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Restore Youthful Cognition and Well-Being

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By Arthur Strand • www.ProHealth.com • March 4, 2016


Restore Youthful Cognition and Well-Being
Aging individuals suffer progressive frailty, cognitive dysfunction, and a diminished sense of well-being. These conditions correlate with declining dopamine levels in the aging brain.1-3

Dopamine functions as a neurotransmitter, where it signals nerve cells to regulate mood, cognition, and bodily function.4

From the time a person is born, dopamine plays a major role in reward behavior.5 So much so that dopamine response can dictate cravings for sugary foods, recreational drugs, ethanol, tobacco, gambling, and/or sex.6

All of these behaviors can prompt a dopamine release in the brain that creates individualistic pleasure addictions.7-13

The dilemma is that as we age, dopamine depletion causes us to lose neurological functions that enable us to enjoy and function in everyday life.

Restoring dopamine to more youthful ranges is vital for healthy longevity.

Role of Dopamine in Addictive Behaviors


Narcotics like cocaine have long been associated with intense dopamine-fueled euphoria.14 Less recognized is the impact that alcohol, nicotine, and activities like gambling play in the brain's dopamine release.

This can be seen in the form of "binge drinking," where ethanol initially prompts dopamine release, which motivates the drinker to imbibe increasing quantities of ethanol to enhance their dopamine high.15

Compulsive gamblers feel a surge of dopamine every time a card is flipped, causing gambling binges to go on for days in some cases without regard to sleep or food. This is especially true when gambling is combined with nicotine, which prompts even greater flows of euphoric dopamine.

Perhaps one of the most common dopamine-fueled cravings people have today is for sugary foods. Despite knowing the toxic effect of glucose overload, people excessively consume sweets because of the dopamine release it generates in the brain.

Activities that promote the rapid release of dopamine are often dangerous and addicting.16 Yet some very intelligent people succumb to these euphoric effects even though their lives are adversely impacted.

Clearly, safer methods are needed to restore brain dopamine to a more youthful "feel-good" range.

Dopamine and Brain Aging


Dopamine levels decline as we age past 45 years.17 When this happens, people no longer "feel" as young as they used to. This sometimes manifests as clinical depression.18,19 For the most part, however, aging people find that their motivation, their cognitive function, and their ability to enjoy pleasurable events all diminish.

Loss of dopamine also causes people to lose their sense of well-being, i.e. they don't feel the same as they once did.20 This is often accompanied by reduced bodily coordination that may progress to frailty.21,22

If we did not know what caused the age-related decline in brain dopamine, this would be a depressing situation for us all.

How to Boost Brain Dopamine


Fortunately, a prime reason for dopamine depletion was long ago discovered. It involves a dopamine-degrading enzyme in the brain called MAO-B, which stands for monoamine oxidase-B.

In youth, MAO-B is crucial in regulating just the right amount of dopamine in the brain.23 As humans age, however, MAO-B levels increase too much.24,25 The result of excess MAO-B is a dopamine deficit.

A natural method has been discovered to inhibit excess MAO-B in the brain. Placebo-controlled human studies show meaningful improvements in response to this novel dopamine restoration approach.

Dopamine is known as the "feel-good" neurotransmitter and it is a key factor in preserving a range of cognitive functions and promoting longevity. 26-29

By age 45, the brain's levels of dopamine begin to diminish.28 This not only makes people feel older, but is also involved in accelerated brain aging.

Dopamine depletion is largely caused by rising levels of the MAO-B enzyme. The ensuing dopamine deficiency strikes the brain's signaling system. The tragic result is cognitive decline, destruction of brain cells, reduction of youthful vigor/sexual desire, progression toward Parkinson's/neurological disorders, and a decrease in life span.25,30-34

Laboratory studies have shown that the inhibition of MAO-B not only preserves brain function by protecting dopamine, but it also has longevity benefits.34

In a search for a safe method to block the insidious MAO-B enzyme, scientists have identified a bioactive extract of wild green oat that not only inhibits MAO-B and the resulting breakdown of dopamine, but enhances dopaminergic neurotransmission that normally declines with aging. These protective actions enable more dopamine availability for use by brain cells.

