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Noradrenaline Storage & ReleaseIn order to understand how green tea works we need to take a quick look at noradrenaline storage, release, and metabolism. Noradrenaline is synthesized in the sympathetic nerves and stored in storage vesicles. When sufficiently stimulated, the vesicles migrate to the end of the nerve and release noradrenaline into the synaptic cleft. As you probably already know, the noradrenaline binds to the adrenergic receptors and stimulates thermogenesis. Next in the chain of events is noradrenaline metabolism, which involves two uptake mechanisms. |
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Noradrenaline MetabolismUptake 1: After stimulating the adrenergic receptors, 85-90% of the noradrenaline is taken back up into the sympathetic nerves (uptake 1) and stored in vesicles or metabolized by monoamine oxidase (specifically, MAO-A) in the mitochondria. The importance of uptake 1 (neuronal uptake) is reflected by the warnings against combining sympathomimetics (ephedrine, phentermine, etc.) that increase noradrenaline release with MAO inhibitors -- the risk of overstimulation would be much too high. Uptake 2: Some of the noradrenaline diffuses away from the receptors and is transported by extra-neuronal cells (uptake 2) and metabolized by catechol-O-methyl-transferase (COMT). Green tea increases noradrenaline in the synaptic cleft and safely increases thermogenesis because of its ability to prevent COMT from metabolizing noradrenaline. This is safe because COMT plays a much smaller role in catecholamine dynamics than MAO. COMT exists in both a soluble and a membrane-bound form. The soluble form of COMT is found in organs and it does not have as high of an affinity for catecholamines as the membrane-bound form.
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* There is more information on how caffeine enhances thermogenesis in the following posts: How ECA Works has illustrations and there is referenced information in The "A" in ECA and my Thermogenic FAQ. |
How Green Tea Stimulates ThermogenesisThe thermogenic effect of green tea involves two mechanisms: I.) green tea contains a catechin, EGCG, which inhibits catechol O-methyltransferase (COMT), an enzyme that degrades noradrenaline II.) the caffeine in green tea increases intracellular cAMP accumulation by inhibiting the enzyme, phosphodiesterase. See "How ECA Works" for more info on the importance of caffeine. I have already discussed the effects of caffeine in several posts, so I will focus on COMT. Interestingly, the medical literature showing that green tea inhibits COMT dates back over two decades (7-NA). By inhibiting COMT, green tea prolongs the life of noradrenaline in the synaptic cleft. (This lets noradrenaline stimulate the receptors for a longer time before it is metabolized). The in vivo (human) study by Dulloo et al. (1) found that, compared to placebo and caffeine, green tea significantly increased total 24 hour urinary noradrenaline excretion. The researchers commented on the significance of this:
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DiscussionAlthough this research is exciting, the fact remains that green tea does NOT normalize the release of noradrenaline (the primary obesity-causing defect) -- it prolongs the action of whatever amount of noradrenaline that your body is able to release. For this reason, Dulloo concluded that the thermogenic effect of green tea is "likely to be highly dependent upon the release of endogenous NA [noradrenaline]." Clearly, green tea (by itself) is going to be a "your mileage may vary" situation. However, tissue studies performed by Dulloo et al. showed that green tea produced a significant synergistic effect when it was combined with ephedrine or ephedrine/caffeine (2). Since green tea prolongs the action of noradrenaline, you would think that it would have a stimulatory effect. However, Dulloo et al. noted that green tea caused no significant differences in heart rate. The most logical explanation for this is that the stimulatory effect of increased noradrenaline action is being countered by other mechanisms. For example, green tea contains the amino acid, theanine, which has been found to lower blood pressure (8). Green tea also has a vasorelaxing effect (9, 10). One recent study found that regular tea consumption had no significant effect on blood pressure (11), but it is difficult to achieve a therapeutic dose without taking concentrated supplements. Further complicating the picture, however, is the fact that they also found that green and black tea caused a short term increase in blood pressure (11). I hope there will be further research aimed at determining the optimal dosage for the ephedrine/caffeine/green tea combination. It seems likely that the addition of green tea will make it possible to normalize sympathetic tone with a less stimulating stack. In addition, green tea (without ephedrine/caffeine) may permit people with hypertension to obtain a mild increase in fat oxidation and thermogenesis. Clearly, additional research is needed to expand our understanding of the effect of green tea on blood pressure. Hypertensives that want to take green tea should definitely work with a doctor and monitor their blood pressure. Green tea is an extremely logical supplement for obese people. In addition to its weight loss effect, green tea protects against a number of conditions that are VERY common among the obese:
