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Breast implants are a popular area of plastic surgery. This leads us to the debate on the type of implants that are best and the government’s role in the decision The debate on silicone and saline implants is a hot one. For a long period of time, silicone was dominant, but health concerns led to saline coming to the front. Silicone first became a popular enlargement resource after World War II. Doctors would shoot silicone directly into women’s breasts to create enlargement. This direct approach resulted in numerous complications including cysts, sores and systematic illness. These complications led to the reduction of interest in silicone, but it would make a comeback. In the early 1960s, two Houston plastic surgeons developed the first contained silicone implants with Dow Corning. To say the two plastic surgeons, Thomas Cronin and Frank Gerow, revolutionized plastic surgery would be a minor understatement. The procedure because very popular and there was practically more demand than there were plastic surgeons to satisfy it. The implant was made of a harder silicone sack covering soft silicone gel. The implant was very popular because it held form better than saline implants. The implants, however, were not regulated at the time. As time passed, the Federal Drug Administration was given oversight and concerns started to arise regarding problems associated with leaks or complete failures of the implants. This was particularly true for second generation implants which were designed to be as soft as possible per surgeon requests, a situation that led them to be very thin and result in failures. One version had a polyurethane coating that actually degraded into a carcinogen, a product quickly pulled from the market. The debate on silicone implants is heated, but surprisingly bereft of facts. What is clear is silicone implants leak silicone into the body. Silicone in the body is assumed to be a bad thing, but the exact correlation to specific diseases and problems are not clear. The primary reason is there has not been sufficient time to study the issue long-term and get verifiable results. Many women, however, have shown distinct negative health problems when suffering from leaking silicone implants, complaining of chronic fatigue, neurological and rheumatologic problems. While studies have found conflicting results, it is clear women who have had ruptured silicone implants removed tend to show improved health. The debate continues to this day, but the FDA restricted the use of silicone implants to medically necessary procedures as of 1992. With the restrictions on silicone implants, saline implants have come on the scene. Originally developed in the 1960s, the implants were overshadowed by silicone until the 1992 ban. Saline implants have a rubberized surface and are filled with a saline solution. In general, they are considered safer than silicone because leaking results in fewer health risks as saline is not toxic in the body. That being said, there have been some complaints regarding saline implants. Specifically, the implants can be difficult to manipulate into the correct form, they can wrinkle and can bottom out – a situation where they sag at the bottom. While these are concerns you should discuss with your plastic surgeon, what is clear is the saline implants do not involve the risks associated with silicone implants. There is an ongoing debate regarding implants. Since the FDA has banned silicone, it is a debate being won by saline breast implants. penile enlargement program penile enlargment pump penile enlargment review penis enlargement pills review cheap penile enlargment pills penis elargement surgery pnis enlargement herb pennis enlargement pump

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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. truth about penis enlargement buy penis enlargment pills surgical penis enlargment penis elargement does pennis enlargement work penile enlargement doctor vimax buy penis enlargement pills surgical penile enlargement penis enlargment traction device

Sex provides the very much required excitement in our life. It is a factor which can strengthen or weaken a relationship between two sex partners. Erectile dysfunction is one of the reasons which have caused strained relationships. It is defined as man’s inability to get enough erection to have successful sexual intercourse. If this problem is encountered occasionally then there is nothing much to worry about. Whereas, if it is a regular problem identified as impotency, then it is a serious health concern. The probability of having erectile dysfunction increases with age. Although this problem can be seen at any age but as per data 5 to 25% of men get affected by it in the age group of 40 to 65 years. This can shoot up to 50% by the age of 70 years. Erectile dysfunction can be caused due to physical or psychological factors or both. The erection process involves a sequence of events within the body involving brain, spinal column, veins and arteries in the penis. Erection will not be possible if this process gets disrupted at any stage. Any kind of damage to nerves, arteries, smooth muscles due to diseases like diabetes, neurological disease, kidney disease etc can also result in erectile dysfunction. According to statistics, these kinds of diseases account for about 70 percent cases of erectile dysfunction. It can also be caused as a side effect of some surgery which damages nerves around penis or medication of common diseases like blood pressure. Around 20% cases of erectile dysfunction are due to psychological factors like stress, guilt, depression and anxiety. A variety of treatments are available to overcome impotency. One can choose from various alternatives like psychotherapy, drug therapy, vacuum devices, or surgery. The most widely accepted method is the drug therapy. These drugs used for curing erectile dysfunction can either be consumed orally or injected directly into the penis. Drugs like Generic Cialis and Generic Viagra including Kamagra are becoming immensely popular. If we take example of France, Cilalis has replaced Viagra in most of the France pharmacies. It is available in about 100 countries. You can buy generic Cialis from FDA approved medical stores or licensed online pharmacies. Generic Cialis is taken an hour before indulging into sexual activities to get the required sexual stimulation. It won’t be wrong to say that drugs like Generic Cialis have been instrumental in restoring self respect and excitement in many lives. pennis enlargement before and after picture vigrx penis enlargment pill buy penis enlagement pills natural penis enlargement plastic surgery penis enhancement penis elargement surgery photo penis elargement herb pennis enlargement doctor penis enlargment traction device