In human studies, the effects of wild green oat extract resulted in increased focus and concentration, processing speed, executive function, and working memory as well as other parameters of enhanced dopaminergic transmission.35,36

The discovery of the specific actions of wild green oat extract represents a significant advance in the technology of age management. It provides a method for halting some of the most destructive aspects of neurological aging, thus helping improve cognitive function and enhancing the quality of life.37

What You Need to Know

Restore Youthful Cognition
  • Deprenyl is a MAO-B inhibiting drug with powerful life-extending properties. Deprenyl has been well known and thoroughly researched for more than 30 years.
  • Studies reveal that deprenyl extends life span in animal models by as much as 34%.
  • Antiquated regulations in the United States have kept this potential life span-enhancer from the American public.
  • Only people who already show symptoms of Parkinson's disease are permitted access to deprenyl and its benefits.
  • Innovative researchers have, however, discovered a safe and natural alternative that operates by the same mechanism as deprenyl—inhibition of the dopamine-degrading MAO-B enzyme.
  • Studies with the extract of a wild green oat strain show both MAO-B-inhibition and the improvements in brain activity and function that such inhibition produces.
  • Human studies with wild green oat extract confirm superior cognitive and memory function in both healthy people and those with early loss of cognition.
  • There is reason to anticipate that longer life spans may arise from this modest MAO-B inhibition, as has been shown with deprenyl.


A Drug that Safely Inhibits MAO-B


Until recently, one of the best solutions to combat dopamine depletion was a prescription drug called deprenyl. Discovered in Hungary, deprenyl boosts dopamine levels by decreasing the damaging MAO-B enzyme while increasing life span in animals by a stunning 34%.38-42

For the past 27 years, Life Extension® has been reporting on the longevity benefits of deprenyl.

Despite impressive laboratory and clinical data, deprenyl has been denied to the general public due to FDA restrictions that limit deprenyl prescriptions only for those afflicted with Parkinson's disease. The tragedy of this restriction is that people over age 45 are deprived of this drug's unique anti-aging mechanisms.43 Deprenyl is the only drug compound ever discovered that both prolongs life and preserves cognition in higher animals.42,44,45

Searching for an alternative MAO-B inhibitor that could be made available without prescription, researchers identified a patented extract from wild green oat that works along the same pathways as deprenyl.

Unlike the commercial oats that are eaten for breakfast, wild green oat extract is derived from the green, unripe part of the oat plant. Like deprenyl, wild green oat extract inhibits the damaging MAO-B enzyme.46

In a series of human studies, this special variety of green oat extract significantly improved concentration and cognitive functions, both in healthy people and in those whose brains are just beginning to fail.35,36 By preserving the "feel-good" aspects of dopamine, green oat extract also shows evidence of effectiveness as a tool in smoking cessation, consistent with the role that dopamine plays in addictive behaviors.47

MAO-B in the Aging Brain


Brain cells communicate with one another and with those in the rest of the body through the use of chemical signals called neurotransmitters.48

Dopamine is one of the brain's most important neurotransmitters. Dopamine is the signal your brain uses to transmit information related to movement control, cognition, concentration, and rewards (such as those involved in accomplishments, sexual activity, and addictions).49

Sadly, dopamine levels in the human brain begin to diminish between the ages of 45 and 60.50-52 This produces many of the subtle early changes seen in cognitive dysfunction. If left unchecked, this can eventually lead to dementia and early death by Parkinson's disease.50,53

Why do we lose dopamine as we age?


Part of the answer lays in mitochondrial damage that occurs in the region of the brain (substantia nigra) that produces dopamine.54,55Life Extension consumers long ago gained mitochondrial protection by using nutrients like coenzyme Q10 and PQQ (pyrroloquinoline quinone).

A more insidious cause of dopamine depletion are rising levels of MAO-B in the aging brain. Excess MAO-B enzyme activity relentlessly destroys dopamine with advancing age, causing a progressive dopamine loss that falls dramatically over age 60.50-52,56,57

The age-related increase in MAO-B occurs in key areas throughout the brain, which explains why a "dopamine deficiency" manifests as so many different outward symptoms such as frailty, cognitive impairment, and loss of youthful sense of well-being. Collectively, this decline of dopamine contributes to cerebral senescence.

Age-related symptoms of dopamine deficit include high rates of depression, loss of sexual vigor, and motor control problems resembling (and sometimes progressing to) Parkinson's disease.50

Rising levels of MAO-B also increase mitochondrial damage and destruction of brain cells.25,58 That's because in addition to MAO-B breaking down dopamine, it also produces hydrogen peroxide, an unstable molecule that is a massive source of destructive oxygen free radicals.59,60 Because the MAO-B molecule resides on the membranes of mitochondria, the outflow of reactive oxygen species can directly damage mitochondrial membranes, leading to inefficient energy use, additional cellular damage, and eventually, death of the cell.61,62

Deprenyl Extends Life Span via MAO-B Inhibition

Deprenyl has been intensely studied from 1988 to the present, with particular focus on its long-term effects in animals.28 A surprising outcome of these studies has been the observation that, time after time, in a wide range of animal models, deprenyl is not only neuroprotective, but significantly increases life span, when given at the proper dose level.

