Don’t Die Trying to Boost Brain Dopamine

Dopamine is your main feel-good compound.

Cocaine, nicotine, alcohol, sugar, opioids (and pleasurable emotional experiences) increase dopamine levels in the brain.

America’s deadly addictions are often related to the desire for a dopamine rush.

When people binge on sweets, alcohol, or many narcotics, they are often seeking to fulfil their “cravings” for a dopamine “high.”

Once largely confined to the young, older people are now abusing alcohol and drugs, as aging reduces their dopamine levels.

Dopamine deficits contribute to a diminished sense of wellbeing. This causes people to turn to dopamine-boosting agents, be it sugar, narcotics, or alcohol.

This is particularly hard for smokers, who are addicted to the mild dopamine release they get when lighting a cigarette.

The brain uses dopamine for more than mood elevation. It also enables youthful cognitive performance and body coordination.¹

Dopamine depletion is linked with neuro-degenerative diseases (beyond Parkinson’s) along with shortened lifespans.^2,3

This article describes a low-cost method to safely restore more dopamine, without unpleasant up-and-down spikes.

As people age past 45 years, dopamine brain levels decline by 13% each decade thereafter. ⁴

Dopamine is produced by specialized cells that die off with aging.⁵

When only 30% of dopamine-producing cells remain, symptoms of Parkinson’s disease manifest.⁶

If dopamine-producing cells decline to 10% of normal, the outcome is death.^7,8

Long before this happens, people feel their youth shrivel as they are unable to enjoy the same feelings of pleasure and wellbeing as when their dopamine levels were higher.

There are proven ways to block the enzyme that breaks down dopamine in the brain and help protect dopamine-producing cells against neurotoxicity.

Inhibiting the Dopamine-Depleting Enzyme

Dopamine is abundantly produced in young brains and then precisely controlled by enzymes called MAOs (monoamine oxidases).

As people age, levels of the MAO-B enzyme increase and deplete too much dopamine.^9-11 This is partially why people start to feel their age as youthful dopamine levels wane.

A solution is to ingest compounds that inhibit the MAO-B enzyme.

MAO-B-inhibiting compounds enable more feel-good dopamine to be available to brain cells.

Prescription drugs like deprenyl function as MAO-B inhibitors and are used as adjunctive treatment for Parkinson’s disease.

Parkinson’s is characterized by severe dopamine depletion and accelerated death of dopamine-producing brain cells.

MAO-B Inhibitor Increases Lifespan

Since the 1980s, Life Extension® has encouraged readers to ask their doctor to consider prescribing a drug called deprenyl, which is an MAO-B inhibitor.

We made this recommendation based on published studies emanating from Europe showing lifespan increases in animals given deprenyl. ^3,12-16

When elderly rats were treated with deprenyl, remaining lifespan doubled.³

Aged dogs given deprenyl had twice the survival rate compared with placebo-treated dogs.¹⁷

Mice that were immune suppressed lived up to about 200% longer on deprenyl.¹⁸ Most elderly humans suffer immune senescence.^19,20

In addition to longer lifespans, some deprenyl-supplemented animals displayed more youthful energy levels and dramatically heightened sexual activity.³

This outpouring of scientific data from Europe had Americans clamoring to get their hands on deprenyl.

While deprenyl had been used in Europe to treat Parkinson’s disease beginning in the 1970s, the FDA did not approve it for Americans until 1989.²¹

Life Extension® and Parkinson’s support groups fought a multi-year battle to force the FDA to approve deprenyl.

Plant-Derived MAO-B inhibitors

Despite losing patent status decades ago, deprenyl still costs more than it should in the United States. And most physicians are unwilling to prescribe deprenyl for anti-aging purposes (i.e., “off-label”).

In 2016, Life Extension® introduced a green oat extract that has demonstrated MAO-B-inhibiting properties. This green oat extract was for some.

Even with its cost, green oat extract remains popular because of its dopamine-boosting properties.

The good news is that another plant-derived MAO-B inhibitor has been discovered that costs far less.

Medicinal Plant Inhibits MAO-B

One of the top 50 medicinal plants used in Korea and China is the bark of the Amur Cork Tree. It has a difficult-to-pronounce name:

Phellodendron amurense

It’s been used for centuries in Asia to treat infections of the urinary and digestive tracts, as well as other sources of acute inflammation.

When studied in vitro against other plants, an extract of the Amur Cork Tree ranked as one of the most potent and selective inhibitors of MAO-B.^22,23 It showed more than 80% inhibition of the activity of the MAO-B enzyme, which is comparable to deprenyl.²³

Based on these properties, we are suggesting people start off with 500 mg daily of low-cost Amur Cork Tree bark.

