The Durk Pearson & Sandy Shaw®
Life Extension NewsTM
Volume 17 No. 4 • May 2014


Monetary Incentive-Induced Reward Learning Enhanced, Depressive Symptoms Decreased in Human Pilot Study

The results of a recent randomized, double-blind, placebo-controlled study involving 74 human subjects suggest that it might be a good idea to offer your employees (if you have them) free green tea to enhance their response to incentives such as raises or bonuses. The study1 found that participants receiving green tea for 5 weeks had improved reward learning (decreasing the reaction time in a monetary incentive delay task) compared to those receiving a placebo. Plus, the subjects showed improved mood scores on a measure of depressive symptoms.

Impairment of reward learning is associated with depression. Receiving a raise or bonus or similar incentive is not going to provide a rewarding boost to mood when depression has reduced your ability to respond to rewards (a state called anhedonia). Thus, the results of this study might be of particular interest to entrepreneurs trying to find ways to increase the rewarding effect of monetary incentives. The incentive trials allowed participants to earn money or to avoid losing money by pressing a button during the presentation of a cue (shown for a period of 4.5 to 9.5 seconds). The reaction time (time to push the button following the presentation of the cue) was taken as a measure of depression when response time was retarded.

The results showed significantly enhanced reward learning (faster response to the cue indicating an available reward) in those receiving the green tea. The tea was administered as 400 mg of green tea powder dissolved in hot water three times a day (one serving 30 minutes after each of three meals) and contained 45.6% of polyphenols as EGCG.

In discussing the mechanisms that might be responsible for the improvement in reward learning, the authors note that dopamine deficiency has been proposed as an important cause of anhedonia, an individual’s loss of response to rewarding stimuli in depression. “The mesolimbic and nigrostriatal DA [dopamine] system appears to be related primarily to reward system function and responsiveness to the environment.”1 “It has been reported that the active component of green tea, EGCG, inhibited psychostimulants-induced hyperactivity in part by modulating dopaminergic transmission.”1 “A recent study showed that green tea extract treatment can reduce hypothalamic-pituitary-adrenal (HPA) axis hyperactivity in response to stress in mice.”1 (See “Would You Like To Enjoy Life More?” in the March 2014 issue of Life Enhancement.)

Effects of EGCG on Brain Activity and Mood

Another recent paper2 reports on potential benefits of the green tea polyphenol EGCG on brain activity and mood. They refer to an earlier study showing a modest but significant association between green tea consumption and lower psychological distress. Green tea, of course, contains considerable amounts of EGCG but also other components that could have effects on psychological distress, such as theanine and caffeine.

In this human study, there were 31 volunteers (mean age 27.74 years, SD (standard deviation) 9.28, with 12 males and 19 females). This was, therefore, a small study but the researchers measured a number of interesting parameters that are not generally included in studies of mood, specifically EEG data that included theta, alpha, and beta activity. The treatment (with placebo controls) consisted of 300 mg of Teavigo,® a caffeine-free purified and refined extract of Camelia sinensis (tea) that consisted of approximately 94% EGCG and 6% vitamin C (in the form of ascorbyl palmitate). The researchers note that the results of testing for cognitive and cardiovascular functioning was to be published elsewhere, while this paper reports on mood and resting state EEG.

The EGCG treatment was reported to significantly increase calmness and reduce stress as assessed by the Bond-Lader mood scale. More interestingly, compared with placebo, “EGCG administration was associated with a significant overall increase in alpha, beta, and theta activity (data not shown) more dominant in midline frontal and central regions.”2 The data were summarized in Figure 1b of the paper.

The researchers state that: “Previously an increase in both alpha and theta activity has been observed during non-directed meditation …” and they speculate that, “the changes in these same waveforms in the EGCG condition may reflect a relaxed yet attentive state due to the intervention.” (Keep in mind that this is speculative. Moreover, the EGCG was combined with ascorbyl palmitate and it has been reported that vitamin C increases the bioavailability of EGCG.3)


Mechanisms Identified for Protective Effect of EGCG Against Cognitive Dysfunction Resulting from Amyloid Beta Buildup As Occurs in Alzheimer’s

A recent study of a mouse model of Alzheimer’s disease4 reports that mice pretreated with EGCG for three weeks before receiving intracerebroventricular administration of amyloid beta had reduced toxic effects as compared to animals receiving the amyloid beta but not being pretreated with EGCG. The authors suggest, on the basis of their data, that, “EGCG may be a beneficial agent in the prevention of development or progression of AD [Alzheimer’s disease].”4

The mice receiving EGCG were given doses of 1.5 or 3 mg/kg body weight in their drinking water.

One of the measures of cognition used by the authors was the Morris water maze test, where treatment with amyloid beta resulted in significantly slower arrival times at the platform location (where the mice escaped the need to continually tread water), whereas pretreatment with EGCG (either dose) significantly inhibited the effects of amyloid beta on escape latencies.

The apoptotic death of neurons induced by amyloid beta was reported to be prevented by pretreatment with EGCG. The researchers explain that activation of MAP kinase and NFkappaB as well as the activation of alpha, beta, and gamma-secretase are implicated as causes of amyloid beta-induced neuronal cell apoptosis and that pretreatment with EGCG significantly inhibited the expression of these molecules. Other mechanisms were discussed in the paper.

EGCG Suppresses Gluconeogenesis in Liver Cells, Protecting Against Major Pathway Leading to Excess Blood Sugar in Type 2 Diabetes

Failure of feedback mechanisms to inhibit gluconeogenesis in the liver (eating is supposed to shut down gluconeogenesis, as glucose derived from food acts as a negative feedback signal) is a major reason for excess blood sugar in type 2 diabetics. The release of GLP-1 (glucagon like peptide 1) is a molecule involved in the feedback inhibition of eating to tell liver cells to stop gluconeogenesis. In a fairly recent paper,5 researchers were able to show in mouse liver cells that EGCG suppressed gluconeogenesis by activating 5’-AMP-activated protein kinase (AMPK), an important regulator of energy metabolism that responds to eating by (for one thing) suppressing gluconeogenesis. (The authors point out that the activation of AMPK is associated with EGCG-induced apoptosis in cancer cells, but that is another story.)

The results of this study suggest that EGCG could, as the authors note in their summary (last paragraph in the paper), point to a new therapeutic approach for the management of diabetes.5


  1. Zhang et al. Effect of green tea on reward learning in healthy individuals: a randomized, double-blind, placebo-controlled pilot study. Nutr J. 12:84 (2013).
  2. Scholey et al. Acute neurocognitive effects of epigallocatechin gallate (EGCG). Appetite. 58:767-70 (2012).
  3. Green et al. Common tea formulations modulate in vitro digestive recovery of green tea catechins. Mol Nutr Food Res. 51:1152-62 (2007).
  4. Lee et al. Green tea (-)-Epigallocatechin-3-gallate inhibits beta-amyloid-induced cognitive dysfunction through modification of secretase activity via inhibition of ERK and NFkappaB pathways in mice. J Nutr. 139:1987-93 (2009).
  5. Collins et al. Epigallocatechin-3-gallate (EGCG), a green tea polyphenol, suppresses hepatic gluconeogenesis through 5’-AMP-activated protein kinase. J Biol Chem. 282(41):30143-9 (2007).

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