How can I lower my risk for cataracts?

Answer: Maybe switch to a plant-based diet.

Am J Clin Nutr. 2011 May;93(5):1128-35. Epub 2011 Mar 23.

Diet, vegetarianism, and cataract risk.

Appleby PN, Allen NE, Key TJ.

Abstract

BACKGROUND:

Age-related cataract is a major cause of morbidity. Previous studies of diet and cataract risk have focused on specific nutrients or healthy eating indexes but not on identifiable dietary groups such as vegetarians.

OBJECTIVE:

We investigated the association between diet and cataract risk in a population that has a wide range of diets and includes a high proportion of vegetarians.

DESIGN:

We used Cox proportional hazards regression to study cataract risk in relation to baseline dietary and lifestyle characteristics of 27,670 self-reported nondiabetic participants aged ≥40 y at recruitment in the Oxford (United Kingdom) arm of the European Prospective Investigation into Cancer and Nutrition (EPIC-Oxford) by using data from the Hospital Episode Statistics in England and Scottish Morbidity Records.

RESULTS:

There was a strong relation between cataract risk and diet group, with a progressive decrease in risk of cataract in high meat eaters to low meat eaters, fish eaters (participants who ate fish but not meat), vegetarians, and vegans. After multivariable adjustment, incidence rate ratios (95% CIs) for moderate meat eaters (50-99 g meat/d), low meat eaters (<50 g meat/d), fish eaters, vegetarians, and vegans compared with high-meat eaters (≥100 g meat/d) were 0.96 (0.84, 1.11), 0.85 (0.72, 0.99), 0.79 (0.65, 0.97), 0.70 (0.58, 0.84), and 0.60 (0.38, 0.96), respectively (P < 0.001 for heterogeneity). Associations between cataract risk and intakes of selected nutrients and foods generally reflected the strong association with diet group.

CONCLUSION:

Vegetarians were at lower risk of cataract than were meat eaters in this cohort of health-conscious British residents.

Read the complete scientific paper:

Diet, vegetarianism, and cataract risk

How can I reduce cognitive decline?

Answer: Maybe eat blueberries and strawberries.

Ann Neurol. 2012 Apr 26. doi: 10.1002/ana.23594.

Dietary intakes of berries and flavonoids in relation to cognitive decline.

Devore EE, Kang JH, Breteler MM, Grodstein F.

Abstract

OBJECTIVE:

Berries are high in flavonoids, especially anthocyanidins, and improve cognition in experimental studies. We prospectively evaluated whether greater long-term intakes of berries and flavonoids are associated with slower rates of cognitive decline in older women.

METHODS:

Beginning in 1980, a semiquantitative food frequency questionnaire was administered every 4 years to Nurses’ Health Study participants. In 1995-2001, we began measuring cognitive function in 16,010 participants, aged ≥70 years; follow-up assessments were conducted twice, at 2-year intervals. To ascertain long-term diet, we averaged dietary variables from 1980 through the initial cognitive interview. Using multivariate-adjusted, mixed linear regression, we estimated mean differences in slopes of cognitive decline by long-term berry and flavonoid intakes.

RESULTS:

Greater intakes of blueberries and strawberries were associated with slower rates of cognitive decline (eg, for a global score averaging all 6 cognitive tests, for blueberries: p-trend = 0.014 and mean difference = 0.04, 95% confidence interval [CI] = 0.01-0.07, comparing extreme categories of intake; for strawberries: p-trend = 0.022 and mean difference = 0.03, 95% CI = 0.00-0.06, comparing extreme categories of intake), after adjusting for multiple potential confounders. These effect estimates were equivalent to those we found for approximately 1.5 to 2.5 years of age in our cohort, indicating that berry intake appears to delay cognitive aging by up to 2.5 years. Additionally, in further supporting evidence, greater intakes of anthocyanidins and total flavonoids were associated with slower rates of cognitive decline (p-trends = 0.015 and 0.053, respectively, for the global score).

