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The most exciting event in Slovenia last week was when a group of young army recruits spat on the national flag and sang the anthem of the now defunct former Yugoslavia. They were sent to a military psychiatrist for observation. Indeed, economically speaking, a preference for any other part of the late Federation over Slovenia would indicate mental deformity. Slovenia is by far the most prosperous and pacific of the lot. Income per capita increased by 7% between 1995-2000 and reached 75% of the EU's average. Yugoslavia and Macedonia would require half a century to reach this level at current growth rates. Slovenia's public debt is negligible (c. 26% of GDP), its unemployment rate is almost American (less than 7%), its budget deficit a mere 1.4% of GDP. Slovenia's gross national savings is almost a quarter of its GDP - as is its gross domestic investment (28%). It is a respected member of both the World Bank and the IMF. The former has disbursed c. $250 million for purposes such as structural reforms and environmental cleanups. The latter praises its monetary targeting, the managed float of its tolar, and the lack of major (budget and current account) imbalances. This, despite erratic monetary management by the Bank of Slovenia, which, together with the introduction of VAT, the oil price shock, and a totally CPI-indexed financial environment, led to escalating inflation (c. 9% annually, up from 6%). Thus, should Slovenian officials fail in their efforts to secure agricultural and regional development concessions from their counterparts in Brussels, Slovenia runs the risk of becoming a net creditor of the EU. Slovenia, contrary to most other current members, is openly unhappy with the "Big Bang" enlargement of the Union. It has successfully concluded 22 out 29 chapters to be agreed with the EU prior to accession and it is afraid of being held back by an unrealistic, politically motivated, process of enlargement which will stress the EU's deficient institutions to their breaking point. Slovenia is small. It is the size of pre-1967 Israel or New Jersey. With less than 2 million citizens (88% of which are ethnic Slovene), its population grows by a paltry 0.14% p.a. Still, had it not constituted the northern boundary of a war prone and unstable region, Slovenia might have attracted more FDI (it has one of the lowest rates among the candidate countries), bordering as it does and integrated as it is with the (relatively) large and disinflated economies of Italy, Hungary, and Austria. Many Slovenes actually live in Jorg Haider's part of Austria (Carinthia). Italians owned property (confiscated by the communists) in Slovenia before the Second World War (the source of a simmering grudge in Italy). Italians, Austrians, and Germans invest in Slovenian banks, insurance companies, and industry. Together with Poland, Hungary, and the Czech Republic (among others), it is a member of the now reawakened CEFTA (Central European Free Trade Agreement). Only 4% of Slovenia's GDP derives from agriculture (vs. 61% from services). Still, Slovenia, to its great ire, is often associated with the Balkan. But the bad neighborhood is not the only obstacle. Slovenia's privatization was as crony-infested as elsewhere in the Eastern Bloc and its legislation still incorporates investment-deterring anachronisms (restricted land and media ownership, an over-regulated labour market, lack of corporate governance). Capital account liberalization was implemented only recently. Close to half of the economy (including a chunk of the favoritism-ridden and inefficient banking system) is in the hands of the state. The private sector, though, is thriving. Growth rates (4% this year) are double the European average and GDP per capita is almost equal to Greece's or Portugal's. Slovenia's international trade amounts to 60% of its GDP. Two thirds of it is with the EU (half of this with Germany and Austria, the former colonial mater). Its trade with Russia, the USA (3% of the total each), and even with other republics of the disintegrated Yugoslavia is marginal. It still purchases raw materials from Macedonia and Yugoslavia - and sells back to them the finished products (as it used to do in former Yugoslavia). But this does not amount to much. The decoupling is intentional - Slovenia considers itself an integral part of Western Europe. All it inherited from Communism, it feels, was polluted rivers and coastal water, acid rain, and depleted forests. Still, such exposure to the EU makes Slovenia susceptible to the Union's business cycles. Shortsightedly perhaps, it does not have a trade representation or an economic attaché in the USA. Of all its erstwhile confederates, Slovenia maintains tenuous political contacts only with Croatia. It just resolved a long standing dispute with Croatia regarding the Krsko nuclear power plant. Both countries agreed to continue discussions regarding the final demarcation of the hotly disputed (in Slovenia) border between the two countries as a prelude to the introduction of the Schengen agreement. Overtures are made to post-Milosevic Yugoslavia. Slovene legislation is eagerly copied by Macedonia. Gradually, albeit reluctantly, Slovenia comes to be regarded as a role model by its southern neighbors who strive to emulate its success. best penis enhancement pills penis enlagement procedure natural penis enlagement penis enlagement secret penis enlargment pill magna rx pnis enlargement tool manual penis enlargement exercise penis elargement pic

