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ED, Heart Disease May Be Deadly Duo

March 17, 2010 by · Leave a Comment 

By Bill Hendrick
WebMD Health News

Reviewed by Laura J. Martin, MD
Latest Mens Health News

* ED, Heart Disease May Be Deadly Duo
* Drug for Enlarged Prostate Approved
* Discrimination May Lead to Smoking in Boys
* Men in Europe Trace Roots to Near East Migrants
* Women’s Scent Triggers Hormone Surge in Men
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March 15, 2010 — Erectile dysfunction is a major warning sign for cardiovascular disease and early death.

The finding comes from placebo-controlled studies comparing randomly selected men with ED and cardiovascular disease and men without ED.

The men with ED and cardiovascular disease were:

* 1.9 times more likely to die from cardiovascular disease
* Twice as likely to have a heart attack
* 1.2 times more likely to be hospitalized for heart failure
* 1.1 times more likely to have a stroke

The researchers say they found that medications like ramipril, an angiotensin-converting enzyme (ACE) inhibitor used to treat high blood pressure and heart failure, can reduce cardiovascular events but don’t seem to influence the course or development of ED.

“Erectile dysfunction is something that regularly should be addressed in the medical history of patients,” Michael Bohm, MD, lead author of the study and chairman of internal medicine at the University of Saarland in Germany, says in a news release. “It might be a symptom of early atherosclerosis.”

The study included 1,549 male cardiovascular patients in 13 countries. Each was asked if he had ED, and men who answered in the affirmative were then categorized as having mild, mild-to-moderate, moderate, or severe ED. The average follow-up was five years.

Patients in one trial involving 400 men were randomly assigned to take ramipril, telmisartan — an angiotensin II receptor antagonist used to treat hypertension and heart failure — or a combination.

In another, ACE inhibitor-intolerant patients were randomly assigned to take a placebo or telmisartan.

Patients with ED were older and had a higher prevalence of hypertension, stroke, diabetes, and lower urinary track surgery than men without ED. And 55% of men had ED when they entered the trials.

Researchers say deaths from all causes occurred in 11.3% of patients who had ED at the start, but in only 5.6% of people with no ED or only mild problems at baseline.

They report that 16.2% of ED patients died from cardiovascular problems, suffered heart attacks or strokes, or were hospitalized for heart failure. Only 10.3% of men with no or mild ED had similar outcomes.

As ED worsened, risk of death from all causes increased, suggesting that ED identifies men whose cardiovascular disease might be dangerously advanced.

Bohm says that ED is closely associated with conditions that occur in atherosclerosis and vascular problems, such as plaque buildup, which often precedes heart attacks and strokes.

“Men with ED going to a general practitioner or a urologist need to be referred for a cardiology workup to determine existing cardiovascular disease and proper treatment,” Bohm says. “ED is an early predictor of cardiovascular disease.”

Men with ED are often treated for impotence but not underlying cardiovascular disease, he says, thus placing “a whole segment of men” at increased risk of death.

Therefore, men and their doctors need to view ED as a risk factor, just as they do high blood pressure and cholesterol, he says.

The study is published in the March 15 issue of Circulation: Journal of the American Heart Association.

Asparagus root lowers cholesterol, nurtures heart

January 25, 2010 by · Leave a Comment 

CM NEWS – Asparagus roots, or tian dong (天冬 or 天門冬) can lower cholesterol and blood lipid, thus help prevent atherosclerosis and other cardiovascular diseases, a new study says.
Hyperlipidemia and hypercholesteremia are major risk factors for atherosclerosis and cardiovascular diseases. Atherosclerotic cardiovascular disease is rapidly becoming a major cause of death in many societies throughout the world due to changed dietary habits and occupational stress. In recent years, natural compounds found in plants are gaining scientific attention for their potential therapeutic value in fighting multifactorial atherosclerotic disorders.

A study done at the Department of Biosciences, Sardar Patel University in India investigated the hypocholesteremic and antioxidant potential of the asparagus root root in both normal and hypercholesteremic animals. The results are published in medical journal Evidence-based Complementary and Alternative Medicine.

What is atherosclerosis? The hallmark of atherosclerosis is the accumulation of cells containing excessive lipids (i.e. foam cells) within the arterial wall. The major risk factors for the development ofatherosclerosis are hypercholesteremia and elevated low-density lipoprotein cholesterol (LDL-C) concentration. Persistent hypercholesteremia results from prolonged circulation of lipid-rich lipoproteins that increase oxidative stress leading to oxidative modification of LDL to oxy-LDL.

In the present study, normal and hypercholesteremic male albino rats were administered with root powder of asparagus (5 and 10 g% dose levels) along with normal and hypercholesteremic diets, respectively, for a duration of 4 weeks.

