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Green Tea Extract (EGCG)

Dosage and Safety

For all those of you who have been thinking about adding green tea extract/EGCG to their TNI protocol, here's a safety statement from DSM Nutritional Products Ltd., the producer of Teavigo, offering information on the safe upper intake level, including different rat studies and clinical trials with people.

http://www.teavigoinfo.com/pdf/safety-statement.pdf  (see attachment below).

A suggested dosage is 5mg of EGCG/kg/day.

Ray Sahelian just wrote about green tea, caught the info below:
Epigallocatechin 3-o-gallate, EGCG, is the major catechin found in green tea. Another catechin is GCG, gallocatechin-3-gallate. Other catechins include epicatechin gallate (ECG), epigallocatechin (EGC), and epichtechin (EC). The relative concentration of the five major tea catechins are EGCG > ECG > EC > EGC > C.

Questions

I read an article online that made these claims, "Did you know that most of the free-radical fighters in green tea never make it to your bloodstream? But there's a solution. To get a better grasp on the healthy catechins in your green tea, flavor your cup with a squeeze of citrus juice. The antioxidants in green tea famous for lowering your risk of chronic disease -- quickly lose their power in your intestine. In fact, as much as 80% of the catechins in green tea are never absorbed. The solution to boosting absorption is as simple as flavoring your tea with freshly squeezed and strained lemon, orange, lime, or grapefruit juice. The vitamin C in citrus may help with absorption by increasing the acidity in your small intestine. Other unidentified substances in the juice probably lend a hand, too. Researchers found a 50-50 mix had the greatest catechin-preserving effect, and lemon did it best, closely followed by orange, lime, and, in last place, grapefruit."
Nikki (on Einstein Syndrome)


Neurosci Lett. 2010 Mar 8;471(3):134-8. Epub 2010 Jan 22.

Fish oil enhances anti-amyloidogenic properties of green tea EGCG in Tg2576 mice.

Giunta B, Hou H, Zhu Y, Salemi J, Ruscin A, Shytle RD, Tan J.

Department of Psychiatry and Behavioral Medicine, Neuroimmunology Laboratory, University of South Florida, College of Medicine, Tampa, FL
33613, USA. bgiunta@health.usf.edu <bgiunta@health.usf.edu>

Abstract

Extracellular plaques of beta-amyloid (Abeta) peptides are implicated in Alzheimer's Disease (AD) pathogenesis. Abeta formation is precluded by alpha-secretase, which cleaves within the Abeta domain of APP generating soluble APP-alpha (sAPP-alpha). Thus, alpha-secretase upregulation may be a target AD therapy. We previously showed green tea derived EGCG increased sAPP-alpha in AD mouse models. However, the comparable effective dose of EGCG in humans may exceed clinical convenience and/or safety. Epidemiological studies suggested fish oil consumption is associated with reduced dementia risk. Here we investigated whether oral co-treatment with fish oil (8mg/kg/day) and EGCG (62.5mg/kg/day or 12.5mg/kg/day) would reduce AD-like pathology in Tg2576 mice. In vitro co-treatment of N2a cells with fish oil and EGCG enhanced sAPP-alpha production compared to either compound alone (P<0.001). Fish oil enhanced bioavailability of EGCG versus EGCG treatment alone (P<0.001). Fish oil and EGCG had a synergetic effect on inhibition of cerebral
Abeta deposits (P<0.001) suggesting moderate supplementation with EGCG and fish oil having significant therapeutic potential for the treatment of AD.

PMID: 20096749 [PubMed - indexed for MEDLINE]



Nutr. 2009 Oct;139(10):1987-93. Epub 2009 Aug 5.

Green tea (-)-epigallocatechin-3-gallate inhibits beta-amyloid-induced cognitive dysfunction through modification of secretase activity viainhibition of ERK and NF-kappaB pathways in mice.


Lee JW, Lee YK, Ban JO, Ha TY, Yun YP, Han SB, Oh KW, Hong JT.

College of Pharmacy, Chungbuk National University 12, Gaesin-dong, Heungduk-gu, Cheongju, Chungbuk 361-763, Korea.

