ASPIRIN

>
> If you take an aspirin or a baby aspirin 
> once a day, take it
> at night. The reason: aspirin has a  24-hour
> "half-life". Therefore, if
> most heart attacks happen  in the wee hours of the
> morning, the aspirin would
> be  strongest in your system.
>
> FYI, aspirin lasts a really long  time in
> your medicine
> chest...years. (when it gets old, it  smells like
> vinegar.)
>
> Please read on.
> 
> WHY ASPIRIN BY YOUR BED
> Save lives ...
>
> It  is important to always have ASPIRIN in the
> home!!!
>
>  Why have Aspirin by your bedside ?
>
> ABOUT HEART ATTACKS 
>
> There are other symptoms of an heart attack
> besides  the pain on
> the left side. One must also be aware of an intense 
> pain on the
> chin, as well as nausea and lots of sweating, 
> However these symptoms may also occur less
> frequently. 
>
> NOTE : There may be no pain in the chest
> during an  heart
> attack.
>
> The majority of people (about 60%)  who had an
> heart attack
> d

uring their

> Sleep, did not  wake up. However, if it
> occurs, the chest pain
> may wake you 
> Up from your deep sleep.
>
> If that happens,  IMMEDIATELY DISSOLVE TWO
> ASPIRINS IN YOUR
> MOUTH and
>  Swallow them with a bit of water.
>
> Afterwards, phone a  neighbor or a family
> member who lives very
> close by and 
> State "HEART ATTACK!!!" And that you have
> taken 2 ASPIRINS 
>
> Take a seat on a chair or sofa and wait for
> their  arrival and
> ...DO NOT LIE DOWN !!!
>
> A Cardiologist  has stated that, if each
> person, after receiving
> this  e-mail,
> Sends it to 10 people, probably a life can be
> saved! 
>
> I have already shared the information!!! What
> about  you?
> Forward this message
> : IT MAY SAVE LIVES !!! !!! 
>
> Life isn't about waiting for the storm to
> pass... 
> it's about learning to dance in the rain.

Brian F. Gage, M.D.

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In patients with atrial fibrillation, warfarin prevents 64% of strokes.¹ Thus, warfarin has become the recommended treatment for candidates for anticoagulation therapy who have atrial fibrillation and at least one additional risk factor for stroke.²

Despite clear and consistent recommendations,³ warfarin is prescribed to only two thirds of appropriate candidates.⁴ Several factors contribute to suboptimal use of warfarin therapy: drug and dietary interactions, inconvenience of monitoring the international normalized ratio (INR), risk of hemorrhage, and concerns about real-world effectiveness, which averages 35%.⁴ Thus, new oral anticoagulants are needed.

Dabigatran etexilate, an oral thrombin inhibitor, appears to be an anticoagulant that could fill this niche. After conversion to its active form, dabigatran competitively inhibits thrombin. This conversion is carried out by a serum esterase that is independent of cytochrome P-450. Therefore, dabigatran should be less susceptible to dietary and drug interactions and to genetic polymorphisms that affect warfarin. Furthermore, neither anticoagulation monitoring nor dose adjustments are necessary with dabigatran.

The results of a large, multicenter, randomized trial comparing dabigatran with warfarin are reported in this issue of the Journal.⁵ The Randomized Evaluation of Long-Term Anticoagulation Therapy (RE-LY) (ClinicalTrials.gov number, NCT00262600 [ClinicalTrials.gov] ) steering committee and investigators enrolled 18,113 patients who had atrial fibrillation and were at risk for stroke. Two doses of dabigatran (110 mg twice daily and 150 mg twice daily), administered in a blinded fashion, were compared with adjusted-dose warfarin administered in an unblinded manner. Because warfarin use was not blinded and patients taking warfarin had regular follow-up evaluations for purposes of INR monitoring, reporting bias could have affected the detection of outcome events. To minimize this risk, each event was adjudicated by two independent investigators who were unaware of the treatment assignments, and all hospital records were reviewed to ensure complete detection of events.

The primary outcome of RE-LY was systemic embolism or stroke (including hemorrhagic stroke). The rate of the primary outcome (expressed as the percent per year) was significantly lower with dabigatran at a dose of 150 mg twice daily (1.11%) than with either dabigatran at a dose of 110 mg twice daily (1.53%) or warfarin (1.69%). The rate of nonhemorrhagic (i.e., ischemic or unspecified) stroke also was significantly lower with 150 mg of dabigatran (0.92%) than with either 110 mg of dabigatran (1.34%) or warfarin (1.20%). To prevent one nonhemorrhagic stroke, the number of patients who would need to be treated with dabigatran at a dose of 150 mg twice daily, rather than warfarin, is approximately 357.

