Bodybuilding reduces lipodystrophy in patients with HIV

A common disease among HIV patients is lipodystrophy, which is characterized by irregular distribution of body fat, which causes the accumulation or loss of same in some areas. At the end of sessions, both lipodystrophy and high cholesterol and triglycerides showed improvement.

The author of the study, the physical educator Pedro Pinheiro Neto Paes says that nowadays, with the use of antiretroviral drugs, patients live longer and better with the AIDS virus, but prolonged use of medication has side effects such as lipodystrophy. Furthermore, it is common to high cholesterol and triglycerides. Because of lipodystrophy in the case of a maldistribution of body fat, the teacher thought the exercise as a way to combat the disease in order to verify the relationship between physical activity and negative variables altered by antiretroviral therapy.

Research volunteers for health education and physical activity in promoting quality of life of people living with HIV / AIDS conducted 36 training sessions spread over 12 weeks. Each session was made by heating, strength training and relaxation. At the end of the process, all variables showed a decrease negative. And besides, they also adopted a practice of regular physical activity that positively influenced the quality of life of this group of people. It was observed that lipodystrophy and triglycerides were the problems with most significant improvement.

What the author of the study highlights, however, is the improvement of self-esteem reported by them. The practice outside of our training sessions promoted the reintegration into society through physical activity, which was a great gain qualitative research. Although the quantitative effects have been very positive, the biggest complaint of them is still prejudice, which is decreased with this social integration. For the educator, it is important to encourage physical activity in this group because it shows an alternative therapy. That is, gives results and does not involve drugs.

When you think about losing fat, is usually the first association with aerobic exercises, including literature, but we went the other way: the strength training, says study author. He said this was one of the differentials of their study, who worked with high loads of strength: the patients came to lift more than 80% of its maximum capacity for each individual year, during the specific training.

Neto explains that aerobic exercises require much practice time for fat loss and ergogenic factor (calories burned) occurs mainly during the activity. Meanwhile, the activity of force causes the metabolic rate increases, and fat loss occurs throughout the day. And in addition to fat loss, there is still gain muscle mass.

Many note that water retention occurs due to the use of Deca Durabolin. This isn’t something you can do about, but the good news is that the total aromatase rate is just 20 percent of testosterone. You can limit the amount of water retention that occurs by using an anti-estrogen supplement. You may need to increase your anti-estrogen dose to limit the retention, but it could also mean that you are eating too many calories. Over-eating carbohydrates is common, and this leads to water holding. This happens with or without this anabolic steroid, so diet control remains extremely important. A remarkable property of Deca is its capability to develop collagen synthesis in addition to bone mineral content, which is an enormous benefit to athletes with joint maladies such as inflammation and connective tissue problems. Since it is a progestin, it aids the immune mediated anti-inflammatory process, and in so doing alleviates joint pain.

Deca results effectively stimulates weight gain in AIDS patients suffering from its wasting effect, athletes, and bodybuilders. Deca is the preferred anabolic steroid to use for cutting and bulking cycles. While the shorter estered version of Deca Durabolin or the chemical name of Nandrolone Phenylpropionate, is the preference to use for cutting cycles.

The fact that Deca Durabolin has a very long active life requires the administration of injections at intervals of one week, irrespective of total dose. Due to this fact, Deca Durabolin is routinely used for a period of no less than ten weeks, and customarily for twelve weeks.

Many users have noted they are dissatisfied when they first start taking Deca Durabolin. Despite being an anabolic steroid, you will not see large results straight away. The steroid just does not work that way. This is a slow process and you will need some patience. There are steroids out there that will do it quicker, but then there will also be more water retention rather than muscle mass. Dianabol and Anadrol over lead to weight gains of 20-30 pounds in a few weeks, but that is not going to be 20 to 30 pounds of muscle! Deca is stable and will lead to muscle mass increase instead of other weight, as long as you use it properly.

Side Effects:
Erectile dysfunction is considered one of the side effects that can result from Deca Durabolin. This can occur even when using testosterone supplements. Some individuals just believe that their bodies struggle to respond to this hormone, no matter how much they use. However, there are high chances that you are doing something wrong if you notice this issue with each use of the steroid. You could try to increase the amount of testosterone, but this can make the problem worse. You will now have more estrogenic activity in the body, which affects the dysfunction. Anti-estrogens can affect the sexual performance, especially those that are aromatase inhibitors.

It is extremely important to keep your estrogen to testosterone ratio at a healthy and correct level. Sexual dysfunction can occur if you have large testosterone doses without the aromatase inhibitors. The same effect can be gained from the exact opposite, while large amounts of aromatase inhibitors and large levels of testosterone can also cause the effect. You need to find the right balance for yourself.

Anabolic steroid and HIV therapy

Sometimes, athletes who use anabolic steroids may share the needles, syringes or other equipment they use to inject these drugs. By sharing needles, syringes or other equipment, a person becomes a high risk for HIV transmission. HIV is the virus that causes AIDS. If a person shares needles, syringes and other equipment to inject steroids into the vein (IV), in the muscles or under the skin, small amounts of blood from the person infected with HIV may be injected into the bloodstream of the next person to use the equipment.

HIV attacks the body's defense system, making the body less able to fight off infections and cancers. There's no vaccine or cure for HIV or AIDS. People who may have been exposed to HIV should be tested. If they find out they have the virus, they can start treatment early. You can't tell just be looking at someone if he or she has HIV. And, since someone can be infected with HIV for many years without having any symptoms, some people may not know they have HIV. Anyone who has ever shared a needle to shoot any drugs even once could become infected with HIV and should be tested.

These have shown some benefit in a variety of human disorders, including HIV-related muscle wasting and other catabolic conditions such as chronic obstructive pulmonary disease, severe burn injuries, and alcoholic hepatitis. Because of their diverse biological actions, anabolic steroids have been used to treat a variety of other conditions, including bone marrow failure syndromes, constitutional growth retardation in children, and hereditary angioedema.

Anabolic steroid side effect, safety, risks and danger:
Anabolic steroid therapy is associated with various side effects that are generally dose related, therefore, illicit use of mega doses for the purpose of bodybuilding and enhancement of athletic performance can lead to serious and irreversible organ damage. The most common side effects of anabolic steroids are some degree of masculinization in women and children, behavioral changes (eg, aggression), liver damage, and alteration of blood lipid levels and coagulation factors. Anabolic steroids could also raise levels of homo cysteine. Bodybuilders who used the muscle-building anabolic steroids have increased levels of homo cysteine, an amino acid tied to increased mortality, heart disease risk and blood vessel damage.

HIV (human immunodeficiency virus) is the virus that causes AIDS (acquired immune deficiency syndrome). The HIV retrovirus may be passed from one person to another when infected blood, semen, vaginal secretions or other bodily fluids come in contact with an uninfected person's broken skin or mucous membranes. People with HIV have what is called HIV infection and are fit and well. Some of these people will develop AIDS as a result of their HIV infection. Growth hormone is a popular bodybuilding and performance enhancing aid, and the use of recombinant human growth hormone (rHGH, or simply GH) to treat various conditions in HIV infection has been debated with excitement for years. Indeed it is licensed for the treatment of wasting syndrome in advanced stages of AIDS. GH is also a commonly used bodybuilding and performance enhancing drug, which can be purchased on the black market; used to help both muscle anabolism / strength and reduction in body fat levels. Both of these applications have possible significance in the treatment of HIV.

Other than in the treatment of wasting disease, results from the studies using rHGH to treat body changes associated with HIV and/or drugs used to treat HIV have been very favourable. One which has been studied extensively is the use of rHGH in reducing HIV-associated adipose redistribution syndrome (HARS). However, the positive effects of HGH treatment in HIV may be more direct. Several studies have proposed that rHGH may bolster the immune system in ways that might improve clinical outcomes in HIV. HIV-associated adipose redistribution syndrome (HARS)
HARS is a type of lipodystrophy (abnormal distribution of body fat), where there is accumulation of excess truncal fat and visceral adipose tissue, as opposed to regular gynoid (glutes and hips) or android (abdomen) deposition. This is observed in HIV infected people, moreso as virus load increases. Although not a debilitating condition in itself (indeed extra body fat can prolong life if followed by wasting), HARS is unpleasant for the individual, giving reduced confidence in body image; another negative aspect of the disease.

rHGH therapy has been shown to significantly reduce HARS, leading to an improved body image, and significant improvement in psychological well-being. Numerous studies have demonstrated the benefits of this, leading to rHGH being licesenced for the treatment of HARS in some countries. It should also be noted that improvement in psychological well-being could also contribute to a positive clinical outcome, in that it reduces the effects of wasting.

Immune system:
Of most interest in HIV therapy are the possible benefits of rHGH use on the immune system, since HIV's primary adverse effect is reduction in the immune system. It has been clearly demonstrated that rHGH does benefit the immune system, but the method by which it helps is still under debate. One theory is that rHGH may stimulate renewal of the thymus gland, an important organ in the immune system. This may, in turn, lead to improved immune health in people with HIV. Studies are now examining whether or not renewing thymus tissue leads to better health and longer survival.

