In the 1980s-1990s, published studies in Europe showed remarkable life span increases in animals given a drug called deprenyl.
In elderly rats treated with deprenyl, remaining life span doubled in response to the drug. Aged dogs given deprenyl had twice the survival rate compared with placebo-treated dogs. Mice that were immune-suppressed lived up to about 200% longer on deprenyl. (Most elderly humans suffer immune suppression).
Not only were life spans lengthened, but some deprenyl-supplemented animals displayed more youthful energy levels, as related to sexual activity.
This outpour of scientific data from Europe had aging Americans clamoring to get their hands on deprenyl. It started being used in Europe to treat Parkinson’s disease in the 1970s, but the FDA did not approve deprenyl until 1989.
When deprenyl was finally approved, it cost Americans 4 times more money than what Europeans were paying for the identical drug. Unwilling to pay this extortionist price, Americans began ordering personal-use supplies from Europe.
The FDA struck back and launched criminal investigations against those seeking to make deprenyl more affordable. The FDA did this at the behest of the drug company that owned the patent on deprenyl.
One individual made a liquid form of deprenyl that sold quite well until he was arrested by the FDA and sent to prison for almost 13 years. Back in those days, deprenyl was the most sought-after anti-aging drug.
Some of our supporters still use deprenyl, though getting a physician to prescribe it for anti-aging purposes is sometimes impossible. This article will describe how Americans can now derive the anti-aging mechanism of deprenyl in a low-cost nutrient.
Deprenyl is a drug the FDA approved to treat early-stage Parkinson’s disease. It was enthusiastically greeted by neurologists when first approved in the United States, but its therapeutic effect on advanced Parkinson’s patients was disappointing.
That’s because a significant drop in dopamine occurs before symptoms of Parkinson’s disease become evident. Therefore, most Parkinson’s patients have already lost so many dopamine-producing neurons that deprenyl is of little value.
Deprenyl enhances the anti-Parkinson effects of standard drugs. Its primary mechanism is to inhibit an enzyme in the brain that destroys dopamine.
Longevity enthusiasts realized 30 years ago that if low-dose deprenyl is initiated before the onset of Parkinson’s symptoms, the brain might be protected against Parkinson’s and other neurodegenerative diseases.
By inhibiting this dopamine-degrading enzyme, it was theorized, people might not only live longer, but behave younger.
This same enzyme (MAO-B) may be involved in the destruction of dopamine-producing neurons.
Dopamine Levels in the Brain
Prior to age 45 in people, dopamine levels remain fairly stable. After that, dopamine in the human brain decreases by about 13% each decade.
When the dopamine-producing neuron content in the brain reaches about 30% of normal, Parkinson’s symptoms may be present.
When dopamine levels reach 10% of normal, death ensues.
This has led to the hypothesis that if we live long enough, we will all develop Parkinson’s symptoms due to dopamine depletion in our brains.
How Deprenyl Works in the Brain
Monoamine oxidase B (MAO-B) is an enzyme in the brain that degrades neurotransmitters like dopamine.
As humans age, MAO-B levels begin to increase and degrade precious dopamine and other neurotransmitters.
Deprenyl is a selective inhibitor of MAO-B. As little as 5 mg twice a week of deprenyl is all aging humans may need to maintain their dopamine at youthful levels.
Parkinson’s patients were prescribed 10 mg a day of deprenyl. The inventor of the drug (Dr. Joseph Knoll) believed this dose was too high.
It was long ago hypothesized that low-dose deprenyl might help prevent degenerative brain diseases and improve the quality of life. This is evidenced by increased “mounting frequency” in old male rats treated with deprenyl compared to untreated controls.
Dopamine is a primary “feel-good” neurotransmitter that progressively depletes as humans age. By restoring dopamine and other neurotransmitter levels using low-dose deprenyl, aging humans may regain some of their youthful sense of well-being.
Deprenyl has demonstrated intriguing anti-aging properties. Animals given relatively low doses of the drug live much longer than control groups not receiving deprenyl.
Need to Suppress MAO-B in Aging Brains
The enzyme monoamine oxidase B (MAO-B) serves a function in youth by keeping neurotransmitter levels from elevating too high. As we age past 45 years, however, MAO-B levels begin a steady rise that results the depletion in dopamine seen in elderly individuals.
MAO-B also may inflict toxic damage to brain cells via several well-defined mechanisms.
Excess MAO-B not only deprives us of our youthful emotions by depleting dopamine, but also impairs cognitive functions by decreasing acetylcholine while simultaneously accelerating brain aging.
People today should take steps to suppress MAO-B levels as they age past 45 years. Those who are already taking low-dose deprenyl (5 mg twice a week) may be deriving enormous benefits by protecting against MAO-B toxicity.
The problem is that most doctors will not prescribe deprenyl to non-Parkinson’s patients. Insurance companies are unlikely pay for “off-label” use.
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