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If you’ve ever witnessed someone suffer a stroke, you understand the humbling nature of this disease. It can reduce the mightiest human being to an immobile, helpless creature. Impairment of crucial functions like speech, walking, and control of bowel and bladder can wrench control from the body in a moment. Even perpetually youthful TV personality Dick Clark was struck down by stroke at age 75, despite the outward appearance of perfect health. Clark’s stroke resulted in a six-week hospital stay and, judging from fragmented reports, significant disability. Stroke can be like a devastating fire that strikes without warning, leaving only smoldering rubble. Stroke can so ravage basic bodily functions that often all you can hope for is to regain a portion through rehabilitation. The disease process that underlies stroke requires decades—30 or 40 years—to develop. With that much lead time, why aren’t we better able to detect or stop this crippling disease? The truth is that we are able to predict many, if not most, strokes. Advances in imaging technology allow detection of atherosclerotic plaque that cause stroke years before it becomes a threat. Progress in deciphering the causes of stroke has also leapt forward. Unfortunately, your neighborhood physician still focuses on diagnosing the crisis rather than anticipating it. Physicians prefer to deal with catastrophes and are just not that interested in prevention. Most physicians ask: “Is it time to operate or not?” The medical community obsesses over procedures like carotid endarterectomy (surgical removal of plaque) or carotid stents. Even when a person is afforded the warnings of a “mini-stroke”, or transient ischemic attack (TIA), little more is done once it’s determined that surgery is not necessary—even though this person has high risk for future stroke (50% over 10 years). Let’s flip-flop this approach to stroke. Procedures represent a failure of prevention! Where do strokes come from? Stroke develops when some portion of the brain is deprived of blood. This usually results from a tiny bit of debris that dislodges from an atherosclerotic plaque along the walls of an artery (the same sort that accumulates in coronaries causing heart attack). The sources of debris have been a subject of controversy, but new imaging technologies have settled the question. Any blood vessel that leads from the heart to the brain can be a source. The two carotid arteries on both sides of your neck are a frequent source, as these arteries are prone to develop plaque. (Our discussion will be confined to what are called thromboembolic, or ischemic, strokes, i.e, strokes that occur from plaque that fragments, sending debris to the brain, and will not include the far less common hemorrhagic strokes due to rupture of small vessels in the brain, nor will we discuss atrial fibrillation and other heart causes of stroke. The thromboembolic strokes we discuss cause around 88% of all strokes.) Over the last 10 years, the aorta has been recognized as another important source of stroke. The aorta is the main artery of the body whose branches go to the head, arms, and legs. Atherosclerotic plaque is a live tissue that, through poor diet, inactivity, high cholesterol, overweight, etc., grows and becomes progressively more unstable. At some point, plaque fragments. Little bits break away, traveling to the brain. Fractured plaque also exposes its deeper structures to flowing blood, triggering blood clot formation, which in turn can also fragment and go to the brain. Atherosclerotic plaque is a prerequisite for the most common causes of stroke. If the majority of strokes originate from plaque, why not measure plaque to determine if you’re at risk for stroke? How can we easily, safely, and accurately measure plaque in the carotid arteries and aorta? And if plaque can be measured, can it be shrunk or inactivated to reduce or eliminate risk for stroke? How can plaque be measured? Just 20 years ago, the only practical method of identifying plaque in the carotids or aorta was through angiography, requiring catheters inserted into the body to inject x-ray dye. Angiography was impractical as a screening measure. CT scanning and magnetic resonance imaging (MRI) are emerging as exciting methods of imaging both carotids and aorta. Unfortunately, most centers and physicians are much more focused on the diagnostic uses of these technologies for people who have already suffered stroke or other catastrophe, and application of these devices for preventive uses is still evolving. One exception is when aortic calcification or aortic enlargement is incidentally noted on the increasingly popular CT heart scans; this is an important finding that can signal presence of aortic plaque. The one test that is widely available and can be performed in just about any center is carotid ultrasound. It’s simple, painless, and precise. Two basic observations can be made: 1. Plaque detection—Atherosclerotic plaque can be clearly visualized. If plaque blocks more than 70% of the diameter of the vessel, or if there are “soft” (unstable) elements in plaque, then stroke risk may be high enough to justify surgery or stents. However, if there are plaques that are less severe, substantial risk for stroke may still be present that can be reduced with preventive measures. 2. Carotid intimal-medial thickness—This is a measure of the thickness of the lining of the carotid artery in areas not involved by plaque, but often precedes the development of mature plaque. Carotid intimal-medial thickness also provides an index of body-wide potential for atherosclerotic plaque that can place you at risk for stroke. The aorta, for instance, cannot be well imaged by surface ultrasound but can still be a source for stroke. Increased carotid intimal-medial thickness and carotid plaque are closely associated with likelihood of aortic plaque. The Rotterdam Study of 4000 participants demonstrated that if carotid intimal-medial thickness is greater than normal (1.0 mm), then you can be at risk for stroke (and heart attack), even if no carotid plaques are detected. Carotid ultrasound is the one test you should consider that provides the most information with least effort. Ultrasound is harmless, painless, and can be obtained just about anywhere. Even if your doctor disagrees with your request for a carotid ultrasound, an increasing number of mobile services are popping up nationwide that make this test available for around $100. One important point: many scanners and interpreters will only report whether plaque is present or not. While this is important information, you should request that the carotid-intimal medial thickness be made as well. Not all centers can make this simple measure (because of software requirements), but it doesn’t hurt to try. Any amount of carotid plaque is reason to follow a preventive program, even if the plaque is insufficient to justify surgery. Can plaque be reduced? Can we shrink plaque in carotid arteries and aorta and thereby reduce, perhaps eliminate, these sources of stroke? That question is gaining momentum as effective therapies become available that pack real punch for reducing plaque. Study after study has now documented that plaque can be reduced and, with it, risk for stroke. Reduction in plaque of 10–20% is possible within a year or two. Let’s consider the most potent influences on carotid and aortic plaque