How can I reduce my cognitive decline due to aging?

Answer: Try drinking coffee–especially if you’re a woman.

Neurology. 2007 Aug 7;69(6):536-45.

The neuroprotective effects of caffeine: a prospective population study (the Three City Study).

Ritchie K, Carrière I, de Mendonca A, Portet F, Dartigues JF, Rouaud O, Barberger-Gateau P, Ancelin ML.

Abstract

OBJECTIVE:

To examine the association between caffeine intake, cognitive decline, and incident dementia in a community-based sample of subjects aged 65 years and over.

METHODS:

Participants were 4,197 women and 2,820 men from a population-based cohort recruited from three French cities. Cognitive performance, clinical diagnosis of dementia, and caffeine consumption were evaluated at baseline and at 2 and 4 year follow-up.

RESULTS:

Caffeine consumption is associated with a wide range of sociodemographic, lifestyle, and clinical variables which may also affect cognitive decline. Multivariate mixed models and multivariate adjusted logistic regression indicated that women with high rates of caffeine consumption (over three cups per day) showed less decline in verbal retrieval (OR = 0.67, CI = 0.53, 0.85), and to a lesser extent in visuospatial memory (OR = 0.82, CI = 0.65, 1.03) over 4 years than women consuming one cup or less. The protective effect of caffeine was observed to increase with age (OR = 0.73, CI = 0.53, 1.02 in the age range 65 to 74; OR = 0.3, CI = 0.14, 0.63 in the range 80+). No relation was found between caffeine intake and cognitive decline in men. Caffeine consumption did not reduce dementia risk over 4 years.

CONCLUSIONS:

The psychostimulant properties of caffeine appear to reduce cognitive decline in women without dementia, especially at higher ages. Although no impact is observed on dementia incidence, further studies are required to ascertain whether caffeine may nonetheless be of potential use in prolonging the period of mild cognitive impairment in women prior to a diagnosis of dementia.

J Alzheimers Dis. 2011;27(3):553-66.

Gender differences in tea, coffee, and cognitive decline in the elderly: the cardiovascular health study.

Arab L, Biggs ML, O’Meara ES, Longstreth WT, Crane PK, Fitzpatrick AL.

Abstract

Although caffeine can enhance cognitive function acutely, long-term effects of consumption of caffeine-containing beverages such as tea and coffee are uncertain. Data on 4,809 participants aged 65 and older from the Cardiovascular Health Study (CHS) were used to examine the relationship of consumption of tea and coffee, assessed by food frequency questionnaire, on change in cognitive function by gender. Cognitive performance was assessed using serial Modified Mini-Mental State (3MS) examinations, which were administered annually up to 9 times. Linear mixed models were used to estimate rates of change in standard 3MS scores and scores modeled using item response theory (IRT). Models were adjusted for age, education, smoking status, clinic site, diabetes, hypertension, stroke, coronary heart disease, depression score, and APOE genotype. Over the median 7.9 years of follow-up, participants who did not consume tea or coffee declined annually an average of 1.30 points (women) and 1.11 points (men) on standard 3MS scores. In fully adjusted models using either standard or IRT 3MS scores, we found modestly reduced rates of cognitive decline for some, but not all, levels of coffee and tea consumption for women, with no consistent effect for men. Caffeine consumption was also associated with attenuation in cognitive decline in women. Dose-response relationships were not linear. These longitudinal analyses suggest a somewhat attenuated rate of cognitive decline among tea and coffee consumers compared to non-consumers in women but not in men. Whether this association is causal or due to unmeasured confounding requires further study.

Eur J Clin Nutr. 2007 Feb;61(2):226-32. Epub 2006 Aug 16.

Coffee consumption is inversely associated with cognitive decline in elderly European men: the FINE Study.

van Gelder BM, Buijsse B, Tijhuis M, Kalmijn S, Giampaoli S, Nissinen A, Kromhout D.

