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How can I lower my cholesterol and LDL levels?

January 21, 2012 by Leave a Comment

Answer: Try eating dark chocolate.

Eur J Clin Nutr. 2011 Aug;65(8):879-86. doi: 10.1038/ejcn.2011.64.

Effects of cocoa products/dark chocolate on serum lipids: a meta-analysis.

Tokede OA, Gaziano JM, Djoussé L.

Abstract

Cocoa products, which are rich sources of flavonoids, have been shown to reduce blood pressure and the risk of cardiovascular disease. Dark chocolate contains saturated fat and is a source of dietary calories; consequently, it is important to determine whether consumption of dark chocolate adversely affects the blood lipid profile. The objective was to examine the effects of dark chocolate/cocoa product consumption on the lipid profile using published trials. A detailed literature search was conducted via MEDLINE (from 1966 to May 2010), CENTRAL and ClinicalTrials.gov for randomized controlled clinical trials assessing the effects of flavanol-rich cocoa products or dark chocolate on lipid profile. The primary effect measure was the difference in means of the final measurements between the intervention and control groups.

In all, 10 clinical trials consisting of 320 participants were included in the analysis. Treatment duration ranged from 2 to 12 weeks. Intervention with dark chocolate/cocoa products significantly reduced serum low-density lipoprotein (LDL) and total cholesterol (TC) levels (differences in means (95% CI) were -5.90 mg/dl (-10.47, -1.32 mg/dl) and -6.23 mg/dl (-11.60, -0.85 mg/dl), respectively). No statistically significant effects were observed for high-density lipoprotein (HDL) (difference in means (95% CI): -0.76 mg/dl (-3.02 to 1.51 mg/dl)) and triglyceride (TG) (-5.06 mg/dl (-13.45 to 3.32 mg/dl)). These data are consistent with beneficial effects of dark chocolate/cocoa products on total and LDL cholesterol and no major effects on HDL and TG in short-term intervention trials.

Filed Under: high_cholesterol_and_LDL_levels, managing minor conditions and injuries, physical Tagged With: , , , ,

How can I reduce my blood pressure?

January 21, 2012 by Leave a Comment

Answer: Try eating more garlic.

BMC Cardiovasc Disord. 2008 Jun 16;8:13.

Effect of garlic on blood pressure: a systematic review and meta-analysis.

Ried K, Frank OR, Stocks NP, Fakler P, Sullivan T.

Abstract

BACKGROUND:

Non-pharmacological treatment options for hypertension have the potential to reduce the risk of cardiovascular disease at a population level. Animal studies have suggested that garlic reduces blood pressure, but primary studies in humans and non-systematic reviews have reported mixed results. With interest in complementary medicine for hypertension increasing, it is timely to update a systematic review and meta-analysis from 1994 of studies investigating the effect of garlic preparations on blood pressure.

METHODS:

We searched the Medline and Embase databases for studies published between 1955 and October 2007. Randomised controlled trials with true placebo groups, using garlic-only preparations, and reporting mean systolic and/or diastolic blood pressure (SBP/DBP) and standard deviations were included in the meta-analysis. We also conducted subgroup meta-analysis by baseline blood pressure (hypertensive/normotensive), for the first time. Meta-regression analysis was performed to test the associations between blood pressure outcomes and duration of treatment, dosage, and blood pressure at start of treatment.

RESULTS:

Eleven of 25 studies included in the systematic review were suitable for meta-analysis. Meta-analysis of all studies showed a mean decrease of 4.6 +/- 2.8 mm Hg for SBP in the garlic group compared to placebo (n = 10; p = 0.001), while the mean decrease in the hypertensive subgroup was 8.4 +/- 2.8 mm Hg for SBP (n = 4; p < 0.001), and 7.3 +/- 1.5 mm Hg for DBP (n = 3; p < 0.001). Regression analysis revealed a significant association between blood pressure at the start of the intervention and the level of blood pressure reduction (SBP: R = 0.057; p = 0.03; DBP: R = -0.315; p = 0.02).

