Human growth hormone, insulin, FT4, and FT3

25 Nov 2021

Human growth hormone, insulin, FT4, and FT3

Human growth hormone, insulin, FT4, and FT3

1.    Why you need insulin during a growth hormone course

2.    Causes of diabetes because of a course of growth hormone

3.    How to avoid problems in the future

4.    Human growth hormone impact

5.    Insulin impact

6.    Which insulin should be used and in what dosage

7.    Alternative solutions for insulin use

8.    Human growth hormone without using insulin

9.    Introductory theory on FT3 and FT4

10. The correct regimen

Why you need insulin during a growth hormone course

Growth hormone is a strong doping agent for athletes. It is needed for everything that requires strength and endurance. Bodybuilding is one of its most important uses. There is a common opinion that taking growth hormone will lead to insulin resistance and diabetes in the long term. This side effect is possible with the use of growth hormone. Risks are the highest with regular high doses over 5 milligrams per day.

HGH enhances and accelerates the processes of gluconeogenesis and glycogenolysis in the liver, which leads to the increase of glucose (sugar) level in the blood. Gluconeogenesis is when the body gets glucose from non-carbohydrate sources, while glycogenolysis is the conversion of glycogen into glucose. There is no exact data as to which of these processes is more strongly affected by human growth hormone.

Causes of diabetes because of a course of growth hormone

Diabetes mellitus is caused by a dysfunction of the pancreas, which, with constantly elevated glucose levels, fails to cope with the task of producing insulin. If you increase the concentration of human growth hormone in the body with the drugs, insulin levels rise as well. This is the body's response to excess glucose. If growth hormone is used constantly, the pancreas becomes depleted. The next step is the inability of the pancreas to produce insulin. This is what diabetes mellitus is.

Diabetes mellitus is a complex and life-threatening disease that is associated with metabolic disorders. The body stops absorbing glucose from food. The consequence is the destruction of the circulatory system, blindness and paralysis, as well as gangrene of the lower extremities. Even a hyperglycemic coma is possible.

How can this be avoided? A person should keep a balance of use of insulin and growth hormone. Thus, the more growth hormone administered exogenously, the more insulin is needed to compensate for rising glucose levels.

Insulin is a pancreatic hormone that helps glucose enter the body's cells and reduces its concentration in the blood. Insulin is a conductor of glucose from the blood to the organs where it is needed. A lack of insulin prevents cells from absorbing glucose, and as a result, the concentration increases in the blood.

Lack of endogenous insulin leads to a persistent increase in blood glucose levels when high doses of growth hormone are used. The result is problems with the work of a number of organs and body systems. Diabetes mellitus disrupts literally all types of metabolism. This applies to protein, fat, carbohydrate and water-salt metabolism.

How to avoid problems in the future

There is no need for additional insulin if the growth hormone dose is less than 5 milligrams per day.

The effect of growth hormone on carbohydrate metabolism was described in 1920.

The role of insulin in the regulation of carbohydrate metabolism is well defined. Decreased and increased levels of growth hormone lead to changes in carbohydrate metabolism. 

Obesity and impaired glucose metabolism were observed at different stages of hypopituitarism. People with acromegaly often have diabetes mellitus and insulin resistance. The ability of insulin to reduce blood glucose levels in animals with the pituitary gland removed was 10-100 times higher. That is, the pituitary gland is involved in the regulation of tissue sensitivity to insulin. When the growth hormone was obtained in its pure form (in 1949), it was proved that this particular pituitary hormone has a diabetogenic effect. Ingestion of large doses of growth hormone increases blood glucose levels. This is caused by a decrease in tissue sensitivity to insulin, including fat and muscle tissue.

Human growth hormone impact

Human growth hormone stimulates the pancreas to release insulin. Excess hgh is accompanied by increased insulin levels and increased insulin release due to high glucose levels. Lack of growth hormone determines insulin deficiency in the body and decreased insulin release. A role for human growth hormone in the regulation of insulin secretion has also been confirmed. Early studies can’t help to determine the primary or secondary effect on insulin secretion through hyperglycemia, and whether growth hormone directly affects tissues, or whether it is due to the effect of insulin on them.