The thymus is necessary for developing new T-lymphocytes, which are key immune cells in the defense against disease, and numbers of which steadily reduce in HIV as infection progresses. In particular the thymus gland is involved in the development of CD4+ and CD8+ cells, and it is the CD4+ level which is a very critical marker in HIV outcome. Without some thymus activity, immune reconstitution that produces a wide range of functional CD4+ cells is not believed to be possible. Thus, the state of the thymus in HIV disease and how therapies affect it are of great interest to those researching ways to restore the immune system.

Napolitano et al (2002) researched rHGH and its impact on the thymus in HIV. Doses ranged from 1.5 (4.5IU) to 3.0mg (9IU) per day for 6–12 months in healthy HIV volunteers. After six months, marked increases in thymus mass were noted, beyond what has been seen using anti-HIV therapy alone. This increase was sustained during the course of rHGH therapy and correlated with a higher CD4+ count, suggesting that the thymus is functioning properly and helping make new T-cells, further suggesting a stronger immune system. When rHGH was stopped, there was a loss of thymus mass; however, CD4+ cell count increases seen over the course of therapy were sustained despite this loss of mass.

Napolitano later (2003) did a twenty-person study using 3mg (9IU) rHGH a day injected under the skin (subcutaneous injection). This was followed by 1.5mg (4.5IU) rHGH a day for another six months, for a total of one year of daily therapy. Of the 20 volunteers (all of whom stayed on anti-HIV therapy during the study), ten took one year of rHGH according to the schedule described above while the other ten were merely observed. After one year, the group on rHGH stopped therapy and were observed for a second year, while the group who hadn't taken rHGH therapy then started one year of it. The size of the thymus increased in those on rHGH during the first year, but not among the second group. Those on rHGH had a significant increase in thymus mass while those only on anti-HIV therapy actually had a slight decrease. Interestingly the most pronounced increase in both naïve and total CD4+ cell counts were seen among those on rHGH with a rise in the hormone IGF-1 (insulin-like growth factor-1) which is also associated with immune function. In subjects with pronounced increase in IGF-1 levels due to rHGH use, naïve cells increased by 95% and CD4+ increased by 25%.

The anabolic steroids and Hepatitis C

The anabolic steroids have been studied as a treatment for wasting caused by HIV and have been shown to be safe and effective, helping the formation of lean muscle mass. To be most effective, anabolic steroid treatment should be combined with an exercise program of resistance (weight) training. Studies have mostly been restricted to men because of concerns about the side-effects of steroid treatment for women. It is estimated that as many as 40% of HIV-positive men who are ill because of HIV have low levels of testosterone (hypogonadism). Low testosterone can result in decreased appetite, depression, poor metabolism of food, and sexual problems, including the inability to obtain and maintain an erection.

A blood test can show if you have low levels of testosterone and your doctor may prescribe either a short course of oral testosterone replacement therapy, testosterone patches or testosterone gel. Although testosterone is usually considered to be the male sexual hormone, it also occurs naturally in women. Testosterone patches have been examined as a treatment for wasting caused by HIV in women. It was found that weight and quality of life improved for some of the women, and the development of male characteristics was not reported. Side-effects from testosterone replacement therapy are rare, but can include the shutting down of natural testosterone production, shrinking of the testicles, hair loss, increased sexual desire, and aggression. In women, male characteristics, such as the deepening of the voice, and facial hair may develop. Hepatitis C is usually transmitted through blood-to-blood contact. Needles, syringes and other equipment used to inject drugs, and equipment used to sniff drugs such as straws or banknotes, should never be shared.

The sexual transmission of hepatitis C is now an issue of concern. It used to be thought that this was very rare. However, there have been recent reports of increasing numbers of gay men testing positive for hepatitis C. Many of these men are HIV positive and their only risk activity appears to be unprotected anal sex. Sexual activity that carries a risk of contact with blood, such as rougher anal sex, use of sex toys and fisting, seems to have a particular risk of hepatitis C transmission. Group sex, especially in the context of drug use, is also an important risk factor. Using condoms correctly, every time you have sex, not sharing sex toys or washing them between use, and not sharing pots of lubricant can reduce the risk. Mother-to-baby transmission of hepatitis C is thought to be uncommon, but the risk is increased if the mother is also HIV positive. A high hepatitis C viral load increases the risk that a mother will pass on hepatitis C to her baby and, as with HIV, a caesarean delivery reduces the risk. It’s best not to share razors, hair and nail clippers, nail scissors or toothbrushes if you have hepatitis C.

Very few people experience symptoms when they are first infected with hepatitis C. When they do occur, symptoms include jaundice, diarrhoea and feeling sick. In the longer term, about 50% of people with hepatitis C will experience some symptoms. The most common ones are feeling generally unwell, extreme tiredness, weight loss, depression and intolerance of fatty food and alcohol. Although a small proportion of people infected with hepatitis C clear the infection naturally, about 85% will go on to develop chronic hepatitis C. About a third of people will develop severe liver disease within 15 to 25 years. The severity of disease can be affected by the strain of hepatitis C you are infected with. Men, people who drink alcohol, people who are infected with hepatitis C when they are already into middle age, and people with HIV seem to experience faster hepatitis C disease progression. Hepatitis C can cause liver fibrosis (hardening) and cirrhosis (scarring). This damages the liver to such an extent that it cannot work properly, causing jaundice, internal bleeding and swelling of the abdomen. Chronic infection with hepatitis C can cause liver cancer (hepatocellular carcinoma, or HCC). HCC is especially likely to happen in people with cirrhosis, particularly if they drink heavily. There’s also some evidence that smoking can speed up the rate of cirrhosis and increase the risk of liver cancer. Surgery is the most effective form of treatment for liver cancer, but  other options include chemotherapy and treatment with drugs.

You should be tested soon after your diagnosis with HIV to see if you are also infected with hepatitis C. Unlike hepatitis B, there is no vaccine against hepatitis C. If you are in a group at high risk of infection with hepatitis C, it’s recommended that you have regular tests to see if you have been infected. A test is available to measure hepatitis C viral load. Unlike the HIV viral load test, this is not an indicator of when to start treatment. However, it is used to show how effective treatment any hepatitis C is being and how long it should continue. Liver function tests can give an indication of the extent to which hepatitis C has damaged your liver. Liver ultrasounds and biopsies may also be used. People co-infected with HIV and hepatitis C are more likely to develop liver damage than people who are only infected with hepatitis C. However, hepatitis C does not increase your risk of becoming ill due to HIV or responding less well to HIV treatment.

HIV treatment can be used safely and effectively if you are co-infected with HIV and hepatitis C. HIV treatment that suppresses viral load and increases your CD4 cell count can slow the rate of HCV-related liver damage. However, you may be at greater risk of experiencing the liver side-effects which some anti-HIV drugs can cause, and you and your doctor should have this in mind when selecting which anti-HIV drugs to take. It also seems to be the case that people co-infected with HIV and hepatitis C are at greater risk of developing some of the metabolic disorders which anti-HIV drugs can cause (particularly insulin resistance and diabetes).

Drugs are available for the treatment of hepatitis C and you should receive your treatment and care from doctors who are expert in the treatment of both HIV and hepatitis C. This may mean that, as well as seeing an HIV doctor, you also need to see a specialist liver doctor. If you have both HIV and hepatitis C, you should be assessed to see if you would benefit from starting hepatitis C treatment. If you and your doctor decide that you will start hepatitis C treatment now, and your CD4 cell count is between 350 and 500, you should start hepatitis C treatment first, then start HIV treatment. If your CD4 cell count is between 350 and 500 and you don’t yet need treatment for hepatitis C, you should start HIV treatment. If your CD4 cell count is under 350, you should start HIV treatment before starting hepatitis C treatment. A number of anti-HIV drugs have interactions with drugs used to treat hepatitis C. The choice of anti-HIV drugs you take will need to be made with these possible interactions in mind.

Before you start treatment for hepatitis C, it is important to know which strain, or genotype, of hepatitis C you have been infected with, as this can predict your response to treatment and the amount of time you will need to take treatment for. There are several hepatitis C genotypes. Type 1 is most common in the UK, and unfortunately responds least well to the currently available treatments for hepatitis C. Genotype 4 is also harder to treat. People with genotypes 2 or 3 respond better to treatment. However, there are new HCV drugs available, and more in development, which should improve the chances of a cure for people with harder-to-treat genotypes.

Factors such as your age, gender, how long you have had hepatitis C, the degree of liver damage and whether cirrhosis has developed are also important in predicting if treatment is likely to be effective. Unlike HIV treatment, treatment for hepatitis C is not lifelong. It consists of 24 or 48 weeks of treatment, and the length of treatment you receive will depend on the hepatitis C genotype you are infected with. A test after twelve weeks of treatment can predict if you are going to respond to treatment. Drugs are available for the treatment of hepatitis C. The backbone of treatment consists is pegylated interferon and ribavirin. These are taken in combination with an anti-HCV protease inhibitor. This sort of triple combination has been found to be much more effective than dual therapy with pegylated interferon and ribavirin alone. The aim of hepatitis C treatment is to eradicate infection with hepatitis C completely. Other aims of treatment include normalising liver function, reducing liver inflammation and reducing further damage to the liver. If you are ill because of HIV, then the aim of hepatitis C treatment is likely to focus on improving your tolerance of anti-HIV drugs, reducing the risk of death from liver problems and improving your overall quality of life. Hepatitis C treatment can have unpleasant side-effects, including a high temperature, joint pain, weight loss, nausea and vomiting and depression. Other side-effects include disturbances in blood chemistry.