Source

Centre for Prevention and Health Services Research, National Institute for Public Health and the Environment, Bilthoven, The Netherlands. Boukje.van.Gelder@rivm.nl

Abstract

OBJECTIVE:

To investigate whether coffee consumption is associated with 10-year cognitive decline in elderly men, as results of previous studies obtained hitherto have been controversial and prospective information on this association has been lacking.

DESIGN, SUBJECTS AND SETTING:

Six hundred and seventy six healthy men born between 1900 and 1920 from Finland, Italy and the Netherlands participated in a 10-year prospective cohort study. Cognitive functioning was assessed using the Mini-Mental State Examination (0-30 points, with a higher score indicating better cognitive performance). Coffee consumption was estimated in cups per day. A mixed longitudinal model was used to investigate the association between baseline coffee consumption and 10-year cognitive decline. Multiple adjustments were made.

RESULTS:

Men who consumed coffee had a 10-year cognitive decline of 1.2 points (4%). Non-consumers had an additional decline of 1.4 points (P<0.001). An inverse and J-shaped association was observed between the number of cups of coffee consumed and cognitive decline, with the least cognitive decline for three cups of coffee per day (0.6 points). This decline was 4.3 times smaller than the decline of non-consumers (P<0.001).

CONCLUSIONS:

Findings suggest that consuming coffee reduces cognitive decline in elderly men. An inverse and J-shaped association may exist between the number of cups of coffee consumed and cognitive decline, with the least cognitive decline for men consuming three cups of coffee per day.

Caffeine is good for rats too!

Neuroscience. 2011 Dec 2. [Epub ahead of print]

Chronic caffeine consumption prevents cognitive decline from young to middle age in rats, and is associated with increased length, branching, and spine density of basal dendrites in CA1 hippocampal neurons.

Vila-Luna S, Cabrera-Isidoro S, Vila-Luna L, Juárez-Díaz I, Bata-García JL, Alvarez-Cervera FJ, Zapata-Vázquez RE, Arankowsky-Sandoval G, Heredia-López F, Flores G, Góngora-Alfaro JL.

Abstract

Chronic caffeine consumption has been inversely associated with the risk of developing dementia and Alzheimer’s disease. Here we assessed whether chronic caffeine treatment prevents the behavioral and cognitive decline that male Wistar rats experience from young (≈3 months) to middle age (≈10 months). When animals were young they were evaluated at weekly intervals in three tests: motor activity habituation in the open field (30-min sessions at the same time on consecutive days), continuous spontaneous alternation in the Y-maze (8 min), and elevated plus-maze (5 min). Afterward, rats from the same litter were randomly assigned either to a caffeine-treated group (n=13) or a control group (n=11), which received only tap water. Caffeine treatment (5 mg/kg/day) began when animals were ≈4 months old, and lasted for 6 months. Behavioral tests were repeated from day 14 to day 28 after caffeine withdrawal, a time period that is far in excess for the full excretion of a caffeine dose in this species. Thirty days after caffeine discontinuation brains were processed for Golgi-Cox staining. Compared with controls, we found that middle-aged rats that had chronically consumed low doses of caffeine (1) maintained their locomotor habituation during the second consecutive day exposure to the open field (an index of non-associative learning), (2) maintained their exploratory drive to complete the conventional minimum of nine arm visits required to calculate the alternation performance in the Y-maze in a greater proportion, (3) maintained their alternation percentage above chance level (an index of working memory), and (4) did not increase the anxiety indexes assessed by measuring the time spent in the open arms of the elevated plus maze. In addition, morphometric analysis of hippocampal neurons revealed that dendritic branching (90-140 μm from the soma), length of 4th and 5th order branches, total dendritic length, and spine density in distal dendritic branches were greater in the basal but not the apical dendrites of CA1 pyramidal neurons from rats chronically treated with caffeine, in comparison with their age- and littermate-matched controls. Altogether, the present findings strengthen the epidemiological observations suggesting that prolonged caffeine intake prevents the cognitive decline associated with aging, and open the possibility that this process could be mediated by promoting the growth of dendrites and spines in neurons of the adult mammalian brain.