To date, deprenyl remains the only drug that has been shown to increase longevity in at least four different mammalian species.41,42

In rats, deprenyl treatment:
  • Extended average life span to 198 weeks. This is remarkable in that this average exceeds the estimated maximum age at death of a normal rat, 182 weeks.91,92 In this study, the longest-living control rat died at 164 weeks, while the longest-living deprenyl-treated rat lived to 226 weeks. That's a nearly 25% increase over the typical maximum age at death.
  • Extended average life spans by up to 34% when started at 24 months (late middle age for a rat).40,93
  • Extended life span significantly even when started late (at 23 to 25 months of age).94
  • Restored sexual activity in 64 of 66 2-year-old (elderly) rats (Untreated animals did not have full scale sexual activity past age 2).92
  • Decreased brain MAO-B activity by 85%.95

In mice, deprenyl treatment increased survival in immunocompromised animals by about 200% compared with controls,96,97 while in hamsters, deprenyl produced a three-month delay in the onset of long-term memory impairment, compared with controls.98

And in elderly dogs, deprenyl treatment started while the animals were in late mid-life led to 80% survival of treated animals to the end of a 26-month study, while just 39% of placebo dogs were alive. Interestingly, when the first dopamine-treated dog died, 12.2% of the placebo animals had already succumbed.78


The Vicious Cycle of Increasing Levels of MAO-B


As the MAO-B enzyme begins to invade our brain and devour our precious reserves of dopamine, our life span begins to shorten.50,63-66 Why?

It turns out that excess MAO-B not only destroys functioning brain cells, but replaces these healthy cells with non-neuronal "zombie cells" (called glia cells) that continue to manufacture even more MAO-B.25,67,68

You can see that once started, this becomes a vicious cycle that increasingly depletes dopamine production and destroys functioning brain cells and progressively leads to a shortened life span. Without intervention, the aggression of the MAO-B enzyme can result in an early death.

Wild Green Oat Extract Inhibits MAO-B


A patented extract from wild green oat has shown potent MAO-B-inhibiting properties. A series of human studies have demonstrated neurological-enhancing effects.

Wild green oats are younger plants (different) than those used for cereal grains. They have a long history of traditional therapeutic use in supporting mental health and cognitive function.47,69 Extracts of this "oat herb" are now widely used for indications that include anxiety, tension, stress, excitation, and other neurologic problems.69

Given the brain protective and longevity benefits of deprenyl, European scientists turned to wild green oats in search of a natural MAO-B inhibitor. A patented extract of wild green oat was developed after researchers screened 36 different varieties of wild oats for their ability to inhibit MAO-B.46

Once scientists identified the specific strain of wild green oat with the most potent biological activity, laboratory assays were conducted using various concentrations of the extract (based on standardized concentrations of isovitexin, a bioactive flavone molecule).

What they found was a 50% inhibition of the MAO-B enzyme by wild green oat extract at small concentrations.46 These findings show that this specific strain of wild green oat extract, by inhibiting the MAO-B enzyme, could have the potential of raising dopamine levels in the brain.

Demonstration of significant MAO-B inhibition by wild green oat extract would not only be a safe and inexpensive means to improve cognitive function in aging adults, it would also be likely to have favorable impacts on life span itself.

Wild Green Oat Extract in Lab Studies


Once the potency of wild green oat extract had been standardized, a study of laboratory rats was conducted to examine actual changes in behavior as a result of MAO-B inhibition from ingestion of the extract.

Animals were fed for seven weeks with either a normal diet or one supplemented with two different dosages (low and high) of the wild green oat extract. All three groups then underwent a series of behavioral tests.69

In this study, the animals showed impressive gains in learning and memory formation. Animals supplemented with the lower dose made significantly fewer mistakes in learning, learned tasks faster, and demonstrated accelerated memory formation, compared with either control or high-dose rats. As an important added benefit, low-dose supplemented rats showed increased social interest in other animals and improvement of their reactions to social signals from others.

This response highlights the essential value of raising the "feel-good" aspects of dopamine levels by properly inhibiting MAO-B. These results are consistent with findings in the literature on the use of pharmaceutical MAO-B inhibitors in Parkinson's disease patients.69

In another study in rats, scientists used an electroencephalogram (EEG) to evaluate the impact of wild green oat extract supplementation on specific areas of brain activity. The researchers were looking to measure changes in neurotransmitters as a result of ingesting wild green oat extract.70 These changes can be "mapped" and compared to those produced by known drugs that would produce similar behavioral outcomes.

