Announcing Greater Rewards™ Capsules

Would You Like To
Enjoy Life More?

Would you like to feel a greater reward in life for everything that you accomplish?
Read on! You can have a more rewarding life!
There are two different types of people. Which type are you?
Which type would you like to be?

By Durk Pearson & Sandy Shaw®

Wealth is not his that has it but his that enjoys it.
— Benjamin Franklin

T he Stanford marshmallow experiment explores the two different types of people in the world: (1) those who plan and think ahead and are able to delay immediate gratification if there is a substantially larger reward later and (2) those who grab a small reward at once (impatient decision making) rather than wait for a larger reward later. The way children as experimental subjects responded to an offered immediate reward (one marshmallow) as compared to a larger but delayed reward (two marshmallows) in the Stanford marshmallow experiment was significantly associated with very important outcomes in life such as educational attainment, income, SAT scores, body mass index, and other measures of general success in life.

The Marshmallow Experiment

The study took place in the late 60’s and early 1970’s, led by Walter Mischel, who was at that time a professor of psychology at Stanford University.A1 Children (4–6 years old) were left with a marshmallow and told that if they didn’t eat the marshmallow and waited for the experimenter to return in about 15 minutes, they would get two marshmallows (the original one plus another). The simple choice was between a small reward immediately (if the child ate the marshmallow before the experimenter returned) or a greater reward if the child waited for 15 minutes. Of 600 children that participated in the experiments, a minority ate the marshmallow immediately and of those that tried to wait for the fifteen minutes, one third of them succeeded in getting the second marshmallow. It was reported that age had a lot to do with the ability to wait for the larger reward.

The Difference Between Those Who Waited And Those Who Didn’t

J. Adam Fenster / University of Rochester
A follow-up study in 1988C reported that, “preschool children who delayed gratification longer in the self-imposed delay paradigm, were described more than 10 years later by their parents as adolescents who were significantly more competent.” The second follow-up in 1990 reported that delayed gratification was associated with higher SAT scores. Especially interesting was the result of a 2011 brain imaging study of a sample from the original child research subjects (now in middle age), which found that those who had delayed gratification longer had more activity in the prefrontal cortex (importantly involved in executive functions such as planning).

Scientists know far more about the brain mechanisms involved in delaying gratification now than they did when these experiments were done. Interestingly, an important enzyme that degrades dopamine, a major constituent of the brain’s reward and reward seeking systems is involved and people with different versions of the gene encoding the enzyme have been identified to differ in their ability to delay gratification. Moreover, food components that can alter the function of the enzyme specified by that gene have also been identified, that have been shown to increase the ability to defer gratification.

Introducing (drumroll!!) Our New GREATER REWARDS Formulation for a More Rewarding Life!

We are proud to introduce our new Greater Rewards capsules. One of the principal ingredients is EGCG. EGCG is the major polyphenolic catechin in green and white tea and is able to do many things. EGCG’s ability to promote the Dopaminergic Reward System by inhibiting COMT (catechol-O-methyltransferase), an enzyme that metabolizes catecholamines (degrading dopamine and adrenaline/noradrenalineA1) can be a powerful element of human behavior and, indeed, of the pursuit of happiness. Therefore, we designed a formulation containing EGCG (and several other important co-factors) specifically for the purpose of promoting Greater Rewards and the Rewarding Life. You can get more rewards out of life by taking this new formulation. Experimental evidence supports the notion that by inhibiting COMT, EGCG can provide you with a close simulation of the naturally inherited COMT allelic version that gives you more rewards out of life by providing higher levels of dopamine than other allelic versions of COMT. This is an example of the sort of modifications people will have the opportunity to take advantage of—to go beyond their inherited version of some biological molecules to better versions that other people were lucky to be born with. You can put more rewards into your daily life!