CONCLUSION:

Our meta-analysis suggests that garlic preparations are superior to placebo in reducing blood pressure in individuals with hypertension.

Read the complete scientific review:

Effect of garlic on blood pressure: A systematic review and meta-analysis



Filed Under: high blood pressure, Managing common health problems, physical Tagged With: , ,

How can I improve my congestive heart failure condition?

January 21, 2012 by Leave a Comment

Answer: Talk to your doctor about eating more dark chocolate.

Eur Heart J. 2011 Dec 15.

Cardiovascular effects of flavanol-rich chocolate in patients with heart failure.

Flammer AJ, Sudano I, Wolfrum M, Thomas R, Enseleit F, Périat D, Kaiser P, Hirt A, Hermann M, Serafini M, Lévêques A, Lüscher TF, Ruschitzka F, Noll G, Corti R.

Abstract

Aims

Flavanol-rich chocolate (FRC) is beneficial for vascular and platelet function by increasing nitric oxide bioavailability and decreasing oxidative stress. Congestive heart failure (CHF) is characterized by impaired endothelial and increased platelet reactivity. As statins are ineffective in CHF, alternative therapies are a clinical need. We therefore investigated whether FRC might improve cardiovascular function in patients with CHF.

Methods and results

Twenty patients with CHF were enrolled in a double-blind, randomized placebo-controlled trial, comparing the effect of commercially available FRC with cocoa-liquor-free control chocolate (CC) on endothelial and platelet function in the short term (2 h after ingestion of a chocolate bar) and long term (4 weeks, two chocolate bars/day). Endothelial function was assessed non-invasively by flow-mediated vasodilatation of the brachial artery. Flow-mediated vasodilatation significantly improved from 4.98 ± 1.95 to 5.98 ± 2.32% (P = 0.045 and 0.02 for between-group changes) 2h after intake of FRC to 6.86 ± 1.76% after 4 weeks of daily intake (P = 0.03 and 0.004 for between groups). No effect on endothelial-independent vasodilatation was observed. Platelet adhesion significantly decreased from 3.9 ± 1.3 to 3.0 ± 1.3% (P = 0.03 and 0.05 for between groups) 2 h after FRC, an effect that was not sustained at 2 and 4 weeks. Cocoa-liquor-free CC had no effect, either on endothelial function or on platelet function. Blood pressure and heart rate did not change in either group.

Conclusion

Flavanol-rich chocolate acutely improves vascular function in patients with CHF. A sustained effect was seen after daily consumption over a 4-week period, even after 12 h abstinence. These beneficial effects were paralleled by an inhibition of platelet function in the presence of FRC only.Trial Registration ClinicalTrials.gov Identifier: NCT00538941.

Filed Under: congestive heart failure, managing less common health problems, physical Tagged With: , ,

How can I improve my chronic fatigue?

January 21, 2012 by Leave a Comment

Answer: Try eating dark chocolate.



Nutr J. 2010 Nov 22;9:55.

High cocoa polyphenol rich chocolate may reduce the burden of the symptoms in chronic fatigue syndrome.

Sathyapalan T, Beckett S, Rigby AS, Mellor DD, Atkin SL.

Abstract

BACKGROUND:

Chocolate is rich in flavonoids that have been shown to be of benefit in disparate conditions including cardiovascular disease and cancer. The effect of polyphenol rich chocolate in subjects with chronic fatigue syndrome (CFS) has not been studied previously.

METHODS:

We conducted a double blinded, randomised, clinical pilot crossover study comparing high cocoa liquor/polyphenol rich chocolate (HCL/PR) in comparison to simulated iso-calorific chocolate (cocoa liquor free/low polyphenols(CLF/LP)) on fatigue and residual function in subjects with chronic fatigue syndrome. Subjects with CFS having severe fatigue of at least 10 out of 11 on the Chalder Fatigue Scale were enrolled. Subjects had either 8 weeks of intervention in the form of HCL/PR or CLF/LP, with a 2 week wash out period followed by 8 weeks of intervention with the other chocolate.