The rates of hemorrhagic stroke with the 110-mg and 150-mg dabigatran doses (0.12% and 0.10%) were significantly lower than that with warfarin (0.38%). Given these rates, the number of patients who would need to be treated with dabigatran (rather than warfarin) to prevent one hemorrhagic stroke is approximately 370. The rate of extracranial hemorrhage was similar in all three groups: 2.51% with 110 mg of dabigatran, 2.84% with 150 mg of dabigatran, and 2.67% with warfarin.

The quality of warfarin management in RE-LY was assessed by measuring the percentage of time (excluding the first week of therapy) during which the INR was within the therapeutic range, which averaged 64%. This value is similar to the percentage of time within the therapeutic range in warfarin groups of contemporary trials: 64% in ACTIVE (Atrial Fibrillation Clopidogrel Trial with Irbesartan for Prevention of Vascular Events) W^6,7 and 66% to 68% in the SPORTIF (Stroke Prevention Using an Oral Thrombin Inhibitor in Atrial Fibrillation) trials.^8,9 The slightly lower rate of INR control in RE-LY reflects the higher enrollment of RE-LY participants who had not received long-term vitamin K–antagonist therapy. On the basis of a published equation,⁷ one can estimate that RE-LY participants who were randomly assigned to receive warfarin would have needed to have an INR within the therapeutic range approximately 79% of the time to have a stroke rate as low as that in the group receiving 150 mg of dabigatran. Even with patients' self monitoring or pharmacogenetic dosing, such tight control is unlikely.

Myocardial infarction and gastrointestinal side effects were significantly more common with dabigatran than with warfarin. Rates of myocardial infarction were 0.72% and 0.74% with 110 mg and 150 mg of dabigatran, respectively, and 0.53% with warfarin; approximately 500 patients would have to receive dabigatran for 1 patient to have an event. Whether thrombin inhibition contributes to the risk of myocardial infarction is unclear. As compared with warfarin, ximelagatran (another oral thrombin inhibitor that is not available for clinical use) was associated with a significantly increased risk of myocardial infarction in patients who had acute deep-vein thrombosis¹⁰ or were undergoing joint arthroplasty.¹¹ However, in another study, ximelagatran prevented reinfarction after an acute myocardial infarction.¹² In RE-LY, rates of dyspepsia (including abdominal pain) were elevated with dabigatran (11.8% in the 110-mg group and 11.3% in the 150-mg group) as compared with warfarin (5.8%), and it contributed to the greater second-year rate of dropout with dabigatran (approximately 21%) than with warfarin (16.6%).

RE-LY participants underwent monitoring of aspartate aminotransferase and alanine aminotransferase to detect possible hepatotoxicity. The fraction of participants whose aminotransferase levels were elevated to more than three times the upper limit of the normal range was approximately 2% in each dabigatran group — no higher than in the warfarin group and one third that associated with ximelagatran.^8,9 In RE-LY, the fraction of patients requiring hospitalization for a hepatobiliary disorder was equivalent in the three treatment groups. The median duration of follow-up in RE-LY was 2.0 years, so the hepatic risks of long-term use are unclear, but they are being quantified in a follow-up study (NCT00808067 [ClinicalTrials.gov] ). Also unclear is how often aminotransferases should be monitored during the initial months of therapy and whether subsequent monitoring will be needed.

Dabigatran is not without important drug interactions. P-glycoprotein inhibitors — including verapamil, amiodarone, and especially quinidine — raise dabigatran serum concentrations considerably. This interaction may have contributed to the trend toward greater efficacy of dabigatran in the subgroup of patients taking amiodarone, but it could elevate the risk of hemorrhage in such patients.