Abstract

Alzheimer's disease (AD) is characterized by the extracellular deposition of beta-amyloid peptide (Abeta) in cerebral plaques. Abeta is
derived from the beta-amyloid precursor protein (APP) by the enzymes alpha-, beta- and gamma-secretase. Compounds that enhance
alpha-secretase, but inhibit beta- or gamma-secretase activity, have therapeutic potential in the treatment of AD. Green tea, or its major
polyphenolic compound, has been shown to have neuroprotective effects. In this study, we investigated the possible effects of
(-)-epigallocatechin-3-gallate (EGCG) on memory dysfunction caused by Abeta through the change of Abeta-induced secretase activities. Mice were pretreated with EGCG (1.5 or 3 mg/kg body weight in drinking water) for 3 wk before intracerebroventricular administration of 0.5 microg Abeta(1-42). EGCG dose-dependently reduced the Abeta(1-42)-induced memory dysfunction, which was evaluated using passive avoidance and water maze tests. Abeta(1-42) induced a decrease in brain alpha-secretase and increases in both brain beta- and gamma-secretase activities, which were reduced by EGCG. In the cortex and the hippocampus, expression of the metabolic products of the beta- and
gamma-secretases from APP, C99, and Abeta also were dose-dependently suppressed by EGCG. Paralleled with the suppression of beta- and
gamma-secretases by EGCG, we found that EGCG inhibited the activation of extracellular signal-regulated kinase and nuclear transcription
factor-kappaB in the Abeta(1-42)-injected mouse brains. In addition, EGCG inhibited Abeta(1-42)-induced apoptotic neuronal cell death in the brain. To further test the ability of EGCG to affect memory, EGCG (3 mg/kg body weight) was administered in drinking water for 1 wk to
genetically developed preseniline 2 (PS2) mutant AD mice. Compared with untreated mutant PS2 AD mice, treatment with EGCG enhanced memory function and brain alpha-secretase activity but reduced brain beta- and gamma-secretase activities as well as Abeta levels. Moreover, EGCG inhibited the fibrillization of Abeta in vitro with a half maximal inhibitory concentration of 7.5 mg/L. These studies suggest that EGCG may be a beneficial agent in the prevention of development or progression of AD.

PMID: 19656855 [PubMed - indexed for MEDLINE]



Brain Res. 2009 Jan 23;1250:164-74. Epub 2008 Nov 1.

(-)-Epigallocatechin-3-gallate prevents lipopolysaccharide-induced elevation of beta-amyloid generation and memory deficiency.

Lee YK, Yuk DY, Lee JW, Lee SY, Ha TY, Oh KW, Yun YP, Hong JT.

College of Pharmacy, Chungbuk National University 12, Heungduk-gu, Cheongju, Chungbuk 361-763, Republic of Korea.

Abstract

Neuroinflammation has been known to play a role in the pathogenesis of AD. Our previous study showed that lipopolysaccharide (LPS) induced memory impairment through the accumulation of Abeta via the increase of beta- and gamma-secretase. In this study, we investigated the possible preventive effect of (-)-epigallocatechin-3-gallate (EGCG) on memory deficiency caused by LPS through the inhibition of Abeta(1-42) generation. Oral treatment with EGCG (1.5 and 3 mg/kg, for 3 weeks) into drinking water ameliorated LPS (1 microg/mouse, i.c.v.)-induced memory deficiency in a dose dependent manner. In addition, EGCG also dose-dependently inhibited LPS-induced elevation of Abeta level through attenuation of LPS-induced beta- and gamma-secretase activities and expression of its metabolic products; C99 and Abeta. Moreover, EGCG prevented LPS-induced neuronal cell death as well as the expression of
inflammatory proteins, inducible nitric oxide synthetase and cyclooxygenase-2. This study therefore suggests that EGCG prevents
LPS-mediated apoptotic cell death through the inhibition of the elevation of Abeta via the inhibition of beta- and gamma-secretases, and
thus EGCG can be a useful agent against neuroinflammation-associated development or progression of AD.

PMID: 18992719 [PubMed - indexed for MEDLINE]


Neurosci Lett. 2010 Mar 8;471(3):134-8. Epub 2010 Jan 22.
 
Fish oil enhances anti-amyloidogenic properties of green tea EGCG in Tg2576 mice.


Giunta B, Hou H, Zhu, Salemi J , Ruscin A, Shytle RD, Tan J

Department of Psychiatry and Behavioral Medicine, Neuroimmunology Laboratory, University of South Florida, College of Medicine, Tampa, FL
33613, USA. bgiunta@... <bgiunta@...>
 
Abstract

Extracellular plaques of beta-amyloid (Abeta) peptides are implicated in Alzheimer's Disease (AD) pathogenesis. Abeta formation is precluded by alpha-secretase, which cleaves within the Abeta domain of APP generating soluble APP-alpha (sAPP-alpha). Thus, alpha-secretase upregulation may be a target AD therapy. We previously showed green tea derived EGCG increased sAPP-alpha in AD mouse models. However, the comparable effective dose of EGCG in humans may exceed clinical convenience and/or safety.  Epidemiological studies suggested fish oil consumption is associated with reduced dementia risk. Here we investigated whether oral co-treatment with fish oil (8mg/kg/day) and EGCG (62.5mg/kg/day or 12.5mg/kg/day) would reduce AD-like pathology in Tg2576 mice. In vitro co-treatment of N2a cells with fish oil and EGCG enhanced sAPP-alpha production compared to either compound alone (P<0.001). Fish oil enhanced bioavailability of EGCG versus EGCG treatment alone (P<0.001). Fish oil and EGCG had a synergetic effect on inhibition of cerebral Abeta deposits (P<0.001) suggesting moderate supplementation with EGCG and fish oil having significant therapeutic potential for the treatment of AD.