INTERPRETATION:

Higher intake of flavonoids, particularly from berries, appears to reduce rates of cognitive decline in older adults.

How can I reduce my risk of getting periodontitis?

Answer: Try eating more Omega-3 fatty acids.

J Am Diet Assoc. 2010 Nov;110(11):1669-75.

n-3 fatty acids and periodontitis in US adults.

Naqvi AZ, Buettner C, Phillips RS, Davis RB, Mukamal KJ.

Abstract

BACKGROUND:

Periodontitis is a common, chronic inflammatory disease. Although n-3 fatty acids have anti-inflammatory properties, it is unclear whether n-3 fatty acids can treat or prevent periodontitis.

METHOD:

We studied 9,182 adults aged 20 years and older who participated in the National Health and Nutrition Examination Survey between 1999 and 2004. Periodontitis was assessed by dental exam and was defined as >4 mm pocket depth and >3 mm attachment loss in any one tooth. Intake of n-3 fatty acids was assessed by 24-hour dietary recall. We used multivariable logistic regression to estimate the associations between periodontitis and intakes of docosahexaenoic acid (DHA), eicosapentaenoic acid (EPA), and linolenic acid (LNA).

RESULTS:

The weighted prevalence and 95% confidence interval (CI) of periodontitis was 8.2% (95% CI 7.0 to 9.4). Compared with the lowest tertiles, the adjusted odds ratios for periodontitis associated with the highest tertiles of dietary n-3 intake were 0.78 (95% CI 0.61 to 1.00; P=0.009) for DHA, 0.85 (95% CI 0.67 to 1.08; P=0.10) for EPA, and 0.86 (95% CI 0.60 to 1.23; P=0.28) for LNA. The associations were little changed by multivariable adjustment or exclusion of individuals reporting use of dietary supplements containing DHA, EPA, or LNA.

CONCLUSIONS:

In this nationally representative sample, higher dietary intakes of DHA and, to a lesser degree, EPA, were associated with lower prevalence of periodontitis. Interventional studies are needed to confirm the potential protective effects of n-3 fatty acids on periodontitis.

How can I reduce my risk of coronary heart disease?

Answer: Eat dark chocolate.

Clin Nutr. 2011 Apr;30(2):182-7. Epub 2010 Sep 19.

Chocolate consumption is inversely associated with prevalent coronary heart disease: the National Heart, Lung, and Blood Institute Family Heart Study.

Djoussé L, Hopkins PN, North KE, Pankow JS, Arnett DK, Ellison RC.

Abstract

BACKGROUND &#38; AIMS:

Epidemiologic studies have suggested beneficial effects of flavonoids on cardiovascular disease. Cocoa and particularly dark chocolate are rich in flavonoids and recent studies have demonstrated blood pressure lowering effects of dark chocolate. However, limited data are available on the association of chocolate consumption and the risk of coronary heart disease (CHD). We sought to examine the association between chocolate consumption and prevalent CHD.

METHODS:

We studied in a cross-sectional design 4970 participants aged 25-93 years who participated in the National Heart, Lung, and Blood Institute (NHLBI) Family Heart Study. Chocolate intake was assessed through a semi-quantitative food frequency questionnaire. We used generalized estimating equations to estimate adjusted odds ratios.

RESULTS:

Compared to subjects who did not report any chocolate intake, odds ratios (95% CI) for CHD were 1.01 (0.76-1.37), 0.74 (0.56-0.98), and 0.43 (0.28-0.67) for subjects consuming 1-3 times/month, 1-4 times/week, and 5+ times/week, respectively (p for trend <0.0001) adjusting for age, sex, family CHD risk group, energy intake, education, non-chocolate candy intake, linolenic acid intake, smoking, alcohol intake, exercise, and fruit and vegetables. Consumption of non-chocolate candy was associated with a 49% higher prevalence of CHD comparing 5+/week vs. 0/week [OR = 1.49 (0.96-2.32)].