In conclusion, as compared with adjusted-dose warfarin, dabigatran given at a dose of 150 mg twice daily prevented more strokes and dabigatran at a dose of 110 mg twice daily caused fewer hemorrhages. The 150-mg dose appears to be more efficacious and the 110-mg dose appears to be safer, especially in patients taking amiodarone or other P-glycoprotein inhibitors. A future subgroup analysis could test the hypothesis that the 110-mg dose also is safer in patients who are petite or elderly or who have renal impairment. Patients who had a creatinine clearance of less than 30 ml per minute or liver disease were excluded from RE-LY and should not receive the drug. Noncompliant patients also were excluded from RE-LY, and they might receive less (if any) benefit from dabigatran, because the longer half-life of warfarin could provide them with a more consistent anticoagulant effect. Because of dabigatran's twice-daily dosing and greater risk of nonhemorrhagic side effects, patients already taking warfarin with excellent INR control have little to gain by switching to dabigatran. In contrast, many other patients who have atrial fibrillation and at least one additional risk factor for stroke could benefit from dabigatran. In summary, although there are qualifications, we can rely on RE-LY.

No potential conflict of interest relevant to this article was reported.

Source Information

From Washington University, St. Louis.

This article (10.1056/NEJMe0906886) was published on August 30, 2009, at NEJM.org.

Summary and Comment Is 140/90 Low Enough for Nondiabetic Hypertensive Patients? A study supports a more aggressive approach to BP reduction. Most guidelines recommend 140/90 mm Hg as the blood pressure target for nondiabetic patients with hypertension. But, no randomized trials of systolic blood pressure (SBP) reduction to 130 mm Hg have been conducted in this population. With funding from three pharmaceutical manufacturers, Italian investigators randomized 1111 nondiabetic hypertensive patients to tight (<130 src="http://general-medicine.jwatch.org/math/ge.gif" alt="≥" _base_href="http://general-medicine.jwatch.org" border="0">55) had baseline SBP levels of 150 mm Hg after receiving antihypertensive therapy for at least 12 weeks and had at least one other cardiovascular risk factor. Treatment was open-label and individualized and included previous (background) therapy plus various combinations of furosemide, hydrochlorothiazide, ramipril, telmisartan (Micardis), amlodipine, bisoprolol, and clonidine. Clinicians measured blood pressure by auscultation every 4 months and reported the average of three seated readings after 10 minutes of rest. In the tight-control group, one SBP reading >130 mm Hg at any visit led to intensification of treatment; in the usual-control group, one SBP reading <130> At baseline, blood pressures were equal in the two groups, and roughly 20% of patients in each group had LVH. After 2 years, 27% and 72% of patients in the usual- and tight-control groups, respectively, had SBP <130> Comment: Left ventricular hypertrophy is not a clinical endpoint, but it is a powerful predictor of cardiovascular events. According to this study, an aggressive approach to blood pressure reduction can be well-tolerated and might lower the incidence of adverse cardiovascular outcomes. Larger and longer studies will be required to measure individual cardiovascular outcomes directly and to test this hypothesis in patients at lower baseline risk. — Bruce Soloway, MD Published in Journal Watch General Medicine August 27, 2009 Citation(s): Verdecchia P et al. Usual versus tight control of systolic blood pressure in non-diabetic patients with hypertension (Cardio-Sis): An open-label randomised trial. Lancet 2009 Aug 15; 374:525. Medline abstract (Free)

Summary and Comment

Statin Reload Beneficial in Percutaneous Coronary Intervention

The ARMYDA-RECAPTURE results demonstrate that the protective effects of statin loading before PCI extend to ACS patients who are already taking statins.

[PDF]Dit artikel kan ik niet markeren. De erfelijkheid speelt een grotere rol naarmate men ouder wordt. Dat is niet wat je zou verwachten.Door onderzoek met een en meereiïge tweelingen is een en ander duidelijk gebleken.

The heritability of general cognitive ability increases linearly ...

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August 11, 2009 — Even moderately elevated cholesterol levels in midlife are strongly associated with later risk for Alzheimer's disease (AD) and vascular dementia (VaD), new research suggests.

Lead author Alina Solomon, MD, from the University of Kuopio, Finland, used data from the Kaiser Permanente Northern California Medical Group to investigate the relationship between midlife cholesterol and dementia and found that even cholesterol levels of 200 to 239 mg/dL increase risk.

"Both physicians and patients need to know that elevated cholesterol increases the risk not only for heart disease but also for dementia," Dr. Solomon told Medscape Psychiatry. "The most important finding was that even moderately elevated cholesterol at midlife can increase the risk of both AD and VaD later in life," she added. "This emphasizes the fact that AD and VaD may have more in common than was previously thought. Several studies have pointed out that there is a degree of overlap between the 2 dementia types in terms of risk factors, clinical symptoms, and neuropathology. Vascular factors can be associated with AD as well — not just with vascular forms of dementia."