Within the first hour of oral administration, the supplemented animals demonstrated positive changes in their electrical brain activity.70 The most impressive changes were seen in electrical frequencies that are known to be controlled by dopamine.

This confirmed previous studies showing that the wild green oat extract activates the dopamine-signaling system. In fact, the EEG signatures induced by the extract closely resembled those of known antidementia drugs.

Human Study Reveals Similar Finding


Scaling up from the animal studies, a similar investigation into EEG changes resulting from ingestion of wild green oat extract has now been conducted on humans. This enabled researchers to further validate the dopamine-promoting effects of wild green oat extract.36

In a human study testing concentration skills, a group of healthy males and females, aged 30 to 60 years, took a single dose of wild green oat extract at 1,250 or 2,500 mg or placebo. Using a specialized EEG brain mapping, positive changes were shown in the green oat groups during concentration tests in an area of the brain essential for cognitive function (the left frontotemporal lobe).

This EEG brain mapping also showed significant increases in the power of theta brainwaves that are involved in focusing attention and detection ofsignals.71

Signal detection, as measured by theta wave power, is an essential component of the process by which we recognize familiar faces and objects, skills that are all too often lost to neurodegenerative diseases.72,73 Theta brain activity is an important marker of cognitive health. It is well known that Alzheimer's patients have heartbreaking difficulties recognizing the faces of loved ones.74,75

Wild Green Oat Reduces Mental Errors

Wild Green Oat Reduces Mental Errors

A study was conducted among a group of elderly people, some of whom showed signs of mild cognitive impairment while others in the group showed no cognitive impairment. The researchers wanted to look for measurements of cognitive performance after taking wild green oat .35

Subjects were randomly assigned to receive single doses of the oat extract once a week. The three doses in the study were 0 mg (control group), 1,600 mg, or 2,400 mg. This was a "crossover" design, so that each subject was rotated through all three dosages and received each treatment arm on separate occasions, allowing each participant to function as a control.

Using the Stroop Color-Word Test, subjects were tested for a range of cognitive functions including memory, executive function, catching errors, appropriate response, and attention. It focuses on two key areas of the brain's cortex. In the test, participants must look at a card covered with words that name colors. The difficulty is that each word is printed in a color that does not match the word (e.g., the word "RED" printed in blue). They are first asked to read all the words as quickly and accurately as possible. They are then asked to name the color of each word, disregarding the word name itself.76,77 While the test sounds simple, it is highly diagnostic with regard to cognitive abilities and brain health.

In this study, those not given the wild green oat extract made an average of 3.39 errors on the test. The study subjects receiving 1,600 mg of wild green oat extract group made only 1.2 errors, a significant improvement of 65%.

In the group of subjects that had no diagnosis of mild cognitive impairment, the improvement was even more dramatic, with patients taking the wild green oat extract averaging just 0.55 errors compared to placebo recipients, who averaged 2.13 errors. This represented a significant 74% improvement in this test of mental acuity for those taking wild green oat extract.

In this study, even those patients with mild cognitive impairment had a 26% reduction in a score that measured how distraction affects mental performance and the ability to concentrate (lower scores reflect better performance).

The conclusion from this study is analogous to lab experiments involving deprenyl that suggest that the earlier MAO-B inhibition is initiated the better chances of preserving brain function during aging.78

Interestingly, the higher dose (2,400 mg) of green oat extract did not show this cognitive improvement, indicating that excessively supressing MAO-B does not elicit desired effects.76 This is analogous to deprenyl, where lower doses are shown to be more beneficial in some studies.79

Boosting Cognitive Function


Wild green oat extract has been associated with improving mental processing time and speed.

In a soon-to-be published study, 42 healthy middle-to-older aged adults (mean age 59), with self-reported age-related cognitive decline, were given a single dose (800 mg) of wild green oat extract. Before and after the dose, they were given a battery of neuro-cognitive tests administered by computer.80

Supplemented subjects showed significantly faster responses to stimuli compared with placebo recipients, taking less time to plan and complete specific tasks. Supplemented subjects also performed significantly better on memory-related tasks, making fewer errors in recalling words after a delay, and achieving greater accuracy in remembering spatial arrangements of objects.

Those who were given wild green oat extract showed a 180% increase in speed in the "global speed of performance test" compared to those given only the placebo.

These human trials represent a promising advance in the preservation of brain health.