Arthritis and HIV-infected patients

Musculoskeletal syndromes that occur in HIV-infected patients include manifestations of drug toxicity, reactive arthritis, Reiter's syndrome, infectious arthritis, and myositis. Principles to keep in mind when evaluating an HIV-infected patient with a musculoskeletal syndrome include the following:

Any musculoskeletal syndrome in non-HIV infected patients can occur in HIV-infected patients, such syndromes may not be related to the HIV infection.
HIV infection can alter clinical presentation and course. Reactive arthritis, inflammatory arthritis, or musculoskeletal infections may be more severe in presentation and course in HIV-infected persons. In some cases, musculoskeletal infections may be more insidious and subtle in onset.
Ruling out or correctly diagnosing infections is especially important to prevent the spread of infection in an immunocompromised patient.
The probability of an opportunistic infection as a cause for a musculoskeletal complaint depends on the stage of the patient's HIV disease. At early stages (CD4 count above 300), opportunistic infections are unlikely, although resistance to common bacterial pathogens may be reduced.
Generally, diagnostic tests and treatment regimens for musculoskeletal syndromes are the same as when the syndromes occur in non-HIV infected patients, except that the patient's HIV-related medications may cause side effects and interactions that impact differential diagnosis and limit therapeutic options, and there should be a very high threshold to using immunosuppressive drugs.

Some risk factors for HIV infection are also risk factors for other conditions that may present as musculoskeletal syndromes. Examples include injection drug use and arthritis associated with hepatitis B virus infection or endocarditis, sexual promiscuity and the arthritis syndromes associated with sexually transmitted infections such as gonorrhea and chlamydia, and hemophilia and hemarthrosis. Clinicians need to examine HIV-infected patients who present with acute or subacute musculoskeletal pains for evidence of infection in the joints and muscles. Careful examination of the skin may reveal a fungal infection that has spread to the joints. Septic arthritis may be difficult to differentiate from reactive arthritis, but cultures of the synovial fluid and blood will be sterile in cases of reactive arthritis. Septic arthritis in HIV-infected injection drug users (IDUs) is most commonly due to Staphylococcus aureus and usually responds well to treatment. In patients with advanced HIV disease who are not IDUs, clinicians must always consider opportunistic infections in joints, bones, and muscles. HIV-infected patients with muscle pain and weakness must be evaluated for idiopathic polymyositis, myositis secondary to zidovudine (AZT) toxicity, and infectious pyomyositis. Although many clinicians believe that HIV infection predisposes patients to musculoskeletal infections and has a negative impact on the outcome of the therapy, this hypothesis is not yet proved.
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Both Reiter's syndrome and septic bursitis can cause a monarticular arthritis in an HIV-infected patient. Evaluation of synovial fluid is necessary to rule out infection and make a diagnosis. Clues to help the clinician differentiate between infectious and reactive arthritis in patients with HIV disease include a history of urethritis, cervicitis, diarrhea, or conjunctivitis, and findings of psoriasiform lesions, nail changes and enthesopathy (inflammation of tendinous insertions), as these may accompany a reactive arthritis.

The onset of reactive arthritis in HIV-positive patients usually occurs in the foot and ankle, and the common types of inflammation are enthesopathy (involving the Achilles tendon, plantar fascia, or anterior and posterior tibial tendons) and multidigit dactylitis. Synovitis is rare but may occur in joints of the lower extremities. In the upper extremities, dactylitis and enthesopathy occur in the tendinous insertions in the lower part of the arms. Cutaneous symptoms include psoriasiform rashes, keratoderma blennorrhagicum, and onychodystrophy.

In reactive arthritis, the synovial fluid is usually inflammatory, with a few thousand white blood cells and a synovial glucose level that is at least two thirds the serum glucose level. Gram stain or culture of synovial fluid is the only reliable way to make the diagnosis of a septic arthritis or bursitis. If the diagnosis is entertained, aspiration and culture should be performed immediately. If the synovial fluid is purulent, it may be prudent to initiate broad antibiotic coverage while waiting for the results of definitive synovial fluid cultures. Also, if the synovial fluid is initially unobtainable (as in axial joint infection), it is prudent to initiate antibiotic coverage. Blood cultures should be obtained during the work-up of the arthritis, as they may become positive before the synovial fluid cultures. HIV-infected patients who are at high risk for septic arthritis include IDUs and hemophiliacs. Clinicians must always consider and rule out acute infectious synovitis in these patients.

Gram-positive bacteria, such as S. aureus and Streptococcus pneumoniae, commonly found in non-HIV infected patients with septic arthritis and bursitis, are causative factors in most reported cases of septic arthritis and bursitis in HIV-infected persons. Infections with organisms not common to the skin have also been reported. One report described osteomyelitis in HIV-infected patients, but usually it results from direct extension from a septic joint. Clinicians must frequently re-examine HIV-infected patients treated for septic arthritis for evidence of worsening or unchanging symptoms and signs. If bone pain and fever continue despite antibiotic coverage, extension of the infection to the surrounding bone should be considered, surgical debridement may be necessary.

In most HIV-infected patients with acute joint or bursa infections, broad antibacterial coverage to cover common skin organisms (including staphylococcal and streptococcal infections) should be initiated. Patients with advanced HIV disease occasionally have opportunistic joint infections, such as sporotrichosis, cryptococcosis and Mycobacterium avium intracellulare. Often these patients have extraarticular features suggestive of such infections, including typical skin lesions. These opportunistic infections often present with a more indolent course than that of a bacterial septic arthritis. If extra articular features of fungal infection are present or hyphae or budding yeasts are seen on direct synovial fluid examination, the patient should receive standard doses of intravenous amphotericin B.

The HIV Wasting Syndrome

Wasting syndrome is defined as weight loss in excess of 10% from baseline that is associated with chronic diarrhea, fever, or weakness. Between 1987 and 1991, wasting was the second most common AIDS-associated condition reported to the CDC and the only AIDS-associated illness noted in 7.1% of reported cases. Unpublished data from the CDC's Adult-Adolescent Spectrum of Disease Program, which studied AIDS deaths in 10 cities, found that between 1990 and 1994, wasting occurred in 21.6% of cases. This was the fourth most common AIDS-associated condition, after PCP, MAC, and esophageal candidiasis. CDC statistics from 1995 document wasting as the third most common AIDS-indicator condition, after severe immunosuppression and PCP. Wasting is more prevalent in people of low socioeconomic status and women. For a variety of reasons, clinicians often treat wasting syndrome inadequately. They can be overwhelmed by the difficulties and competing side effects of antiretroviral regimens and OI therapies. Physicians receive very little nutrition education as part of their formal training. Additionally, effective pharmacologic intervention in wasting is just beginning to evolve.

The degree of wasting and malnutrition correlates with progression of AIDS. Data from the Multicenter AIDS Cohort Study showed that development of AIDS, fever, thrush, and a CD4 lymphocyte count of less than 100/mm3 were independently associated with continuing loss of body mass. Another study found that measurements of lean body mass, albumin, and transferring predict survival, independent of CD4 count. Starvation causes death when people reach 66% of ideal body weight or 54% of ideal body cell mass; patients with AIDS die at a similar level of weight loss. Because wasting is associated with disease progression, prevention and treatment of wasting should be an integral part of the care of patients infected with HIV. Studies are in progress to document the effect of reversing wasting on disease progression, morbidity and mortality.

Pathophysiology of Wasting:

Not all pathogenetic mechanisms of wasting in HIV have been fully elucidated, but many factors that promote progressive weight loss are understood. Wasting is a product of:  perturbations of metabolism and resting energy expenditure caused by the body's immunologic response to HIV and its secondary infections;  inadequate nutrition, secondary to poor oral intake, and malabsorption of nutrients, caused by diarrhea and alteration of levels of endogenous anabolic hormones, especially in men.

Perturbations of Metabolism: Resting energy expenditure (REE) increases with HIV infection. Even asymptomatic individuals with early infection have been shown to have an REE of 9% to 12% above seronegative controls. In HIV-associated hypermetabolism, maintenance of body weight requires an increase in caloric intake but, in the absence of OIs, most HIV-positive individuals can maintain adequate intake. Patients with AIDS have REEs of 25% to 34% above controls in some studies, and REE increases even when nutritional intake is poor. Paradoxically, in normal subjects REE decreases when caloric intake declines.

The development of an OI, with its concomitant rise in REE, usually leads to loss of weight, mostly lean body mass. Conversely, weight gain achieved through alimentation alone is mostly adipose tissue. This physiologic preference for fat over lean body mass is more acute in men than women, but all patients with AIDS face a persistent loss of lean body mass that is difficult to replace. The body, instead of reacting to a scarcity of nutrients by preserving lean body mass, combines hypermetabolism with accelerated protein breakdown and negative nitrogen balance to produce wasting.

Limited data are available on the potential role of cytokines in patients with AIDS and more research is needed. However, the mechanism of metabolic dysregulation that inappropriately increases REE and favors adipose tissue over lean body mass may in part be related to the cytokines elaborated in response to HIV and OIs. Tumor necrosis factor (TNF), interleukin (IL)  and 6 and interferon alpha, beta, and gamma have all been implicated in metabolic dysregulation. TNF induces weight loss and suppresses appetite in animal models. In addition, these various cytokines may act synergistically to cause futile cycling and inappropriate use of substrates.