RESULTS:

Ten subjects were enrolled in the study. The Chalder Fatigue Scale score improved significantly after 8 weeks of the HCL/PR chocolate arm [median (range) Exact Sig. (2-tailed)] [33 (25 – 38) vs. 21.5 (6 – 35) 0.01], but that deteriorated significantly when subjects were given simulated iso-calorific chocolate (CLF/CP) [ 28.5 (17 – 20) vs. 34.5 (13-26) 0.03]. The residual function, as assessed by the London Handicap scale, also improved significantly after the HCL/PR arm [0.49 (0.33 – 0.62) vs. 0.64 (0.44 – 0.83) 0.01] and deteriorated after iso-calorific chocolate [00.44 (0.43 – 0.68) vs. 0.36 (0.33 – 0.62)0.03]. Likewise the Hospital Anxiety and Depression score also improved after the HCL/PR arm, but deteriorated after CLF/CP. Mean weight remained unchanged throughout the trial.

CONCLUSION:

This study suggests that HCL/PR chocolate may improve symptoms in subjects with chronic fatigue syndrome.

Read the complete scientific paper:

High cocoa polyphenol rich chocolate may reduce the burden of the symptoms in chronic fatigue syndrome

Filed Under: chronic fatigue, managing less common health problems, physical Tagged With: , , ,

How can I manage my Parkinson’s disease symptoms better?

January 19, 2012 by Leave a Comment

Answer: Check with your neurologist about increasing your caffeine intake.

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J Alzheimers Dis. 2010;20 Suppl 1:S205-20.

Effects of caffeine in Parkinson’s disease: from neuroprotection to the management of motor and non-motor symptoms.

Prediger RD.

Abstract

Parkinson’s disease (PD) is the second most common neurodegenerative disorder affecting approximately 1% of the population older than 60 years. Classically, PD is considered to be a motor system disease and its diagnosis is based on the presence of a set of cardinal motor signs (rigidity, bradykinesia, rest tremor) that are consequence of a pronounced death of dopaminergic neurons in the substantia nigra pars compacta. Nowadays there is considerable evidence showing that non-dopaminergic degeneration also occurs in other brain areas which seems to be responsible for the deficits in olfactory, emotional and memory functions that precede the classical motor symptoms in PD. The present review attempts to examine results reported in epidemiological, clinical and animal studies to provide a comprehensive picture of the antiparkinsonian potential of caffeine.

Convergent epidemiological and pre-clinical data suggest that caffeine may confer neuroprotection against the underlying dopaminergic neuron degeneration, and influence the onset and progression of PD. The available data also suggest that caffeine can improve the motor deficits of PD and that adenosine A2A receptor antagonists such as istradefylline reduces OFF time and dyskinesia associated with standard ‘dopamine replacement’ treatments. Finally, recent experimental findings have indicated the potential of caffeine in the management of non-motor symptoms of PD, which do not improve with the current dopaminergic drugs.

Altogether, the studies reviewed provide strong evidence that caffeine may represent a promising therapeutic tool in PD, thus being the first compound to restore both motor and non-motor early symptoms of PD together with its neuroprotective potential.

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Handb Exp Pharmacol. 2011;(200):267-310.

Impacts of methylxanthines and adenosine receptors on neurodegeneration: human and experimental studies.

Chen JF, Chern Y.

Abstract

Neurodegenerative disorders are some of the most feared illnesses in modern society, with no effective treatments to slow or halt this neurodegeneration. Several decades after the earliest attempt to treat Parkinson’s disease using caffeine, tremendous amounts of information regarding the potential beneficial effect of caffeine as well as adenosine drugs on major neurodegenerative disorders have accumulated.

In the first part of this review, we provide general background on the adenosine receptor signaling systems by which caffeine and methylxanthine modulate brain activity and their role in relationship to the development and treatment of neurodegenerative disorders. The demonstration of close interaction between adenosine receptor and other G protein coupled receptors and accessory proteins might offer distinct pharmacological properties from adenosine receptor monomers.