The study is published in the August issue of Dementia and Geriatric Cognitive Disorders.

More than 9000 Subjects

Performed in collaboration with Rachel A. Whitmer, PhD, from Kaiser Permanente in Oakland, California, the study included 9844 subjects who had undergone detailed health evaluations during 1964 to 1973, when they were 40 to 45 years old.

Data from 1994 showed that 469 participants had AD, and 127 had VaD. The researchers adjusted for age, education, race/ethnic group, sex, midlife diabetes, hypertension, body mass index, and late-life stroke. They used cholesterol levels lower than 200 mg/dL as a reference point.

The analysis showed AD hazard ratios of 1.23 for midlife borderline cholesterol (200 – 239 mg/dL) and 1.57 for high cholesterol (≥240 mg/dL). Quartile analysis showed that hazard ratios were 1.31 for cholesterol levels of 221 to 238 mg/dL and 1.58 for levels of 249 to 500 mg/dL.

VaD hazard ratios were 1.50 for borderline cholesterol and 1.26 for high cholesterol.

Dr. Solomon said that the results were not entirely surprising, as previous studies have shown a link between high cholesterol and dementia risk. However, she added, this study is the largest to date, includes a heterogeneous population, and considers VaD as well as AD as an outcome.

Unanswered questions for future investigations include the roles of different cholesterol types, the significance of cholesterol changes after midlife in relation to dementia risk, and the effect of lipid-lowering treatment on dementia risk.

According to Dr. Solomon, the mechanisms behind the cholesterol-dementia association are not entirely clear.

"Our results remained significant even after taking into account several vascular-related factors and conditions, so other mechanisms may be involved as well. The brain is the most cholesterol-rich organ in the human body, but compared to serum cholesterol, far less is known about brain cholesterol and the interactions between the 2 cholesterol pools," she said.

What Is Bad for the Heart Is Bad for the Brain

Robert Stewart, MD, head of epidemiology at the Institute of Psychiatry, King's College London, United Kingdom, told Medscape Psychiatry that the Solomon study data are "convincing" and "consistent with those from other studies which have screened community populations for this disorder."

"In general, there is now a large body of evidence which indicates that what is bad for the heart is bad for the brain — that is, that that the well-known risk factors for coronary heart disease and stroke are also risk factors for dementia (whether this is classified as AD or VaD)," Dr. Stewart said.

"So the real message for clinicians is not to do anything differently, but to be aware that what they should be doing already — identifying and treating high cholesterol, high blood pressure, [and] diabetes and promoting healthy diet and active lifestyles — is likely to have more benefits than originally envisaged and should reduce risk of dementia as well as reducing risk of cardiovascular disease."

The authors have disclosed no relevant financial relationships.

Dement Geriatr Cogn Disord. 2009;28:75–80.

