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Dietary method for reducing fluctuations in PD (1987)

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3 Replies

What are good updates to this 1987 study which is open access?

Dietary method for reducing fluctuations in Parkinson's disease.

Pincus JH, et al. Yale J Biol Med. 1987 Mar-Apr.

Abstract.

Motor fluctuations and non-response to carbidopa-levodopa (Sinemet) therapy are major problems in the long-term management of Parkinson's disease. Levodopa manipulation, addition of adjuvants, and drug holidays are often unsuccessful. Others have shown that the clinical state of stabilized Parkinsonians can be reversed with intravenous administration of large neutral amino acids. Reasoning that dietary protein might precipitate motor oscillations and non-response, a low-protein daytime diet (7 g) was offered to fifteen patients. Eighty-six percent of this sample demonstrated immediate sensitivity to Sinemet. While on a low-protein diet, patients' clinical function was predominantly choreatic. Eight patients required a 10-60 percent reduction in their daily levodopa dose in order to minimize this choreatic tendency. Discontinuation of adjuvants did not compromise motor independence. Conversely, while on a high-protein diet (160 g), patients were predominantly immobile with markedly elevated plasma amino acid and levodopa levels. Consequently, elimination of dietary protein from breakfast and lunch can offer an effective and easily modified method for the amelioration of motor fluctuations and non-response to Sinemet in Parkinson's disease during working hours.

PMID 3577210

PMCID PMC2590325

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felixned profile image
felixned

Interesting, I experimentally arrived to the same conclusion: no protein for breakfast and lunch provides better response to Sinemet. The best response achieved when I fast.

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aspergerian in reply to felixned

Felixned,

Thank for describing your experience.

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aspergerian

Here is a clue regarding how after a ~large meal, not only am I tired as blood flows into my mesentery but also: my levodopa and dopamine functions are diminished.

Postprandial somnolence.

en.m.wikipedia.org/wiki/Pos...

In individuals with normal carbohydrate metabolism, insulin levels rise concordantly to drive glucose into the body's tissues and maintain blood glucose levels in the normal range.[7] Insulin stimulates the uptake of valine, leucine, and isoleucine into skeletal muscle, but not uptake of tryptophan. This lowers the ratio of these branched-chain amino acids in the bloodstream relative to tryptophan[8][9] (an aromatic amino acid), making tryptophan preferentially available to the large neutral amino acid transporter at the blood–brain barrier.[10][9] Uptake of tryptophan by the brain thus increases. In the brain, tryptophan is converted to serotonin,[11] which is then converted to melatonin. Increased brain serotonin and melatonin levels result in sleepiness.[12][13].

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