growth that need to be considered in a plaque-reducing program. (I assume that you are a non-smoker—if you are a smoker, you first need to concentrate on quitting.) Hypertension Considerable experience documents the power of blood pressure-lowering for prevention of stroke. The most recently updated guidelines, the JNC–VII, recommends a blood pressure of 407 mg/dl heightens stroke risk six-fold. C-reactive protein (CRP) This measure of inflammation is proving to be a useful marker for identifying people at risk for stroke, with increased risk beginning at a level of 0.5 mg/l. High CRP also predicts more rapidly growing carotid plaque. Homocysteine Homocysteine is an important marker of increased likelihood of both carotid and aortic plaque, as well as stroke. In 1997, the European Concerted Action Project reported more than a doubling of stroke when homocysteine levels exceeded 12 mol/l. As homocysteine increases to 20 μmol/l, risk for stroke and heart attack increases an amazing 10-fold over that at a level of 9 μmol/l. Asymmetric dimethylarginine (ADMA) ADMA is recently discovered amino acid whose blood levels can skyrocket up to 10-fold in the presence of hypertension, metabolic syndrome, diabetes, high cholesterol and triglycerides, obesity, and high homocysteine levels. ADMA blocks the action of the amino acid, l-arginine. This mimicry reduces the availability of nitric oxide, a powerful dilator and protector of arteries. ADMA levels in the top 10% predict a six-fold heightened risk for future stroke, and ADMA levels in people with strokes are double that in other people. A carotid ultrasound study in 116 subjects showed that higher blood levels of ADMA are associated with more severe carotid plaque. Because of ADMA’s shared role across a variety of abnormal conditions, correction or blocking the action of ADMA has been suggested as a unique therapeutic tool to reduce stroke risk. Cholesterol Data suggest that lowering cholesterol with statin cholesterol-lowering drugs slows carotid plaque growth and reduce stroke risk approximately 22%. An interesting study from the Cardiovascular Institute at Mt. Sinai School of Medicine in New York using the precise measuring ability of MRI of the carotids and thoracic aorta showed an impressive 20% regression of plaque area with simvastatin (Zocor®) taken for two years. Although guidelines for cholesterol treatment recommend reduction of LDL cholesterol to 100 mg/dl in high-risk persons, a report from the Walter Reed Army Medical Center in Washington, DC, showed that carotid plaque was more effectively reduced when LDL cholesterol of 70 mg/dl or lower was achieved with statin cholesterol drugs. Lower LDL cholesterol may, therefore, be better. Treatment Strategies to Reduce Carotid and Aortic Plaque The essential question: How do we reduce carotid and aortic plaque? If we make this the focus of our efforts, many pieces begin to fall into place. If you’ve had any measure of carotid or aortic plaque such as a carotid ultrasound or aortic calcification on a CT heart scan, you know that you’re at increased risk for stroke. You also have a baseline for future comparison to gauge whether your program is working or not. Because most people have not one but several causes of carotid and aortic plaque, there is no one single treatment that effectively eliminates risk for stroke. Instead, most people require a comprehensive program of healthy diet, exercise, supplements, and medication when indicated. Here, we focus on the nutritional supplements that can be critical components of your plaque-reduction program. Fish oil Fish oil is a cornerstone of your stroke prevention program. Epidemiological observations suggest a strong relationship of fish intake and reduction of stroke risk. Carotid ultrasound studies demonstrate less carotid plaque with greater intakes of fish. A cleverly designed University of Southampton study made the fascinating observation that fish oil transforms the structure of carotid plaque. 150 people with severe carotid plaque scheduled for carotid endarterectomy (surgical removal of the plaque) were given fish oil, sunflower oil, or no treatment over several months while waiting for their procedure. (Delays in the British health system permitted this unique design.) Plaque was removed at surgery and examined. Participants taking fish oil had reduced inflammation in plaque and thicker tissue covering the fatty core, markers of more stable plaque. Those taking sunflower oil or no treatment had unstable plaques with greater inflammation and thinner, less sturdy covering tissue. This suggests that fish oil stabilizes carotid plaque, making it less likely to rupture and fragment. A standard capsule of fish oil (containing 300 mg of EPA + DHA) contains the same amount of omega-3s as a 3 oz serving of cod or halibut; three capsules (900 mg DHA + EPA) contain the equivalent of a serving of farm-raised salmon. The dose that seems to provide greatest protection from stroke, lowers triglycerides (that form abnormal lipoproteins; see above), and reduces fibrinogen, is four capsules per day (1200 mg EPA + DHA). Coenzyme Q10 (CoQ10) Although there are no data specifically addressing whether CoQ10 reduces plaque, it is a marvelously effective way to reduce blood pressure, one of the crucial factors causing carotid and aortic plaque growth. A pooled analysis of eight studies showed that, on average, CoQ10 in daily doses of 50–200 mg reduced systolic blood pressure by 16 mm Hg, diastolic pressure by 10 mm Hg. Data suggest that CoQ10 can reverse abnormal heart muscle thickening (hypertrophy), another manifestation of high blood pressure, strongly suggesting that CoQ10 has benefits beyond just reducing pressure. Supplements to correct the metabolic syndrome Weight loss is, without question, the most immediate and direct path to correction of this dangerous pre-diabetic condition. A drop of even 10–20 lbs yields improvements across the board: increased sensitivity to insulin, increased HDL, and reductions in triglycerides, CRP, fibrinogen, small LDL particles, and blood pressure. Diet and exercise are fundamental components of an effort to lose weight; low carbohydrate or reduced glycemic index diets (e.g., South Beach or Mediterranean) rich in fibers are clearly effective. Several supplements can amplify weight-reduction efforts and be useful adjuncts to your lifestyle program. Among them: White bean extract White bean extract blocks intestinal absorption of carbohydrates by 66%. 