How can I manage my gout condition better?

Answer: Try changing your diet: cut back on foods associated with an increased risk for gout (e.g. beer and spirits, foods rich in purines, fructose) and consume more of those foods associated with a decreased risk for gout (e.g. coffee).

Surprisingly, the dietary intervention studies haven’t been done yet to test whether dietary changes reduce gout flares, but it makes sense for you to see if changing your diet helps.

Read this scientific article for ideas to try:

Update on the management of hyperuricemia and gout.

Bull NYU Hosp Jt Dis. 2008;66(3):231-9.

Update on the management of hyperuricemia and gout.

Pillinger MH, Keenan RT.

Abstract

Gout is the most common inflammatory arthritis in the United States, with more than three million sufferers. Management of gout has changed relatively little in the past 50 years, despite the fact that many gout patients have contraindications to one or more currently available gout therapies. However, recent insights into gout pathophysiology suggest that time is ripe for a change. This article reviews recent updates in the management of gout, including new insights into dietary management that may permit better control of hyuperuricemia. Also reviewed are the biological and clinical data behind newly-developed drugs for gout that are likely to receive serious consideration for FDA approval, and clinical use, in the foreseeable future.

Here’s the abstract of another scientific review opinion paper that gives some good suggestions to try:

Curr Opin Rheumatol. 2010 Mar;22(2):165-72.

A prescription for lifestyle change in patients with hyperuricemia and gout.

Choi HK.

Abstract

PURPOSE OF REVIEW:

This review summarizes the recent data on lifestyle factors that influence serum uric acid levels and the risk of gout and attempts to provide holistic recommendations, considering both their impact on gout as well as on other health implications.

RECENT FINDINGS:

Large-scale studies have clarified a number of long-suspected relations between lifestyle factors, hyperuricemia, and gout, including purine-rich foods, dairy foods, various beverages, fructose, and vitamin C supplementation. Furthermore, recent studies have identified the substantial burden of comorbidities among patients with hyperuricemia and gout.

SUMMARY:

Lifestyle and dietary recommendations for gout patients should consider overall health benefits and risk, since gout is often associated with the metabolic syndrome and an increased future risk of cardiovascular disease (CVD) and mortality. Weight reduction with daily exercise and limiting intake of red meat and sugary beverages would help reduce uric acid levels, the risk of gout, insulin resistance, and comorbidities. Heavy drinking should be avoided, whereas moderate drinking, sweet fruits, and seafood intake, particularly oily fish, should be tailored to the individual, considering their anticipated health benefits against CVD. Dairy products, vegetables, nuts, legumes, fruits (less sugary ones), and whole grains are healthy choices for the comorbidities of gout and may also help prevent gout by reducing insulin resistance. Coffee and vitamin C supplementation could be considered as preventive measures as these can lower urate levels, as well as the risk of gout and some of its comorbidities.

How can I reduce my risk of dying from prostate cancer?

Answer: Try drinking coffee–regular or decaffeinated.

J Natl Cancer Inst. 2011 Jun 8;103(11):876-84.

Coffee consumption and prostate cancer risk and progression in the Health Professionals Follow-up Study.

Wilson KM, Kasperzyk JL, Rider JR, Kenfield S, van Dam RM, Stampfer MJ, Giovannucci E, Mucci LA.

Abstract

BACKGROUND:

Coffee contains many biologically active compounds, including caffeine and phenolic acids, that have potent antioxidant activity and can affect glucose metabolism and sex hormone levels. Because of these biological activities, coffee may be associated with a reduced risk of prostate cancer.