Premature ejaculation is the most common sexual dysfunction in the under 40’s. It is almost impossible to say under what time scale ejaculation can be classed as premature as it is largely dependent on how long it takes your partner to climax. Thus if the man can last for 10 minutes but his partner needs 15 then it stands to reason that he needs to learn to last for longer. The fact that female arousal and orgasm require more time than male arousal is being increasingly recognized, and this may result in increased recognition and definition of premature ejaculation as a problem. It is thought that premature ejaculation is purely psychological with no known physical reason for early ejaculation. It is a controllable and the need to control it is largely dependent on how miserable early ejaculation makes an individual feel and how important prolonged love making is too their partner and their relationship. Most men tend to find that premature ejaculation is just an irritation which makes them ‘come’ with the first couple of minutes of lovemaking with little sexual satisfaction for either partner. Learning to control premature ejaculation is all about understanding your different levels of arousal and recognizing when you are close to your point of no return. Once you recognize how you feel when you are close to ejaculation and you understand what sexual activities get you that point quicker than others you will be at a stage where a few small changes to the way you make love will enable you to stay highly aroused, without ejaculating, for longer. You want to learn to control premature ejaculation the natural way, taking drugs will just impair your self awareness and distract you while you working towards ejaculatory control. Making love isn’t something you want to be masked with drugs, it’s something special, something sensual and something that should be enjoyed to the full. The best sex is when men learn to think about lovemaking with their whole body and not just their penis. It’s all about the complete arousal, the appreciation by every inch of the body. The early stages of lovemaking are equally as important as the last with the continual build of sexual tension just adding to the heightened and ultimate pleasure that controlling premature ejaculation can bring. You just need to learn that little step, to take your mind off the penis and concentrate on the complete unadulterated, sensual experience. One little pointer in your quest for control is to use masturbation as a way of learning when you are about to ejaculate and how to control it. By varying how you caress your penis you can learn to understand all your stages of sexual arousal, understand when you have reached a point of no return and learn how to control premature ejaculation. natural penis elargement and lengthening medical penis enhancement free exercise tip for penis enlargement penis enlargement doctor natural pnis enlargement technique truth about penile enlargement pills natural penis enlargement free penis enlagement exercise penis enlargment traction device

Erectile dysfunction is a common problem for more than half of men with diabetes. A recent study from the Brady Urological Institute at Johns Hopkins suggests that an over-supply of a simple blood sugar could be a major cause of erectile dysfunction in diabetic men. Describing the mechanism of erection, the research team has determined that high glucose in diabetes mellitus is an interrupting factor of this process. Erection begins when a sexual stimulus activates the enzyme neuronal nitric oxide synthase (nNOS) that causes short-term release of nitric oxide (NO) at the nerve endings in the penis. This initial release of NO causes short-term and rapid increases in penile blood flow and short-term relaxation of the penile smooth muscle, initiating an erection. The resulting expansion of penile blood vessels and smooth-muscle relaxation allows more blood to flow into the penis. This increased blood flow (shear stress) activates the eNOS in penile blood vessels causing sustained NO release, continued relaxation and full erection. O-GlcNAc, a blood sugar present in hyperglycemic (high blood sugar) circumstances, hinders this normal chain of events by inhibiting the activation of eNOS, and consequently reducing the release of NO and preventing the smooth muscle in the penis from relaxing. Without this relaxation, there is no shear stress to stoke the production of more NO and therefore, no normal, sustained erection. This is not the same type of erectile dysfunction seen in non-diabetics, and it is less effectively treated with conventional drugs like Viagra. The mechanism described above stresses the critical importance of vascular function in the erectile response. It may suggest new ways of treating erectile dysfunction by targeting specifically this mechanism in penile erection.