The Durk Pearson & Sandy Shaw®
Life Extension NewsTM
Volume 12 No. 5 • October 2009


[O]f those men who have overturned the liberties of republics, the greatest number have begun their career by paying an obsequious court to the people; commencing demagogues, and ending tyrants.
— Alexander Hamilton, Federalist No. 1

Health Care Stats
For the year 2006, the total health care spending (U.S.) was estimated at $2.2 trillion, while, for that same year, the total estimated out-of-pocket expenses was $302.5 billion (with the rest out of taxpayers’ pockets); spending on complementary and alternative medicine was $33.9 billion, with natural products representing $14.8 billion (est.) of the spending on complementary and alternative medicine.
— Science Stats, Science News, August 29, 2009
(sources: 2007 National Health Interview Survey,
Centers for Medicare and Medicaid Services)

Universal [health] coverage is so expensive that Congress can’t get there without taxing Democrats.
— Michael Barone, Rasmussen Reports

A nation of sheep will beget a government of wolves.
— Edward R. Murrow

More on Tea (Camellia sinensis):
Cholesterol and Triglyceride Regulation, and Neuroprotection

Postprandial Triglycerides Reduced by Tea Catechins

Although elevated fasting levels of serum lipids can be significant risk factors for cardiovascular disease, much emphasis is now being focused on postprandial (after meal) lipid levels, which may be even more important risk factors.1

A recent paper1 reports that tea catechins attenuated the postprandial increase in plasma triacylglycerol (triglyceride) levels following a fat load in a randomized, triple-crossover design study of nine male subjects with mild or borderline hypertriacylglycerolemia (high triglycerides). A semi-purified extract of green tea was used for preparation of test beverages (10 mg tea catechins as control, 224 mg of tea catechins as moderate dose, and 674 mg as high dose). “Expressed as a percentage of control, the average reductions in IAUC [increment area under the curve] after a moderate and a high-catechin dosage were 15.1% and 28.7%, respectively. However, no significant effect on IAUC was observed between the control and the moderate dosage of tea catechins.”1

“The assumption that exaggerated lipaemia in the postprandial phase may be implicated in the early development of atherosclerosis is now widely accepted . . . .”

The authors referred to the results of other studies for possible mechanisms by which the tea catechins decreased postprandial plasma triacylglycerol in their own study. One such potential mechanism is the marked ability of green tea catechins to inhibit gastric and pancreatic lipases, thus limiting intestinal lipid absorption. Our ShapeShifter Teas Booster Caps™ contain 660 mg of green tea catechins per capsule, of which 330 mg is EGCG.

Suppression by Tea Catechins With a Galloyl Moiety on Postprandial Hypertriglyceridemia in Rats

In this study,2 a lipid emulsion was administered orally to rats along with epigallocatechin gallate (EGCG) at a dose of 100 mg/kg. The result showed that, compared to the lipid emulsion group that received placebo, there was a significant inhibition by EGCG in the plasma increase in triacylglycerol. In a second experiment, rats receiving the lipid emulsion along with 50–200 mg/kg of a tea extract comprised largely of catechins with a galloyl moiety, had suppressed increases in plasma TG (triglyceride) levels 1 and 2 hours after administration compared to those receiving distilled water. The suppression of the TG AUC (area under the curve) by the tea extract was statistically significant at 200 mg/kg. “Its plasma TG-lowering effect is thought to be produced by at least two different mechanisms, i.e., inhibition of the absorption of fat from the intestine, and activation of the catabolism of TG in the bloodstream.” In this study, the authors attribute the decrease in TG increase to the first mechanism (reduced absorption) because “the administration of catechins without the lipid emulsion had no effect on the plasma TG level.” Our ShapeShifter Teas Booster Caps™ contain 660 mg of green tea catechins per capsule, of which 330 mg. is EGCG.

Neuroprotection by Green Tea Theanine and Catechins

This review3 of neuroprotection by green tea components covers many studies, mostly in vitro mechanistic studies and animal model studies, but also a few human studies.

The author discusses the following: “An epidemiological study showed that the incidence of stroke was significantly lower in people who consume more than five cups of green tea (Camellia sinensis) per day.”

The researcher notes that the green tea component theanine (gamma-glutamylethylamide) is chemically similar to the excitatory neurotransmitter glutamic acid which, when released in excessive amounts (a condition called excitotoxicity), can cause damage such as forebrain ischemic neuronal death. The investigations of the author3 demonstrated that theanine has a neuroprotective effect in transient ischemic neuronal death.

As the author explains, glutamic acid “plays an important role in memory and learning by producing synaptic plasticity, known as long term potentiation (LTP) or long term depression (LTD).

“However, when the intracellular energy source ATP is depleted by injury such as ischemia, depolarization of the neuronal membrane leads to excessive release of glutamic acid and lack of ability to reabsorb this glutamic acid by the glutamate transporter, resulting in an excessive concentration of glutamic acid in the extracellular space.”

Since theanine may be an analog of the excitatory neurotransmitter glutamic acid, the author paid special attention to the effects of theanine as a possible competitor with glutamic acid in the binding of glutamate receptors. He discusses studies, in vitro and in vivo, showing protection by theanine against glutamate excitotoxicity. For example, he examined the neuroprotective effect of theanine against postischemic neuronal death in a transient ischemia model in gerbil hippocampus. The theanine treated animals received 50 µM, 125 µM, or 500 µM theanine before transient forebrain ischemia. “Ischemic neuronal death in field CA1 of the hippocampus was suppressed in the theanine-pretreated groups in a dose-dependent manner, with approximately 60% and 90% survival with theanine 125 µM and 500 µM, respectively.”

The author further discusses studies showing the binding of theanine to glutamate receptor subtypes, such as AMPA, kainate, and NMDA; though theanine’s binding capacity to these receptor subtypes was found to be much lower than that of glutamic acid, the author believes that theanine may still act as a glutamate antagonist. The author urges that more studies be done to clarify this.

References

  1. Unno et al. Effect of tea catechins on postprandial plasma lipid responses in human subjects. Br J Nutr 93:543-7 (2005). Biosci Biotechnol Biochem 69(7):1288-91 (2005).
  2. Kakuda. Neuroprotective effects of the green tea components theanine and catechins. Biol Pharm Bull 25(12):1513-8 (2002).

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