Futile cycling of fat occurs in HIV infection, contributing to increased REE as well as hypertriglyceridemia. Peripheral lipolysis releases free fatty acids from adipose tissue. The free fatty acids are re-esterified into triglycerides in the liver and then packaged into very low density lipoproteins (VLDLs), which are released into circulation. The VLDLs are broken down in the periphery by lipoprotein lipase, resulting in storage of the triglycerides in peripheral adipose tissue again. Each of these steps requires adenosine triphosphate (ATP), thus wasting energy, shuttling fat between the periphery and the liver and back again. Current research concludes that TNF, IL-1, IL-6, and interferon alpha play a role in futile cycling of fat.

Inappropriate use of substrate contributes to increased REE and protein wasting seen in HIV. An example of this is the liver utilizing glucose to synthesize triglycerides, instead of protein, in individuals with negative nitrogen balance. This step consumes energy needed to maintain body cell mass. Using energy to make fat is inappropriate in a patient losing body cell mass. The body should be oxidizing fat, not synthesizing it, in this situation. Bodily energy reserves and substrate such as glucose should be employed to restore lean body mass. TNF, IL-1, IL-6, and interferon alpha appear to be involved in the transformation of glucose into triglycerides in the liver.

Malnutrition: Malnutrition occurs in HIV for many reasons. Both illness and inactivity suppress appetite. Many of the medications used to treat HIV and OIs cause anorexia and a variety of GI side effects. Candidiasis, aphthous ulcers, and CMV disease involving the mouth and esophagus make eating difficult and decrease oral intake.

Many secondary infections including MAC, CMV, cryptosporidium, microspora, protozoa, and bacterial pathogens cause diarrhea and secondary malabsorption of nutrients. HIV causes diarrhea through villous atrophy, crypt hyperplasia, lymphocyte infiltration of bowel epithelium, viral infiltration of the mucosae, and the development of an enteric autonomic neuropathy. Many of the well-known hepatic complications associated with HIV, as well as abnormalities of the pancreas caused by ddI, ddC, pentamidine, CMV, MAC, cryptococcus, toxoplasmosis, and TB contribute to diarrhea and malnutrition. Malnutrition is further exacerbated when patients decrease oral intake in an effort to reduce diarrhea.

Androgen Deficiency: One of the roles of androgenic hormones is to help generate and maintain lean body mass. More than half of men with AIDS have low or inadequate androgenic hormone levels due to HIV's interference with the hypothalamus-pituitary axis, adrenal glands, and the testes. Total and free testosterone levels are both suppressed. This lack of endogenous anabolic stimulation is particularly important in light of the metabolic shift away from preservation of lean body mass. HIV's effect on endogenous androgens in women has not been well studied. Given the high prevalence of wasting syndrome in women, both viral effects on female metabolism and the impact of hormone supplementation need further study.

Treatment of Wasting: Optimally, clinicians should try to prevent wasting syndrome as well as treat it when it occurs. Weight loss is often the first sign of a new AIDS-defining illness. Patients should be weighed at every visit and their weight trends recorded on a graph. Because lean body mass is lost in preference to fat, weight alone can be a misleading indicator of nutritional status and clinical course. Laboratory markers of nutritional status include albumin, transferrin, and cholesterol levels. Some clinicians also use bioelectric impedance analysis, which measures lean body mass, to track nutritional status.

Treating Underlying Illness: A crucial first step is to provide appropriate antiretroviral therapy as well as meticulous prophylaxis and treatment of OIs. Two early studies documented clinical and biochemical improvement in individuals treated with AZT monotherapy; one documented an average 2- to 3-kg weight gain and a second demonstrated rapid, significant, and sustained declines in interferon and triglyceride levels in subjects treated with AZT. A later study documented a decrease in REE of 650 kcal/day in patients with CMV colitis who were treated with ganciclovir. Several studies have documented that patients with active, untreated secondary infections are often unable to gain weight even with hyperalimentation.

Patients with untreated secondary infections involving the mouth and GI tract tend to have poor oral intake, since they often have dysphagia and odynophagia as well as diarrhea and malabsorption. Addressing oral and esophageal complications can improve caloric intake and reduce discomfort (see ACC, March 1995 for a complete discussion of esophageal lesions in HIV).

Nutrition: Maintenance of good nutrition is essential. Lost weight can be very difficult to replace. Calorie needs are in the 25 to 60 kcal/kg/day range; 20% should be protein. Working with a nutritionist is helpful. Patients often have deficiencies of micronutrients. One study found a 31% decrease in progression to AIDS in patients taking regular multivitamins with minerals. This finding may be confounded by a bias in favor of more compliant patients with better diets.

Oral feeding is clearly the nutritional route of choice. Emphasizing intake that is high in calories, protein, and fat is important. Over-the-counter nutritional supplements can help patients who are having difficulty with meals, or while they are being treated for oral or esophageal ulcers. Enteral alimentation can be used if oral or esophageal disease or disabling systemic illness makes eating temporarily impractical. Total parenteral nutrition (TPN) has been hotly debated in AIDS. Using TPN in patients with inadequately treated, active OIs and end-stage disease is of little value. Weight gained, if any, will be primarily fat. TPN is occasionally useful as temporary "bridge" therapy for a discrete period during treatment of intercurrent illness. The clear goal should be a restoration of full oral feeding once the patient can eat again. TPN is generally inappropriate in the terminal care of patients with AIDS.

The two main goals of HIV treatment

The only way to diagnose HIV is to take a test which looks for signs of the virus in the blood. Presence of the virus in the blood is termed as HIV positive (HIV+). If no signs of the virus are found in the blood, the result is considered negative. It is diagnosed on the basis of positive results from two different HIV tests.

The plasma HIV RNA test (a viral load test) is recommended when recent infection is suspected. The test detects the virus in the blood within 9 days of infection; before the body develops detectable antibodies to it.

Antibody tests: The antibody tests check for HIV antibodies that the body produces in response to the infection. In most people, antibodies to the virus are not detectable during a window period of 3 to 12 weeks after infection. Hence, a HIV antibody test is not useful during this period. Retesting should be done after three months to confirm the test results. Some of the antibody tests are as follows:

    Rapid HIV antibody test, the most common HIV test, is done using blood, urine or saliva and can produce results within an hour.
    Enzyme-linked immunosorbent assay is an antibody test that is usually the first one used to detect HIV infection. If the result is positive, the test is usually repeated to confirm the diagnosis.
    Western blot test is one of the oldest but most accurate confirmatory antibody tests. It is done to confirm the results of two positive ELISA tests

Polymerase chain reaction (PCR, a viral load test) test finds either the RNA or the DNA of the HIV in white blood cells even if other tests are negative for the virus. The PCR test is very useful to find a very recent infection, screen blood for HIV before donation and in babies born to mothers infected with the virus. Protein p24, the antigen on HIV that produces an antibody response in the body is produced in excess early in the infection. Antigen p24 tests detect these proteins in the blood. This test is usually not used for general HIV diagnostic purposes. HIV-infected people may not have any symptoms of disease for eight to ten years or longer (asymptomatic period). Their CD4 (T-cell) count should be watched closely during this time. If they have a CD4 count below 200 and if AIDS-related conditions appear, then they are considered to have AIDS.

The two main goals of HIV treatment are:

    to prevent the virus from damaging the immune system
    to halt or delay the progress of the infection

Antiretroviral (ARV) drugs are used for treating and preventing HIV infection. They stop or interfere with the reproduction of the virus in the body. HIV therapy includes combinations of drugs. Antiretroviral therapy (ART) consisting of combination of three or more antiretroviral drugs to suppress the virus. ART does not cure HIV infection. It controls replication of the virus thereby strengthening an individual’s immune system to fight off infections. These drugs must be taken at the right time every day. Incorrect or inconsistent therapy can mutate the virus causing resistance to treatment. In such cases, other medication options must be used. The amount of the virus in the blood (viral load) is measured to monitor the efficacy of the treatment. The goal of treatment is to get an undetectable viral load in lab tests.

There is no cure for HIV. But the progression of the virus in the body can be reduced to a near halt with continued adherence to appropriate antiretroviral therapy. If the infection has progressed to AIDS, treatment may also include drugs to fight and prevent the opportunistic infections.

People with HIV need counseling and psychosocial support in addition to antiretroviral treatment. A high quality of life needs to be maintained with basic hygiene, adequate nutrition and safe water. Testosterone levels decline naturally as a man gets older. Symptoms of low testosterone may appear earlier in some men. This is called hypogonadism and the symptoms include:

    Low libido or sex drive
    Erectile dysfunction or impotence
    Fatigue and lethargy
    Muscle weakness
    Shaving less often, loss of body hair
    Breast growth
    Reduced testicle size
    Skin changes on the skin, smooth, fine wrinkles

Living with HIV – diagnosis, treatment and prevention

The plasma HIV RNA test (a viral load test) is recommended when recent infection is suspected. The test detects the virus in the blood within 9 days of infection; before the body develops detectable antibodies to it. The only way to diagnose HIV is to take a test which looks for signs of the virus in the blood. Presence of the virus in the blood is termed as HIV positive (HIV+). If no signs of the virus are found in the blood, the result is considered negative. It is diagnosed on the basis of positive results from two different HIV tests.