METHODS:

We conducted a prospective analysis of 47,911 men in the Health Professionals Follow-up Study who reported intake of regular and decaffeinated coffee in 1986 and every 4 years thereafter. From 1986 to 2006, 5035 patients with prostate cancer were identified, including 642 patients with lethal prostate cancers, defined as fatal or metastatic. We used Cox proportional hazards models to assess the association between coffee and prostate cancer, adjusting for potential confounding by smoking, obesity, and other variables. All P values were from two-sided tests.

RESULTS:

The average intake of coffee in 1986 was 1.9 cups per day. Men who consumed six or more cups per day had a lower adjusted relative risk for overall prostate cancer compared with nondrinkers (RR = 0.82, 95% confidence interval [CI] = 0.68 to 0.98, P(trend) = .10). The association was stronger for lethal prostate cancer (consumers of more than six cups of coffee per day: RR = 0.40, 95% CI = 0.22 to 0.75, P(trend) = .03). Coffee consumption was not associated with the risk of nonadvanced or low-grade cancers and was only weakly inversely associated with high-grade cancer. The inverse association with lethal cancer was similar for regular and decaffeinated coffee (each one cup per day increment: RR = 0.94, 95% CI = 0.88 to 1.01, P = .08 for regular coffee and RR = 0.91, 95% CI = 0.83 to 1.00, P = .05 for decaffeinated coffee). The age-adjusted incidence rates for men who had the highest (≥6 cups per day) and lowest (no coffee) coffee consumption were 425 and 519 total prostate cancers, respectively, per 100 000 person-years and 34 and 79 lethal prostate cancers, respectively, per 100 000 person-years.

CONCLUSIONS:

We observed a strong inverse association between coffee consumption and risk of lethal prostate cancer. The association appears to be related to non-caffeine components of coffee.

How can I reduce my chances of getting type 2 diabetes?

Answer 1: Try drinking 2-3 cups of coffee a day (de-caff or regular).

Diabetes Care. 2006 Feb;29(2):398-403.

Coffee, caffeine, and risk of type 2 diabetes: a prospective cohort study in younger and middle-aged U.S. women.

van Dam RM, Willett WC, Manson JE, Hu FB.

Abstract

OBJECTIVE:

High habitual coffee consumption has been associated with a lower risk of type 2 diabetes, but data on lower levels of consumption and on different types of coffee are sparse.

RESEARCH DESIGN AND METHODS:

This is a prospective cohort study including 88,259 U.S. women of the Nurses’ Health Study II aged 26-46 years without history of diabetes at baseline. Consumption of coffee and other caffeine-containing foods and drinks was assessed in 1991, 1995, and 1999. We documented 1,263 incident cases of confirmed type 2 diabetes between 1991 and 2001.

RESULTS:

After adjustment for potential confounders, the relative risk of type 2 diabetes was 0.87 (95% CI 0.73-1.03) for one cup per day, 0.58 (0.49-0.68) for two to three cups per day, and 0.53 (0.41-0.68) for four or more cups per day compared with nondrinkers (P for trend <0.0001). Associations were similar for caffeinated (0.87 [0.83-0.91] for a one-cup increment per day) and decaffeinated (0.81 [0.73-0.90]) coffee and for filtered (0.86 [0.82-0.90]) and instant (0.83 [0.74-0.93]) coffee. Tea consumption was not substantially associated with risk of type 2 diabetes (0.88 [0.64-1.23] for four or more versus no cups per day; P for trend = 0.81).

CONCLUSIONS:

These results suggest that moderate consumption of both caffeinated and decaffeinated coffee may lower risk of type 2 diabetes in younger and middle-aged women. Coffee constituents other than caffeine may affect the development of type 2 diabetes.

Here are some similar earlier research findings:

Ann Intern Med. 2004 Jan 6;140(1):1-8.

Coffee consumption and risk for type 2 diabetes mellitus.

Salazar-Martinez E, Willett WC, Ascherio A, Manson JE, Leitzmann MF, Stampfer MJ, Hu FB.