1500 mg twice a day with meals yields, on average, 3–7 lbs of weight loss in the first month of use. The only side-effect is excessive gas, due to unabsorbed starches. Glucomannan This unique fiber taken prior to meals absorbs many times its weight in water and thereby fills your stomach. You consequently take in less food. Most people lose around four lbs per month using 1500 mg prior to each meal. Interestingly, glucomannan also blunts the rise in blood sugar after meals, an effect that, by itself, may lead to weight loss. Be sure to take with plenty of water. DHEA This adrenal hormone is key to maintaining physical stamina, mood, muscle mass in men, and libido in women. A recent randomized, placebo-controlled study at Washington University in 56 subjects showed a 13% decline in abdominal fat (fat that drives resistance to insulin) measured by MRI with 50 mg of DHEA per day at bedtime, along with improved sugar control and lower insulin levels. Pectin, beta-glucan Pectin is the soluble fiber in citrus rinds, green vegetables, and apples, also available as a supplement. Beta-glucan is the soluble fiber of oats and is also available as a supplement. Both are wonderful fibers that provide feelings of fullness, lower cholesterol, slow release of sugars, and can yield modest weight reduction. A USC study in 573 subjects using carotid ultrasound showed that greater intake of healthy fibers like pectin and beta-glucan is associated with less carotid plaque growth. Folic acid, vitamins B6 and B12 Dr. Daniel Hackam at the Stroke Prevention and Atherosclerosis Research Centre in Ontario conducted a study using carotid ultrasound in 101 participants treated with folic acid 2.5 mg, vitamin B6 25 mg, and B12 250 mcg per day. Treatment resulted in plaque reduction, especially when homocysteine levels exceeded 14μmol/l at the start, compared to untreated participants who experienced substantial plaque growth. An attempt to clarify the role of homocysteine treatment was made through a National Institute of Health-sponsored study of stroke prevention. 3680 participants with a prior history of stroke were enrolled and given either a “low-dose” (20 mcg folic acid, 0.2 mg B6, 6 mcg B12) or a “high-dose” (2.5 mg folic acid, 25 mg B6, 400 mcg B12) regimen. Although starting homocysteine levels showed a graded association with stroke risk (higher homocysteine levels predicted greater stroke risk), the treatment groups experienced, on average, only a 2 μmol drop in homocysteine levels and no reduction in stroke risk over two years. The study investigators as well as critics have suggested that the study failed due to an insufficient treatment period and that the doses were too low. (The doses we use in our plaque reduction program are folic acid 2.5–5.0 mg, B6 50–100 mg, B12 1000–2500 mcg.) L-arginine L-arginine can be used to overpower the adverse effects of ADMA. L-arginine is emerging as an important carotid plaque-reversing tool. Early reports in animals showed that l-arginine completely halted growth of aortic plaque, and did so more effectively than lovastatin (a cholesterol-lowering drug). In humans, L-arginine reduces blood pressure, abnormal constriction of carotid and coronary arteries, blocks entry of inflammatory cells into plaque, increases sensitivity to insulin, and heightens exercise capacity. Following coronary angioplasty or stent placement, l-arginine results in up to 36% reduction in plaque growth. The average American takes in 5400 mg of l-arginine through food every day. Supplementing with doses of 3000–12,000 mg per day has proven useful to correct many of these phenomena. (We use a dose of 6000 mg of l-arginine powder, twice a day on an empty stomach, dissolved in water, for our plaque regression program.) Does this result in a reduction of stroke risk? The emerging data suggest that l-arginine is likely to exert a powerful plaque-reducing and stroke-preventing benefit, but we await more clinical trial data. Conclusion Reducing stroke risk by reversing carotid and aortic plaque is becoming an everyday reality, with better tools becoming available. To know whether you’re at risk, the best and most available imaging tool is carotid ultrasound, aiming to identify intimal-medial thickness >1.0 mm, or carotid plaque. Any degree of calcification of the aorta, such as on a CT heart scan, is another useful measure of risk. Treatment to reduce risk is multi-faceted but is based on examining all your sources of risk, including metabolic syndrome, small LDL, lipoprotein(a), and C-reactive protein. Fish oil is the one absolutely crucial ingredient in any stroke prevention program. Other supplements can be used in a targeted fashion, depending on the causes identified for your carotid or aortic plaque. Ideally, repeat scanning of your carotids should be done sometime after your program has begun to assess whether you’ve successfully achieved reversal of plaque growth. com enlargement pnis pnis pump cheap penile enlargement natural penis enlagement herbal natural penis enlarement vimax penis enlargement secret penis enhancement surgery penis elargement program pennis enlargement pic before and after best penile enlargment pills

The common term frequently used for conjunctivitis is "pink eye." However, this term is only properly used to refer to conjunctivitis which is caused by a viral infection of the eye. What we will target here is allergic conjunctivitis, its causes, and some treatments. Allergic conjunctivitis is caused when the mast cells (part of the body's immune system) in the eye react to allergens which the body's immune system deems to be foreign to one's body. There is a large number of mast cells in the eyes, which makes them a common location for these types of allergic reactions. The allergic reaction causes a release of histamines, which is the immune system's way of counteracting the allergen. What follows is enlargement of the blood vessels in the conjunctiva (a thin membrane which covers the white of the eye and the inside of the eyelid). Symptoms of allergic conjunctivitis may include, but are not limited to, slight swelling of the area around the eyes, redness, itching, and tearing (crying). One may also experience nasal symptoms such as congestion, sneezing, runny nose, and itching. While other forms of conjunctivitis may affect only one eye, the allergic form generally manifests itself in both eyes. There are five different types of allergic conjunctivitis. These are: 1. Seasonal Allergic Conjunctivitis (SAC): This is the most common type of the five listed here. It usually occurs when the seasons change and is caused by airborne allergens such as tree, weed, and grass pollens, as well as many different types of mold. Quite often those who suffer from this eye affliction also have allergic rhinitis, also know as "hay fever." This is often the source of SAC. This form of allergic conjuntivitis can be treated with over-the-counter (OTC) medications, as well as prescriptions. 