"Give with a free hand, but give only your own."
 -- J.R.R. Tolkien The Children of Hurin
- Coffee -

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Dr. Ray Shahelien entry: 



[Ponder:  Considering the evidence that a spirochete infection may play a role in many AD cases, and since only whole caffeinated coffee appears to be effective, I have to wonder if coffee has some antibacterial properties for oral spirochetes as green tea does.]

High Blood Caffeine Levels in Older Adults Linked to Avoidance of Alzheimer’s Disease
ScienceDaily (June 4, 2012)
..."Moderate daily consumption of caffeinated coffee appears to be the best dietary option for long-term protection against Alzheimer's memory loss," Dr. Arendash said. "Coffee is inexpensive, readily available, easily gets into the brain, and has few side-effects for most of us. Moreover, our studies show that caffeine and coffee appear to directly attack the Alzheimer's disease process."...

High Blood Caffeine Levels in MCI Linked to Lack of Progression to Dementia.
Alzheimers Dis. 2012 Jan 1;30(3):559-72.
Cao C, Loewenstein DA, Lin X, Zhang C, Wang L, Duara R, Wu Y, Giannini A, Bai G, Cai J, Greig M, Schofield E, Ashok R, Small B, Potter H, Arendash GW.
Source: Department of Pharmaceutical Science, University of South Florida College of Pharmacy, Tampa, FL, USA Department of Molecular Pharmacology and Physiology, University of South Florida College of Medicine, Tampa, FL, USA USF Health Byrd Alzheimer's Institute, Tampa, FL, USA Department of Cell Biology, Microbiology and Molecular Biology, University of South Florida, Tampa, FL, USA.

Although both human epidemiologic and animal model studies have suggested that caffeine/coffee protects against Alzheimer's disease, direct human evidence for this premise has been lacking. In the present case-control study, two separate cohorts consisting of 124 total individuals (65-88 years old) were cognitively assessed and a blood sample taken for caffeine/biomarker analysis. Subjects were then monitored for cognitive status over the ensuing 2-4 year period to determine the extent to which initial plasma caffeine/biomarkers levels would be predictive of changes in cognitive status. Plasma caffeine levels at study onset were substantially lower (-51%) in mild cognitive impairment (MCI) subjects who later progressed to dementia (MCI→DEM) compared to levels in stable MCI subjects (MCI→MCI). Moreover, none of the MCI→DEM subjects had initial blood caffeine levels that were above a critical level of 1200 ng/ml, while half of stable MCI→MCI subjects had blood caffeine levels higher than that critical level. Thus, plasma caffeine levels greater than 1200 ng/ml (≈6 μM) in MCI subjects were associated with no conversion to dementia during the ensuing 2-4 year follow-up period. Among the 11 cytokines measured in plasma, three of them (GCSF, IL-10, and IL-6) were decreased in MCI→DEM subjects, but not in stable MCI→MCI subjects with high plasma caffeine levels. Coffee would appear to be the major or perhaps only source of caffeine for such stable MCI patients. This case-control study provides the first direct evidence that caffeine/coffee intake is associated with a reduced risk of dementia or delayed onset, particularly for those who already have MCI.
PMID: 22430531 [PubMed]

Something must be said for “doing it right”.  Look at your computer keyboard.  Twenty six letters, ten numbers and a smattering of punctuation.  Yet such simplicity becomes the conduit through which the ingenuity of the human mind gets translated by the pedantic instructions of software into all of the complexity of modern day computing.  Just pounding on the keys like a monkey gets you nowhere. When nothing happens you say, while waving your finger in the general direction of the keyboard, see, it’s all nonsense.  You have to do it right.

Midlife coffee and tea drinking and the risk of late-life dementia
Sabina Bossi
Karolinska Institutet
Public release date: 14-Jan-2009
Stockholm, Sweden -- Midlife coffee drinking can decrease the risk of dementia/Alzheimer's disease (AD) later in life. This conclusion is made in a Finnish Cardiovascular Risk Factors, Aging and Dementia (CAIDE) Study published in the January 2009 issue of the Journal of Alzheimer's Disease (Volume 16:1).

...The study found that coffee drinkers at midlife had lower risk for dementia and AD later in life compared to those drinking no or only little coffee. The lowest risk (65% decreased) was found among moderate coffee drinkers (drinking 3-5 cups of coffee/day). Adjustments for various confounders did not change the results. Tea drinking was relatively uncommon and was not associated with dementia/AD.

Midlife Coffee and Tea Drinking and the Risk of Late-Life Dementia: A Population-based CAIDE Study.
Publication: Marjo H. Eskelinen, Tiia Ngandu, Jaakko Tuomilehto, Hilkka Soininen, Miia Kivipelto (2009).Journal of Alzheimer's Disease 16(1), xx-xx.
Abstract: http://www.j-alz.com/issues/16/vol16-1.html

[Did these people drink decaf coffee?]


Google search: site:alzforum.org coffee

Caffeine suppresses amyloid-beta levels in plasma and brain of Alzheimer's disease transgenic mice.
Cao C, Cirrito JR, Lin X, Wang L, Verges DK, Dickson A, Mamcarz M, Zhang C, Mori T, Arendash GW, Holtzman DM, Potter H.
J Alzheimers Dis. 2009;17(3):681-97.
Source: The Byrd Alzheimer's Center & Research Institute, Tampa, FL, USA.

Erratum in J Alzheimers Dis. 2009 Nov;18(3):727. Wang, Lilly [corrected to Wang, Li]..