Antibody tests: The antibody tests check for HIV antibodies that the body produces in response to the infection. In most people, antibodies to the virus are not detectable during a window period of 3 to 12 weeks after infection. Hence, a HIV antibody test is not useful during this period. Retesting should be done after three months to confirm the test results. Some of the antibody tests are as follows:

    Rapid HIV antibody test, the most common HIV test, is done using blood, urine or saliva and can produce results within an hour.
    Enzyme-linked immunosorbent assay (ELISA) is an antibody test that is usually the first one used to detect HIV infection. If the result is positive, the test is usually repeated to confirm the diagnosis.
    Western blot test is one of the oldest but most accurate confirmatory antibody tests. It is done to confirm the results of two positive ELISA tests

Polymerase chain reaction (PCR, a viral load test) test finds either the RNA or the DNA of the HIV in white blood cells even if other tests are negative for the virus. The PCR test is very useful to find a very recent infection, screen blood for HIV before donation and in babies born to mothers infected with the virus.

Protein p24, the antigen on HIV that produces an antibody response in the body is produced in excess early in the infection. Antigen p24 tests detect these proteins in the blood. This test is usually not used for general HIV diagnostic purposes.

HIV-infected people may not have any symptoms of disease for eight to ten years or longer (asymptomatic period). Their CD4 (T-cell) count should be watched closely during this time. If they have a CD4 count below 200 and/or if AIDS-related conditions appear, then they are considered to have AIDS.

The two main goals of HIV treatment are:

  -  to prevent the virus from damaging the immune system
  -  to halt or delay the progress of the infection

Antiretroviral (ARV) drugs are used for treating and preventing HIV infection. They stop or interfere with the reproduction of the virus in the body.

HIV therapy includes combinations of drugs. Antiretroviral therapy (ART) consisting of combination of three or more antiretroviral drugs to suppress the virus. ART does not cure HIV infection. It controls replication of the virus thereby strengthening an individual’s immune system to fight off infections. These drugs must be taken at the right time every day. Incorrect or inconsistent therapy can mutate the virus causing resistance to treatment. In such cases, other medication options must be used. The amount of the virus in the blood (viral load) is measured to monitor the efficacy of the treatment. The goal of treatment is to get an undetectable viral load in lab tests.

There is no cure for HIV. But the progression of the virus in the body can be reduced to a near halt with continued adherence to appropriate antiretroviral therapy. If the infection has progressed to AIDS, treatment may also include drugs to fight and prevent the opportunistic infections. People with HIV need counselling and psychosocial support in addition to antiretroviral treatment. A high quality of life needs to be maintained with basic hygiene, adequate nutrition and safe water.

Can treatment prevent HIV from advancing to AIDS? Treatment with anti-HIV medications prevents the virus from multiplying and destroying the immune system, thus helping the body fight off infections and cancers and preventing HIV from advancing to AIDS.

HIV-virus and making use of anabolic steroids

People who are suffering from the dreaded HIV-virus and making use of anabolic steroids to prevent AIDS wasting tend to gain modest gains in terms of muscle mass and weight, according to a new review.  Anabolic steroids are synthetic substances similar to the male sex hormone testosterone that promote growth of skeletal muscle and the development of male sexual characteristics. Although most recently in the news for their misuse by professional athletes, anabolic steroids have legitimate medical application for men with low testosterone and people with certain types of anemia. Two anabolic steroids available in the United States, Nandrolone Decanoate and Oxandrolone, have been used to help increase weight and muscle mass in small studies of people with wasting. Conversely, anabolic steroid use has been associated with increased rates of HIV in those who share needles or use non sterile needles when they inject steroids.

A synthetic anabolic steroid derived from Dihydrotestosterone, Winstrol or Stanozolol has been approved by the U.S. Food and Drug Administration for human use. This steroid with a high oral bioavailability survives first-pass liver metabolism when ingested because of a C17 a-alkylation.

Classified as a controlled substance under the Anabolic Steroids Control Act of 1990 and assigned to Schedule III, this drug has the chemical name of 17-methyl-2′ H -5(alpha)-androst-2-eno [3,2- c ]pyrazol-17(beta)-ol and the molecular weight of 344.5392 g/mol at the base.

Why Is Winstrol Used:
Winstrol is medically prescribed to treat anemia and hereditary angioedema. It is also recommended for improving muscle growth and increasing bone density. Winstrol may also be prescribed for improving the production of red blood cells in the body and stimulating the appetite of debilitated or weakened individuals. It may also be recommended to treat health conditions like urticaria, Raynaud’s phenomenon, cryptofibrinogenemia, and lipodermatosclerosis. Winstrol use can also be associated with strengthened tendons and ligaments and to increase lymphocyte count and CD8+ cell numbers and to decrease CD4+ and CD3+ in postmenopausal women who are diagnosed with autoimmune disorders or osteoporosis.

Winstrol is generally used by those into bodybuilding, athletics, and power lifting to lose fat while retaining lean muscle mass. Winstrol is commonly made a part of cutting cycles for preserving lean body mass while metabolizing adipose. Winstrol has the unique ability of reducing the level of sex hormone-binding globulin (SHBG) that binds to sex hormones for creating a positive and synergetic effect with other anabolic steroids used in an anabolic steroid cycle. This performance enhancing drug is also used by athletes to run faster and preserve muscle tissue during dieting. Winstrol is also admired in the bodybuilding circles for decreasing the level of high-density lipoproteins and increasing the level of low-density lipoproteins. This drug can even stimulate immediate-early gene expression in a manner that is independent of the androgen receptor.

In addition to these advantages, this drug is also used by athletes and bodybuilders because of its diuretic properties since Winstrol can improve the excretion of water from the body while improving body strength, without causing an increase in the level of body weight. Athletes absolutely admire this drug as it helps them utilize more amounts of testosterone for burning excess fat tissues and stimulates the production of prostaglandin E2 and the matrix metalloproteases collegenase and stromelysin in skin fibroblasts. The use of Winstrol can also be associated with the inhibition of growth factor stimulated DNA synthesis and fibroblasts.

Winstrol is ideally used by men in doses of 25-100 mg per day and 5-15 mg per day by women for a period not exceeding eight weeks at a stretch. This drug may be stacked for a bulking cycle with Testosterone, Dianabol or Anadrol or with Trenbolone or Halotestin during a dieting phase. A big majority of athletes even stack Winstrol with Equipoise, Deca Durabolin or Primobolan.

Anabolic steroids and retrospective studies of HIV

Anabolic steroids are orally-ingested, synthetic (man-made) drugs that act like testosterone. They cause growth and development of male sexual organs, secondary sex characteristics, and increases in muscle size and strength. They are used for treating delayed puberty in boys, anemia, low muscle mass due to AIDs or HIV, breast cancer, and for replacing testosterone in men with low testosterone levels. Anabolic steroids often are abused by athletes for increasing muscle mass and performance. Non-athletes and non-competitive body builders also abuse anabolic steroids for cosmetic reasons. Anabolic steroids have many side effects because testosterone, which they mimic, has many effects in the body. The long list if side effects from anabolic steroids include shrinking of testicles, breast enlargement (gynecomastia), low sperm count, increased hair growth, deeper voice and reduced breast size in women, high blood pressure, heart attack, stroke, high cholesterol, rage, violence and aggression. Liver disease and liver cancer also can occur.

Anabolic steroids increase blood levels and effects of cyclosporine by decreasing the breakdown of Cyclosporine. They also reduce the breakdown of Warfarin (Coumadin), increasing blood levels of Warfarin and the risk of bleeding from warfarin.
High-dose steroid therapy has been proven effective in AIDS-related Pneumocystis pneumonia (PCP) but not in non-AIDS-related cases. We evaluated the effects on survival of steroids in HIV-negative patients with PCP. Retrospective study patients admitted to the ICU with hypoxemic PCP.
HDS were associated with increased mortality in HIV-negative patients with PCP via a mechanism independent from an increased risk of infection. Pneumocystis jiroveci pneumonia (PCP) is a major cause of acute respiratory failure in immunocompromised patients. Malignant disease, steroid treatment, and transplantation of solid organs or bone marrow are the leading causes of T-cell suppression, which is associated with a high risk of opportunistic infections, including PCP. The number of patients with T-cell suppression has risen in recent years, resulting in an increased incidence of PCP. In recent studies, more than 8% of patients with hematological malignancies admitted to the ICU for acute respiratory failure had PCP. Mortality rates of up to 30% have been reported in cancer patients with PCP.

Studies done in the 1990s showed that adjunctive treatment with high-dose steroids (HDS) was associated with a dramatic decrease in mortality during PCP episodes in HIV-positive patients. Corresponding proof of efficacy is not available for HIV-negative patients with PCP, and findings from the three available studies, all retrospective, are conflicting. In a 1998 study in 30 patients, the 16 patients given adjunctive HDS had no difference in mortality but spent less time on mechanical ventilation compared to the 14 patients managed without steroids. The second study, reported in 1999, compared 15 patients with HDS and 8 without HDS and found no significant differences in mortality or ICU stay length. The most recent study was published in 2011 and found no significant difference in mortality between the 59 patients given HDS and the 29 other patients. More over two retrospective studies from our group could not conclude of outcome improvement with adjunctive steroid in that setting. The small sample sizes may have jeopardized the ability of these studies to detect significant differences between patients given HDS and other patients.