PMID: 20096749 [PubMed - indexed for MEDLINE]

 
Nutr. 2009 Oct;139(10):1987-93. Epub 2009 Aug 5.

Green tea (-)-epigallocatechin-3-gallate inhibits beta-amyloid-induced cognitive dysfunction through modification of secretase activity via inhibition of ERK and NF-kappaB pathways in mice.


Lee JW, Lee YK, Ban JO , Ha TY, Yun YP, Han SB, Oh KW , Hong JT.

College of Pharmacy, Chungbuk National University 12, Gaesin-dong, Heungduk-gu, Cheongju, Chungbuk 361-763, Korea.

Abstract

Alzheimer's disease (AD) is characterized by the extracellular deposition of beta-amyloid peptide (Abeta) in cerebral plaques. Abeta is derived from the beta-amyloid precursor protein (APP) by the enzymes alpha-, beta- and gamma-secretase. Compounds that enhance alpha-secretase, but inhibit beta- or gamma-secretase activity, have therapeutic potential in the treatment of AD. Green tea, or its major polyphenolic compound, has been shown to have neuroprotective effects.  In this study, we investigated the possible effects of (-)-epigallocatechin-3-gallate (EGCG) on memory dysfunction caused by Abeta through the change of Abeta-induced secretase activities. Mice were pretreated with EGCG (1.5 or 3 mg/kg body weight in drinking water) for 3 wk before intracerebroventricular administration of 0.5 microg Abeta(1-42). EGCG dose-dependently reduced the Abeta(1-42)-induced memory dysfunction, which was evaluated using passive avoidance and water maze tests. Abeta(1-42) induced a decrease in brain alpha-secretase and increases in both brain beta- and gamma-secretase activities, which were reduced by EGCG. In the cortex and the hippocampus, expression of the metabolic products of the beta- and gamma-secretases from APP, C99, and Abeta also were dose-dependently suppressed by EGCG. Paralleled with the suppression of beta- and gamma-secretases by EGCG, we found that EGCG inhibited the activation of extracellular signal-regulated kinase and nuclear transcription factor-kappaB in the Abeta(1-42)-injected mouse brains. In addition, EGCG inhibited Abeta(1-42)-induced apoptotic neuronal cell death in the brain. To further test the ability of EGCG to affect memory, EGCG (3 mg/kg body weight) was administered in drinking water for 1 wk to genetically developed preseniline 2 (PS2) mutant AD mice. Compared with untreated mutant PS2 AD mice, treatment with EGCG enhanced memory function and brain alpha-secretase activity but reduced brain beta- and gamma-secretase activities as well as Abeta levels. Moreover, EGCG inhibited the fibrillization of Abeta in vitro with a half maximal inhibitory concentration of 7.5 mg/L. These studies suggest that EGCG may be a beneficial agent in the prevention of development or progression of AD.

PMID: 19656855 [PubMed - indexed for MEDLINE]


Brain Res. 2009 Jan 23;1250:164-74. Epub 2008 Nov 1.

(-)-Epigallocatechin-3-gallate prevents lipopolysaccharide-induced elevation of beta-amyloid generation and memory deficiency.
 
College of Pharmacy, Chungbuk National University 12, Heungduk-gu, Cheongju, Chungbuk 361-763, Republic of Korea.

Abstract

Neuroinflammation has been known to play a role in the pathogenesis of AD. Our previous study showed that lipopolysaccharide (LPS) induced memory impairment through the accumulation of Abeta via the increase of beta- and gamma-secretase. In this study, we investigated the possible preventive effect of (-)-epigallocatechin-3-gallate (EGCG) on memory deficiency caused by LPS through the inhibition of Abeta(1-42) generation. Oral treatment with EGCG (1.5 and 3 mg/kg, for 3 weeks) into drinking water ameliorated LPS (1 microg/mouse, i.c.v.)-induced memory deficiency in a dose dependent manner. In addition, EGCG also dose-dependently inhibited LPS-induced elevation of Abeta level through attenuation of LPS-induced beta- and gamma-secretase activities and expression of its metabolic products; C99 and Abeta.  Moreover, EGCG prevented LPS-induced neuronal cell death as well as the expression of inflammatory proteins, inducible nitric oxide synthetase and cyclooxygenase-2. This study therefore suggests that EGCG prevents LPS-mediated apoptotic cell death through the inhibition of the elevation of Abeta via the inhibition of beta- and gamma-secretases, and thus EGCG can be a useful agent against neuroinflammation-associated development or progression of AD.

PMID: 18992719 [PubMed - indexed for MEDLINE]
ċ
TeavigoEGCGSafetyStatement.pdf
(668k)
Paul Doney,
25 Dec 2010, 21:22
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