Reward Responsiveness Is a Key to the Enjoyment of Life

EGCG and the other ingredients in our formulation do not alter your genetic code. They reduce the activity of an enzyme that is a product of your genetic code so that the enzyme degrades less of the important neurotransmitter, dopamine. COMT is a powerful protein that has a lot to do with how you decide between doing something for a small reward right away or foregoing the small reward to pursue a larger reward that you would receive sometime later—the sort of choices you make every day and that can make the difference between success and failure and between more happiness or less.

We all have two copies (alleles) of the COMT gene, one from each of our parents. The Val allele (compared to the Met allele) of COMT is associated with a higher level of enzymatic activity. As COMT degrades dopamine, the higher level of COMT lowers prefrontal cortex dopamine levels. “The G>A mutation that produces a valine-to-methionine (Val/Met) substitution within the catechol-O-methyltransferase (COMT) gene has been widely researched and associated with several behavioral disorder phenotypes …”E In one study,1 researchers conclude that, “[o]ur research suggests that the Val allele predisposes individuals to a low level of baseline activation in the left DPFC [left dorsal prefrontal cortex] which then biases them toward impatient choices.” By “impatient choices” the researchers mean a preference for smaller rewards right away as compared to greater rewards delayed into the future (delayed gratification).

Why Some People Get More Sense of Reward from the Same Action as Other People Do and How To Increase Your Brain’s Perception of Reward

Researchers in one paperE report that “subjects with the Val/Val genotype generated almost similar amounts of PA [positive affect] from a ‘very pleasant event’ as Met/Met subjects did from a ‘bit pleasant event.’“ In other words, the rewarding effect for the Val/Val subjects was less than that for the Met/Met subjects. As the authors explain,E “variation in COMT Val158Met genotype moderates the ability to experience reward from events that happen in the flow of daily life. Ability to experience reward increases with the number of ‘Met’ alleles of the subject, and this differential effect of genotype was greater for events that were experienced as more pleasant.”

In another paper,B 244 volunteers participated in experiments designed to determine reward-responsiveness and risk-taking/reward-seeking (how much risk individuals would accept in the pursuit of reward) behavior. The risk-taking/reward-seeking task, for example, had people inflating a balloon visible on their computer screen with mouse clicks. They received a monetary bonus if they stopped inflating before the balloon burst; otherwise, they lost all their earnings. The researchers hypothesized that the individuals with a greater sensitivity to reward would make riskier decisions in the pursuit of reward. The results, in fact, supported their hypothesis in that the subjects with the Met/Met version of COMT (more sensitive to reward) did make riskier decisions. Importantly, however, the Met/Met (lower rate of dopamine destruction) individuals also earned more money in the long run. Their stronger desire to pursue greater rewards—and not be defeated by occasional loses—better tracked the real risk versus reward situation.

In their paperB the authors provided helpful summations of the current research on reward responsiveness: “… researchers argue that sensitivity to reward may be a crucial factor in performance on cognitive tasks, particularly those assessing executive [higher cognitive] function.”

More Pleasure in Activities of Daily Life

In fact, the researchersB note that “… evidence based on experience sampling methods suggests a COMT-genotype by environment interaction whereby exposure to environmental rewards (pleasant events in daily life) leads to significantly greater positive affect for Met homozygotes than for Val homozygotes.”

Just Knowing You Gave the Right Answer Provides Reward Independently of a Money Payment

“… [E]vidence shows that simply knowing one has answered correctly, in the absence of any feedback, activates ventral striatum, an area associated with mid-brain reward circuitry. Therefore, COMT genotype-dependent differences in cognitive performance may relate to the intrinsic reward associated with correct performance, regardless of explicit incentives.”B Some people are self-starters and self-motivators; they can maintain high levels of effort to be continually productive without constant supervision and feedback from a manager. We strongly suspect that this personality type has a lower rate of dopamine destruction.

