How does growth hormone burn fat

Still, others may head to the gym to work out for hours on end. Even if you do all those things are more, they may not be enough for you to lose weight. Adding a growth hormone to your regimen could be the answer. Human growth hormone is produced by your pituitary gland. In kids, human growth hormone supports growth and development. As you get older, your pituitary gland produces lower levels of this growth hormone. Because research shows that obese adults have less HGH than individuals who maintain a normal weight, many people suspect that the hormone can facilitate weight loss.

That study showed that the use of synthetic HGH injections yielded an 8. Growth hormone does not appear to help older men either. Now in his 50s, Larry has continued to use a steroid-hormone combination on and off since he started more than a decade ago. The steroids give him a muscle boost, while the growth hormone—typically 0. Indeed, a variety of research reveals that HGH can be a potent burner of fat, especially stubborn visceral fat.

Larry is concerned about HGH side effects, particularly the link to increased cancer risk. Among his gym crew, Larry says, HGH has a worse rep than steroids because there is so little research on it.

It makes you think. When Max Sittenfeld, an American anesthesiologist practicing in Costa Rica, began to develop tennis elbow, he turned to the usual remedies. Soon the year-old was taking so many anti-inflammatory drugs his stomach ached. Costa Rica has fewer drug restrictions, so a doctor began growth hormone shots through the Anti Aging and Wellness Clinic in San Jose, gradually increasing the dose. The use of HGH for injury repair has long been a part of sports lore. Whether the tales are true or not, medical science is in need of better treatment for battered joints, says Christopher Mendias, Ph.

By the time athletes are able to return to the field or court, the side that had the ACL tear is about 40 percent weaker. Mendias has just begun studies that involve administering 0. The first participants are all men between ages 18 and 35 undergoing an ACL reconstruction. His hypothesis, somewhat simplified, is that HGH will help preserve the muscle around the joint by activating IGF-1 that stimulates muscular growth while blocking another protein, myostatin, which is triggered by injury and curbs that growth.

The research is funded by the Mark Cuban Foundation, and the Dallas Mavericks owner has publicly stated that he thinks HGH should be legal to aid in joint repair. Danish researchers are also looking into HGH as a treatment for patients with tendinopathy—long-term tendon pain. Mendias has the measured optimism of a scientist; he says the research is still too sparse to draw conclusions. Among his biggest concerns is that the possible side effects are still uncertain. Still other side effects may exist.

But if his research turns out to be successful, it could usher in a new era of better, faster recovery from sports injuries. Low HGH results in weight gain and central obesity, which carry serious health risks. More specifically, the accumulation of fat occurs around the abdomen and internal organs which increases the risk for other metabolic and cardiovascular diseases. Without adequate growth hormone levels, fat accumulates much easier in the region. Therefore, the metabolic changes in GHD are characterized by increased waist circumference and body fat percentage.

Other metabolic parameters which may be negatively affected by the condition are blood pressure and cholesterol levels. On the other hand, obesity is a metabolic condition that can suppress growth hormone secretion and further reduce GH levels in GHD patients. According to scientists, obesity leads to changes in several regulatory hormones that affect HGH synthesis. For example, its counterregulatory hormones insulin and somatostatin are increased while ghrelin levels are reduced which results in suppressed HGH production.

Studies reveal that the obesity-associated suppression of HGH secretion is fully reversible after weight loss. HGH can help you burn fat by stimulating lipolysis. This is a metabolic pathway through which stored fat breaks down into fatty acids. When the molecules are released, the fat cells shrink.

These fatty acids can be burned when your body needs extra energy or they will return to fat storage if unused. One of the most notable enzymes lipases which facilitate the process of fat breakdown is hormone-sensitive lipase HSL. Experiments reveal that growth hormone stimulates HSL which helps your body mobilize fat from the adipose tissues. Normally, HGH has a pulsatile secretion, and fat breakdown begins around hours after a peak. Similar data have been produced in men with abdominal obesity where 9 months of GH treatment was able to improve insulin sensitivity Treatment with GH for 5 wk in obese women was followed by a reduction in body fat mass 18 , and 12 wk of GH treatment combined with a diet and exercise program in postmenopausal women reduced truncal fat, an effect not different from diet and exercise alone There are no long-term data on the effect of GH treatment in women with abdominal obesity, and previous studies have not been able to show that GH is more efficient than weight reduction alone to reduce total body fat in subjects with simple obesity 20 , The primary aim of this study was to explore the effects of GH treatment on insulin sensitivity in postmenopausal women with abdominal obesity, and the secondary aim was to study effects on visceral fat mass and glucose tolerance.

Forty women with a mean age of They were recruited by advertisements in a local newspaper. The criteria for exclusion were DM, cardiovascular disease, claudicatio intermittens, stroke, any malignancy, and any other hormone treatment, including estrogen replacement therapy. Of women who responded to the advertisement, were screened and 40 were then found to be eligible for inclusion Fig.

This study was designed as a month, randomized, double-blind, parallel group trial with subjects receiving placebo or recombinant human GH. After a 1-month run-in period in which concomitant medications were optimized, 40 women were randomized to receive GH or placebo treatment. A computerized randomization was performed by the Sahlgrenska hospital pharmacy. Informed consent was obtained from each patient before entry into the study. The treatment regimen was initially formulated in international units per day and later converted to milligrams per day.

