[Conductor71]

Just to add the pot, I ran across this article on a nifty little peptide we produce in our gut, and we have low levels of it. I found that it has close ties with dopamine and glucose tolerance. Interesting, but there are holes to fill.


Postprandial ghrelin response is reduced in patients with Parkinson's disease and idiopathic REM sleep behaviour disorder: a peripheral biomarker for early Parkinson's disease?

Ghrelin is a 28 amino acid hunger-stimulating peptide and hormone that is produced mainly cells lining the fundus of the human stomach and epsilon cells of the pancreas.[1] Ghrelin levels increase before meals and decrease after meals. It has multiple functions, which include promoting gastrointestinal motility and influencing higher brain functions. Experimental data suggest that ghrelin has neuroprotective potential in the MPTP mouse model of Parkinson's disease (PD). PD patients show delayed gastric emptying and other symptoms that may relate to disturbed excretion of ghrelin.

-It has a role in how we handle chronic stress and is linked to the evil axis (hypothalamus-pituitary axis or HPA). This makes me think of how some have described PD as a state of perpetual fight-freeze-flight.

-recent evidence suggests ghrelin prevents excessive anxiety under conditions of chronic stress.

-It influences our sleep-wake cycles.

-The level of ghrelin increases during the time of day from midnight to dawn in thinner people which suggests there is a flaw in the circadian system of obese individuals (and potentially PWP?)

-High levels are prevalent when animal in starvation mode; think back to research and discussion on intermittent fasting benefits.

-Low levels result in delayed gastric motility.

- After H pylori cure, plasma ghrelin increased profoundly in asymptomatic subjects.

Most importantly:

Ghrelin binds to SNpc cells, electrically activates SNpc DA neurons, increases tyrosine hydroxylase mRNA and increases DA concentration in the dorsal striatum. Exogenous ghrelin administration decreased SNpc DA cell loss and restricted striatal dopamine loss after 1-methyl-4-phenyl-1,2,5,6 tetrahydropyridine (MPTP) treatment.


Ghrelin promotes and protects nigrostriatal dopamine function via a UCP2-dependent mitochondrial mechanism.