CONCLUSIONS:

These data suggest that consumption of chocolate is inversely related with prevalent CHD in a general United States population.

How can I lower my cardiovascular risk factors?

Answer: Try drinking black tea.

Prev Med. 2011 Dec 16.

The effect of black tea on risk factors of cardiovascular disease in a normal population.

Bahorun T, Luximon-Ramma A, Neergheen-Bhujun VS, Gunness TK, Googoolye K, Auger C, Crozier A, Aruoma OI.

Abstract

OBJECTIVES:

A prospective randomized controlled clinical trial determined the effect of Mauritian black tea consumption on fasting blood plasma levels of glucose, lipid profiles and antioxidant status in a normal population.

METHODS:

The study group (71%) consumed 3 x 200ml of black tea infusate/day for 12weeks without additives followed by a 3week wash-out. The control group (29%) consumed equivalent volume of hot water for same intervention period.

RESULTS:

The tea used had high levels of gallic acid derivatives (50±0.4mg/L), flavan-3-ols (42±2mg/L), flavonols (32±1mg/L) and theaflavins (90±1mg/L). Daily 9g supplementation of black tea infusate induced, in a normal population, a highly significant decrease of fasting serum glucose (18.4%; p<0.001) and triglyceride levels (35.8%; p<0.01), a significant decrease in LDL/HDL plasma cholesterol ratio (16.6%; p<0.05) and a non significant increase in HDL plasma cholesterol levels (20.3%), while a highly significant rise in plasma antioxidant propensity (FRAP: 418%; p<0.001) was noted .

CONCLUSION:

Black tea consumed within a normal diet contributes to a decrease of independent cardiovascular risk factors and improves the overall antioxidant status in humans.

How can I reduce my risk of getting Parkinson’s disease?

Answer: Try drinking coffee–and hope you are one of the lucky 25% of the population who carry the gene that strongly protects against Parkinson’s in the presence of enough caffeine/coffee.

This is a brilliant scientific paper is worth the hard slog of reading it:

Genome-wide gene-environment study identifies glutamate receptor gene GRIN2A as a Parkinson’s disease modifier gene via interaction with coffee.

