3 replies to this topic

[J. Galt]

Neurochem Res. 1978 Dec;3(6):763-73.
d-Amphetamine binding to brain lipid.
Goldberg MA, Todoroff T.
Abstract
The interaction of d-amphetamine with several brain tissue components has been investigated. A brain lipid extract and a number of individual phospholipids were found to bind d-amphetamine when measured by means of a hexane-buffer partition coefficient technique. Phosphatidylserine showed the greatest binding and phosphatidylethanolamine and dipalmitoyllecithin were also effective. Phospholipid binding of d-amphetamine was shown to be related to fatty acid composition. Cholesterol and ganglioside did not bind. It is suggested that phospholipid binding of d-amphetamine may play a role in the pharmacological action of this drug.
PMID: 33345 [PubMed - indexed for MEDLINE]

I came across this abstract on PubMed recently and am a bit worried. I have ADHD and mild dyslexia and Adderall daily along with 100-300mg PS. The PS has noticeably improved my memory over the past few months, and it also helps my cortisol levels while on Adderall.

Unfortunately I lack the background to properly interpret this abstract and am hoping that someone can shed light on this.

As I understand it, Adderall is about 75% dextroamphetamine. Is d-amp's high affinity for PS binding a bad thing, particularly in regards to amphetamine neurotoxicity, tolerance, and neurotransmitter depletion/downregulation?

Any insight would be greatly appreciated. Curious hear what you guys think.

[chrono]

Is d-amp's high affinity for PS binding a bad thing, particularly in regards to amphetamine neurotoxicity, tolerance, and neurotransmitter depletion/downregulation?

A good question, but I'm not sure there's much possibility of a helpful answer. The paper you posted is apparently the only research concerning this property, and it's 30 years old. It suggests that endogenous PS may play a role in its MOA, but doesn't really speculate on how; perhaps it plays some role in AMP's uptake into neurons?

But I think it would be even harder to predict how supplemental PS might impact the functioning of AMP. The extra PS in neurons might increase its uptake (and thus function), or the increased systemic PS might bind prematurely and inhibit its uptake into the brain or neurons.

I'm not entirely sure if PS enhances NMDA function appreciably, and thus might cause some concern for the same reason as piracetam. This paper suggests it enhances synaptic transmission generally, and seems to discuss NMDA in particular in the full text:

Phosphatidylserine increases hippocampal synaptic efficacy.
Borghese CM, Gómez RA, Ramírez OA.

In the present study, the effects of phosphatidylserine (BC-PS) on hippocampal synaptic transmission were evaluated. Extracellular potentials evoked by low-frequency stimulation (0.2 Hz) of the perforant path (PP) were recorded from the granule cell layer of the dentate gyrus in 400 microns hippocampal slices. Slices were perfused with either BC-PS alone (10 microM) or BC-PS in combination with DL-2-amino-5-phosphonovaleric acid (APV, 20 microM), or after previous perfusion with dizocilpine (MK-801, 10 microM). BC-PS significantly potentiated PP-evoked responses (mean percent increase +/- SEM, 108 +/- 18%), an effect that was blocked by perfusion of MK-801, but not APV. The increase in hippocampal synaptic efficacy produced by BC-PS is discussed in terms of N-methyl-D-aspartate receptors (NMDA) and the associated channels.

PMID: 8100181 [PubMed - indexed for MEDLINE]

[luv2increase]

I'm really sorry OP, but I don't see anything dangerous at all with the combination of adderall and PS in that study you posted.

[J. Galt]

Thanks for the thoughtful replies.