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Rudman’s study involved 21 men who were representative of the approx. 30% of all men ranging in age from 60 to 80 years old who have a plasma IGF-I concentration that is < 350 U per liter in comparison to a range of 500 to 1500 U per liter in 20 to 40 years old health men. Dr. Rudman said the findings of the study couldn’t be generalized to approx. 2/3 of men >60 years of age who have plasma IGFK-I concentrations of >350 U per liter, nor can it be applied to women in a similar age range. The criteria of the study focused on a subgroup of overly healthy older men.
If obesity is absent, there are no liver disease or one is not below normal weight, a plasma IGF-I concentration of <350 U per liter in older men usually indicates they secrete very little HGH. The explanation for low plasma IGF-I concentration in these men is verified by measuring serum growth hormone levels at 24 hour intervals or to determine the 24 hour urinary excretion of HGH the same was applied. We did not do this, but Ho et al. established that the 24-hour integrated serum growth hormone level was noticeably lower in the men >55 than in the 18 to 33 years old men.
An alternative explanation for low plasma IGF-I concentration is decreased production of plasma IGF-I binding proteins. Most of the IGF-I plasma is bound to these proteins, however, in healthy people who eat a normal diet their concentrations do not vary much.
In the 12 men that were part of Group 1, the study was able to raise the initial low plasma IGF-I concentrations to normal level like those seen in young adult men by the dose of HGH that was administered, and there was no tachyphylaxis or hormone resistance evident. The dose that was given was approx. 0.03 mg per kilogram. This was administered 3x a week, and it was based on the estimated rate of growth hormone secretion in young men and it was similar to or smaller than doses that were administered to children with an HGH deficiency and young adults.
The way these older men’s plasma IGF-I responded to this dosage was similar in scale to those in younger people. These replacement doses, instead of the pharmacological doses, being administered were being confirmed by the plasma IGF-I measurements. These measurements stayed in the range expected for healthy young adults at 500 to 1500 U per liter throughout the treatment period. The study concluded that in aging men that have low plasma IGF-I concentrations hepatic responsiveness there is no impairment of HGH. The decrease in plasma IGF-1 concentrations in these men was the result of an HGH deficiency not an HGH resistance. The increase in plasma IGF-1 levels that occurs when HGH is administered to children that have an HGH deficiency reflects augmented hepatic production of IGF-1, as well as an increased production of one of the binding proteins that transport IGF-1. The degree that the production of IGF-1 binding protein increases by administering HGH hasn’t been studied in adults.
At the beginning of the study, the researchers thought it was unlikely that adverse reactions to HGH would happen because they were using physiologic doses. In addition, larger doses or similar doses hadn’t caused reactions that were undesirable in children or young adults. However, the potential that this dose, when administered for six months to older subjects, could result in the manifestation of hypersomatotropism, such as hypertension, oedema, diabetes, or cardiomegaly. Even though none of these conditions did develop small increases in the fasting plasma glucose concentration and the mean systolic blood pressure of the group of men who received HGH did occur.
The extent of the increase in lean body mass, 8.8% and the decrease in adipose-tissue mass, 14.2% above and below baseline in the aging men receiving HGH for 6 months was comparable to the degree of the responses in children and young adults that were treated with similar or lower doses for a 3-6 month period. This further comparison offers further proof that tissue responsiveness to GH and IGFK-I isn’t changed in older men. Up until this point, the evidence that resulted in this conclusion just came from short-term nitrogen-balance experiments.
Salomon et al. reported that the administration of HGH in a dose of 0.49 unit per kilogram per week - 0.19 mg per kilogram per week for 6 months to adults that are 20 to 50 years of age who had a growth hormone deficiency significantly lowered the serum cholesterol concentration. The study did not change serum cholesterol concentrations. The deviating results could reflect the subjects' age differences, the degree of HGH deficiency, the dose of hormone, or all of these.
In rodents the response to growth hormone was an increase in lean body mass that was the result of increases in the volume of the skin, liver, skeletal muscle, spleen and kidney. In the younger human subjects, growth hormone has been documented to have caused a muscle and kidney enlargement. Other organs have not been assessed. When children with growth hormone deficiency are treated with HGH the reduction in adipose-tissue mass is associated with a redistribution of adipose tissue from the abdominal to peripheral areas. However, it isn’t known whether the increase in lean body mass and the decrease in adipose-tissue mass are both qualitatively and quantitatively similar in young and old human subjects.
The Biosynthetic human growth hormone had no noticeable effect on the bone density of the radius or proximal femur in the aging men. However, it did increase the lumbar vertebrae density by about 1.6%. Although the bone density decrease with advancing age in men could be partially due to the diminished secretion of growth hormone, there will be the need for longer periods of HGH administration before any final conclusions can be drawn concerning its effectiveness in reversing that decrease.
There are questions that still need to be answered: What will be the benefits and what will be the nature and frequency of any adverse effects when a study involves a larger number of elderly subjects and different doses of HGH are studied? What organs are answerable for the increase in lean body mass, and do the functional capacities also change? Only when these types of questions are answered can we explore the potential benefits of HGH in the elderly. Atrophy of muscle and skin plays a role in older people’s frailty so continued investigation of the potential benefits of HGH should be further explored.
Although the study was done using prescription HGH injections the fact remains that the HGH benefits incurred were due to an increase in HGH levels. Fortunately HGH levels can also be raised using HGH releasers. HGH releasers like Genf20 Plus are products that stimulates the secretion of our own internal HGH which is believed to be much more safer and most importantly HGH releasers such as Genf20 Plus can be obtained legally without the need of a prescription.
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