The initial dose of GH was 0. Symptoms and signs of adverse effects were carefully monitored at each visit. The dose was reduced by half in the event of fluid-related side effects.

Oral and written instructions about administration and dose were given. Compliance was assessed by counting the returned empty vials and expressing that number as a percentage of the vials needed for the treatment period.

Body composition assessments of insulin sensitivity and glucose tolerance were made before the start of treatment and after 6 and 12 months of treatment. Computed tomography CT of the abdomen and thigh area was performed, and physical activity and quality of life questionnaires were used at baseline and at 12 months. Physical and laboratory examinations including safety assessments were performed at the start; after 1, 2, 3, 6, 9, and 12 months; and 1 month after discontinuing treatment.

Body weight BW was measured in the morning to the nearest 0. Body height was measured barefoot to the nearest 0. Waist circumference was measured in the standing position with a flexible plastic tape midway between the lower rib margin and the iliac crest, whereas the hip girth was measured at the widest part of the hip. Systolic and diastolic blood pressures were measured after 5 min supine rest with an automatic sphygmomanometer.

The mean of three measurements with a 1-min interval in between was used for evaluation. Total body potassium was measured by counting the emission of 1. A CT technique was used to measure abdominal adipose tissue and thigh muscle. The tube voltage was kV, and the slice thickness was 5 mm.

Four scans were obtained from each participant. Scan 1 was obtained in the mid-thigh region 1 cm below the gluteal fold, scan 2 at the fourth lumbar vertebra level L4 , scan 3 at the mid-liver level, and scan 4 at the fourth cervical vertebra level C4. From scan 1, the tissue areas of the right leg are reported. Tissue areas were determined as previously described 23 with precision errors calculated from double determinations: sc adipose tissue AT 0.

To assess hepatic fat content, the attenuation of the liver and spleen was determined within three circular regions of interest placed in the dorsal aspect of each organ. Attempts were made to avoid vessels, artifacts, and areas of homogeneity.

Hepatic fat content was studied as the liver attenuation absolute values or as the liver-to-spleen attenuation ratio. The effective dose equivalent per examination was less than 0. A euglycemic hyperinsulinemic glucose clamp was performed after an overnight fast, as described previously An iv catheter was placed in an antecubital vein for the infusion of insulin 0.

A second catheter was placed in the contralateral arm for arterialized blood. Blood glucose was monitored every 10 min during the insulin infusion and, during the last 30 min, every 5 min. Euglycemia was maintained 5. The glucose disposal rate GDR was measured for 20 min in steady-state conditions, which were reached after min. The mean insulin concentrations during steady state were All the subjects performed an oral glucose tolerance test OGTT before the start, at 6 and 12 months, respectively, and 1 month after treatment.

A standard dose of 75 g of glucose was administered, and fasting blood samples were obtained at baseline and every 30 min for 2 h. To eliminate any type of interference, OGTT assessments were performed 1 wk after the glucose clamp.

Blood samples were drawn in the morning after an overnight fast. The within-assay CV for total cholesterol and TG determinations was 2. HDL cholesterol was determined after the precipitation of apolipoprotein B apoB -containing lipoproteins with magnesium sulfate and dextran sulfate Thermo Clinical Labsystems , with a CV of 1.

The low-density lipoprotein LDL cholesterol concentration was calculated as described previously All analyses were performed on a Konelab 20 autoanalyzer Thermo Clinical Labsystems.

Physical activity was studied by assessing indices of habitual physical activity at work, sport, and during leisure time using a questionnaire developed by Baecke et al. Quality of life was assessed using the Psychological General Well-Being index, which includes an overall score and six subscores anxiety, depression, well-being, self-control, health, and vitality , described elsewhere All the descriptive statistical results are presented as the mean sem.

The results have been analyzed on an intention-to-treat basis with the exception of the subgroup analysis of GDR and weight including only subjects who fulfilled 1 yr of treatment. Log transformation before statistical analysis was used for variables that did not have a normal distribution. An unpaired t test was used for between-group analyses. All values are expressed as the mean sem. BF and FFM were estimated by total body potassium. At 12 months, the mean dose of GH in the GH group was 0.

There was no significant change in serum IGF-I concentrations between 6 and 12 months in both groups. Twelve women in the GH-treated group experienced side effects related to fluid retention arthralgia, joint stiffness, or peripheral edema. They appeared during the first 4 wk of treatment and were all considered to be of mild to moderate severity.

In 11 subjects, dose adjustments were required, although in one subject the symptoms subsided spontaneously after 9 months. At the end of the trial, only two of the 11 subjects presenting signs of fluid retention had an IGF-I score greater than 2 sd. Five dropouts occurred in the GH-treated group, four of which could be potentially attributed to the GH treatment Fig.

One subject left the trial after 3 months of persistent swelling and numbness despite dose adjustments. One subject developed DM and was excluded from further treatment at 6 months.

In retrospect, the diagnosis of DM was present during OGTT at the first visit, data that were not available until 1 wk after the performed test. One subject complained of profuse perspiration 1 month after the start of treatment and was excluded from the trial after 2 months when estrogen treatment was commenced, although one subject decided to discontinue treatment after 3 months as she experienced increased hair loss. The fifth case was withdrawn after 4 months of treatment because of the diagnosis of an epidermoid tumor in the oral cavity.

The lesion was already present several months before the start of the trial, but the diagnosis was first established by biopsy 2 months later.