2. Perennial Allergic Conjunctivitis (PAC): PAC can occur year-round and is frequently cause by pet or animal dander, dust mites, feathers, and other like substances. Although this form of conjunctivitis can occur all year long, the symptoms may be more severe during seasonal changes. The symptoms are very similar to those of the seasonal form. Again, this type of allergic conjunctivitis can be treated by OTC and prescription medications. One may also avoid pet/animal dander and feathers to lessen the chances of "attacks." The use of an air purifier indoors can also provide relief from irritants which may cause this allergic reaction. Although untreated bouts of seasonal or perennial allergic conjunctivitis rarely lead to long-term complications, they can cause serious problems with other parts of the eye. One can develop an inflammation of the iris, or colored part, of the eye. Please seek appropriate treatment for both of these 3. Vernal Conjunctivitis: This a chronic form of conjunctivitis which occurs most frequently during the spring and fall seasons. It can cause permanent damage to one's vision, making it one of the two most dangerous forms of allergic conjuntivitis. Vernal Conjunctivitis is more likely to occur in males than females, and has both allergic and non-allergic forms. An eye-care speciaist who also specializes in allergies should be able to pinpoint and treat this form of conjuntivitis most effectively. 4. Atopic Keratoconjunctivitis: This is a form of allergic conjunctivitis which is associated with atopic dermatitis (also known as eczema) of the eyelids and face. The symptoms include those of seasonal and perennial allergic conjunctivitis, as well as a stringy or ropy discharge from the eyes. This form of allergic conjunctivitis first manifests itself most frequently in persons in their teens and early 20's. It may also occur in persons who have a history of allegies, especially allergic rhinitis and/or asthma. As with Vernal Conjunctivitis, Atopic Keratoconjunctivitis left untreated can cause permanent damage to one's eyes. 5. Giant Papillary Conjunctivitis: This form of allergic conjunctivitis is most frequently associated with the use of contact lenses. It is believed to be caused by an allergic reaction to proteins which may adhere to the surface of the lenses, prosthetic devices used for the eye, or sutures used in eye surgery. The indications of this form of allergic conjunctivitis can be bumps which occur on the insides of the eyelids. It may also have non-allergy related causes. These last three types of allergic conjunctivitis are best treated by an eye-care specialist. It is not advisable to treat these with any OTC products unless so advised by your physician. In fact, it is best to consult a physician or specialist before treating any eye affliction with O-T-C medications. While they may provide short-term relief, it is not always wise to treat one's eyes without first knowing the exact cause of the allergic conjunctivitis, and the most effective and safest form of treatment. Misuse of OTCs can cause other eye ailments or damage which may or may not be reversible. So always consult the appropriate health care professional before treating yourself. penis enlargment technique vimax best penis enlargement free penis elargement tip cheap penis enlagement pills penile enlargment fact penile enlargment program home penile enlargement pnis enlargement video best penile enlargment pills

Viagra, the anti-impotency medicine that made inroads into the pharmaceutical market after gaining approval from the Food And Drugs Administration, USA (FDA) on March 27, 1998 as a treatment of male erectile dysfunction is currently basking in eternal glory. But this time the drug is not on the focus for its heroic action against male erectile dysfunction but for its sheer brilliance in combating the deadly disease known as pulmonary hypertension. Well, from making the penis engorged with blood in the treatment of erectile dysfunction to redressing poor blood flow to the lungs caused by pulmonary hypertension, Viagra has indeed come a long way. It is really an incredible achievement for Viagra to be able to gain approval from FDA as a pulmonary hypertension cure. Guys! from now on if the consequences of pulmonary hypertension show off in your body, say, the vessels that supply blood to the lungs are constricted and as a result sufficient amount of blood fail to reach your lungs you no need to trouble yourself by worrying over it? Leave all your anxieties behind for as along as Viagra, the erectile dysfunction medicine is with you, you are fully protected and taken care of. You can rely on Viagra for the treatment of your pulmonary hypertension for the drug is clinically approved for the treatment of the malady. In a clinical experiment, 277 people afflicted with erectile dysfunction were selected from 25 countries and were administered with 20, 40 and 80 mg Viagra dosages. The treatment lasted for six weeks and after the period the patients were able to walk with more speediness and agility in comparison to those on placebo. Now, let’s shift to erectile dysfunction. Viagra efficacy against male erectile dysfunction or impotency is universally known and no need to elaborate on that. But what is more conspicuous is that in the treatment of both these diseases, Viagra evolves as a caretaker of the body for its meticulous action in restoring stability, health and as well as in healing all the wounds occurred to it. In your fight against both these ailments, Viagra unyieldingly tries to help you escape from the claws of suffering and pain and eventually emerges a definite winner. Having unraveled Viagra efficacy elaborately, now it is time to dwell at length on the proper way to administer Viagra to the system. Viagra, the anti-impotency drug is to be applied to the body by following a suitable procedure and only then impotency related worries would take a backseat in your life. To assure a speedy and quick recovery from the clutches of erectile dysfunction, start off with the lowest 25 mg Viagra dosage. Viagra can be taken with or without food also and the ideal moment of Viagra administration is 30 minutes to 4 hours before sexual intercourse. But the amount of dosages can be increased according to your body’s response towards Viagra. To add on, any modification in your Viagra treatment, if recommended by a physician, should be immediately followed. prosolution penis enlargement pill does vigrx really work vimax truth about penis enlargement pills magna rx patch easy enlargement free penis surgery way penis enlargment surgery penile enlargment doctor penis enlarement fact best penile enlargment pills

