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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 improve my handwriting and other psychomotor tasks?

January 18, 2012 by Leave a Comment

Answer: Try caffeine (coffee!).


Hum Mov Sci. 2006 Oct;25(4-5):523-35.

The effect of caffeine on handwriting movements in skilled writers.

Tucha O, Walitza S, Mecklinger L, Stasik D, Sontag TA, Lange KW.

Abstract

In laboratory tasks, caffeine has been shown to improve psychomotor performance. The aim of the present experiment was to assess the effects of caffeine on a skilled everyday life task in habitual caffeine consumers. The assessment of handwriting movements of 20 adults was performed following the administration of 0mg/kg (placebo), 1.5mg/kg, 3.0mg/kg or 4.5mg/kg of caffeine. A digitising tablet was used for the assessment of fine motor movements. Participants were asked to perform a simple writing task. Kinematic analysis of handwriting movements showed that, in comparison to placebo administration, high doses of caffeine (i.e., 4.5mg/kg) can produce improvements in handwriting as indicated by more fluent handwriting movements as well as an increase in maximum velocity and maximum positive and negative accelerations. The results suggest that higher doses of caffeine can enhance psychomotor performance.

Filed Under: cognitive, cognitive performance, improve handwriting, improve psychomotor skills 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 reduce my risk of getting depressed?

January 15, 2012 by Leave a Comment

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.

Filed Under: depression Tagged With: , , ,

How can I reduce my risk of getting nonalcoholic fatty liver disease?

January 13, 2012 by Leave a Comment

Answer: Try increasing your intake of caffeine.

Aliment Pharmacol Ther. 2012 Jan;35(1):76-82. doi: 10.1111/j.1365-2036.2011.04916.x.

Caffeine is protective in patients with non-alcoholic fatty liver disease.

Birerdinc A, Stepanova M, Pawloski L, Younossi ZM.

Abstract

Background: Non-alcoholic fatty liver disease (NAFLD), the hepatic manifestation of metabolic syndrome, is the most common cause of primary liver disease. Although recent studies have found that coffee drinking is protective against end stage chronic liver disease, there are scarce caffeine intake data in NAFLD specifically.

Aim: To investigate the effects of dietary behaviour in NAFLD patients, using four continuous cycles of the National Health and Nutrition Examination Surveys (NHANES 2001-2008).

Methods: Using data from four continuous cycles of NHANES, dietary intake questionnaires that list 62 nutrition components. Logistic regression was used to identify independent predictors of NAFLD among nutrition components after adjustment for potential clinical confounders. All analyses were run using sas 9.1 and sudaan 10.0 (SAS Institute Inc., Cary, NC, USA).

Results: Of the 62 nutrient components used for the univariate analysis, 38% were significant (P-value <0.05) in NAFLD with caffeine consumption being higher in the control group (P-value <0.001). The multivariate analysis using demographics, clinical parameters and nutritional components found five factors independently associated with NAFLD [African American Race P-value <0.001); Male gender P-value <0.001); Obesity (BMI ≥ 30) P-value <0.001); Caffeine intake (mg) P-value <0.001) and total plain water consumption (g) P-value ≤0.02)].

Conclusions: Our analysis shows that caffeine intake is independently associated with a lower risk for NAFLD suggesting a potential protective effect. These data necessitate further research to elucidate the mechanism by which caffeine can protect against NAFLD.

Here’s another study reporting the protective powers of coffee (caffeine?) for the liver:

Hepatology. 2011 Oct 10. doi: 10.1002/hep.24731. [Epub ahead of print]

Association of coffee and caffeine consumption with fatty liver disease, nonalcoholic steatohepatitis, and degree of hepatic fibrosis.

Molloy JW, Calcagno CJ, Williams CD, Jones FJ, Torres DM, Harrison SA.

Abstract

Coffee caffeine consumption (CC) is associated with reduced hepatic fibrosis in patients with chronic liver diseases, such as hepatitis C. The association of CC with nonalcoholic fatty liver disease (NAFLD) has not been established. The aim of this study was to correlate CC with the prevalence and severity of NAFLD. Patients involved in a previously published NAFLD prevalence study, as well as additional NASH patients identified in the Brooke Army Medical Center Hepatology clinic, were queried about their caffeine intake. A validated questionnaire for CC was utilized to assess for a relationship between caffeine and four groups: ultrasound negative (controls), bland steatosis/not-NASH*, NASH stage 0-1, and NASH stage 2-4. A total of 306 patients responded to the CC questionnaire. Average milligrams of total caffeine/coffee CC per day in controls, bland steatosis/not-NASH, NASH stage 0-1, and NASH stage 2-4 were 307/228, 229/160, 351/255, and 252/152, respectively. When comparing patients with bland steatosis/not-NASH to those with NASH stage 0-1, there was a significant difference in CC between the two groups (P = 0.005). Additionally, when comparing patients with NASH stage 0-1 to those with NASH stage 2-4, there was a significant difference in coffee CC (P = 0.016). Spearman’s rank correlation analysis further supported a negative relationship between coffee CC and hepatic fibrosis (r = -0.215; P = 0.035). Conclusion: Coffee CC is associated with a significant reduction in risk of fibrosis among NASH patients. (Hepatology 2011).

*  Translation:  NASH = Non-alcoholic steatohepatitis; steatohepatitis = fatty liver. Therefore NASH = Non-alcoholic fatty liver disease = NAFLD!)

Here’s an interesting summing up of where non-alcoholic fatty liver fits into metabolic syndrome:

Ned Tijdschr Geneeskd. 2011;155:A3181.

Treatment of non-alcoholic fatty liver disease

[Article in Dutch]
Koek GH.

Abstract

Non-alcoholic fatty liver disease (NAFLD) comprises benign steatosis and steatohepatitis (NASH) and may lead to liver fibrosis, cirrhosis and hepatocellular carcinoma. Its prevalence is estimated to be 20% in the general population and 50-100% in patients with overweight and obesity. In about 15-30% of patients steatosis evolves to NASH which can only be diagnosed by means of a liver biopsy. NAFLD may be described as the hepatic component of the metabolic syndrome and is a consequence of the Western lifestyle. The pathogenesis is multifactorial; oxidative stress plays a crucial role in maintaining inflammation and progressive fibrosis. Lifestyle modification with weight loss and increased physical activity is the cornerstone of the treatment, which should take place in a multidisciplinary setting. To date, no specific registered drug for NAFLD treatment is available. Supportive drug therapy is mainly focused on aspects of the metabolic syndrome and chronic inflammation.

Filed Under: non-alcoholic fatty liver, physical, preventing specific diseases Tagged With: , ,