This is followed by an outline of the major mechanism underlying neuroprotection against neurodegeneration offered by caffeine and adenosine receptor agents. In the second part, we discuss the current understanding of caffeine/methylxantheine and its major target adenosine receptors in development of individual neurodegenerative disorders, including stroke, traumatic brain injury Alzheimer’s disease, Parkinson’s disease, Huntington’s disease and multiple sclerosis.

The exciting findings to date include the specific in vivo functions of adenosine receptors revealed by genetic mouse models, the demonstration of a broad spectrum of neuroprotection by chronic treatment of caffeine and adenosine receptor ligands in animal models of neurodegenerative disorders, the encouraging development of several A(2A) receptor selective antagonists which are now in advanced clinical phase III trials for Parkinson’s disease.

Importantly, increasing body of the human and experimental studies reveals encouraging evidence that regular human consumption of caffeine in fact may have several beneficial effects on neurodegenerative disorders, from motor stimulation to cognitive enhancement to potential neuroprotection. Thus, with regard to neurodegenerative disorders, these potential benefits of methylxanthines, caffeine in particular, strongly argue against the common practice by clinicians to discourage regular human consumption of caffeine in aging populations.

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J Neurol Sci. 2006 Oct 25;248(1-2):9-15. Epub 2006 Jun 27.

Novel neuroprotection by caffeine and adenosine A(2A) receptor antagonists in animal models of Parkinson’s disease.

Kalda A, Yu L, Oztas E, Chen JF.

Abstract

The adenosine A(2A) receptor has recently emerged as a leading non-dopaminergic therapeutic target for Parkinson’s disease, largely due to the restricted distribution of the receptor in the striatum and the profound interaction between adenosine and dopamine receptors in brain. Two lines of research in particular have demonstrated the promise of the A(2A) receptor antagonists as novel anti-parkinsonian drugs.

First, building on extensive preclinical animal studies, the A(2A) receptor antagonist KW6002 has demonstrated its potential to increase motor activity in PD patients of the advanced stage in a recent clinical phase IIB trial. Second, recently two prospective epidemiological studies of large cohorts have firmly established the inverse relationship between the consumption of caffeine (a non-specific adenosine antagonist) and the risk of developing PD. The potential neuroprotective effect of caffeine and A(2A) receptor antagonists in PD is further substantiated by the demonstration that pharmacological blockade (by caffeine or specific A(2A) antagonists) or genetic depletion of the A(2A) receptor attenuated dopaminergic neurotoxicity and neurodegeneration in animal models of PD.

Moreover, A(2A) receptor antagonism-mediated neuroprotection goes beyond PD models and can be extended to a variety of other brain injuries induced by stroke, excitotoxicity and mitochondrial toxins. Intensive investigations are under way to dissect out common cellular mechanisms (such as A(2A) receptor modulation of neuroinflammation) which may underlie the broad spectrum of neuroprotection by A(2A) receptor inactivation in brain.

Filed Under: managing less common health problems, Parkinson's disease, physical Tagged With: , , ,

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

January 18, 2012 by Leave a Comment

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.
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I’ve extracted the key bits:
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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.

Filed Under: Parkinson's disease Tagged With: ,

How can I reduce my cognitive decline due to aging?

January 18, 2012 by Leave a Comment

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.

Filed Under: cognitive decline, physical, preventing specific diseases Tagged With: , , , , ,

How can I manage my gout condition better?

January 18, 2012 by Leave a Comment

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.

Filed Under: blog, gout, managing less common health problems, physical Tagged With: , , , , ,

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

January 15, 2012 by Leave a Comment

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


Filed Under: mouth and throat cancer, physical, preventing specific diseases Tagged With: , ,

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

January 15, 2012 by Leave a Comment

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.

Filed Under: physical, preventing specific diseases Tagged With: , ,
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