Green Tea & Alzheimer’s Disease
Have you heard the news? Green tea has been shown to potentially prevent and possibly even reverse various types of dementia, including Alzheimer’s Disease! This is HUGE!
What is Alzheimer’s Disease?
Alzheimer’s disease is a neurological disorder in which the damage and death of brain cells causes memory loss and cognitive decline. A neurodegenerative type of dementia, the disease starts mild and gets progressively worse. (Ref. 1.)
So What Causes Alzheimer’s Disease?
Scientists believe that for most people, Alzheimer’s Disease results from a combination of genetic, lifestyle and environmental factors that affect the brain over time. Less than 5 percent of the time, Alzheimer’s is caused by specific genetic changes that virtually guarantee a person will develop the disease. (Ref. 2)
Like all types of dementia, Alzheimer’s is caused by brain cell death. It is a neurodegenerative disease, which means there is progressive brain cell death that happens over a course of time. The total brain size shrinks with Alzheimer’s – the tissue has progressively fewer nerve cells and connections. (Ref. 1.)
Here is a diagram showing the difference between a normal brain (left), and a brain with Alzheimer’s Disease (right).
How Does Green Tea Help?
Impairment and death of brain cells associated with Alzheimer’s Disease is partially caused by the buildup of toxic protein fragments called amyloid beta. (Ref. 2)
Green tea gets to the root of Alzheimer’s disease by three distinct mechanisms:
1. Preventing the formation of amyloid plaques
2. Breaking down existing plaques
3. Creating critical new neurons in the brain
As a result, green tea consumption has now been associated with a 54% reduction in the risk of developing cognitive decline. (Ref 3.)
How Else Can Green Tea Improve My Health?
” Green tea catechins (polyphenol antioxidants) scavenge oxygen-free radicals, restoring cells to health and reducing inflammation. Because inflammation underlies so many age-related afflictions, green tea may have a myriad of applications in preventing disease.” (Ref 4 & 5)
Findings from animal studies suggest that green tea polyphenols promote the repair of damaged DNA. Since DNA damage can lead to cancer, green tea may play an important role in preventing cancer. (Ref. 6)
The EGCG (antioxidant) in green tea has been shown to produce apoptosis (cell death) in experimental prostate cancer, inhibit the growth of squamous cell carcinomas of the head and neck, inhibit the production and limit the invasion of experimentally induced breast cancers, reduce the incidence of carcinogen-induced lung cancers, and sensitise melanoma cells to growth inhibition by other agents. (Ref 7)
Green tea is also well-known to provide substantial defence against an array of diseases, including cardiovascular (Ref 8,9,10), insulin resistance (Ref 11.), obesity (Ref 12.), and autoimmune(Ref 13, 14).
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4. Rahman I, Biswas SK, Kirkham PA. Regulation of inflammation and redox signaling by dietary polyphenols. Biochem Pharmacol. 2006 Nov 30;72(11):1439-52.
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7. Yang CS, Wang X. Green tea and cancer prevention. Nutr Cancer. 2010;62(7):931-7.
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10. Kuriyama S, Shimazu T, Ohmori K, et al. Green tea consumption and mortality due to cardiovascular disease, cancer, and all causes in Japan: the Ohsaki study. JAMA. 2006 Sep 13; 296(10):1255-65.
11. Wu LY, Juan CC, Hwang LS, Hsu YP, Ho PH, Ho LT. Green tea supplementation ameliorates insulin resistance and increases glucose transporter IV content in a fructose-fed rat model. Eur J Nutr. 2004 Apr; 43(2):116-24.
12. Chantre P, Lairon D. Recent findings of green tea extract AR25 (Exolise) and its activity for the treatment of obesity.Phytomedicine. 2002 Jan; 9(1):3-8.
13. Hsu S, Dickinson D. A new approach to managing oral manifestations of Sjogren’s syndrome and skin manifestations of lupus. J Biochem Mol Biol. 2006 May 31; 39(3):229-39.
14. Hsu S, Dickinson DP, Qin H, et al. Inhibition of autoantigen expression by (-)-epigallocatechin-3-gallate (the major constituent of green tea) in normal human cells. J Pharmacol Exp Ther. 2005 Nov; 315(2):805-11.