In a 2000 paper,D researchers (including some of those who did the original marshmallow experiments) followed up by examining later life events in participants who had been part of the original marshmallow experiments. There they reported that children with sensitivity to rejection but who had delayed gratification in the marshmallow studies were (20 years later) buffered from the negative effects of rejection sensitivity. They had fewer interpersonal problems (as compared to rejection sensitive children that didn’t delay gratification) such as aggression and peer rejection and diminished well-being (a low sense of self-worth and higher abusive drug use). Importantly, the children who delayed gratification were less likely as adults to abuse drugs.

The COMT Data May Support an Inverted-U Model of Dopamine Function

An inverted-U model simply means that the effects of low levels of dopamine are different from and often opposite to those of high levels of dopamine. The optimal effects are generally found at the concentration of dopamine at the peak of the inverted U.

The amount of dopamine for optimal effects will depend upon the task at hand. For example, one paperF explains that an inverted-U relationship between the amount of dopamine and prefrontal cortex function could result in performance “in which too little or too much dopamine signaling impairs working memory.” As they further explain, “Val-COMT subjects, with their higher COMT activity [and lower dopamine release], sit to the left of Met-COMT subjects. COMT inhibition will thus tend to move Val-COMT subjects closer to the optimum and enhance performance, while moving Met-COMT subjects beyond the peak and impairing performance.” What this means is that the optimal amount of a COMT inhibitor would depend on the baseline level of COMT-regulated dopamine levels as well as on the sort of task which a subject is working on and on the range over which dopamine release is optimal (the peak). There are gender effects as well. See the next section.

Determining the Optimal Dose of EGCG for a More Rewarding Life

Most neurotransmitters work as a U shaped curve, where the effects are different at the low-end dosages and the high-end dosages, but generally provide desired effects at medium doses. Hence, the optimal amount of dopamine depends on each individual and also on the task at hand and requires a little self-experimentation. Nothing too unusual about that—remember how you learned to use the common neuromodulator caffeine, which at low doses does not give you the energy you want but at too high doses can produce a lot of side effects, such as anxiety and excessive excitation. You quickly learn where in the middle range of caffeine doses you feel most energized but comfortable. One way caffeine works is to inhibit the breakdown of the second messenger cyclic AMP (a signaling molecule for adrenaline and noradrenaline). You can feel these effects.

What Else Does Greater Rewards Contain?

Another ingredient in our Greater Rewards is taurine.

Taurine Increases Dopamine Levels in the Dopamine Reward System

The rat dopamine reward system is organized like that of humans, with the mesolimbic dopamine neurons projecting from the ventral tegmental area to the nucleus accumbens. Researchers looking for receptors involved in the regulation of dopamine in this pathway reportedMA that local perfusion of taurine (by microdialysis) increased dopamine levels in the nucleus accumbens reward center and that this involved taurine acting as an agonist at (activating) glycine receptors. (Yes, these pathways are complex, but the bottom line here is that evidence indicates that taurine may induce elevation of dopamine in the reward system.)

Taurine Involved in Learning and Memory

Interestingly, taurine is found at high concentrations throughout the brain. The extent of its functions such that these high concentrations are required have not been entirely clarified. A very recent 2014 paperMB reported that “taurine uptake is necessary and cooperates with other neurotransmitter systems in the induction of L-LTP [the late phase of Long Term Potentiation, an important process in learning and memory].”MB

An Age-Related Decline in Striatal Taurine Is Correlated with a Loss of Dopaminergic Function

We include taurine because it is known to decline with age in various areas of the mammalian brain and is associated with age-associated decline in spatial learning. Aged and young rats were tested for their performance in the dreaded Morris water maze (you know, the one where the rats are tossed into a tank of water pigmented to be opaque and, desperately treading water, have to find a hidden platform to safely escape from drowning in the water) and examined their performance in finding the platform, as well as the level of striatal taurine. In that study,L the researchers reported that “[s]triatal taurine was the only amino acid that varied as a function of age or learning impairment. Taurine levels were reduced in aged animals, regardless of impairment, although the reduction was only significant in impaired rats.”L