The pathophysiology of PCP may differ between patients with and without HIV infection. Studies have shown that HIV-negative patients with PCP were older and had a larger number of co-morbidities, longer symptom duration at diagnosis and higher neutrophil counts in bronchoalveolar lavage fluid, compared to HIV-positive patients. Conceivably, these differences between the two populations might affect the ability of steroid therapy to provide therapeutic benefits.

Here, our objective was to determine whether HDS produced therapeutic benefits in HIV-negative patients with severe PCP requiring admission to the intensive care unit (ICU). To increase the sample size for our investigation, we included patients from four different sources, namely, three previously published studies and a teaching-hospital ICU database. We analyzed data from three retrospective studies of HIV-negative patients with Pneumocystis jiroveci pneumonia. The first study included HIV-negative patients admitted to two ICUs between 1988 and 1996 for PCP and compared patients who did (n=23) and did not (n=8) receive HDS in addition to standard treatment. The second study described HIV-negative patients with PCP managed in the ICU between 1989 and 1990 and looked for predictors of mortality, 33 of the 39 patients received HDS. Finally, the third study compared 56 cancer patients with PCP to 56 cancer patients with bacterial pneumonia admitted to the ICU between 2001 and 2006 of the patients with PCP, 21 received HDS. Only patients from theses studies who were admitted in ICU were included in the present study. In addition to the data from these three studies, we included data from patients admitted for PCP to the ICU of the Saint Louis Teaching Hospital, Paris, France, between 2006 and 2011. The IRB from Clermont Ferrand approved data collection for the addition of patients from St Louis hospital in this non international study. Medical chart were reviewed by the investigators (VL or AD) for all included patients . For all four sources of patients, inclusion criteria were age over 18 years, ICU admission, and PCP. Only definite case of PCP were considered (positive IF for pneumocystis or MGG coloration in BAL). Exclusion criteria were patients with HIV infection and patients who were not admitted to the ICU. Moreover, colonized patients defined with positive P. jiroveci PCR only, without any pulmonary symptom or treatment of P. jiroveci were not included.

Symptoms of HIV

People with HIV can live long and healthy lives with access to treatment. Since HIV was first reported substantial progress in the research and development of antiretroviral drugs has been made. There are now more than 20 approved antiretroviral drugs. Despite this, people with HIV face many barriers to accessing affordable, effective HIV treatment.

Taking HIV treatment requires effort and commitment as drugs must be taken at exact times each day. Some people may experience serious side-effects or may not respond to certain drugs. Treatment, care and support can help people to adhere to treatment and address any problems they may have with their treatment regimen.
This is the main type of treatment for HIV or AIDS. It is not a cure, but it can stop people from becoming ill for many years. The treatment consists of drugs that have to be taken every day for the rest of a person’s life.

The aim of antiretroviral treatment is to keep the amount of HIV in the body at a low level. This stops any weakening of the immune system and allows it to recover from any damage that HIV might have caused already.

The drugs are often referred to as: antiretrovirals, ARVs, anti-HIV or anti-AIDS drugs. Taking two or more antiretroviral drugs at a time is called combination therapy. Taking a combination of three or more anti-HIV drugs is sometimes referred to as Highly Active Antiretroviral Therapy (HAART).

If only one drug was taken, HIV would quickly become resistant to it and the drug would stop working. Taking two or more antivirals at the same time vastly reduces the rate at which resistance would develop, making treatment more effective in the long term. Our starting, monitoring and switching HIV treatment page has more about drug resistance.

Most people who are infected with HIV experience a short, flu-like illness that occurs two to six weeks after infection. After this, HIV often causes no symptoms for several years. The flu-like illness that often occurs a few weeks after HIV infection is also known as seroconversion illness. It's estimated that up to 80% of people who are infected with HIV experience this illness.

The most common symptoms are:
    fever (raised temperature)
    sore throat
    body rash

Other symptoms can include:
    tiredness
    joint pain
    muscle pain
    swollen glands (nodes)

The symptoms, which can last up to four weeks, are a sign that your immune system is putting up a fight against the virus. These symptoms can all be caused by conditions other than HIV, and do not mean you have the virus. However, if you have several of these symptoms, and you think you have been at risk of HIV infection, you should get an HIV test. After the initial symptoms disappear, HIV will often not cause any further symptoms for many years. During this time, known as asymptomatic HIV infection, the virus continues to spread and damage your immune system. This process can take about 10 years, during which you will feel and appear well.

It is important to remember that not everyone with HIV experiences early symptoms, so you should still take an HIV test if you have put yourself as risk, even if you experience no symptoms.

Late-stage HIV infection:
If left untreated, HIV will weaken your ability to fight infection so much that you become vulnerable to serious illnesses. This stage of infection is known as AIDS, although doctors now prefer to use the term late-stage HIV infection. Typically, a person with late-stage HIV infection has:

    persistent tiredness
    night sweats
    weight loss
    persistent diarrhoea
    blurred vision
    white spots on the tongue or mouth
    dry cough
    shortness of breath
    fever of above 37C (100F) that lasts a number of weeks
    swollen glands that last for more than three months

At this stage, you are at increased risk of life-threatening illnesses such as tuberculosis, pneumonia and some cancers. Many of these, though serious, can be treated and your health is likely to improve if you start HIV treatment.

Testosterone and exercise help weight gain in HIV wasting

Testosterone is the androgen secreted in the male testis and in the female ovaries. It is very important hormone for the proper growth of the human body. In men, testosterone plays a very important role in development of the secondary sexual characters. The sexuality of the men is dependent considerably on the testosterone levels in his body. The men with the less level of testosterone are often found to be weak and usually fail to perform well during the sex, whereas men with high level of testosterone are always healthy and found to excellent during the sexual encounter. It is the testosterone that helps to build the sexual stamina and guides the erection mechanism. But, due to low levels of testosterone many of the men are failing to perform well during the sex.

The main reason for the reduction in the testosterone level is aging. Also few other factors like stress, tensions, injuries to testis, inadequate sleep, and too much exercising decrease the testosterone levels in the body. There are various medications available to increase the levels of testosterone, but please don’t take them as they may affect your health adversely or if at all you want to take them consult the doctor. But, guys you can increase the levels of testosterone even without taking any of these medicines. So, go through the list of the food items mentioned below and have them regularly to increase the testosterone levels:

Eggs: Daily intake of egg is found to be very good source to increase the testosterone levels. Even it has been proved through the research that egg are very good source of proteins that promote the production of the testosterone. Eggs along with the proteins also contain the Vitamin A that stimulates the production of the testosterone. If you are having very low testosterone content then you should certainly start eating egg daily and you would be able to see the difference in few months.

Meat: Non-vegetarian food items are found to be very rich in the testosterone content. You can certainly boost the testosterone levels in the body by including meat in your daily diet. Meat includes the high amount of proteins that in accordance with the minerals like zinc that promotes the production of the testosterone. White meat chicken is one of the healthiest lean meats available that is best to increase the testosterone levels. But, please make a note that keep the meat intake in control otherwise it may also increase the fats and carbohydrates in the body and make you prone to many other hazardous diseases.

Vegetables: The intake of vegetables regularly will never make you prone to the low testosterone levels. Spinach is specifically very good to boost the testosterone levels in the body. The most important benefit of vegetable intake is that it doesn’t promote any hazardous effect to your health like the non-vegetarian food items. Tomatoes also are found to prop up the testosterone levels as they are rich in Vitamin A. Vegetables intake increase the testosterone levels in the body very fast, and you can see the effects in short span of time in comparison to other food items.

Fruits: One of the best methods to increase the production of the testosterone in the body is to eat the fruits regularly. Fruits are the rich source of the vitamins and minerals that prop up the testosterone production in the body. Fruits also are found to decrease the influence of the factors that affects the testosterone production adversely. Fruit intake reduces the production of the dihydrotestosterone that is found to reduce the testosterone levels in the body. The best fruit to induce testosterone levels is Apple, which if you eat regularly for about 2 months will surely increase the testosterone levels in your body. The other fruits are Pineapple, Orange, and Mango that also increases the testosterone level in body.

Milk and Milk Products: Drinking milk daily can help you to improve the testosterone levels in the body. Milk is considered as the whole food so its intake can boost the production of testosterone. Milk contains adequate amount of minerals, vitamins, and proteins that maintains the level of the testosterone in the body and doesn’t allow it to drop below the normal level. Milk products are also rich in nutrients. So, if you having the low level of testosterone, you need to include the milk and milk products in your daily diet routine.

Further evidence that anabolic steroids or resistance exercise (weight training) can help replace lean muscle tissue lost in HIV wasting appears in a study published in this week's edition of the Journal of the American Medical Association. However, using anabolic steroids with an exercise programme did not result in any greater benefit than using one element on its own.

61 HIV-positive men whose body weight had declined by more than 5% in the previous 6 months, and who had low serum testosterone levels (< 12.1 nmol/L (349 ng/dL) were randomly assigned to receive either 100mg Testosterone Enanthate weekly as an intramuscular injection or a placebo injection. They were also randomly assigned to a programme of resistance exercise or to maintain their normal activity levels.