If you’ve ever witnessed someone suffer a stroke, you understand the humbling nature of this disease. It can reduce the mightiest human being to an immobile, helpless creature. Impairment of crucial functions like speech, walking, and control of bowel and bladder can wrench control from the body in a moment. Even perpetually youthful TV personality Dick Clark was struck down by stroke at age 75, despite the outward appearance of perfect health. Clark’s stroke resulted in a six-week hospital stay and, judging from fragmented reports, significant disability. Stroke can be like a devastating fire that strikes without warning, leaving only smoldering rubble. Stroke can so ravage basic bodily functions that often all you can hope for is to regain a portion through rehabilitation. The disease process that underlies stroke requires decades—30 or 40 years—to develop. With that much lead time, why aren’t we better able to detect or stop this crippling disease? The truth is that we are able to predict many, if not most, strokes. Advances in imaging technology allow detection of atherosclerotic plaque that cause stroke years before it becomes a threat. Progress in deciphering the causes of stroke has also leapt forward. Unfortunately, your neighborhood physician still focuses on diagnosing the crisis rather than anticipating it. Physicians prefer to deal with catastrophes and are just not that interested in prevention. Most physicians ask: “Is it time to operate or not?” The medical community obsesses over procedures like carotid endarterectomy (surgical removal of plaque) or carotid stents. Even when a person is afforded the warnings of a “mini-stroke”, or transient ischemic attack (TIA), little more is done once it’s determined that surgery is not necessary—even though this person has high risk for future stroke (50% over 10 years). Let’s flip-flop this approach to stroke. Procedures represent a failure of prevention! Where do strokes come from? Stroke develops when some portion of the brain is deprived of blood. This usually results from a tiny bit of debris that dislodges from an atherosclerotic plaque along the walls of an artery (the same sort that accumulates in coronaries causing heart attack). The sources of debris have been a subject of controversy, but new imaging technologies have settled the question. Any blood vessel that leads from the heart to the brain can be a source. The two carotid arteries on both sides of your neck are a frequent source, as these arteries are prone to develop plaque. (Our discussion will be confined to what are called thromboembolic, or ischemic, strokes, i.e, strokes that occur from plaque that fragments, sending debris to the brain, and will not include the far less common hemorrhagic strokes due to rupture of small vessels in the brain, nor will we discuss atrial fibrillation and other heart causes of stroke. The thromboembolic strokes we discuss cause around 88% of all strokes.) Over the last 10 years, the aorta has been recognized as another important source of stroke. The aorta is the main artery of the body whose branches go to the head, arms, and legs. Atherosclerotic plaque is a live tissue that, through poor diet, inactivity, high cholesterol, overweight, etc., grows and becomes progressively more unstable. At some point, plaque fragments. Little bits break away, traveling to the brain. Fractured plaque also exposes its deeper structures to flowing blood, triggering blood clot formation, which in turn can also fragment and go to the brain. Atherosclerotic plaque is a prerequisite for the most common causes of stroke. If the majority of strokes originate from plaque, why not measure plaque to determine if you’re at risk for stroke? How can we easily, safely, and accurately measure plaque in the carotid arteries and aorta? And if plaque can be measured, can it be shrunk or inactivated to reduce or eliminate risk for stroke? How can plaque be measured? Just 20 years ago, the only practical method of identifying plaque in the carotids or aorta was through angiography, requiring catheters inserted into the body to inject x-ray dye. Angiography was impractical as a screening measure. CT scanning and magnetic resonance imaging (MRI) are emerging as exciting methods of imaging both carotids and aorta. Unfortunately, most centers and physicians are much more focused on the diagnostic uses of these technologies for people who have already suffered stroke or other catastrophe, and application of these devices for preventive uses is still evolving. One exception is when aortic calcification or aortic enlargement is incidentally noted on the increasingly popular CT heart scans; this is an important finding that can signal presence of aortic plaque. The one test that is widely available and can be performed in just about any center is carotid ultrasound. It’s simple, painless, and precise. Two basic observations can be made: 1. Plaque detection—Atherosclerotic plaque can be clearly visualized. If plaque blocks more than 70% of the diameter of the vessel, or if there are “soft” (unstable) elements in plaque, then stroke risk may be high enough to justify surgery or stents. However, if there are plaques that are less severe, substantial risk for stroke may still be present that can be reduced with preventive measures. 