Taurine Supplementation Reverses Age-Associated Cognitive Impairment

“Aging in rats is associated with a taurine-deficient state that is reversible by dietary supplementation,” the same researchers (as those who produced paper L) conclude in a paper they published at about the same time in Mechanisms of Ageing & Development.M “Urinary excretion of taurine was significantly (p<0.05) reduced in aged rats indicating an increased need to conserve taurine.”M In this study, male F344 rats—18 months of age (old) and a group of the same type rats that were 1 month old at the start of the study—were put on a normal rat chow diet (controls), a taurine supplemented diet (same rat chow + 1.5% taurine in their drinking water), a taurine deficient diet that was identical to the rat chow except that a plant protein was substituted for the taurine that would normally be part of the rat chow at 0.02%. The researchers did not explain how or why the tissue content of taurine declines with age. They observed declines in tissue content of tryptophan as well. The effects of taurine supplementation included correction of the age-associated loss of taurine in tissues and a blunting of the age-related decline in serum IGF-1 concentration. IGF-1 (insulin-like growth factor one) is the principle cause of the actions of growth hormone.

Increasing the Bioavailability of EGCG with Vitamin C

“Catechin losses of approximately 80%, including almost total degradation of EGCG, have been observed during simulated digestion of simple tea infusions.”L2 Vitamin C has been found to help maintain catechin content in ready-to-drink tea beverages, so we added vitamin C to our Greater Rewards to help protect the bioavailability of EGCG. At the pH of the small intestine (pH 7–8),L2 catechins undergo chemical changes (they are reported to be deprotonated to form a semiquinone and vitamin C has been found to reduce these reactive catechin semiquinone free radicals back to their native forms before undergoing further degradation).L2

Increasing the Intracellular Concentration of EGCG by Combining EGCG and Quercetin

We also added quercetin to our Greater Rewards formulation because the combination of quercetin and EGCG act together synergistically to inhibit COMT.L3 In LNCaP prostate cancer cells, EGCG and quercetin synergistically enhanced the antiproliferative activity of EGCG. The researchers proposeL3 that the mechanism responsible for the results of their study might be that EGCG primarily inhibited COMT activity while quercetin reduced the amount of the COMT protein.

Why We’ve Added Thiamine to Our Greater Rewards

Another ingredient in our Greater Rewards is thiamine. Why thiamine? Though you are undoubtedly aware that thiamine is an essential vitamin that is probably included in every multi-vitamin supplement (at low RDA levels) on the market, you probably don’t know much about the many effects thiamine has on brain (as well as body) functions. For example, intrastriatal administration of the thiamine metabolites thiamine triphosphate or diphosphate has been shown to induce dopamine release in the rat brainM2 and these thiamine derivatives are known to be present in high concentrations in the human substantia nigra.M3 Moreover, “[p]atients with PD [Parkinson’s disease, which is caused by damage to dopaminergic neurons] that have undergone levodopa therapy [to increase dopamine levels] show significantly higher cerebrospinal fluid (CSF) levels of thiamine diphosphate (TDP) and total thiamine than those patients who are not treated with this drug.”M3 Interestingly, plasma thiamine levels have been shown to be decreased by 76% in type 1 and 75% in type 2 diabetic patients.M3

In a small clinical trial by the same authors,M3 thiamine was reported to improve symptoms associated with Parkinson’s. According to the authors, within days of thiamine treatment, patients reportedly had smiles on their faces, walked normally with longer strides, increased their arm swings, and experienced no tremors. Three of the patients were said to no longer require carbidopa or levodopa treatment but did not experience negative effects on their movements as a result. These are said to be “preliminary” results, suggesting caution in their interpretation.

P53, which regulates cell death in response to DNA damage, has been found to be significantly increased in the caudate nucleus of patients with Parkinson’s disease as compared to controls.M4 Thiamine has been reported to reduce intracellular P53 activity.M4 This is another potential link between thiamine and Parkinson’s disease and the dopaminergic nervous system.

