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Energy drinks may pose risks for people with high blood pressure, heart disease
11-06-2007 · EurekAlert!Downing an 'energy drink' may boost blood pressure as well as energy, researchers said in a small study presented at the American Heart Association's Scientific Sessions 2007.
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Keywords: energy, drinks, pose, risks, people, blood, pressure, heart, disease, drink, risk
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- Double cardiovascular benefit for people with chronic kidney disease
10-04-2007 · EurekAlert!
New research, published today in the Journal of American Society of Nephrology by the George Institute for International Health in Sydney, has found that lowering blood pressure protects stroke victims with chronic kidney disease from further strokes or heart attacks. Given the high risk of cardiovascular complications in people with chronic kidney disease, these results have significant implications for millions of people across the world.
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- New research casts doubt over heart disease treatments
03-14-2007 · EurekAlert!
Some treatments for high blood pressure could be increasing the risk of heart attacks and causing more people to need cardiac pacemakers, according to new research findings published today.
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- Diuretics excel in drug comparison trial involving hypertension/metabolic syndrome
01-28-2008 · EurekAlert!
Diuretics were associated with reduced heart disease in a drug comparison trial involving 23,077 people with both high blood pressure and the metabolic syndrome, a cluster of risk factors for heart disease, report researchers from the University of Texas School of Public Health and Case Western Reserve University in the Jan. 28 issue of the Archives of Internal Medicine, one of the JAMA/Archives journals.
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- Australian-led international study shows blood pressure drugs cut death rate in type 2 diabetes
09-03-2007 · EurekAlert!
The largest-ever study of treatments for type 2 diabetes has shown that a combination of two blood pressure lowering drugs reduced the risk of death, as well as the risks of heart and kidney disease. The ADVANCE (Action in Diabetes and Vascular Disease) Study was led by researchers at the George Institute for International Health in Sydney and the results have been presented at the European Congress of Cardiology in Vienna.
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- Advance in understanding of blood pressure gene could lead to new treatments
02-04-2007 · EurekAlert!
Research by scientists at UCL (University College London) has clearly demonstrated for the first time the structure and function of a gene crucial to the regulation of blood pressure. The discovery could be important in the search for new treatments for illnesses such as heart disease, the UK's biggest killer. In a paper published online today in Nature Medicine, the team, led by Professor Patrick Vallance and Dr James Leiper, UCL Department of Medicine, reveal the role of the human gene dimethylarginine dimethylaminohydrolase (DDAH), showing that loss of DDAH activity disrupts nitric oxide (NO) production. NO is critical in the regulation of blood pressure, nervous system functions and the immune system. The role of DDAH is to break down modified amino acids (Asymmetric dimethylarginine (ADMA) and monomethyl arginine (L-NMMA)) that are produced by the body and have been shown to inhibit NO synthase. These molecules accumulate in various disease states including diabetes, renal failure and pulmonary and systemic hypertension, and their concentration in plasma (the fluid component of blood) is strongly predicative of cardiovascular disease and death. In a healthy human body, the majority of ADMA is eliminated through active metabolism by DDAH. Scientists have hypothesised that if DDAH function is impaired, NO production is reduced, and that this could be an important feature of increased cardiovascular risk. To examine this pathway in more detail, the researchers deleted the DDAH gene in mice. These mice went on to develop hypertension, or high blood pressure. They also designed specific inhibitors (small molecules) which bind to the active site of human DDAH. These small molecule inhibitors also induced hypertension in mice, confirming the importance of DDAH in the regulation of blood pressure. Dr Leiper, UCL Medicine, said: “These genetic and chemical approaches to disrupt DDAH showed remarkably consistent results, and provide compelling evidence that loss of DDAH function increases the concentration of ADMA and thereby disrupts vascular NO signalling. “There has been considerable scientific interest in this pathway and the role of ADMA as a novel risk factor, but so far there's been little evidence to support the idea that it's a cause of disease, rather than just a marker. Genes and their pathways are crucial to our understanding of cardiovascular disease and a better understanding of DDAH-1 could lead to important new treatments. “It could help us to establish if genetic variation predisposes certain people to these diseases, or whether environmental factors exert some of their effects through modulation of DDAH activity. “Our research also shows that this pathway could be harnessed therapeutically