Plasma and hepatic lipid profiles, fecal sterol, bile acid excretion and hepatic antioxidant activity were assessed.

What is asparagus root? A perennial with a woody root stock, asparagus grows from 1 to 5 feet high. The female Asparagus plant is slimmer than the male, which is shorter and stockier.

The dried root of asparagus is used in Chinese and Indian medicines as a tonic, galactogogue, aphrodisiac, rejuvenator, antispasmodic, antiulcerous and antiinflammatory. The medicinal/pharmacological value ofasparagus root is attributed to the presence of steroidal saponins and sapogenins. The root of asaparagus is also used in the treatment of nervous disorders, dyspepsia, diarrhea, dysentery, tumours, hyperdipsia, neuropathy and hepatopathy. This plant is reported to have immunostimulant, antihepatotoxic and antioxytocic activities. Recent reports on asparagus indicate that the root extracts haveantioxidant and antidiarrheal activities in laboratory animals.

Asparagus has also been used in its wild form in Ancient Greece and Rome as a natural diuretic that flushes out the kidneys and helps prevent the formation of kidney stones. It is because that the asparagus acts to increase cellular activity in the kidneys and thus increases the rate of urine production.

Asparagus roots also encourages evacuation of the bowels by increasing fecal bulk with undigested fiber. The roots are considered diuretic and laxative and are said to induce sweating, an they are recommended for gout, dropsy and rheumatism.

Chinese medicine says the asparagus root can increase feelings of compassion and love. In India, Asparagus is used to promote fertility, reduce menstrual cramping and increase milk production in nursing mothers.

In the Eastern and Western world, it has been touted as an aphrodisiac. These customs and beliefs are not mere superstition – the root contains compounds called steroidal glycosides (asparagoside) that directly affect hormone production and may very well influence emotions.

Chinese studies report that the roots may also lower blood pressure. The powdered seeds have antibiotic properties and help to relieve nausea while calming the stomach. Japanese studies report that green Asparagus aids protein conversion into amino acids.

Asparagus is also high in folic acid, which is essential for production of new red blood cells. Other primary chemical constituents of Asparagus include essential oil, asparagine, arginine, tyrosine, flavonoids (kaempferol, quercitin, rutin), resin and tannin.

The researchers found that rats that took diet with asparagus root powder have a reduction in their plasma and hepatic lipid profiles. Other observations include: increased fecal excretion of cholesterol, neutral sterol and bile acid, and increases in hepatic HMG-CoA reductase activity and bile acid content in hypercholesteremic rats.

Further, the asparagus root diet also improved the hepatic antioxidant status (catalase, SOD and ascorbic acid levels). However, there were no significant changes in lipid and antioxidant profiles occurred in rats with normal cholesterol levels.

The researchers explain that the lipid-lowering effects of the asparagus root in hypercholesteremic rats are related primarily to an increased excretion of cholesterol, neutral sterols, bile acid and an increase in hepatic bile acid content. In this context, the phytosterol and saponin contents of asparagus root could be responsible.

On one hand phytosterols are reported to compete and displace cholesterol from the intestinal bile acid micelles and decrease the cholesterol circulation, the researchers say. On the other hand, saponins precipitate cholesterol from micelles and interfere with enterohepatic circulation of bile acids making it unavailable for intestinal absorption of cholesterol leading to a reduction in plasma cholesterol levels.

Although the main component of the Asparagus root is a steroidal saponin, the root also contains alkaloids, flavonoids, sterols, terpenes, tannins, phenolics and mucilage.

In all, the results of the present study indicate that the potent therapeutic phyto-components present in the asparagus root i.e. phytosterols, saponins, polyphenols, flavonoids and ascorbic acid, could be responsible for increased bile acid production, elimination of excess cholesterol and elevation of hepatic antioxidant status in hypercholesteremic conditions.

Do High-fat Diets Make Us Stupid And Lazy? Physical And Memory Abilities Of Rats Affected After 9 Days

September 5, 2009 by · Leave a Comment 

The research, funded by the British Heart Foundation and published in the FASEB Journal, may have implications not only for those eating lots of high-fat foods, but also athletes looking for the optimal diet for training and patients with metabolic disorders.

“We found that rats, when switched to a high-fat diet from their standard low-fat feed, showed a surprisingly quick reduction in their physical performance,” says Dr Andrew Murray, who led the work at Oxford University and has now moved to the University of Cambridge. “After just nine days, they were only able to run 50 per cent as far on a treadmill as those that remained on the low-fat feed.”