New Review Endorses CV Benefits of Fish Oil

Lisa Nainggolan

Authors and Disclosures

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pubmed gastro-enterology 12 ? augustus 09
Abstract
Background: Simvastatin reduces cardiovascular mortality and morbidity but, as with other HMG-CoA reductase inhibitors, can cause significant muscle toxicity and has been associated with elevations of liver transaminases.Methods: Muscle and liver adverse effects of simvastatin 40 mg daily were evaluated in a randomized placebo-controlled trial involving 20,536 UK patients with vascular disease or diabetes (in which a substantial reduction of cardiovascular mortality and morbidity has previously been demonstrated).Results: The excess incidence of myopathy in the simvastatin group was < 0.1% over the 5 years of the trial, and there were no significant differences between the treatment groups in the incidence of serious hepatobiliary disease.Conclusion: Among the many different types of high-risk patient studied (including women, older individuals and those with low cholesterol levels), there was a very low incidence (< 0.1%) of myopathy during 5 years treatment with simvastatin 40 mg daily. The risk of hepatitis, if any, was undetectable even in this very large long-term trial. Routine monitoring of liver function tests during treatment with simvastatin 40 mg is not useful.
Background
The HMG-CoA reductase inhibitor simvastatin is widely used to lower LDL cholesterol and reduce cardiovascular risk.[1] The substantial reductions in cardiovascular morbidity and mortality produced by lowering blood cholesterol with simvastatin were established first in hypercholesterolaemic patients with coronary heart disease (CHD),[2] and subsequently by the Heart Protection Study (HPS) and other trials, in a broad range of high risk patients with and without hypercholesterolaemia or CHD.[3-7] Large long-term randomized trials can provide valuable information on clinically relevant adverse effects of drugs that are too uncommon to be evaluated in the smaller, relatively short-term, trials upon which regulatory approval is typically based. The tolerability of simvastatin early in HPS has been reported,[8] and the safety further summarised in the first report of results.[3] The lack of any detectable effect of simvastatin on the risk of non-cardiovascular mortality, haemorrhagic stroke, cancer, respiratory and neurological morbidity, and the lack of hazard in patients with diabetes or heart failure, as well as those with low blood cholesterol, have been reported in subsequent papers.[4,5,9,10] In this paper, we provide further detail about the effects on muscle and liver adverse events in HPS.
Since their introduction in the 1980s, statins have been recognised to have occasional adverse effects on muscle and liver, with the former of greater clinical importance. Few drugs have toxic effects on skeletal muscle, but all statins occasionally cause myopathy.[11-13] In this context, myopathy is generally defined as unexplained muscle pain or weakness accompanied by a creatine kinase (CK) level >10 times the upper limit of normal (ULN).[11,14] Rhabdomyolysis is a severe form of myopathy (typically with CK >40 × ULN) that may require the patient to be hospitalised, often associated with myoglobinuria that can lead to acute renal failure and death. Though rare with all currently marketed statins, this adverse effect has been the focus of increased concern as a result of the withdrawal of cerivastatin by its manufacturer in 2001 due to a high incidence of rhabdomyolysis.[15]
Treatment with lipid lowering therapy, including statins, tends to increase hepatic transaminases, but clinical hepatitis is uncommon during statin therapy.[16,17] Routine monitoring of liver function has been recommended in the prescribing information for all statins, but its usefulness has subsequently been questioned.[16,18] The size, duration and placebo control of HPS provides the opportunity to assess clinical and biochemical adverse effects on muscle and liver during treatment with simvastatin 40 mg daily, and to use this information to evaluate the value of routine monitoring of liver function tests.

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Home Cardiovascular News print this page back Page summary Text size News quick search Beta-blocker therapy has effects unique to HF with normal or reduced LVEF 7 August 2009 MedWire News: Beta-blocker therapy has unique myocardial effects in heart failure (HF) patients with normal and reduced left ventricular ejection fraction (LVEF), possibly contributing to the different outcomes of therapy for each phenotype, reports a Dutch team. Walter Paulus (VU University Medical Center, Amsterdam, The Netherlands) and colleagues compared myocardial structure, cardiomyocyte function, and myocardial protein composition in HF patients with normal or reduced LVEF, with or without beta-blocker therapy. The study included a total of 71 patients, 32 with normal LVEF, of whom 16 were and 16 were not taking beta blockers, and 39 with reduced LVEF, of whom 22 were on beta-blocker therapy and 17 were not. The researchers assessed collagen volume fraction (CVF), cardiomyocyte diameter (MyD), phosphorylation of myofilamentary proteins, expression of β-adrenergic signaling and calcium handling proteins, and cardiomyocyte function in LV endomyocardial biopsies taken from the patients on suspicion of infiltrative or inflammatory myocardial disease. They report in the European Heart Journal that shared effects of beta-blocker therapy that are “beneficial for cardiomyocyte contractile performance” were enhanced myocyte calcium sensitivity and active force, reduced phosphorylation of troponin I and myosin-binding protein C, and reduced β2-adrenergic receptor expression. Effects of beta-blocker therapy unique to patients with normal LVEF were reduced interstitial fibrosis, regression of cardiomyocyte hypertrophy, elevated resting force of cardiomyocytes before and after protein kinase A (PKA) administration and elevated calcium sensitivity after adding PKA, and reduced expression of stimulatory G protein, whereas reduced inhibitory G protein expression was unique to HF with reduced LVEF. Of note, the lower MyD and higher resting force of cardiomyocytes with beta-blocker treatment in HF with normal LVEF likely relates to the hypertrophied and stiff cardiomyocytes characterisistc of this phenotype, say Paulus and team. Meanwhile, unchanged CVF in HF patients with reduced LVEF signals poor outcome of beta-blocker therapy for those with intense myocardial fibrosis, they summarize, whereas lower G protein inhibition contributes to improve myocardial contractile performance. “Unequal outcome of beta-blocker therapy in HF with normal LVEF and HF with reduced LVEF could related to myocardial effects of beta-blocker therapy, which are unique to either HF with normal or HF with reduced LVEF,” the researchers conclude. MedWire (www.medwire-news.md) is an independent clinical news service provided by Current Medicine Group, a part of Springer Science+Business Media. © Current Medicine Group Ltd; 2009 Eur Heart J 2009; Advance online publication