Hamza TH, Chen H, Hill-Burns EM, Rhodes SL, Montimurro J, Kay DM, Tenesa A, Kusel VI, Sheehan P, Eaaswarkhanth M, Yearout D, Samii A, Roberts JW, Agarwal P, Bordelon Y, Park Y, Wang L, Gao J, Vance JM, Kendler KS, Bacanu SA, Scott WK, Ritz B, Nutt J, Factor SA, Zabetian CP, Payami H.
PLoS Genet. 2011 Aug;7(8):e1002237.
.
I’ve extracted the key bits:
.
Author plain English summary:
Parkinson’s disease (PD), like most common disorders,
involves interactions between genetic make-up and
environmental exposures that are unique to each individual.
Caffeinated-coffee consumption may protect some
people from developing PD, although not all benefit
equally. In a genome-wide search, we discovered that
variations in the glutamate-receptor gene
GRIN2A
modulate
the risk of developing PD in heavy coffee drinkers.
The
study was hypothesis-free, that is, we cast a net across the
entire genome allowing statistical significance to point us
to a genetic variant, regardless of whether it fell in a
genomic desert or an important gene. Fortuitously, the
most significant finding was in a well-known gene, GRIN2A,
which regulates brain signals that control movement and
behavior. Our finding is important for three reasons: First,
it is a proof of concept that studying genes and
environment on the whole-genome scale is feasible, and
this approach can identify important genes that are missed
when environmental exposures are ignored. Second, the
knowledge of interaction between GRIN2A, which is
involved in neurotransmission in the brain, and caffeine,
which is an adenosine-A2A-receptor antagonist, will
stimulate new research towards understanding the cause
and progression of PD. Third, the results may lead to
personalized prevention of and treatment for PD.
Parkinson’s disease is becoming more common as our population ages:
PD is the
second most common neurodegenerative disease after Alzheimer’s
disease; it affects about 5 million individuals in the 10 most
populous nations and is expected to double in frequency by 2030
[3]. Until the 1990’s PD was thought to be purely environmental
with no genetic component. In the last decade, numerous genes
have been identified, some of which can cause PD [4] and others
that are susceptibility loci [5–10]. There are also compelling data
from epidemiology that cigarette smoking and caffeinated-coffee
consumption are associated with reduced risk of developing PD
[11,12] and that exposure to environmental neurotoxins is
associated with increased risk of developing PD [13].
If they were lucky to be in the 25% of people with the protective variant of the GRIN 2A gene, heavy coffee drinkers were 59% less likely to get PD than were light/nil coffee drinkers; if they didn’t have the protective variant of the gene, heavy coffee drinkers were 18% less likely to get PD than were light/nil coffee drinkers:
In a genome-wide gene-environment study we identified
GRIN2A as a genetic modifier of the inverse association of coffee
with the risk of developing PD. The discovery was made in
NGRC, and replicated in independent data. Risk reduction by
heavy coffee use, which was estimated to be 27% on average, was
genotype-specific and varied according to GRIN2A genotype from
18% (P= 361023) for individuals with rs4998386_CC genotype to
59% (P= 6610213) for those with rs4998386_TC genotype. When
coffee intake was categorized in four doses, the dose trend was
more prominent in individuals with rs4998386_T allele than those
with rs4998386_CC genotype, with the 3rd and 4th quartiles
exhibiting only 11% and 39% risk reduction for rs4998386_CC
carriers, vs. 37% and 66% for rs4998386_T carriers.
If they didn’t drink coffee, having the protective variant of the gene offered no protection at all:
compared to the light coffee drinkers with
GRIN2A_rs4998386_CC genotype (the group with highest risk),
heavy coffee use (with CC genotype) reduced risk by 18%
(OR = 0.82, P= 361023), having GRIN2A_rs4998386_T allele
(light coffee) had no effect on risk (OR =1.0, P= 0.99),
but the
combination of heavy coffee use and GRIN2A_rs4998386_TC
genotype was associated with a highly significant 59% risk
reduction (OR = 0.41, P =6610213)
How much caffeine did the study subjects have to drink each day to be called a heavy user? About 238 mg–that’s about two and a half espresso-type coffees a day:
To classify coffee/caffeine intake, each
dataset was treated separately according to the measurements
available. The median ccy or mg was determined for controls
within each dataset (excluding those with zero intake) and used as
the cut-off for heavy drinkers (.median) vs. light drinkers (0 to
#median). The median was 67.5 ccy for NGRC, 74.0 ccy for
PEG, 70.0 ccy for HIHG, and
237.8 mg/day for PAGE
.

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 reduce my risk of getting cancer in the mouth or upper throat?

Answer: Try drinking coffee.

Cancer Epidemiol Biomarkers Prev. 2010 Jul;19(7):1723-36. Epub 2010 Jun 22.

Coffee and tea intake and risk of head and neck cancer: pooled analysis in the international head and neck cancer epidemiology consortium.

Galeone C, Tavani A, Pelucchi C, Turati F, Winn DM, Levi F, Yu GP, Morgenstern H, Kelsey K, Dal Maso L, Purdue MP, McClean M, Talamini R, Hayes RB, Franceschi S, Schantz S, Zhang ZF, Ferro G, Chuang SC, Boffetta P, La Vecchia C, Hashibe M.

Source

Istituto di Ricerche Farmacologiche “Mario Negri”, Università degli Studi di Milano, Milan, Italy.

Abstract

BACKGROUND:

Only a few studies have explored the relation between coffee and tea intake and head and neck cancers, with inconsistent results.

