypertonic conditions showed a 1.7-fold and 3.2-fold increase in [3H]taurine uptake, respectively. In contrast, lipopolysaccharide and diethyl maleate did not significantly affect taurine uptake. The taurine uptake was reduced by pre-treatment with excess taurine (50 mm). The mRNA level of the TAUT in TNF-alpha and following hypertonic treatment was greater than that in control cells, whereas that under excess taurine conditions was lower than in controls. Therefore, taurine transport activity at the BBB appears to be regulated at the transcriptional level by cell damage, osmolality and taurine in the brain.
PMID: 12437590 [PubMed - indexed for MEDLINE]

and


"Small neutral amino acids, such as alanine, glycine, proline and GABA (gamma-aminobutyric acid), are markedly restricted in their entry into the brain. These amino acids are non-essential amino acids and are transported by alanine-preferring or A-type transport protein. The A-type transport protein is not present on the luminal surface of the blood brain barrier. In contrast, these small neutral amino acids appear to be transported out of the brain across the blood-brain-barrier."

from
http://neuroscience..../chapter11.html

Additonally,

"The essential amino acids cannot be synthesized by the brain and, therefore, must be supplied from protein breakdown and diet. Phenylalanine, leucine, tyrosine, isoleucine, valine, tryptophan, methionine and histidine, which are essential amino acids, and also the precursor of dopamine, L-DOPA, enter the brain as rapidly as glucose. These amino acids are transported into the brain by the leucine-preferring or the L-type transport proteins. These compounds compete with each other for entry into the brain. Therefore, an elevation of plasma level of one will inhibit uptake of the others. This competition may be important for certain metabolic diseases such as phenylketonuria (PKU), where high levels of phenylalanine in plasma reduce brain uptake of other essential amino acids. "

Edited by zorba990, 22 August 2015 - 08:37 PM.