Daily food intake was standardized for all four groups at 1.5g of protein per kg of body weight and 40kcal per kg of body weight, a diet very high in protein and carbohydrates. The authors cannot explain why the testosterone and exercise group failed to perform better than the exercise alone or testosterone alone group, despite the expected additive effect of combining the two interventions.

After 16 weeks, muscle strength had improved by 20-30% in all groups apart from the placebo group, and this improvement was statistically significant.

The most popular drugs and human immunodeficiency virus

HIV (human immunodeficiency virus) is a virus that attacks the immune system, making it hard for the body to fight off infection and some diseases. Without treatment, HIV eventually causes AIDS (acquired immunodeficiency syndrome).

Initial HIV symptoms are similar to those of the flu and include fatigue, fever, weight loss, and swollen lymph nodes in the neck, armpits, or groin. Although there currently is no cure for HIV infection, a combination of medicines called highly active antiretroviral therapy, or HAART, helps keeps the immune system healthy for most people. Treatment can also prevent or delay the development of AIDS.

The most popular drugs (excluding alcohol and tobacco) were nitrites (poppers), used by 27% of study participants, and cannabis, cocaine and erectile dysfunction drugs (Viagra¸ Cialis), which were each used by about 20%. Ketamine and MDMA (ecstasy) were used by about 12% of participants, GHB or GBL by 9% and methamphetamine and mephedrone by 7%. All other individual drugs including various opiates, psychedelics, crack and anabolic steroids were used by less than 4% of study participants. Three per cent of the sample reported injecting drug use (68 people) of whom four reported sharing injecting equipment with persons of unknown serostatus.

The pattern for which drugs were most used stayed the same as the number of different drugs increased; in men who had used just one drug in the last three months, poppers were the most popular, closely followed by cannabis; in men who had used three, these two drugs plus cocaine and erectile dysfunction drugs predominated, and in men who had used more than five drugs there was more or less equal use of these drugs plus ketamine, GHB, MDMA and, to a slightly lesser extent, methamphetamine.

Any drug use was especially strongly associated with younger age, smoking, having disclosed they had HIV to partners, and being non-adherent to antiretroviral therapy (ART). Men who reported drug use were also somewhat more likely to have sex with other HIV-positive rather than HIV-negative partners or partners whose HIV status was unknown.

Men who reported using four or more drugs were more likely than other men who used drugs or men who did not use drugs to either not be on ART or to have a viral load over 50 copies/ml, and also to be young and to have a higher proportion of partners who also had HIV.

Compared with men over 60, men under 40 were 70% more likely to use any drug, 50% more likely to have disclosed to partners that they had HIV, 40% more likely to smoke and 30% more likely to be non-adherent to ART.


There was also a strong and consistent correlation between the numbers of different drugs used in the last three months and the various sexual behaviour indicators: the more different drugs people used, the more sex, condom-less sex, risky sex, STIs, group sex and partners they had. For instance, whereas 10% of men who had any drug use had higher-risk condom-less sex, 16% of the men who had used five or more different drugs in the last three months had done so (39 individuals), and whereas 15% of men who had any drug use had been diagnosed with an STI in the last three months, 24% of men who had used five or more drugs had had an STI. This correlation was particularly strong for group sex and number of partners.

In general, men who used drugs were about 40 to 70% more likely to have high-risk sex than men who did not use drugs, while users of ‘club drugs’ like GHB and mephedrone, erectile dysfunction drugs, nitrites (poppers) and cocaine were 90% more likely to have higher-risk sex.

What is Egrifta (Tesamorelin) in life of bodybuilders?

There are a wide variety of drugs that can help bodybuilders achieve major muscle gains and cut fat quickly and efficiently. One of the latest potential bodybuilding drugs is Egrifta the brand name of the drug Tesamorelin.

Traditionally used to help HIV patients reduce body fat around their abdomens, Egrifta is now being tested for use in non-HIV patients. Even more interesting is the fact that some bodybuilders have already gotten a hold of the drug in hopes of vanishing body fat around their waist, and building the ultimate set of abs. So is Egrifta the answer for people who have trouble getting ripped abs? Let’s dive a little deeper into the subject, beginning with the basics of Egrifta.
EGRIFTA (tesamorelin) is an FDA-approved treatment for HIV-related belly fat. More specifically, this injectable prescription medicine cuts down on abdominal fat that’s brought on by lipodystrophy (abnormal body fat composition). The way Egrifta works is by acting on the pituitary cells in the brain so that your body produces more human growth hormone. In short, the drug contains a growth hormone-releasing factor (GRF).

As of right now, Egrifta is not approved for anything other than treating HIV-related abdominal fat deposits. In the past, the drug had been considered a possible solution for improving cardiovascular health in HIV patients, but nothing definitive has been discovered on this front. In fact, there are concerns over whether the product could be just as damaging as it is helpful when treating anything related to the cardiovascular system.

In any case, the only current benefit to using Egrifta is the aforementioned reduction of belly fat in people affected by HIV. But with this being said, many bodybuilders are wondering what the drug can do for their physical appearance.
Those looking to use Egrifta (Tesamorelin) to cut down fat around their mid-section should know right away that there’s no proof it will reduce fat that comes from overeating or not working out.

In regards to using Egrifta, you’re supposed to take a daily injection in the fatty area around the abdomen (never inject the drug directly into a muscle or bruised area). As with pretty much any drug, your chances of properly using Egrifta increase greatly with the help of a doctor, but unless you’ve got HIV, you probably aren’t going to be getting this drug from a doctor.

Moving to the drug’s appearance, Egrifta comes in dry powder form and is packaged in vials; you’re supposed to mix two vials of Egrifta along with one vial of sterile water (comes with the product). Once you’ve mixed the vials together, you’re ready to inject the solution into the aforementioned area to meet daily recommended amounts (2 mg). With everything already being measured out in vials, this cuts down on the confusion for how much Egrifta you’re supposed to take.

The obvious benefit to using Egrifta for bodybuilding purposes is that you could get rid of excess belly fat that normally takes years of religious training and eating clean. Furthermore, the side effects of Egrifta (muscle pain, fluid retention, injection site redness, numbness) are fairly mild in comparison with some of the other fat-cutting drugs that bodybuilders take.

But while all of this sounds great, the unfortunate downside to using Egrifta is that it’s a relatively new drug, so there aren’t a whole lot of non-HIV-related results available. As said before, the drug is currently in FDA trials to measure its effectiveness in non-HIV patients. Of course, it could take years before any solid findings come out of this. Furthermore, there aren’t a ton of bodybuilders out there using Egrifta to cut fat either, so finding experienced users is pretty tough.

Antiretroviral treatment prevents AIDS

Antiretroviral treatment (ART) manages an HIV infection by hampering the ability of the virus to attack the immune system's T-helper cells. ART kills HIV, reducing the risk of opportunistic infections and preventing the number of T-helper cells (CD4 count) dropping, in turn preventing AIDS.

In 2013, the World Health Organisation (WHO) released new recommended guidelines on antiretroviral treatment. They recommend that people start taking ART earlier than before, when their CD4 count is 500 cells/mm3, previously it was 350 cells/mm3. This is due to the wealth of benefits that are seen if people start treatment earlier, including greater success at delaying or eliminating the onset of AIDS.

Significant health gains have been noticed where treatment access has improved, especially among populations with high HIV prevalence. For example, in KwaZulu Natal province in South Africa, life expectancy has risen by 11 years since HIV treatment was scaled up in 2003. An HIV infection will cause a person's health to be compromised if they do not take antiretroviral treatment (ART). Eventually, someone living with HIV who is not taking ART will experience serious health issues and opportunistic infections, leading to AIDS.

People who are taking ART, but who do not adhere to it correctly may find that HIV becomes resistant to their treatment, allowing HIV to reproduce and multiply in their body again. This increases the risk of progressing to AIDS, and is evidence of the cause and effect relationship between HIV and AIDS.

For example, only a quarter of people living with HIV in sub-Saharan Africa have achieved viral suppression (where the level of HIV in their body has become undetectable) because of shortfalls in treatment provision or not adhering to their drugs. In 2012, 1.2 million of the 1.6 million AIDS-related deaths that year were in sub-Saharan Africa.
Even a partially effective HIV vaccine could save millions of lives. Experts have calculated that a vaccine that is 50 percent effective, given to just 30 percent of the population could reduce the number of HIV infections in the developing world by more than half over 15 years. An HIV vaccine that was more than 50 percent effective could cut the infection rate by more than 80 percent.

An HIV vaccine would have a number of key advantages over today’s HIV prevention options. In particular, the protection offered by a vaccine during sex would not depend on the consent of both partners (unlike condom use), and would not require behaviour change (unlike abstinence). An HIV vaccine would also be invaluable for couples wishing to conceive a child while minimising the risk of HIV transmission.

Children could be given an HIV vaccine before ever being exposed to HIV, and ideally this would protect them from all routes of HIV transmission. Vaccinating large numbers of people would probably require relatively little equipment and expertise, and would be much simpler and cheaper than providing antiretroviral treatment for those already infected. An HIV vaccine could be effective in either of two ways. A “preventive” vaccine would stop HIV infection occurring altogether, whereas a “therapeutic” vaccine would not stop infection, but would prevent or delay illness in people who do become infected, and might also reduce the risk of them transmitting the virus to other people. Although a preventive vaccine would be ideal, a therapeutic vaccine would also be highly beneficial.

