We know BCAAs rapidly deplete neurotransmitters. Obviously this should cause significant cognitive issues; many report sluggishness, reduced hedonic tone etc.
I'm wondering if ordinary protein shakes have the same effect. They have large doses of the BCAAs...they have the remaining aminos but perhaps the BCAAS are dominant and are depleting catchefolamines? This would be a huge warning to anyone who uses whey (like I do).
Many here say that you can't take things like tyrosine, you'll develop tolerance. Not really sure what that means in "standard" doses like one gets from food.
Perhaps the solution is to time one's Aminos? Kick the day off with low doses of the neurotransmitter precursors, then go for the complete proteins later on?
Musings but serious food for thought, please everyone jump in.
Protein shakes like Whey don't break down into only free amino acids. They also break down into peptides. Peptides are absorbed so the effect will be less than straight BCAAs.
You want the peptides because they do other things for you.
BCAAs simply block the brain transport system that tyrosine uses to pass the BBB as a dopamine precursor.
So work on the timing an things will go better. e.g. Tyrosine on empty stomach first thing AM and wait at least 2 hours before any BCAAs.
A normal system will increase dopamine from this. If that is what you really want. YMMV IANAD.
Read up on LNAA transport system. You can see that manipulating it can even be used in disease states like :
phenylketonuria
https://www.ncbi.nlm...cles/PMC408272/
"Large neutral amino acids (LNAAs), including phenylalanine (Phe), compete for transport across the blood-brain barrier (BBB) via the l-type amino acid carrier. Accordingly, elevated plasma Phe impairs brain uptake of other LNAAs in patients with phenylketonuria (PKU). Direct effects of elevated brain Phe and depleted LNAAs are probably major causes for disturbed brain development and function in PKU. Competition for the carrier might conversely be put to use to lower Phe influx when the plasma concentrations of all other LNAAs are increased. This hypothesis was tested by measuring brain Phe in patients with PKU by quantitative 1H magnetic resonance spectroscopy during an oral Phe challenge with and without additional supplementation with all other LNAAs. Baseline plasma Phe was ∼1,000 μmol/l and brain Phe was ∼250 μmol/l in both series. Without LNAA supplementation, brain Phe increased to ∼400 μmol/l after the oral Phe load. Electroencephalogram (EEG) spectral analysis revealed acutely disturbed brain activity. With concurrent LNAA supplementation, Phe influx was completely blocked and there was no slowing of EEG activity. These results are relevant for further characterization of the LNAA carrier and of the pathophysiology underlying brain dysfunction in PKU and for treatment of patients with PKU, as brain function might be improved by continued LNAA supplementation."
