One of the most important anti-aging medicines
Deprenyl reduces the age-related decline of dopamine, increasing its availability to preserve youthful brain activity
Deprenyl was originally developed as a ‘psychic energizer’, designed to integrate some amphetamine-like brain effects with anti-depressant effects. It has since been shown to protect nerve cells against a wide, and growing, number of neurotoxins, and has been shown to be a neuroprotection/neurorescue agent when nerve cells are exposed to damaging or stressful conditions.
Professor Joseph Knoll proved that Deprenyl improves the availability of dopamine, slows its age-related decline and helps maintain healthy brain cells by acting as a selective MAO-B inhibitor.
Professor Knoll emphasized that the nigrostriatal tract, the tiny DA-using nerve cluster in the basal ganglia (‘old brain’), typically dies off at an average rate of 13% per decade starting around age 45 in humans. This fact sets the human lifespan at about 115 years, since by that age the nigral neuron population would have dropped below 10% of its original number, at which time death ensues even if in all other respects the organism were healthy.
Therefore, human longevity is in-part governed by the rate of dopamine decline. Its support and enhancement means not only longer life, but lucid mental capabilities too. In fact, four different rat studies and one dog study have shown Deprenyl to be an effective life-extension agent.
Based on the sum total of research, Knoll has suggested that if Deprenyl were used from the 40s on, and only modestly lowered the nigrostriatal neuron death rate – say, from 13% to 10% per decade – then the average human lifespan might increase by 15 years.
Deprenyl has become a standard treatment for Parkinson’s disease, and thanks to its aphrodisiac effects, helps to improve sexual function and desire (much more so for men than woman).
Although Parkinson's disease remains the only FDA approved indication for Deprenyl in the USA, with a number of ongoing clinical studies evaluating its efficacy in Alzheimer's disease, anecdotal reports from both physicians and patients of dramatic improvement in an impressive number of diseases have been accumulating.
Conditions for which Deprenyl appears to be therapeutic or ameliorative include: cerebral infarction (stroke), hormone inadequacy, amyotrophic lateralizing sclerosis (lou gherig's disease), fatigue, chronic pain, gastric ulcers, senile dementia, sexual dysfunction, multiple sclerosis, learning difficulties, blepharospasm, hypertension depression and cancer.
Dr. Clyde Reynolds, a clinician who specializes in the metabolic therapy of cancer in Washington State, discovered that cancer patients invariably have imbalances of the neurotransmitters, epinephrine, norepinephrine and serotonin. Dr. Reynolds has found that Deprenyl is highly effective in restoring the normal levels and normal balance of these neurotransmitters. He believes that normalization of the balance of these neurotransmitters is an absolute necessity for the effective treatment of all cancers.
Parkinson and Alzheimer's disease patients are often treated with very high doses of 20mg daily (usually along with other drugs). Anti-aging doses (dependant on age and condition) are more likely to be 2.5mg to 5mg once, twice or three times a week, or, 1mg to 3mg per day, with regular breaks. Deprenyl tablets are selegiline hydrochloride, which is deprenyl bonded to an in-organic molecule. However, liquid deprenyl citrate (LDC) is selegiline bonded to an organic molecule, one reason why the liquid deprenyl citrate is considered to be superior. This form is generally recognized as the most pure and potent form of deprenyl available. It also allows precise titration for anti-aging purposes, as each ml drop in the bottle is equivalent to 1mg deprenyl citrate. The manufacturer recommends 1mg two times a week for 30 to 35 years olds up to 10mg daily for 80 year olds plus (an age/ dosage list in English is enclosed with order). Ward Dean, M.D., recommends reducing deprenyl doses after several months to lower levels and taking occasional sabbaticals.
Possible gastrointestinal symptoms, such as nausea, heartburn, upset stomach, etc. Some studies have found side effects such as irritability, hyper-excitability, psychomotor agitation and insomnia. These effects are probably due to Deprenyl catecholamine-enhancing effect, over-activating DA/NA neural systems at the expense of calming/sleep-inducing serotonergic systems, so taking magnesium and tryptophan or 5-HTP may suffice to counter these ‘psychic’ effects.
Deprenyl Tablets - Jumex
Chemical: Selegiline Hydrochloride
Excipients: Lactose, cornstarch, polyvinyl pyrrolidone, monohydric citric acid, magnesium stearate.
Adverse Effects and Precautions: Selegiline is often given as an adjunct to levodopa therapy and many of the adverse effects reported can be attributed to enhanced levodopa activity- dosage of levodopa may have to be reduced. Adverse effects have included hypertension, nausea, confusion, psychosis, hallucinations, and increased dyskinesias. Unlike non-selective monoamine oxidase inhibitors such as phenelzine, selegiline is reported not to interact with tyramine in food at usual doses.
Interactions: Although selegiline is less likely than non-selective monoamine oxidase inhibitors to interact with tyramine in food, like other monoamine oxidase inhibitors it can produce life-threatening reactions when given with pethidine. Zornberg GL, et al. severe adverse interaction between pethidine and selegiline. Lancet 1991- 337: 246. Correction. ibid.- 440.
Uses and Administration: Selegiline hydrochloride is a selective inhibitor of monoamine oxidase type B, an enzyme involved in the metabolic degradation of dopamine in the brain. It enhances the effects of levodopa and is used in Parkinson's disease as an adjunct to levodopa therapy, usually when fluctuations in mobility have become a problem. It is administered in a daily dose of 10 mg, either as a single dose in the morning or in 2 divided doses of 5 mg at breakfast and lunchtime. Addition of selegiline to levodopa therapy may enable the dosage of levodopa to be reduced by an average of 30%. Selegiline may also be given alone in early Parkinson's disease in an attempt to slow disease progression (see under Parkinsonism, below). A dose of 10 mg of the hydrochloride daily has been suggested for this purpose.