It is also reported that thiamine absorption decreases with age.M4

Next, We Also Added Hesperidin for Neurogenesis: Stir Gently, Count the Number of Surviving Neural Progenitors, and Feel the Zest

Neurogenesis is the creation of new neurons that takes place in adult mammals in particular areas of the brain. This process enables adults to maintain the ability to learn throughout life. But the mechanisms that make neuro-genesis possible become less effective with age,M4B thus rendering older people less able to produce new neurons and, consequently, less able to deal with complex cognitive activities necessary for rewarding adaptation to ever-changing conditions. As people age, they tend to use compensatory mechanisms to help deal with their less effective cognitive functions. For example, when faced with complex problems, older people generally use more areas of the brain than do younger people.

There is quite a bit known now about how neurogenesis works. It has been found possible to improve the process so that it functions more like that in young individuals by using specific nutrients, food components, herbs, or certain drugs. We have added hesperidin, a flavonoid widely found in fruits and vegetables, for its ability to promote the survival of neural progenitors that are developing into mature neurons.M5 The effect of hesperidin on neural progenitors in cell culture was due to increased survival rather than increasing proliferation.M5 An earlier paper M52 by the same authors found hesperidin to reduce neuronal death by 50% after 48 hours of 10 μM hesperidin treatment in culture. Hesperidin-primed astrocytes were protected against neural progenitor death.M5 A significant advantage of having a larger population of young newly developed neurons is that they tend to be more youthful (have more energy, are more active and more responsive to stimuli, and learn more easilyM6) than mature adult neurons, thus helping maintain that youthful zest for life.

Is the world moving too fast for you? Do something about it by nurturing your newborn neurons!

OVEREATING May Be a Way to Increase Low Dopaminergic Activity in Certain Areas of Your Brain

A new paperG examined the effects of the glycemic index of food eaten by subjects (12 overweight or obese men aged 18–35) on cerebral blood flow as a measure of brain activity. “Compared with an isocaloric low-GI meal, a high-GI meal decreased blood glucose, increased hunger, and selectively stimulated brain regions associated with reward and craving in the late postprandial period, which is a time with special significance to eating behavior at the next meal.”G Strikingly, the striatal dopamine D2 receptor (important for reward) was significantly lower in obese individuals than in their non-obese but otherwise matched controls, suggesting the possibility that overeating may be a way to increase dopamine release as a compensation for the low dopamine D2 receptor level.

One implication of this plausible but controversial hypothesis (evidence is inconsistent) is that decreasing COMT activity via supplementation with EGCG, quercetin, and other co-factors could be a way of increasing dopaminergic release that may reduce the desire to overeat. The ability to inhibit impulsive eating that might result from less activity of COMT may be beneficial for reducing the risk of overweight or obesity. Those who delayed their gratification on the marshmallow test (later found to have slower destruction of dopamine) had lower adult body mass indices.

The authorsG explained that they used ASL, a novel imaging technique that provides a quantitative measure of cerebral blood flow instead of the usual imaging technique, BOLD, which provides acute changes in blood flow, not absolute differences. The authors conclude that, “a reduced consumption of high GI carbohydrates (specifically, highly processed grain products, potatoes, and concentrated sugar) may ameliorate overeating and facilitate maintenance of a healthy weight in overweight and obese individuals.” We are excited by these data that suggest (but do not prove) that increasing dopaminergic reward by inhibiting COMT may make it easier to avoid the impulsive overeating that sustains overweight and obesity.

The accompanying editorial that commented on paper #GGC thought that the activation of the brain might be associated with an increase in glucose by the high GI meal, the main brain fuel, rather than increased dopaminergic activity. Still, a rewarding effect involving dopamine in conjunction with an increase in glucose is also plausible.GC1,GC2 Only additional research will provide more definitive answers.