However, it is difficult to obtain all of these health benefits if one does not take green tea supplements -- without supplements, you would have to drink at least ten cups of green tea every day! |
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1.) Dulloo AG, Duret C, Rohrer D, Girardier L, Mensi N, Fathi M, Chantre P, Vandermander J "Efficacy of a green tea extract rich in catechin polyphenols and caffeine in increasing 24-h energy expenditure and fat oxidation in humans" Am J Clin Nutr 1999, Vol 70 (6), Pg 1040-5. PMID: 0010584049. 2.) Dulloo AG, Seydoux J, Girardier L, Chantre P, Vandermander J "Green tea and thermogenesis: interactions between catechin-polyphenols, caffeine and sympathetic activity" Int J Obes Relat Metab Disord 2000, Vol 24 (2), Pg 252-8. PMID: 0010702779. 3-BK.) Feldman, RS; Meyer, JS, and Quenzer, LF "Principles of Neuropsychopharmacology" Sinauer Associates, Inc. 1997. 4-NA.) Astrup A, Buemann B, Toubro S, Raben A "Defects in substrate oxidation involved in the predisposition to obesity" Proc Nutr Soc 1996, Vol 55 (3), Pg 817-28. PMID: 0009004326. 5-NA.) Astrup A, Raben A, Buemann B, Toubro S "Fat metabolism in the predisposition to obesity" Ann N Y Acad Sci 1997, Vol 827 Pg 417-30. PMID: 0009329772. 6.) Astrup A, Madsen J, Holst JJ, Christensen NJ "The effect of chronic ephedrine treatment on substrate utilization, the sympathoadrenal activity, and energy expenditure during glucose-induced thermogenesis in man" Metabolism 1986, Vol 35 (3), Pg 260-5. PMID: 0003512957. 7-NA.) Borchardt RT and Huber JA "Catechol O-methyltransferase. 5. Structure-activity relationships for inhibition by flavonoids" J Med Chem 1975, Vol 18 (1), Pg 120-2. PMID: 0001109569. 8.) Yokogoshi H, Kato Y, Sagesaka YM, Takihara-Matsuura T, Kakuda T, Takeuchi N "Reduction effect of theanine on blood pressure and brain 5- hydroxyindoles in spontaneously hypertensive rats" Biosci Biotechnol Biochem 1995, Vol 59 (4), Pg 615-8. PMID: 0007539642. 9.) Huang Y, Zhang A, Lau CW, Chen ZY "Vasorelaxant effects of purified green tea epicatechin derivatives in rat mesenteric artery" Life Sci 1998, Vol 63 (4), Pg 275-83. PMID: 0009698036. 10.) Huang Y, Chan NW, Lau CW, Yao XQ, Chan FL, Chen ZY "Involvement of endothelium/nitric oxide in vasorelaxation induced by purified green tea (-)epicatechin" Biochim Biophys Acta 1999, Vol 1427 (2), Pg 322-8. PMID: 0010216249. 11.) Hodgson JM, Puddey IB, Burke V, Beilin LJ, Jordan N "Effects on blood pressure of drinking green and black tea" J Hypertens 1999, Vol 17 (4), Pg 457-63. PMID: 0010404946. 12.) Sato Y, Nakatsuka H, Watanabe T, Hisamichi S, Shimizu H, Fujisaku S, Ichinowatari Y, Ida Y, Suda S, Kato K and others. "Possible contribution of green tea drinking habits to the prevention of stroke" Tohoku J Exp Med 1989, Vol 157 (4), Pg 337-43. PMID: 0002741170. 13.) Uchida S, Ozaki M, Akashi T, Yamashita K, Niwa M, Taniyama K "Effects of (-)-epigallocatechin-3-O-gallate (green tea tannin) on the life span of stroke-prone spontaneously hypertensive rats" Clin Exp Pharmacol Physiol Suppl 1995, Vol 1 Pg S302-3. PMID: 0009072402. 14.) Kono S, Ikeda M, Tokudome S, Kuratsune M "A case-control study of gastric cancer and diet in northern Kyushu, Japan" Jpn J Cancer Res 1988, Vol 79 (10), Pg 1067-74. PMID: 0003143695. 15.) Ruch RJ, Cheng SJ, Klaunig JE "Prevention of cytotoxicity and inhibition of intercellular communication by antioxidant catechins isolated from Chinese green tea" Carcinogenesis 1989, Vol 10 (6), Pg 1003-8. PMID: 0002470525. 16.) Karawya MS, Abdel Wahab SM, El-Olemy MM, Farrag NM "Diphenylamine, an antihyperglycemic agent from onion and tea" J Nat Prod 1984, Vol 47 (5), Pg 775-80. PMID: 0006512531. 17.) Muramatsu K, Fukuyo M, Hara Y "Effect of green tea catechins on plasma cholesterol level in cholesterol-fed rats" J Nutr Sci Vitaminol (Tokyo) 1986, Vol 32 (6), Pg 613-22. PMID: 0003585557. 18-NA.) Chisaka T, Matsuda H, Kubomura Y, Mochizuki M, Yamahara J, Fujimura H "The effect of crude drugs on experimental hypercholesteremia: mode of action of (-)-epigallocatechin gallate in tea leaves" Chem Pharm Bull (Tokyo) 1988, Vol 36 (1), Pg 227-33. PMID: 0003378286. 19.) Yokozawa T and Dong E "Influence of green tea and its three major components upon low-density lipoprotein oxidation" Exp Toxicol Pathol 1997, Vol 49 (5), Pg 329-35. PMID: 0009455677. 20-BK.) Greenspan, FS and Gardner, DG "Basic & Clinical Endocrinology" Lange Medical Books/McGraw-Hill 2000. 21-BK.) Munson, PL; Mueller, RA, and Breese, GR "Principles of Pharmacology. Basic Concepts & Clinical Applications." Chapman & Hall 1996. 22.) Deriaz O, Dionne F, Perusse L, Tremblay A, Vohl MC, Cote G, Bouchard C "DNA variation in the genes of the Na,K-adenosine triphosphatase and its relation with resting metabolic rate, respiratory quotient, and body fat" J Clin Invest 1994, Vol 93 (2), Pg 838-43. PMID: 0007509349. |
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