The basic idea behind all HIV vaccines is to encourage the human immune system to fight HIV. The immune system works using a combination of cells and chemicals called antibodies. Early vaccine research focused on teaching the immune system to produce antibodies that would block HIV entering human cells. However, products designed to work this way failed in clinical trials because the antibodies worked only against lab-cultured HIV, not against the wild strains of the virus. Research has found a very small number of HIV-infected people produce 'broadly neutralising antibodies' to HIV. These antibodies, which neutralise a high percentage of the different types of HIV, are now the basis for new research into vaccine development.

Other research has focused on encouraging the immune system to produce cells to fight HIV. Nevertheless, many scientists believe such “cell-mediated” approaches will not be very effective on their own, even as therapeutic vaccines. It seems likely that a really effective vaccine will have to take a two-pronged approach involving both cells and antibodies.

HIV and Nutrition

HIV and nutrition are intimately linked. HIV infection can lead to malnutrition, while poor diet can in turn speed the infection’s progress. As HIV treatment becomes increasingly available in the poorest parts of the world, critical questions are emerging about how well the drugs work in people if they are short of food. Uncertainty also surrounds the role of vitamins and other supplements. And for those already receiving treatment, side effects such as body fat changes are a daily concern.

Understandably, HIV positive people and those who care for them are interested in whatever might benefit their health.
 HIV and AIDS is well known for causing severe weight loss known as wasting. In Africa, the illness was at first called “slim” because sufferers became like skeletons. Yet body changes are not only seen during AIDS, less dramatic changes often occur in earlier stages of HIV infection.

Whereas starving people tend to lose fat first, the weight lost during HIV infection tends to be in the form of lean tissue, such as muscle. This means there may be changes in the makeup of the body even if the overall weight stays the same.

In children, HIV is frequently linked to growth failure. One large European study found that children with HIV were on average around 7 kg (15 lbs) lighter and 7.5 cm (3 inches) shorter than uninfected children at ten years old. One factor behind HIV-related weight loss is increased energy expenditure. Though no one knows quite why, many studies have found that people with HIV tend to burn around 10% more calories while resting, compared to those who are uninfected. People with advanced infection or AIDS (particularly children) may expend far more energy.

But faster metabolism is not the only problem. In normal circumstances, a small rise in energy expenditure may be offset by eating slightly more food 4 or taking less exercise.  There are two other important reasons why people with HIV may lose weight or suffer childhood growth failure.

The first factor is decreased energy intake or, to put it simply, eating less food. Once HIV has weakened the immune system, various infections can take hold, some of which can affect appetite and ability to eat. For example, sores in the mouth or throat may cause pain when swallowing, while diarrhea or nausea may disturb normal eating patterns. Someone who is ill may be less able to earn money, shop for food or prepare meals. Stress and psychological issues may also contribute.

Secondly, weight loss or growth failure can occur when the body is less able to absorb nutrients – particularly fat – from food, because HIV or another infection (such as cryptosporidium) has damaged the lining of the gut. Diarrhea is a common symptom of such malabsorption. Current antiviral drug treatments control HIV infection and prevent severe wasting, as well as other AIDS-related conditions. Emaciated people tend to regain weight once they begin treatment, and stunted children start to grow faster. Nevertheless, the drugs do not eliminate wasting.

Studies have found that relatively small weight loss (between 5% and 10% over six months) is quite common among people with HIV who are taking treatment and not trying to lose weight. Although this might not seem like much, losses of this size have been linked to an increased risk of illness or death, as discussed below.  In addition, some antiretroviral drugs have been linked to a problem called lipodystrophy. Whereas HIV-related wasting tends to deplete lean tissue, lipodystrophy involves changes in fat distribution. Prolonged treatment is sometimes associated with losing fat from the face, limbs or buttocks, or gaining fat deep within the abdomen, between the shoulder blades, or on the breasts.

Antiretroviral treatment can also contribute to lipid abnormalities by raising LDL cholesterol, lowering HDL cholesterol, and raising triglyceride levels in the blood. This may result in higher risks of heart disease, stroke and diabetes. Other side effects of antiretroviral treatment include insulin resistance, which can occasionally lead to diabetes.

Antibody Building and HIV Infection

Scientists at the National Institutes of Health have identified long-sought and elusive broadly neutralizing antibodies to HIV in a pair of papers. These proteins produced by the immune system are crucial for creating a preventive vaccine, and could also have therapeutic uses developed in the coming years or decades.

Variations in individuals' immune systems can dramatically affect responses to infection—HIV is no exception. The result generally can be shown as a bell curve, with a group of people whose disease progresses rapidly, a broad middle segment who progress typically, and a small group of "elite controllers" whose immune systems are quite effective at containing HIV viral replication.

The quest to figure out why has focused primarily on the adaptive immune system, because CD4+ and CD8+ T cells have a clearly demonstrated capacity to kill cells infected with HIV. But that response only arises some days, weeks and even months after a person has been exposed to HIV and the virus has integrated itself into cellular DNA, establishing lifelong infection. The adaptive immune response can only contain an established infection, it cannot prevent that infection from occurring at its onset.

B cells are the first line of defense against infection. They attack at the initial exposure to a pathogen, and can prevent the establishment of infection—and HIV is no exception. But there are a number of reasons why it has proved difficult to identify their contribution to neutralizing the deadly virus.

HIV transmission is not very efficient. Exposed persons may avoid infection for a variety of mechanical (barrier) and biological reasons, such as the virus's failure to penetrate to the surface of mucosal tissue or dendritic cell difficulties in latching onto the virus to carry it to a lymph node. So it is challenging to conclusively identify the contribution of a specific immune response that can prevent an initial infection.

Over the years, it has become clear that there are factors other than CD4+ and CD8+ T cells that help to control the virus in at least a portion of those infected with HIV.

Researchers have identified several antibodies that can neutralize the virus. Most of them bind weakly to small, often deep, pockets on the virus. In most instances, once infection becomes established rapidly mutating HIV evolves resistance to those narrowly focused antibodies, often by adding glycans or sugars to its outer envelope, which shields or blocks antibody access to the binding site.

What is needed is an antibody that binds strongly to a surface site on the virus, and which cannot be easily blocked. It is also important that the binding site is greatly conserved across the many strains of HIV.

Researchers at NIH Vaccine Research Center (VRC) decided to look at neutralizing antibodies in the blood of persons who are able to better control HIV infection. Elite controllers were not part of the mix because they seem to control HIV through their adaptive immunological system T cell mechanisms.

Using sophisticated reverse-engineering techniques, the researchers identified three proteins that are broadly neutralizing, which they labeled VRC01, VRC02 and VRC03. They also isolated the B cells that produced them.

The first two antibodies have very similar chemical structures and bind to HIV's gp120 trimer spike on its surface. The virus uses the trimer to link up with a CD4 receptor, which is the first of many steps taken to enter and infect a host cell. The antibody and gp120 spike bind in a way that is, in part, similar to the way that the spike and CD4 receptor bind.

As a result, VRC01 and VRC02 binding is particularly long and strong compared with the bonds formed by other antibodies. Further, the binding site on the gp120 spike is well exposed and not likely to become blocked by the addition of sugars to the viral envelope.

The two antibodies neutralized 91 percent of the 190 different HIV isolates that the team tested. Those isolates represent all of the various clades or strains of HIV present worldwide, says John Mascola, one of the VRC research team leaders. Also, the antibodies were able to neutralize all of the limited number of HIV variants that are transmitted sexually—a key point, because 80 percent of all new infections result from sexual activity.

VRC01 and VRC02 occur naturally and are produced by what are called RSC3 memory-specific B cells, an extremely rare component of the immune system. Using flow cytometry, the NIH team could isolate only 29 of those cells from among the 25 million cells that they screened. Furthermore, the proteins produced by those B cells often are immature and it appears that the proteins must undergo a series of combinations before they become functional VRC01 or VRC02.

X-ray crystallography allowed the researchers "to identify the [antibody's] binding site down to the atomic level structure…. It is a particularly invariant part of the CD4 binding site, which is exposed," Mascola says. He calls that knowledge "a blueprint from which to design new vaccines. It allows us to try to design a protein that mimics and presents that specific site to the immune system" to stimulate B cells "to crank out the antibody."

Mascola acknowledges the complex nature of the VRC01 and VRC02 antibodies and their low naturally occurring numbers may prove to be an obstacle to developing a vaccine. It is too early to understand all of the issues surrounding the stimulation of antibody production and the concentration necessary to afford protection from infection.

The VRC research team has designed vaccine antigens that already are in preclinical study in small animals. If those prove successful, the work may advance into a monkey model, although it is not completely clear how monkeys can control the simian version of HIV and not progress to advanced disease. The identification of VRC01 and VRC02 may also help to advance a better understanding of the disease in monkeys.

Mascola says these discoveries also may lead to development of a "therapeutic vaccine" or immune-based therapy that helps train the immune system of an HIV-infected person to better control the virus without the use of drugs.

It may be possible to mass-produce these antibodies for passive administration as an adjunct or substitute for current small molecule drugs used to treat HIV. And if production costs can be reduced sufficiently there may be a role for them in topical microbicides as a preventative for HIV exposure.