2. Carotid intimal-medial thickness—This is a measure of the thickness of the lining of the carotid artery in areas not involved by plaque, but often precedes the development of mature plaque. Carotid intimal-medial thickness also provides an index of body-wide potential for atherosclerotic plaque that can place you at risk for stroke. The aorta, for instance, cannot be well imaged by surface ultrasound but can still be a source for stroke. Increased carotid intimal-medial thickness and carotid plaque are closely associated with likelihood of aortic plaque. The Rotterdam Study of 4000 participants demonstrated that if carotid intimal-medial thickness is greater than normal (1.0 mm), then you can be at risk for stroke (and heart attack), even if no carotid plaques are detected. Carotid ultrasound is the one test you should consider that provides the most information with least effort. Ultrasound is harmless, painless, and can be obtained just about anywhere. Even if your doctor disagrees with your request for a carotid ultrasound, an increasing number of mobile services are popping up nationwide that make this test available for around $100. One important point: many scanners and interpreters will only report whether plaque is present or not. While this is important information, you should request that the carotid-intimal medial thickness be made as well. Not all centers can make this simple measure (because of software requirements), but it doesn’t hurt to try. Any amount of carotid plaque is reason to follow a preventive program, even if the plaque is insufficient to justify surgery. Can plaque be reduced? Can we shrink plaque in carotid arteries and aorta and thereby reduce, perhaps eliminate, these sources of stroke? That question is gaining momentum as effective therapies become available that pack real punch for reducing plaque. Study after study has now documented that plaque can be reduced and, with it, risk for stroke. Reduction in plaque of 10–20% is possible within a year or two. Let’s consider the most potent influences on carotid and aortic plaque growth that need to be considered in a plaque-reducing program. (I assume that you are a non-smoker—if you are a smoker, you first need to concentrate on quitting.) Hypertension Considerable experience documents the power of blood pressure-lowering for prevention of stroke. The most recently updated guidelines, the JNC–VII, recommends a blood pressure of 407 mg/dl heightens stroke risk six-fold. C-reactive protein (CRP) This measure of inflammation is proving to be a useful marker for identifying people at risk for stroke, with increased risk beginning at a level of 0.5 mg/l. High CRP also predicts more rapidly growing carotid plaque. Homocysteine Homocysteine is an important marker of increased likelihood of both carotid and aortic plaque, as well as stroke. In 1997, the European Concerted Action Project reported more than a doubling of stroke when homocysteine levels exceeded 12 mol/l. As homocysteine increases to 20 μmol/l, risk for stroke and heart attack increases an amazing 10-fold over that at a level of 9 μmol/l. Asymmetric dimethylarginine (ADMA) ADMA is recently discovered amino acid whose blood levels can skyrocket up to 10-fold in the presence of hypertension, metabolic syndrome, diabetes, high cholesterol and triglycerides, obesity, and high homocysteine levels. ADMA blocks the action of the amino acid, l-arginine. This mimicry reduces the availability of nitric oxide, a powerful dilator and protector of arteries. ADMA levels in the top 10% predict a six-fold heightened risk for future stroke, and ADMA levels in people with strokes are double that in other people. A carotid ultrasound study in 116 subjects showed that higher blood levels of ADMA are associated with more severe carotid plaque. Because of ADMA’s shared role across a variety of abnormal conditions, correction or blocking the action of ADMA has been suggested as a unique therapeutic tool to reduce stroke risk. Cholesterol Data suggest that lowering cholesterol with statin cholesterol-lowering drugs slows carotid plaque growth and reduce stroke risk approximately 22%. An interesting study from the Cardiovascular Institute at Mt. Sinai School of Medicine in New York using the precise measuring ability of MRI of the carotids and thoracic aorta showed an impressive 20% regression of plaque area with simvastatin (Zocor®) taken for two years. Although guidelines for cholesterol treatment recommend reduction of LDL cholesterol to 100 mg/dl in high-risk persons, a report from the Walter Reed Army Medical Center in Washington, DC, showed that carotid plaque was more effectively reduced when LDL cholesterol of 70 mg/dl or lower was achieved with statin cholesterol drugs. Lower LDL cholesterol may, therefore, be better. Treatment Strategies to Reduce Carotid and Aortic Plaque The essential question: How do we reduce carotid and aortic plaque? If we make this the focus of our efforts, many pieces begin to fall into place. If you’ve had any measure of carotid or aortic plaque such as a carotid ultrasound or aortic calcification on a CT heart scan, you know that you’re at increased risk for stroke. You also have a baseline for future comparison to gauge whether your program is working or not. Because most people have not one but several causes of carotid and aortic plaque, there is no one single treatment that effectively eliminates risk for stroke. Instead, most people require a comprehensive program of healthy diet, exercise, supplements, and medication when indicated. Here, we focus on the nutritional supplements that can be critical components of your plaque-reduction program. Fish oil Fish oil is a cornerstone of your stroke prevention program. Epidemiological observations suggest a strong relationship of fish intake and reduction of stroke risk. Carotid ultrasound studies demonstrate less carotid plaque with greater intakes of fish. A cleverly designed University of Southampton study made the fascinating observation that fish oil transforms the structure of carotid plaque. 