We base this on our direct interactions with the Hungarian inventor of deprenyl (Dr. Joseph Knoll). He insisted that deprenyl was being overdosed in Parkinson’s patients at 10 mg a day.

Dr. Knoll recommended that Parkinson’s patients take 5 mg a day (or less) of deprenyl to achieve optimal MAO-B inhibition.

He also told us that for anti-aging purposes, a dose of 5 mg of deprenyl twice a week would likely yieldbenefits. Amur cork tree, in the dose of 500 mg, can be taken daily.

Protect Dopamine-Producing Brain Cells

Inhibiting dopamine-degrading MAO-B can yield immediate and long-term health benefits.

To guard against eventual loss of dopamine, it is critical to also protect dopamine-producing cells in the brain.

Excess activity of MAO-B causes toxic byproducts to form, including hydrogen peroxide, free radicals, and aldehydes.^11,24,25

These compounds can wreak havoc in brain cells, contributing to neurotoxicity.²⁴

Amur Cork Tree has been shown to be neuro-protective in cell and animal models of neuro-degeneration.^26-28

Guard Your Brain Against Excess MAO-B

Loss of dopamine function plays a primary role in the development of certain neurodegenerative disorders.^2,3

Normal aging results in elevated MAO-B, causing our brains to be dopamine depleted.²⁹

People over age 45 should intervene by taking 5 mg of the drug deprenyl two to three times a week, 500 mg of Amur Cork Tree bark powder daily, or 800 mg of green oat extract daily.

An advantage to Amur Cork Tree bark is its low price and centuries of documented medicinal use in Asia.

In this Month’s Issue…

Glucosamine has been used for decades to rebuild cartilage and relieve joint discomfort. Recent findings reveal that people supplementing with glucosamine have a 22% lower risk of cardiovascular death.

The article on page 26 of this issue describes beneficial mechanisms of glucosamine to support cartilage regeneration, and cleanse cells of toxic debris via autophagy.

Milk thistle has long been known for its liver-protecting properties. Research described on page 56 reveals it also helps lower blood glucose levels.

Zinc is taken to boost immune function, but it also plays a critical role in maintaining strong bones, as the article on page 72 describes.

A detailed article about the dopamine-enhancing properties of Amur Cork Tree bark powder can be found on page 46 of this month’s issue.

Thank You for Your Support of Research on Aging!

We use proceeds from supplement sales to fund research projects aimed at slowing and reversing biological aging.

As results from these clinical trials are reported, I look forward to enlightening Life Extension® readers about novel methods for living longer and healthier.

For longer life,

William Faloon

References

1. Available at: https://www.webmd.com/mental-health/what-is-dopamine. Accessed February 1, 2021.
2. Masato A, Plotegher N, Boassa D, et al. Impaired dopamine metabolism in Parkinson’s disease pathogenesis. Mol Neurodegener. 2019 Aug 20;14(1):35.
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4. Knoll J. Deprenyl (selegiline): the history of its development and pharmacological action. Acta Neurol Scand Suppl. 1983;95:57-80.
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19. Weiskopf D, Weinberger B, Grubeck-Loebenstein B. The aging of the immune system. Transpl Int. 2009 Nov;22(11):1041-50.
20. Available at. Accessed November 9, 2015.
21. Mazzio E, Deiab S, Park K, et al. High throughput screening to identify natural human monoamine oxidase B inhibitors. Phytother Res. 2013 Jun;27(6):818-28.
22. Zarmouh NO, Messeha SS, Elshami FM, et al. Natural Products Screening for the Identification of Selective Monoamine Oxidase-B Inhibitors. European J Med Plants. 2016 May;15(1).
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24. Naoi M, Maruyama W, Inaba-Hasegawa K. Type A and B monoamine oxidase in age-related neurodegenerative disorders: their distinct roles in neuronal death and survival. Curr Top Med Chem. 2012;12(20):2177-88.
25. Sun Y, Lenon GB, Yang AWH. Phellodendri Cortex: A Phytochemical, Pharmacological, and Pharmacokinetic Review. Evid Based Complement Alternat Med. 2019;2019:7621929.
26. Xian YF, Lin ZX, Ip SP, et al. Comparison the neuropreotective effect of Cortex Phellodendri chinensis and Cortex Phellodendri amurensis against beta-amyloid-induced neurotoxicity in PC12 cells. Phytomedicine. 2013 Jan 15;20(2):187-93.
27. Kim Y, Jung I, Lee S. Effects of Phellodendron amurense extract on the Alzheimer’s disease model. Journal of Physiology & Pathology in Korean Medicine. 2005;19(1):130-8.
28. Available at: https://www.sciencedirect.com/topics/neuroscience/monoamine-oxidase-b. Accessed February 1, 2021.