Another very recent paperH reported that administering oleoylethanolamine, a gastrointestinal lipid messenger that is a satiety signal suppressed by high fat intake, to high-fat fed mice, resulted in an increase in dopamine release in the brain dopamine reward circuitry. The researchers concluded that their findings suggest that a high fat diet decreased gut-induced dopamine signaling in the brain and, hence, overeating was an attempt to increase the dopamine release with its rewarding effect. When the high fat-fed mice were given oleoylethanolamine, it increased oral intake of low fat food. Thus, the authors suggest, increasing dopamine release in the brain reward circuitry could be a way to increase the reward value of less palatable, but healthier, foods. Studies in obese humans have also reported dopamine receptor deficiency in the dorsal striatum.H Once again, a study appears to indicate that excess calorie intake is linked to a deficiency of brain dopamine reward signaling.

Another Explanation for Why “Comfort” Foods Might Increase Dopamine Release in the Brain

Another reason for eating high fat foods (“comfort food”) might be to experience increased reward as a result of increased dopamine release. Some evidence to support this is derived from the fact that a short-term high fat diet induces expression and activity of the TLR4/NFkappaB signaling pathway.H1 Another paper reports that NFkappaB inhibits COMT (catechol-O-methyltransferase),H2 the enzyme discussed above that degrades dopamine in the brain’s reward circuitry. By decreasing the activity of COMT, increased NFkappaB expression would decrease dopamine degradation, thereby increasing dopamine signaling, a plausible mechanism for increasing the reward of eating high fat foods. It may be, therefore, that EGCG and co-factors could reduce the reward of high fat foods compared to healthier alternatives by decreasing the activity of COMT.

An earlier studyJ reported that oligofructose (a prebiotic) promotes satiety in rats fed a high fat diet and that this involved glucagon-like peptide-1 (GLP-1). We wonder whether there was an increase in dopamine release in the brain’s reward circuitry such as seems to have occurred with oleoylethanolamine, another satiety signal (see paragraph above). If so, it would suggest that oligofructose consumption is another way to reduce overeating by increasing the rewarding effect of food. The authors note: “The addition of OFS [oligofructose] in the diet protects against the promotion of energy intake, body weight gain, fat mass development, and serum triglyceride accumulation induced by a high fat diet.”J Referring to another paper, they point out: “A significantly reduced daily food ingestion in oligofructose (OFS)-fed rats is a phenomenon contributing to the improvement of steatosis [fatty liver] and glycemia in obese Zucker fa/fa rats or diabetic rats, respectively.”

COMT Is a Gene Contributing to Sex Differences in the Brain

Interestingly, extensive studies of genetic associations between COMT and cognition and various psychiatric disorders indicate that COMT affects male and female brains somewhat differently.K For example, the low dopamine destruction activity Met allele was reported to be associated with obsessive-compulsive disorder (OCD) in men, but not in women.K The COMT-OCD relationship is said to be (as of 2008, the year this paper was published) “arguably the clearest evidence to date for a sexually dimorphic autosomal genetic association with a psychiatric disorder.”K In a separate paper, the results of 5000 participants in a longitudinal study on cognitive development in children between 8 and 10 included finding that the Met allele was associated with better cognitive function in several domains, but largely in or limited to boys. The study showed, for example, that boys homozygous for Met (having two Met alleles) had a verbal IQ 3 points higher than Val homozygotes, but that girls homozygous for Met had verbal IQ less than 1 point higher than girls homozygous for Val. Moreover, pubertal boys homozygous for Met had verbal IQ 10 points higher than boys homozygous for Val.K In another study described here,K the Val allele was associated with sensation-seeking in women. (This may be an example of a behavioral attempt to increase dopamine reward when dopamine destruction is naturally higher. This is a speculation on our part.)

How Does EGCG Inhibit COMT?