Project: Prevention of lower urinary tract symptoms (LUTS) in elderly males; the effects of an increased urine output on symptoms and bladder functioning	Print View
Titel Preventie van lagere urineweg syndromen bij oudere mannen; het effect van een verhoogde urinelozing op de symptomen en het functioneren van de blaas Abstract Problems with the storage and voiding of urine (Lower Urinary Tract Symptoms (LUTS)) are a major burden for the ageing male population. It has been estimated that approximately 30% of men aged 50 and over have mild or severe micturition problems. LUTS are very bothering, and a major indication for surgery. The aspects of quality of life, which have been reported to be affected the most, are sleep, worry about the disease, mobility, leisure, daily activities and sexual activities. Despite many years of research, the pathophysiology of LUTS remains unexplained. Obstruction of the urethra, by Benign Prostatic Hyperplasia (BPH) - a benign enlargement of the prostate - is frequently considered to be the major cause of LUTS. However, the BPH-hypothesis is increasingly being doubted since several studies have shown that there is only a weak correlation between prostate enlargement, urethral obstruction and LUTS. It appears that both BPH and obstruction are common phenomena in elderly men. Instead, it is assumed that the bladder plays a key role in the pathophysiology of LUTS. This hypothesis is supported by the almost equal prevalence of obstruction in both symptomatic and asymptomatic elderly men: a strong bladder may thus be able to build up enough pressure to overcome the obstruction and, on the other hand, a weak bladder can cause micturition problems without a present obstruction. Improvement of bladder function would therefore be a promising objective of prevention. In support of this, several animal studies have clearly shown that bladder function can be improved. Just like skeletal muscle, the bladder seems to adapt to the demands placed upon it. A diuretics-induced 3-fold increase in urine output in rabbits caused within two weeks a 100% increase in contractility, a 50% increase in bladder weight and an increase of both the capacity and the compliance of the bladder. The authors suggest that the increase in bladder mass and contractility is the result of an increase in functional smooth muscle capable of increased tension generation per cross-sectional area. This is in contrast to the contractile defects that accompany bladder hyperthrophy secondary to partial outlet obstruction. Ohnishi et al. found that diuresis-induced bladder hyperthrophy protected the rat bladder from these contractile dysfunctions. We wonder whether the same mechanism of adaptation can be achieved in humans and wether this has a positive effect on LUTS. In a human population, diuresis can be induced by surplus intake of water and thus the use diuretics will be unnecessary. To our knowledge, no scientific papers have described any relationship between water intake and LUTS so far. Drinking water would be a very practical and cheap advice to prevent complaints and expensive treatments. We therefore propose a trial in which we will study the effects of additional water intake on LUTS in elderly males. Lower Urinary Tract Symptoms (LUTS) are a very common but difficult problem to manage in general practice. Prevention of LUTS is impossible, since the pathophysiology is still unclear. Bladder functioning is considered to be a key factor in the development of LUTS, independently of a present urethral obstruction. Improvement of bladder functioning could therefore be a promising objective in the prevention of LUTS in elderly men. Several animal studies have shown that, as a result of a 3-fold increase in urine output, the bladder contractility and the bladder weight increased significantly. In addition, diuresis-induced hyperthorphy protected the rat bladder from the contractile defects that usually follow partial outflow obstruction. Apparently the bladder is able to adapt to demands placed upon it just like skeletal muscle. We want to investigate if the same mechanism of adaptation can be achieved in a human population. We will screen elderly men (55-75 years) in general practices on symptom score (8-19) according to the International Prostate Symptoms Score (IPSS). Men who are diagnosed as LUTS patients or men who receive medical treatment will be excluded. The urine output will be increased by drinking 2 litres of additional water per day. A control group will receive placebo intervention in the form of a syruplike substance. We will analyse the effects of an increased urine output on symptoms, urinary flow, bladder pressure and bladder weight