High-fat diets, such as those that are prevalent in Western countries, are known to be harmful in the long term and can lead to problems such as obesity, diabetes and heart failure. They are also known to be associated with a decline in cognitive ability over long time spans. But little attention has been paid to the effect of high-fat diets in the short term.

Physical endurance – how long we can keep exercising – depends on how much oxygen can be supplied to our muscles and how efficiently our muscles release energy by burning up the fuel we get from the food we eat. In particular, using fat as a fuel is less efficient than using glucose from carbohydrates, but the metabolic changes induced by different diets are complex and it has been controversial whether high-fat feeding for a short time would increase or decrease physical performance.

The Oxford team set out to investigate whether rats fed a high-fat diet for just a few days showed any change in their physical and cognitive abilities.

All 42 rats were initially fed a standard feed with a low fat content of 7.5 per cent. Their physical endurance was measured by how long they could run on a treadmill and their short-term or ‘working’ memory was measured in a maze task. Half of the rats were then switched to a high-fat diet where 55 per cent of the calories came from fat. After four days of getting used to the new diet, the endurance and cognitive performance of the rats on the low- and high-fat diets was compared for another five days.

“With the standard feed, 7.5 per cent of the calories come from fat. That’s a pretty low-fat diet, much like humans eating nothing but muesli,” says Dr Murray. “The high-fat diet, in which 55 per cent of the calories came from fat, sounds high but it’s actually not extraordinarily high by human standards. A junk food diet would come close to that.”

“Some high-fat, low-carb diets for weight loss can even have fat contents as high as 60 per cent. However, it’s not clear how many direct conclusions can be drawn from our work for these diets, as the high-fat diet we used was not particularly low in carbs,” he adds.

On the fifth day of the high-fat diet (the first day back on the treadmill), the rats were already running 30 per cent less far than those remaining on the low-fat diet. By the ninth day, the last of the experiment, they were running 50 per cent less far.

The rats on the high-fat diet were also making mistakes sooner in the maze task, suggesting that their cognitive abilities were also being affected by their diet. The number of correct decisions before making a mistake dropped from over six to an average of 5 to 5.5.

The researchers also investigated what metabolic changes the high-fat diet was inducing in the rats. They found increased levels of a specific protein called the ‘uncoupling protein’ in the muscle and heart cells of rats on the high-fat diet. This protein ‘uncouples’ the process of burning food stuffs for energy in the cells, reducing the efficiency of the heart and muscles. This could at least partly explain the reduction in treadmill running seen in the rats.

The rats that were fed a high fat diet and had to run on the treadmill also had a significantly bigger heart after nine days, suggesting the heart had to increase in size to pump more blood around the body and get more oxygen to the muscles.

While this research has been done in rats, the Oxford team and Andrew Murray’s new group in Cambridge are now carrying out similar studies in humans, looking at the effect of a short term high-fat diet on exercise and cognitive ability.

The results will be important not only in informing athletes of the best diets to help their training routine, but also in developing ideal diets for patients with metabolic disorders such as diabetes, insulin resistance or obesity. People with such conditions can have high levels of fat in the blood and show poor exercise tolerance, some cognitive decline, and can even develop dementia over time.

“These are startling results,” says Professor Kieran Clarke, head of the research team at Oxford University. “It shows that high-fat feeding even over short periods of time can markedly affect gene expression, metabolism and physical performance. By optimising diets appropriately we should be able to increase athletes’ endurance and help patients with metabolic abnormalities improve their ability to exercise and do more.”

“In little more than a week, a change in diet appears to have made the rats’ hearts much less efficient,” says Professor Jeremy Pearson, Associate Medical Director of the British Heart Foundation, who funded the research. “We look forward to the results of the equivalent studies in human volunteers, which should tell us more about the short-term effects of high-fat foods on our hearts. We already know that to protect our heart health in the long-term, we should cut down on foods high in saturated fat.”

Haemostasis or normal blood clotting is essential for survival

September 5, 2009 by · Leave a Comment 

From public health scares about the risk of deep vein thrombosis (DVT) on long-distance flights to high rates of pulmonary embolism (PE) in patients recovering from major surgery, venous thromboembolism (VTE) is a well-publicised, serious health issue.1, 2
expand…
Patients undergoing major orthopaedic surgery for total hip or total knee replacement or surgery for fracture of the hip are at particularly high risk of DVT. Undertreatment remains a problem, despite ample evidence that primary preventive therapy effectively reduces the risk of DVT, PE, and fatal PE.3, 57

Thrombosis complications also play a major role in cardiovascular disease. Blood clots in coronary arteries cause acute coronary syndrome, and blood clots that form in the heart are the major cause of stroke in people with atrial fibrillation.4, 5