A recent paperA2 reviewed how EGCG prevents dopamine degradation by the enzyme COMT (catecholamine-O-methyltransferase). COMT degrades dopamine to form 3-O-methyldopa (3-OMD). Inhibiting COMT reduces the levels of 3-OMD. It has been suggested that EGCG can bind with a high affinity to the catalytic site of human COMT, functioning similarly to an irreversible noncompetitive inhibitor. In this way, EGCG would prevent both dopamine and its precursor L-DOPA from reaching the COMT catalytic site to be degraded to 3-OMD.A2 (EGCG, quercetin, and other co-factors may be a beneficial addition to the regimen of Parkinson’s disease patients taking L-dopa to increase brain dopamine levels in the striatum.)

Expectation of Future Rewards:
How Government Policy Destroys Work Ethic by Reducing Expectation of Future Rewards

The form (alleles) of COMT that we inherited has a major impact on how we select between a small reward that we get in the very near future and a larger reward that we have to wait for a longer time into the future to get. Having the Met allele (a lower activity of COMT means less degradation of dopamine, hence, higher levels of dopamine) results in a higher reward whether you choose goals in the short term, the medium term, or the long term. At least that is how it would work if the future rewards reflected a higher payoff for putting off a small reward now. The higher value is what is known as the future discount. That price is supposed to reflect the difference between the value you place on getting a small reward now rather than a larger one later in the future. What has happened with the Fed downward manipulation of interest rates is that it has set an artificially low price on the future discount, the value of the delay when you work for a larger reward later rather than a smaller reward now. For example, there is less incentive to save money because the Fed has set interest rates so low. Indeed, the Fed has explicitly stated that they have set interest rates artificially low to encourage spending and to discourage savings!

Where COMT could foster behavior to seek a larger reward for a long-term investment of hard work and inventiveness, the Fed makes it difficult to realize that reward for the long term. It essentially promotes the consumptive use of resources in the short term and offers disincentives to save for future investment.

We hope that by offering an innovative way to increase the rewards of the dopaminergic reward system by inhibiting COMT with EGCG and co-factors, people will once more turn their eyes to the future and to the potential of working over a longer term for larger rewards. Our long-term reward would be to see a better world and to have helped a little to make it happen, while the short-term reward (of less importance) would be (hopefully) some extra income.

Live Long & Prosper with a Rewarding Life from Greater Rewards!

Dosage of EGCG to Use

We base our recommended dose of EGCG on the amount found in the number of cups of green tea consumed by millions of people daily worldwide and that have been so consumed for thousands of years. Each capsule contains about as much EGCG as is contained in a cup of fresh brewed green tea. As with any natural product, too much can have undesired effects. In the case of COMT, excessive inhibition could theoretically result in decreased methylation of catechol estrogens, resulting in conversion to estrogenic metabolites with a pro-cancer effect. We do not think this is likely, however, as the long-term safety of drinking green tea does not suggest a potential to increase cancer—in fact, it is quite the opposite in that studies suggest reduced risk of various cancers with green tea consumption. The general safety profile of natural products tends to follow a “U” or “J” shaped curve, where the effects are different at the lowest and highest doses as compared to the most beneficial effects usually occurring at the middle doses.

We always consider potential downsides of the use of any natural product when taking it alters natural physiological processes. Remember chapter 8 in Life Extension, a Practical Scientific Approach where we ask “Is Anything Perfectly Safe?” the answer we gave was a single word: “No.” You don’t need the FDA to tell you to always fasten your seatbelt. If you want to live an exceptionally long time, it really pays to be careful.

We suggest that you start out by taking 1 capsule of Greater Rewards 2 times per day on an empty stomach. Then try 1 capsule 3 times per day. Over a few days, gradually increase your consumption to up to 2 capsules 3 times per day, depending how you feel. We take 2 capsules 3 times per day on an empty stomach.

You may want to vary the amount that you take depending on what you will be doing on any particular day. For example, if you tend to choke on tests or during competitive performances (such as golf tournaments), you might—or might not—want to reduce or skip your intake for that day. Different people have different COMT genotypes, and hence one size does not fit all people or all activities.

References

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