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Re: DLPA and enkephalins » samplemethod

Posted by Larry Hoover on June 24, 2003, at 10:44:18

In reply to Re: adapton or DLPA experiences Avid Abulia » Larry Hoover, posted by samplemethod on June 23, 2003, at 7:54:03

> Can someone please give evidence that it is actually the d-form (and not the l-form) of phenylalanine that is an inhibitor of enkephalin breakdown?
>
> Cheers

There's a bunch of similar, repetitive older research (samples here), and one recent reference, showing that at least one doctor has been paying attention.

I'm out of here for a while.

Lar

Acupunct Electrother Res. 1982;7(2-3):157-72.

D-phenylalanine and other enkephalinase inhibitors as pharmacological agents: implications for some important therapeutic application.

Ehrenpreis S.

A number of compounds have been shown to inhibit the degradation of enkephalins. As expected, these compounds produce naloxone reversible analgesia and potentiate the analgesia produced by enkephalins and by acupuncture. One of these, D-phenylalanine, is also anti-inflammatory. D-phenylalanine has proven to be beneficial in many human patients with chronic, intractable pain. It is proposed the enkephalinase inhibitors may be effective in a number of human "endorphin deficiency diseases" such as depression, schizophrenia, convulsive disorders and arthritis. Such compounds may alleviate other conditions associated with decreased endorphin levels such as opiate withdrawal symptoms.


Acupunct Electrother Res. 1985;10(3):203-8.

Pharmacology of enkephalinase inhibitors: animal and human studies.

Ehrenpreis S.

We have shown that a number of compounds which inhibit the degradation of met-enkephalin can produce naloxone-reversible analgesia in mice. These compounds also potentiate the analgesia produced by acupuncture, foot shock, and transcutaneous nerve stimulation in animals and humans. The potency of their effectiveness as analgesics or potentiators parallels their potency as inhibitors of mouse brain enkephalinase. D-Phenylalanine (DPA), one of these enkephalinase inhibitors, has been used successfully for the management of chronic intractable pain in humans and to potentiate the treatment of many painful conditions by acupuncture. Other aspects of pharmacology of DPA will be discussed, including its effects on the cardio-vascular system, behavior, and lack of development of tolerance and dependence when used chronically in animals and humans.


Med Hypotheses. 2000 Oct;55(4):283-8.

DL-phenylalanine markedly potentiates opiate analgesia - an example of nutrient/pharmaceutical up-regulation of the endogenous analgesia system.

Russell AL, McCarty MF.

Brampton Pain Clinic, Bramalea, Ontario, Canada.

In the author's clinical experience, concurrent treatment with DL-phenylalanine (DLPA) often appears to potentiate pain relief and also ease depression in patients receiving opiates for chronic non-malignant pain. An analysis of this phenomenon suggests that it may be mediated, at least in part, by up-regulation of the 'endogenous analgesia system' (EAS), a neural pathway that projects caudally from medullary nuclei to the dorsal horn of the spinal column; when stimulated by chronic pain or therapeutic measures such as opiates or acupuncture, the EAS suppresses activation of second-order pain-receptive neurons in the dorsal horn, and thereby alleviates pain. Since serotonin and enkephalins are key neurotransmitters in the EAS, it is reasonable to predict that measures which promote serotonin activity (such as 5-hydroxytryptophan and serotonin-reuptake inhibitors) as well as enkephalin activity (such as D-phenylalanine, an enkephalinase inhibitor) should potentiate EAS-mediated analgesia - a view consistent with much previous medical research. Comprehensive support of the EAS with well-tolerated nutrients and pharmaceuticals may amplify the analgesic efficacy of chronic opiate therapy, while enabling dosage reductions that minimize opiate side-effects. Analogously, this approach may complement the efficacy of acupuncture and other analgesic measures that activate the EAS.

 

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