The normal physiological response that prevents significant blood loss following vascular injury is called haemostasis.6 Familiarity with haemostasis lays the groundwork for a thorough understanding of the major disease states associated with thrombosis, such as venous thromboembolism (VTE), atherothrombosis (thrombosis triggered by plaque rupture), and cardioembolic stroke.
Blood vessel injury triggers the following sequence:

  • The vessel constricts to reduce blood flow
  • Circulating platelets adhere to the vessel wall at the site of trauma
  • Platelet activation and aggregation, coupled with an intricate series of enzymatic reactions involving coagulation proteins, produces fibrin to form a stable haemostatic plug

This finely tuned process serves to maintain the integrity of the circulatory system.10 However, the process can go out of balance, leading to significant morbidity and mortality.11

Vessel wall chart: clot initiation, formation and fibrinolysis Coagulation schematic

Abnormal haemostasis

Excessive coagulation leads to the formation of a thrombus, potentially obstructing blood flow. This is a common problem, especially in hospitalised or immobilised patients. Venous thromboembolic disease, for example, is a major problem in the European Union, where it causes more than one million events or deaths every year.12

Excessive bleeding results when certain coagulation factors are lacking, as in patients with haemophilia.13


The coagulation cascade

Coagulation involves a complex set of protease reactions involving roughly 30 different proteins.14 The final result of these reactions is to convert fibrinogen, a soluble protein, to insoluble strands of fibrin. Together with platelets, the fibrin strands form a stable blood clot.

An evolving model

For decades, the coagulation cascade was conceptualised as having two distinct points of initiation, labelled the extrinsic and intrinsic pathways.15 Over time, however, it has become clear that these pathways do not function in the body as parallel, independent systems.

The finding that the tissue factor-factor VIIa complex from the extrinsic pathway activates factors in both systems suggests that they are linked. This discovery, combined with an evolving understanding of the role of different cells, in particular blood platelets, has led to a cell-based model of coagulation. Unlike the older, intrinsic/extrinsic cascade model, the cell-based model includes the important interactions between cells directly involved in haemostasis (ie, tissue factor-bearing cells and platelets) and coagulation factors. This model more accurately represents the interaction between cellular activity and coagulation proteins that leads to blood clot formation.15

The intrinsic and extrinsic pathway model

This model divides the initiation of coagulation into distinct parts: the extrinsic pathway and the intrinsic pathway.6 The extrinsic pathway is the primary initiator of coagulation, while the intrinsic pathway leads to the successive activation of Factors IX and X. Activated Factor X (Factor Xa) plays a central role in the coagulation cascade, as it occupies a point where the intrinsic and extrinsic pathways converge.

The cell-based model

The cell-based model identifies the membranes of tissue factor–bearing cells and platelets as the sites where activation of specific coagulation factors occurs.15 This model posits a three-phase process — initiation, amplification, and thrombin action. Initiation occurs after vascular injury, when tissue factor–bearing cells bind to and activate Factor VII. This leads to production of a small amount of thrombin. Thrombin then activates platelets and cofactors during the amplification phase. The prothrombinase complex (comprising Factor Xa and cofactors bound to activated platelets) is responsible for the burst of thrombin production leading to the third phase of clot formation.

Propagation of clotting: the central role of Factor Xa

Factor Xa plays a central role in the coagulation process in both the older, extrinsic/intrinsic model as well as the more recently proposed cell-based model.

The coagulation cascade is triggered when injury to a blood vessel allows blood to come in contact with tissue factor (TF)–bearing cells. Factor Xa, with activated Factor V (Va) as a cofactor, propagates coagulation by converting prothrombin (Factor II) to thrombin (Factor IIa).15 Factor Xa is the primary site of amplification in the process: one molecule of Factor Xa catalyses the formation of approximately 1000 thrombin molecules.16 For this reason, development of medications that inhibit Factor Xa is an active and promising area of pharmaceutical research.17

Final step: fibrin formation

In the final step of the series of protease reactions leading to clot formation, thrombin triggers conversion of the soluble protein fibrinogen to insoluble fibrin strands. Thrombin also activates Factor XIII, which stabilises the clot by cross-linking the fibrin. The resulting fibrin mesh traps and holds cellular components of the clot (platelets and/or red blood cells).6

Fibrinolysis: restoring blood flow

Fibrinolysis, as the term implies, is the process that dissolves fibrin. It leads to clot dissolution. Plasminogen is the precursor of plasmin, which breaks up fibrin clots. During initial clot formation, plasminogen activators are inhibited. Over time, endothelial cells begin to secrete tissue plasminogen activators to start dissolving the clot as the structural integrity of the blood vessel wall is restored. Medications that convert plasminogen to plasmin are used to treat acute, life-threatening thrombotic disorders, such as myocardial infarction.6

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