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[agwoodliffe]

About 4 years ago, I got the NutrEval test from Genova diagnostics, including the urinary Amino Acids profile. One of the most notable things it showed was a high amount of both Cystathionine and Cysteine, yet low Cystine in the urine. I naturally assumed this meant a hyperactive trans-sulfuration activity.

Recently, after reading about the positive effects of N-Acetylcysteine on OCD-like behaviours, I thought what the hell. I was amazed to find that it has had a significantly positive effect on me, quite contrary to what I had expected. I therefore assume that there had in fact been an excessive draining in the Cysteine pathway.

Does anyone have any idea why this phenomena might occur?

[mrd1]

There is an abundance of literature implicating glutamatergic abnormalities in addiction.47,48 More recently, data are emerging suggesting a role of oxidative stress in the pathophysiology of addiction to drugs of abuse.32,49–51 Research has explored the modulation of glutamatergic pathways by NAC in pre-clinical models.52,53 N-acetylcysteine has been shown to reverse the decline in cystine–glutamate exchange through the cystine–glutamate antiporter and thereby assist in the restoration of glutamatergic pathways in addiction.32,52 These properties have made it a potential prospect for the treatment of addiction.

In addition to modulating glutamate levels through the cystine–glutamate antiporter, NAC has also been shown to alter DA release. Following amphetamine treatment to rat striatal slices, NAC has been shown to facilitate vesicular DA release at low doses in striatal neurons and inhibit release at millimolar concentrations.29 In monkeys, NAC has been shown to protect against reductions in DA transporter levels following repeated methamphetamine administration,30 suggesting one mechanism whereby increased DA release was facilitated in the previous study. Glutathione has also been shown to increase glutamate agonist–evoked DA release in mouse striatal neurons.23

I love this stuff I take 2000mg a day!