MAO-B and Brain Disease

Both Parkinson's and Alzheimer's diseases have now been found to be associated with elevated MAO-B activity, even greater than those found in healthy people of the same age. This suggests a potential causative effect, due to the decreased dopamine availability, or the increased oxidant stress caused by MAO-B or both.53,60,68

One study found that MAO-B activity in Alzheimer's patients was higher than in controls in all brain regions studied: up to 70% higher in white matter, and 20-50% higher in gray matter regions.99 Another study showed that Alzheimer's brains had up to 3-fold increased MAO-B activity compared with controls, with the bulk of the excess located in precisely the areas of greatest loss to Alzheimer's patients, areas concerned with emotional processing, cognition, and personality.100

Aging people even without clear-cut diagnoses of neurodegenerative diseases also show evidence of substantial loss of brain cells, which may contribute to loss of cognitive performance and premature mortality.101-104 Given the cell-killing effects of excessive MAO-B, it seems likely that this brain shrinkage is related to increased activity of that enzyme, suggesting a potential mechanism for the life span-increasing effects of compounds that inhibit MAO-B.105-107


Improved Blood Flow to the Brain


Wild green oat extract has demonstrated improvements in tests of systemic endothelial function and cerebral vascular responsiveness, as shown in a recent human study.

The study evaluated healthy adults older than 60 years, providing them with 1,500 mg a day of wild green oat extract or placebo.81

By the end of the 12-week study period, the group receiving wild green oat extract had a significant 41% increase in measurement of flow mediated dilation, indicating an improvement in endothelial function.

The study also showed that cerebral vascular responsiveness increased significantly by 42%, suggesting the middle cerebral artery's ability to dilate in response to stress increased.

The ability of wild green oat extract to improve endothelial function as well as cerebral vasodilator function is a property that should capture the attention of anyone wishing to protect and improve their brain health and cognitive function.

"This is the first study in humans to show sustained improvement of cerebral vasodilator function following a chronic dietary supplementation," researchers state.

Impairments of blood flow to the heart and brain are common ailments of aging.82,83

Compromised cerebral vasodilator function has been reported as an independent predictor of stroke and transient ischemic attack.84

Impaired endothelial function is a well-established biomarker for future cardiovascular disease and cardiac events. 85-87

The tests used in this study assessed blood flow markers to the brain and other parts of the body. Wild green oat extract supplementation improved outcomes in both of these tests of vascular function.

Green Oats and Smoking Cessation


Dopamine controls our sense of accomplishment and the cycle of addiction.

When a tobacco user smokes or ingests nicotine, it binds to brain receptors that results in the release of dopamine, producing a satisfying, even euphoric, initial sensation.47,88,89

But once the stimulus goes away, the user is left with a relative dopamine deficiency, which produces cravings and eventually dependence on yet another dose of nicotine.88,90

Japanese scientists realized that this sequence of events was ripe for intervention with a product that worked along dopamine pathways. Wild green oat extract was selected as a test product.47

A group of male smokers, who all used different cigarette brands, was given 300 mg wild green oat extract taken after each meal ( 900 mg per day) for 28 days. Average cigarette consumption prior to supplementation was almost 20 cigarettes (one pack) per day, but after the end of the study, average consumption fell to just 8.9 cigarettes per day. This was an astounding 54% decrease in tobacco intake versus baseline.

Scientists are aware that dopamine is involved in both addiction and reward stimulus in the brain. This study demonstrated how wild green oat extract could significantly reduce smoking by improving dopaminergic transmission.

The discovery that the dopamine-enhancing effects of wild green oat extract can reduce cigarette consumption may be a revolutionary advance in the science of smoking cessation.

Summary


Aging exposes our brain to increased MAO-B, which results in dopamine deficit, loss of brain cells, cognitive decline, and risk for early death.

Deprenyl, a selective inhibitor of MAO-B, has been proven to ameliorate dopamine deficiency and improve cognitive functions. Numerous animal studies demonstrate that regular deprenyl administration produces increases in life span.

The FDA does not allow Americans the use of deprenyl for the treatment of any longevity-related disease, or any disease for that matter except for Parkinson's.

Fortunately, diligent research has yielded an exciting alternative. An extract from a specific strain of wild green oat has demonstrated MAO-B-inhibiting activity. Animal studies have established improvements in dopamine-related behavior and brain activity.

Human studies confirm significantly better performance on tasks of cognition and memory in response to this wild green oat extract, as would be expected from an MAO-B-inhibiting compound.

Improved indicators of blood flow to the brain and other parts of the body, along with a reduction in addictive behavior are among the quality-of-life enhancing properties of this natural extract from select wild green oats. Reprinted with kind permission of Life Extension

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