METHODS:

We pooled individual-level data from nine case-control studies of head and neck cancers, including 5,139 cases and 9,028 controls. Logistic regression was used to estimate odds ratios (OR) and 95% confidence intervals (95% CI), adjusting for potential confounders.

RESULTS:

Caffeinated coffee intake was inversely related with the risk of cancer of the oral cavity and pharynx: the ORs were 0.96 (95% CI, 0.94-0.98) for an increment of 1 cup per day and 0.61 (95% CI, 0.47-0.80) in drinkers of >4 cups per day versus nondrinkers. This latter estimate was consistent for different anatomic sites (OR, 0.46; 95% CI, 0.30-0.71 for oral cavity; OR, 0.58; 95% CI, 0.41-0.82 for oropharynx/hypopharynx; and OR, 0.61; 95% CI, 0.37-1.01 for oral cavity/pharynx not otherwise specified) and across strata of selected covariates. No association of caffeinated coffee drinking was found with laryngeal cancer (OR, 0.96; 95% CI, 0.64-1.45 in drinkers of >4 cups per day versus nondrinkers). Data on decaffeinated coffee were too sparse for detailed analysis, but indicated no increased risk. Tea intake was not associated with head and neck cancer risk (OR, 0.99; 95% CI, 0.89-1.11 for drinkers versus nondrinkers).

CONCLUSIONS:

This pooled analysis of case-control studies supports the hypothesis of an inverse association between caffeinated coffee drinking and risk of cancer of the oral cavity and pharynx.

IMPACT:

Given widespread use of coffee and the relatively high incidence and low survival of head and neck cancers, the observed inverse association may have appreciable public health relevance.


Read the complete scientific article:

COFFEE AND TEA INTAKE AND RISK OF HEAD AND NECK CANCER: POOLED ANALYSIS IN THE INTERNATIONAL HEAD AND NECK CANCER EPIDEMIOLOGY CONSORTIUM


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 risk of getting depressed?

Answer: Try drinking coffee.

Arch Intern Med. 2011 Sep 26;171(17):1571-8.

Coffee, caffeine, and risk of depression among women.

Lucas M, Mirzaei F, Pan A, Okereke OI, Willett WC, O’Reilly ÉJ, Koenen K, Ascherio A.

Abstract

BACKGROUND:

Caffeine is the world’s most widely used central nervous system stimulant, with approximately 80% consumed in the form of coffee. However, studies that analyze prospectively the relationship between coffee or caffeine consumption and depression risk are scarce.

METHODS:

A total of 50,739 US women (mean age, 63 years) free of depressive symptoms at baseline (in 1996) were prospectively followed up through June 1, 2006. Consumption of caffeine was measured from validated questionnaires completed from May 1, 1980, through April 1, 2004, and computed as cumulative mean consumption with a 2-year latency period applied. Clinical depression was defined as self-reported physician-diagnosed depression and antidepressant use. Relative risks of clinical depression were estimated using Cox proportional hazards regression models.

RESULTS:

During 10 years of follow-up (1996-2006), 2607 incident cases of depression were identified. Compared with women consuming 1 or less cup of caffeinated coffee per week, the multivariate relative risk of depression was 0.85 (95% confidence interval, 0.75-0.95) for those consuming 2 to 3 cups per day and 0.80 (0.64-0.99; P for trend<.001) for those consuming 4 cups per day or more. Multivariate relative risk of depression was 0.80 (95% confidence interval, 0.68-0.95; P for trend=.02) for women in the highest (≥550 mg/d) vs lowest (<100 mg/d) of the 5 caffeine consumption categories. Decaffeinated coffee was not associated with depression risk.

CONCLUSIONS:

In this large longitudinal study, we found that depression risk decreases with increasing caffeinated coffee consumption. Further investigations are needed to confirm this finding and to determine whether usual caffeinated coffee consumption can contribute to depression prevention.