to limit production of NO in certain situations where too much nitric oxide is a bad thing; for example, hypotension and septic shock. These are some of the biggest problems in intensive care medicine and there is a huge unmet need for drug treatments.” The study, which was carried out at UCL's Rayne Institute, was funded by grants from the British Heart Foundation, the Wellcome Trust and the Medical Research Council. Professor Jeremy Pearson, Associate Medical Director of the British Heart Foundation, said: "The unexpected finding in the 1980s that a simple gas, nitric oxide (NO), is made by cells in the blood vessel wall and is a powerful control of blood vessel relaxation led to the award of the Nobel Prize in 1998 to its discoverers. "More recently, there has been increasing evidence that impairment of NO production is likely to be an important factor in the development of heart and circulatory disease, but the mechanisms responsible are not fully understood. "This study suggests for the first time that the loss of the activity of the enzyme DDAH-1 leads to reduced NO production and may cause heart and circulatory disease. These findings are likely to be important in the search for new ways to optimise the health of our blood vessels." ### Notes for Editors 1. For more information, please contact Ruth Metcalfe in the UCL Media Relations Office on tel: +44 (0)20 7679 9739, mobile: +44 (0)7990 675 947, out of hours: +44 (0)7917 271 364, e-mail: r.metcalfe@ucl.ac.uk2. 'Disruption of methylarginine metabolism impairs vascular homeostasis' is published in the February issue of the journal Nature Medicine. Advance online publication is embargoed to 18.00 GMT (13.00 US Eastern) Sunday 4 February 2007. Journalists can obtain copies of the paper by contacting the UCL Media Relations Office.3. The study was funded by the British Heart Foundation, the Wellcome Trust and the Medical Research Council. About UCL Founded in 1826, UCL was the first English university established after Oxford and Cambridge, the first to admit students regardless of race, class, religion or gender, and the first to provide systematic teaching of law, architecture and medicine. In the government's most recent Research Assessment Exercise, 59 UCL departments achieved top ratings of 5* and 5, indicating research quality of international excellence. UCL is the fourth-ranked UK university in the 2006 league table of the top 500 world universities produced by the Shanghai Jiao Tong University. UCL alumni include Mahatma Gandhi (Laws 1889, Indian political and spiritual leader); Jonathan Dimbleby (Philosophy 1969, writer and television presenter); Junichiro Koizumi (Economics 1969, Prime Minister of Japan); Lord Woolf (Laws 1954, Lord Chief Justice of England & Wales); Alexander Graham Bell (Phonetics 1860s, inventor of the telephone), and members of the band Coldplay.
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- Framingham study shows parents who live long pass on
03-12-2007 · EurekAlert!
Researchers from the long-standing Framingham Heart Study (FHS), a program of the National Heart, Lung, and Blood Institute (NHLBI) of the National Institutes of Health, report that people whose parents live longer were more likely to avoid developing high blood pressure, high cholesterol, and other risk factors for cardiovascular disease in middle age than their peers whose parents died younger.
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- One pill may be better than two for treating patients with high blood pressure
05-11-2007 · EurekAlert!
Adults with high blood pressure and additional risk factors for heart disease may benefit more from taking one tablet rather than two, if their current treatment combines the lipid-lowering medication atorvastatin with the blood pressure-lowering medication amlodipine.
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- Blood protein offers clues to heart attack in seemingly healthy people
07-02-2007 · EurekAlert!
We've all wondered how a seemingly healthy person can actually be at high risk for heart disease or a heart attack. Now researchers have uncovered a new clue to this mystery. The culprit: myeloperoxidase, a protein secreted by white blood cells that both signals inflammation and releases a bleach-like substance that damages the cardiovascular system.
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- High blood pressure pill cuts risk of Parkinson's disease
02-06-2008 · EurekAlert!
People taking a widely used group of drugs known as calcium channel blockers to treat high blood pressure also appear to be cutting their risk of Parkinson's disease, according to a study published in the Feb. 6, 2008, online issue of Neurology, the medical journal of the American Academy of Neurology.
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- Researchers find heart disease in a marathon runner -- Is too much exercise a bad thing?
03-14-2007 · EurekAlert!
Doctors at the University of Maryland Medical Center were puzzled when a 51-year-old physician colleague who looked the picture of health -- no cardiovascular risks, a marathon runner who had exercised vigorously each day for 30 years -- had flunked a calcium screening scan of his heart. He was at high risk for blocked blood vessels and a possible heart attack. The researchers conclude his heavy exercise regime may have played a role in his heart disease.
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