Abstract

BACKGROUND:

In small, short-term studies, acute administration of caffeine decreases insulin sensitivity and impairs glucose tolerance.

OBJECTIVE:

To examine the long-term relationship between consumption of coffee and other caffeinated beverages and incidence of type 2 diabetes mellitus.

DESIGN:

Prospective cohort study.

SETTING:

The Nurses’ Health Study and Health Professionals’ Follow-up Study.

PARTICIPANTS:

The authors followed 41 934 men from 1986 to 1998 and 84 276 women from 1980 to 1998. These participants did not have diabetes, cancer, or cardiovascular disease at baseline.

MEASUREMENTS:

Coffee consumption was assessed every 2 to 4 years through validated questionnaires.

RESULTS:

The authors documented 1333 new cases of type 2 diabetes in men and 4085 new cases in women. The authors found an inverse association between coffee intake and type 2 diabetes after adjustment for age, body mass index, and other risk factors. The multivariate relative risks for diabetes according to regular coffee consumption categories (0, <1, 1 to 3, 4 to 5, or > or =6 cups per day) in men were 1.00, 0.98, 0.93, 0.71, and 0.46 (95% CI, 0.26 to 0.82; P = 0.007 for trend), respectively. The corresponding multivariate relative risks in women were 1.00, 1.16, 0.99, 0.70, and 0.71 (CI, 0.56 to 0.89; P < 0.001 for trend), respectively. For decaffeinated coffee, the multivariate relative risks comparing persons who drank 4 cups or more per day with nondrinkers were 0.74 (CI, 0.48 to 1.12) for men and 0.85 (CI, 0.61 to 1.17) for women. Total caffeine intake from coffee and other sources was associated with a statistically significantly lower risk for diabetes in both men and women.

CONCLUSIONS:

These data suggest that long-term coffee consumption is associated with a statistically significantly lower risk for type 2 diabetes.



Read this paper for a possible metabolic explanation for why coffee (or caffeine) protects against Type 2 diabetes:

Coffee and Caffeine Improve Insulin Sensitivity and Glucose Tolerance in C57BL/6J Mice Fed a High-Fat Diet.

How can I reduce my chances of getting endometrial cancer?

Answer: Drink coffee.


Int J Cancer. 2011 Dec 20. doi: 10.1002/ijc.27408.

Coffee drinking and risk of endometrial cancer: Findings from a large up-to-date meta-analysis.

Abstract

Several epidemiological studies have examined the association between coffee drinking and risk of endometrial cancer. To provide a quantitative assessment of this association, we conducted a meta-analysis of observational studies published up to October 2011 through a search of MEDLINE and EMBASE databases and the reference lists of retrieved article. Pooled relative risks (RRs) with 95% confidence intervals (CIs) were calculated using a random-effects model, and generalized least square trend estimation was used to assess dose-response relationships. A total of 16 studies (10 case-control and 6 cohort studies) on coffee intake with 6,628 endometrial cancer cases were included in the meta-analysis. The pooled RR of endometrial cancer for the highest versus lowest categories of coffee intake was 0.71 (95% CI: 0.62-0.81; p for heterogeneity = 0.13). By study design, the pooled RRs were 0.69 (95% CI: 0.55-0.87) for case-control studies and 0.70 (95% CI: 0.61-0.80) for cohort studies. By geographic region, the inverse association was stronger for 3 Japanese studies (pooled RR=0.40; 95% CI: 0.25-0.63) than 5 studies from USA/Canada (pooled RR=0.69; 95% CI: 0.60-0.79) or 8 studies from Europe (pooled RR=0.79; 95% CI: 0.63-0.99). An increment of 1 cup/d of coffee intake conferred a pooled RR of 0.92 (95% CI: 0.90-0.95). In conclusion, our findings suggest that increased coffee intake is associated with a reduced risk of endometrial cancer, consistently observed for cohort and case-control studies. More large studies are needed to determine subgroups to obtain more benefits from coffee drinking in relation to endometrial cancer risk.

