I reviewed one article so far for my lit review based around the role of phenylalanine content in nutrasweet having an effect on recurrent undiagnosable abdominal pain.
What'd my brain go and do to me?
Come up with more research ideas. This isn't funny anymore.
Questions like: If folks with PTSD have smaller than normal hippocampuses, how would folks with chronic pain compare?
Does this abdominal pain activate the HPA axis?
If it does, are the cortisol levels consistently high like folks without PTSD respond to stress? Or are they comparable to the low cortisol levels of folks with PTSD?
What role does cortisol have in lowering serotonin levels? (Cortisol increases metabolism, providing less protein, therefore less tryptophan, therefore less serotonin?)
Now, if insulin is what pushes the competing large amino acids of tryptophan (phenylalanine is one of them), to make way for tryptophan to use its transport system (the same system that phenylalanine likes to use), then if folks who switch from regular soda to diet soda (or high carb diet to low carb?!), thereby lowering insulin levels, thereby allowing phenylalanine to use more transport systems, and then lowering serotonin?
Scott, I see you as an almost perfect, upstanding kid with a wicked sense of humor that brought his Mom flowers on Mothers' Day and her birthday.
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I'm holding mack accountable for my newfound hesitation to drink Diet Coke. I can't drink regular the sugar bothers me so what am I left with???? Water?!?!?!
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quote: What role does cortisol have in lowering serotonin levels? (Cortisol increases metabolism, providing less protein, therefore less tryptophan, therefore less serotonin?)
I think this sounds right, which is why going to low carbs is also less ideal for folks with low seratonin conditions. I thought cortisol is an insulin agonist. So Cortisol keeps the tryptophan from being as available, and also keeps the insulin from encouraging the tryptophan->seratonin transformation. I'm throwing around words that may imply causation that I don't really know to be the case.
quote: Hypersecretion of cortisol is a common feature of depressive illness, and may also be a feature of alcoholism and obesity. Such patients may fail to suppress their cortisol levels during a low-dose dexamethasone suppression test.
Drugs such as phenytoin, phenobarbitone, carbamezepine, and rifampicin will induce hepatic enzymatic clearance of dexamethasone. This will reduce its plasma concentration, and may cause false positive responses.
Estrogens increase the cortisol-binding globulin concentration in the circulation, and where total cortisol is measured in serum, false positives may be seen. (? stop estrogen-containing drugs and delay investigation for 6 weeks to allow the cortisol-binding globulin to return to baseline. This may not be necessary in the case of transdermal estrogens).
I'm always interested in info that suggests a reason for the apparent prevalence of low seratonin syndromes and pain syndromes in women.
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