150 people with severe carotid plaque scheduled for carotid endarterectomy (surgical removal of the plaque) were given fish oil, sunflower oil, or no treatment over several months while waiting for their procedure. (Delays in the British health system permitted this unique design.) Plaque was removed at surgery and examined. Participants taking fish oil had reduced inflammation in plaque and thicker tissue covering the fatty core, markers of more stable plaque. Those taking sunflower oil or no treatment had unstable plaques with greater inflammation and thinner, less sturdy covering tissue. This suggests that fish oil stabilizes carotid plaque, making it less likely to rupture and fragment. A standard capsule of fish oil (containing 300 mg of EPA + DHA) contains the same amount of omega-3s as a 3 oz serving of cod or halibut; three capsules (900 mg DHA + EPA) contain the equivalent of a serving of farm-raised salmon. The dose that seems to provide greatest protection from stroke, lowers triglycerides (that form abnormal lipoproteins; see above), and reduces fibrinogen, is four capsules per day (1200 mg EPA + DHA). Coenzyme Q10 (CoQ10) Although there are no data specifically addressing whether CoQ10 reduces plaque, it is a marvelously effective way to reduce blood pressure, one of the crucial factors causing carotid and aortic plaque growth. A pooled analysis of eight studies showed that, on average, CoQ10 in daily doses of 50–200 mg reduced systolic blood pressure by 16 mm Hg, diastolic pressure by 10 mm Hg. Data suggest that CoQ10 can reverse abnormal heart muscle thickening (hypertrophy), another manifestation of high blood pressure, strongly suggesting that CoQ10 has benefits beyond just reducing pressure. Supplements to correct the metabolic syndrome Weight loss is, without question, the most immediate and direct path to correction of this dangerous pre-diabetic condition. A drop of even 10–20 lbs yields improvements across the board: increased sensitivity to insulin, increased HDL, and reductions in triglycerides, CRP, fibrinogen, small LDL particles, and blood pressure. Diet and exercise are fundamental components of an effort to lose weight; low carbohydrate or reduced glycemic index diets (e.g., South Beach or Mediterranean) rich in fibers are clearly effective. Several supplements can amplify weight-reduction efforts and be useful adjuncts to your lifestyle program. Among them: White bean extract White bean extract blocks intestinal absorption of carbohydrates by 66%. 1500 mg twice a day with meals yields, on average, 3–7 lbs of weight loss in the first month of use. The only side-effect is excessive gas, due to unabsorbed starches. Glucomannan This unique fiber taken prior to meals absorbs many times its weight in water and thereby fills your stomach. You consequently take in less food. Most people lose around four lbs per month using 1500 mg prior to each meal. Interestingly, glucomannan also blunts the rise in blood sugar after meals, an effect that, by itself, may lead to weight loss. Be sure to take with plenty of water. DHEA This adrenal hormone is key to maintaining physical stamina, mood, muscle mass in men, and libido in women. A recent randomized, placebo-controlled study at Washington University in 56 subjects showed a 13% decline in abdominal fat (fat that drives resistance to insulin) measured by MRI with 50 mg of DHEA per day at bedtime, along with improved sugar control and lower insulin levels. Pectin, beta-glucan Pectin is the soluble fiber in citrus rinds, green vegetables, and apples, also available as a supplement. Beta-glucan is the soluble fiber of oats and is also available as a supplement. Both are wonderful fibers that provide feelings of fullness, lower cholesterol, slow release of sugars, and can yield modest weight reduction. A USC study in 573 subjects using carotid ultrasound showed that greater intake of healthy fibers like pectin and beta-glucan is associated with less carotid plaque growth. Folic acid, vitamins B6 and B12 Dr. Daniel Hackam at the Stroke Prevention and Atherosclerosis Research Centre in Ontario conducted a study using carotid ultrasound in 101 participants treated with folic acid 2.5 mg, vitamin B6 25 mg, and B12 250 mcg per day. Treatment resulted in plaque reduction, especially when homocysteine levels exceeded 14μmol/l at the start, compared to untreated participants who experienced substantial plaque growth. An attempt to clarify the role of homocysteine treatment was made through a National Institute of Health-sponsored study of stroke prevention. 3680 participants with a prior history of stroke were enrolled and given either a “low-dose” (20 mcg folic acid, 0.2 mg B6, 6 mcg B12) or a “high-dose” (2.5 mg folic acid, 25 mg B6, 400 mcg B12) regimen. Although starting homocysteine levels showed a graded association with stroke risk (higher homocysteine levels predicted greater stroke risk), the treatment groups experienced, on average, only a 2 μmol drop in homocysteine levels and no reduction in stroke risk over two years. The study investigators as well as critics have suggested that the study failed due to an insufficient treatment period and that the doses were too low. (The doses we use in our plaque reduction program are folic acid 2.5–5.0 mg, B6 50–100 mg, B12 1000–2500 mcg.) L-arginine L-arginine can be used to overpower the adverse effects of ADMA. L-arginine is emerging as an important carotid plaque-reversing tool. Early reports in animals showed that l-arginine completely halted growth of aortic plaque, and did so more effectively than lovastatin (a cholesterol-lowering drug). In humans, L-arginine reduces blood pressure, abnormal constriction of carotid and coronary arteries, blocks entry of inflammatory cells into plaque, increases sensitivity to insulin, and heightens exercise capacity. Following coronary angioplasty or stent placement, l-arginine results in up to 36% reduction in plaque growth. The average American takes in 5400 mg of l-arginine through food every day. Supplementing with doses of 3000–12,000 mg per day has proven useful to correct many of these phenomena. (We use a dose of 6000 mg of l-arginine powder, twice a day on an empty stomach, dissolved in water, for our plaque regression program.) Does this result in a reduction of stroke risk? The emerging data suggest that l-arginine is likely to exert a powerful plaque-reducing and stroke-preventing benefit, but we await more clinical trial data. Conclusion Reducing stroke risk by reversing carotid and aortic plaque is becoming an everyday reality, with better tools becoming available. To know whether you’re at risk, the best and most available imaging tool is carotid ultrasound, aiming to identify intimal-medial thickness >1.0 mm, or carotid plaque. Any degree of calcification of the aorta, such as on a CT heart scan, is another useful measure of risk. Treatment to reduce risk is multi-faceted but is based on examining all your sources of risk, including metabolic syndrome, small LDL, lipoprotein(a), and C-reactive protein. Fish oil is the one absolutely crucial ingredient in any stroke prevention program. Other supplements can be used in a targeted fashion, depending on the causes identified for your carotid or aortic plaque. Ideally, repeat scanning of your carotids should be done sometime after your program has begun to assess whether you’ve successfully achieved reversal of plaque growth.