Recent epidemiologic studies suggest that caffeine may be protective against Alzheimer's disease (AD). Supportive of this premise, our previous studies have shown that moderate caffeine administration protects/restores cognitive function and suppresses brain amyloid-beta (Abeta) production in AD transgenic mice. In the present study, we report that acute caffeine administration to both young adult and aged AD transgenic mice rapidly reduces Abeta levels in both brain interstitial fluid and plasma without affecting Abeta elimination. Long-term oral caffeine treatment to aged AD mice provided not only sustained reductions in plasma Abeta, but also decreases in both soluble and deposited Abeta in hippocampus and cortex. Irrespective of caffeine treatment, plasma Abeta levels did not correlate with brain Abeta levels or with cognitive performance in individual aged AD mice. Although higher plasma caffeine levels were strongly associated with lower plasma Abeta1-40 levels in aged AD mice, plasma caffeine levels were also not linked to cognitive performance. Plasma caffeine and theophylline levels were tightly correlated, both being associated with reduced inflammatory cytokine levels in hippocampus. Our conclusion is two-fold: first, that both plasma and brain Abeta levels are reduced by acute or chronic caffeine administration in several AD transgenic lines and ages, indicating a therapeutic value of caffeine against AD; and second, that plasma Abeta levels are not an accurate index of brain Abeta levels/deposition or cognitive performance in aged AD mice.
PMID: 19581723 [PubMed]

Coffee and its consumption: benefits and risks.
Butt MS, Sultan MT.
Crit Rev Food Sci Nutr. 2011 Apr;51(4):363-73.
Source: National Institute of Food Science and Technology, University of Agriculture, Faisalabad, Pakistan.
PMID: 21432699 [PubMed]

Alzheimer's disease and coffee: a quantitative review.
Barranco Quintana JL, Allam MF, Serrano Del Castillo A, Fernández-Crehuet Navajas R.
Neurol Res. 2007 Jan;29(1):91-5.
Source: Department of Preventive Medicine and Public Health, Faculty of Medicine, University of Cordoba, Cordoba, Spain.

PURPOSE: To estimate the pooled risk of coffee consumption for Alzheimer's disease (AD).
MATERIAL AND METHODS: We have reviewed all observational studies that evaluated the association between AD risk and coffee consumption. Four studies were identified: two case-control studies and two cohorts. These studies were carried out between 1990 and 2002.
RESULTS: There was an obvious protective effect of coffee consumption in the pooled estimate [risk estimate: 0.73 (95% confidence interval: 0.58-0.92)]. However, the homogeneity test was highly significant (p<0.01), indicating heterogeneity across the pooled studies. Pooled analysis applying the random effect model was 0.79 with 95% confidence interval overlapping unity (95% confidence interval: 0.46-1.36). Three studies assessed coffee consumption by interview questionnaire. The risk of AD in coffee consumers versus non-consumers in studies that used interview questionnaire had a pooled risk estimate of 0.70 with 95% confidence interval 0.55-0.90.
CONCLUSION: Although our pooled estimates show that coffee consumption is inversely associated with the risk of AD, the four studies had heterogeneous methodologies and results. Further prospective studies evaluating the association between coffee consumption and AD are strongly needed.
PMID: 17427282 [PubMed]

Caffeinated coffee, decaffeinated coffee, and the phenolic phytochemical chlorogenic acid up-regulate NQO1 expression and prevent H₂O₂-induced apoptosis in primary cortical neurons.<
Kim J, Lee S, Shim J, Kim HW, Kim J, Jang YJ, Yang H, Park J, Choi SH, Yoon JH, Lee KW, Lee HJ.
Neurochem Int. 2012 Apr;60(5):466-74. Epub 2012 Feb 15.
Source WCU Biomodulation Major, Department of Agricultural Biotechnology, Seoul National University, Seoul 151-742, Republic of Korea.

Abstract: Neurodegenerative disorders are strongly associated with oxidative stress, which is induced by reactive oxygen species including hydrogen peroxide (H₂O₂). Epidemiological studies have suggested that coffee may be neuroprotective, but the molecular mechanisms underlying this effect have not been clarified. In this study, we investigated the protective effects of caffeinated coffee, decaffeinated coffee, and the phenolic phytochemical chlorogenic acid (5-O-caffeoylquinic acid), which is present in both caffeinated and decaffeinated coffee, against oxidative neuronal death. H₂O₂-induced apoptotic nuclear condensation in neuronal cells was strongly inhibited by pretreatment with caffeinated coffee, decaffeinated coffee, or chlorogenic acid. Pretreatment with caffeinated coffee, decaffeinated coffee, or chlorogenic acid inhibited the H₂O₂-induced down-regulation of anti-apoptotic proteins Bcl-2 and Bcl-X(L) while blocking H₂O₂-induced pro-apoptotic cleavage of caspase-3 and pro-poly(ADP-ribose) polymerase. We also found that caffeinated coffee, decaffeinated coffee, and chlorogenic acid induced the expression of NADPH:quinine oxidoreductase 1 (NQO1) in neuronal cells, suggesting that these substances protect neurons from H₂O₂-induced apoptosis by up-regulation of this antioxidant enzyme. The neuroprotective efficacy of caffeinated coffee was similar to that of decaffeinated coffee, indicating that active compounds present in both caffeinated and decaffeinated coffee, such as chlorogenic acid, may drive the effects.
PMID: 22353630 [PubMed]

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Updated: July 2, 2012
Inception: July 2, 2012