How can I protect my mouse against Alzheimer’s disease?

Answer: Feed it coffee or caffeine. In fact, coffee seems to be better.


J Alzheimers Dis. 2010;20 Suppl 1:S117-26.

Caffeine and coffee as therapeutics against Alzheimer’s disease.

Abstract

Epidemiologic studies have increasingly suggested that caffeine/coffee could be an effective therapeutic against Alzheimer’s disease (AD). We have utilized a transgenic mouse model for AD in well-controlled studies to determine if caffeine and/or coffee have beneficial actions to protect against or reverse AD-like cognitive impairment and AD pathology. AD mice given caffeine in their drinking water from young adulthood into older age showed protection against memory impairment and lower brain levels of the abnormal protein (amyloid-beta; Abeta) thought to be central to AD pathogenesis. Moreover, “aged” cognitively-impaired AD mice exhibited memory restoration and lower brain Abeta levels following only 1-2 months of caffeine treatment. We believe that the cognitive benefits of chronic caffeine administration in AD mice are due to caffeine itself, and not metabolites of caffeine; this, because our long-term administration of theophylline to AD mice provided no cognitive benefits. In acute studies involving AD mice, one oral caffeine treatment quickly reduced both brain and plasma Abeta levels – similarly rapid alterations in plasma Abeta levels were seen in humans following acute caffeine administration. “Caffeinated” coffee provided to AD mice also quickly decreased plasma Abeta levels, but not “decaffeinated” coffee, suggesting that caffeine is critical to decreasing blood Abeta levels. Caffeine appears to provide its disease-modifying effects through multiple mechanisms, including a direct reduction of Abeta production through suppression of both beta- and gamma-secretase levels. These results indicate a surprising ability of moderate caffeine intake (the human equivalent of 500 mg caffeine or 5 cups of coffee per day) to protect against or treat AD in a mouse model for the disease and a therapeutic potential for caffeine against AD in humans.

J Alzheimers Dis. 2011;25(2):323-35.

Caffeine synergizes with another coffee component to increase plasma GCSF: linkage to cognitive benefits in Alzheimer’s mice.

Abstract

Retrospective and prospective epidemiologic studies suggest that enhanced coffee/caffeine intake during aging reduces risk of Alzheimer’s disease (AD). Underscoring this premise, our studies in AD transgenic mice show that long-term caffeine administration protects against cognitive impairment and reduces brain amyloid-β levels/deposition through suppression of both β- and γ-secretase. Because coffee contains many constituents in addition to caffeine that may provide cognitive benefits against AD, we examined effects of caffeinated and decaffeinated coffee on plasma cytokines, comparing their effects to caffeine alone. In both AβPPsw+PS1 transgenic mice and non-transgenic littermates, acute i.p. treatment with caffeinated coffee greatly and specifically increased plasma levels of granulocyte-colony stimulating factor (GCSF), IL-10, and IL-6. Neither caffeine solution alone (which provided high plasma caffeine levels) or decaffeinated coffee provided this effect, indicating that caffeine synergized with some as yet unidentified component of coffee to selectively elevate these three plasma cytokines. The increase in GCSF is particularly important because long-term treatment with coffee (but not decaffeinated coffee) enhanced working memory in a fashion that was associated only with increased plasma GCSF levels among all cytokines. Since we have previously reported that long-term GCSF treatment enhances cognitive performance in AD mice through three possible mechanisms (e.g., recruitment of microglia from bone marrow, synaptogenesis, and neurogenesis), the same mechanisms could be complimentary to caffeine’s established ability to suppress Aβ production. We conclude that coffee may be the best source of caffeine to protect against AD because of a component in coffee that synergizes with caffeine to enhance plasma GCSF levels, resulting in multiple therapeutic actions against AD.