Dementia: Double-blind studies (1,2) indicate that selegiline may produce beneficial effect in-patients with Alzheimer's disease but it has been suggested that improvements in mood and cognitive function may be due to a reduction in tension and depression. (3) 1. Piccinin GL, et al. neuropsychological effects of L-deprenyl in Alzheimer's type dementia. Clin Neuropharmacol 1990- 13: 147-63. 2. Mangoni A, et al. Effects of a MAO-B inhibitor in the treatment of Alzheimer disease. Eur Neurol 1991- 31: 100-107. 3. Anonymous. Drugs for Alzheimer's disease. Drug Ther Bull 1990- 28: 42-4.
Depression: Several studies have suggested that like non-selective monoamine oxidase inhibitors such as phenelzine, selegiline may be of some benefit in depression. Mendlewicz and Youdim reported a marked improvement in 14 patients with unipolar or bipolar depression who received selegiline hydrochloride 5 mg three times daily for 40 days compared with 13 patients given placebo. (1) Similarly, Birkmayer et al. reported benefit in an uncontrolled study in 102 outpatients and 53 inpatients with unipolar depression who received selegiline hydrochloride 5 to 10 mg daily in association with phenylalanine 250 mg daily- about 70% of these patients, in whom conventional antidepressants were not effective, were reported as having complete remission. (2) The benefit was not thought to be due to the amphetamine metabolites of selegiline. Benefit has also been reported in-patients with atypical depression who received selegiline hydrochloride in doses of 10 to 40 mg daily. (3) At high doses the specificity of inhibition is reported to be lost and restriction of tyramine in the diet becomes necessary as with more conventional monoamine oxidase inhibitors- in this study there was little evidence of such a loss of specificity. 1. Mendlewicz J, Youdim MBH. L-Deprenil, a selective monoamine oxidase type B inhibitor, in the treatment of depression: a double-blind evaluation. Br J Psychiatry 1983- 142: 508-11 2. Birkmayer W, et al. L-Deprenyl plus L-phenylalanine in the treatment of depression. J Neural Transm 1984- 59: 81-7. 3. Quitkin FM, et al. l-Deprenyl in atypical depressives. Arch Gen Psychiatry 1984- 41: 777-81.
Parkinisim: Early attempts to prolong the actions of dopamine in the brain by administration of monoamine oxidase inhibitors were unsuccessful because of intolerable side effects and the risk of potentially catastrophic hypertension. However, the discovery that monoamine oxidase (MAO) exists in at least 2 forms, A and B, and the realization that dopamine in the brain is metabolized predominantly by MAO-B led to the identification of selegiline, which could delay oxidative diminution of dopamine in the brain without provoking a `cheese-reaction'. (1) When given to patients experiencing fluctuations in levodopa's effect due to `wearing-off' or `end-of-dose' effects selegiline ameliorates the fluctuations in about 50 to 70% of patients, and permits a reduction in levodopa dosage of up to about 30%. (2,3) However the benefit is usually modest, and declines after 6 to 12 months in most patients with complete loss of benefit usually in 12 to 24 months. (2) More severe fluctuations in mobility associated with the `on-off' effect in advanced Parkinsonism are unlikely to respond to adjuvant selegiline. (3) More recently much interest and controversy has surrounded the possibility that selegiline given in early Parkinson's disease may retard disease progression. Several uncontrolled studies had reported that long-term administration of selegiline with levodopa prolonged the period of responsiveness to the latter and resulted in increased life expectancy of parkinsonian patients. (4,5) Furthermore, a theoretical basis for benefit exists in the model of Parkinsonism caused by methylphenyltetrahydropyridine (MPTP) which relies on conversion by monoamine oxidase type B to the active methylphenylpyridinium (MPP (+)) radical to produce damage to the striatum. (3,6) More recently, controlled studies by Tetrud and Langston (in 54 patients) (7) and by the Parkinson Study Group (the DATATOP study, involving 800 patients) (8) have shown a significant prolongation in the time to reach a level of disability requiring commencement of levodopa therapy. Although some critics have suggested that selegiline is simply providing symptomatic relief in disease which continues to progress (9-11) the promising preliminary results have been suggested by others to justify the prescription of selegiline 10 mg daily to patients, especially younger ones, in the early stages of Parkinson's disease, in the hope of impeding progression. (12)
- Anonymous. Deprenyl in Parkinson's disease. Lancet 1982- ii: 695-6.
- Anonymous. Pergolide and selegiline for Parkinson's disease. Med Lett Drugs Ther 1989- 31: 81-
- Golbe LI, et al. Selegiline and Parkinson's disease: protective and symptomatic considerations. Drugs 1990- 39: 646-51.
- Birkmayer W, et al. (-)-Deprenyl leads to prolongation of L-Dopa efficacy in Parkinson's disease. Mod Probl Pharmacopsychiatry 1983- 19: 170-6.
- Birkmayer W, et al. Increased life expectancy resulting from addition of L-deprenyl to Madopar treatment in Parkinson’s disease: a long term study. J Neural Transm 1985- 64: 113-27.
- Steventon G, et al. Monoamine oxidase B and Parkinson's disease. Lancet 1990- 335: 180. 7.