Growth hormone has the opposite effect to that of insulin on fat cells. Basal and drug-induced glucose consumption by cells, its oxidation and lipogenesis are decreased. The ability of growth hormone to decrease the insulin sensitivity of fat cells (adipocytes) and stimulate lipolysis underlies the diabetogenic effect. Regulation of insulin sensitivity is possible through the increase of intracellular calcium concentration. Human growth hormone has a similar effect on liver cells.

Growth hormone provides an anti-insulin effect on the cellular level, i.e. it decreases insulin sensitivity. The effect of growth hormone on the pancreas means an increase in the number of cells, as well as an increase in insulin gene activity, insulin secretion and synthesis.

One study should be mentioned. The results stated that a significant impairment of growth in children with diabetes occurs when this disease is combined with liver pathology, hypothyroidism and poor metabolic control. Growth hormone levels in diabetic patients are normal and may even rise, but levels of circulating insulin-like growth factor, as well as high molecular weight IGF-binding protein, are below normal. This index does not return to normal even at puberty.

There is partial resistance to growth hormone action at the receptor level on liver cells. Reduced response of IFG1 release in response to growth hormone administration in children with diabetes. The development of growth hormone resistance is closely related to insulin concentrations. Insulin increases liver production of IGF1 by influencing growth hormone receptors or further acting on post-receptor processes. The reduced number of growth hormone receptors comes to a normal value after 3 months of insulin therapy. The level of IGF1 depends on the level of insulin in the blood.

Insulin impact

Insulin also affects the biological activity of IGF1. Deficiency of IGF1 and its low biological activity lead to impaired growth in diabetes mellitus. Intensive insulin therapy restores serum IGF1 levels. Sometimes it is possible to restore the growth of children with diabetes. The intensity of growth of girls with diabetes at pubertal age is clearly associated with the concentration of growth hormone, and for boys the relationship with testosterone is characteristic.

The above is true for children with diabetes, but it can also be applied to athletes who use human growth hormone, especially those who take it in high doses for a long period of time.

Thus, the use of insulin in conjunction with growth hormone is appropriate. This is especially true when using high doses of growth hormone for a long period of time to gain muscle mass. In the period before competitions, when there should be no fat, the use of insulin may play a bad joke on an athlete, especially of those who use carbohydrate-free diet. This threatens not only bad form, but also hypoglycemia with all the negative consequences.

Which insulin should be used and in what dosage

The next question is about the dosages and types of insulin to use. The traditional dosing regimen is to use hgh with short or ultra-short insulin in a 1:1 ratio. This means that for every 5 ml of growth hormone, 5 units of insulin should be used. This is either short or ultra-short insulin.

Why choose these types of insulin?

Here the answer is quite simple. Hypoglycemia (a drop-in blood glucose levels) occurs quickly and predictably. This process is easily stopped by the intake of normal carbohydrate foods.

If higher doses of growth hormone and insulin are taken, hypoglycemia is stopped by a combination of simple or complex carbohydrates, based on the rate of 5-10 g of carbohydrates for each unit of insulin. The exact amount of carbohydrates is selected individually, considering how you feel or the data obtained from blood tests, glucose and insulin content in the dynamics.

Alternative solutions for insulin use

There is another option of using growth hormone with insulin. It is very little known and not popularWe are talking about the use of an ultralong type of insulin, in particular Lantus.

Insulin increases IGF1 production by the liver and enhances its biological activity. This effect is extremely important for obtaining high levels of anabolism and fast and high-quality gain of muscle mass.

In addition, Lantus-type insulin shows 10 times greater affinity to IGF1 receptors compared to other insulins.

The peak concentration of human growth hormone in the blood is 3-5 hours after injection. Blood sugar levels will be high for the duration of the injection, when the peak of action of short and, especially, ultra-short insulin is almost over (about 20-40 minutes). The action of ultra-long insulin like Lantus stretches for 24 hours without a peak of activity. That is, it smoothly and gradually reduces the blood glucose level after increasing this level with a shot of growth hormone. Thus, it helps the body to cope with excessive glucose without stopping the pancreas from producing its own insulin. 

Lantus dosage is selected gradually, starting with 20 IU per day, and increasing gradually by 5-10 IU. Efficacy is also evaluated by self-feeling or glucose tests in dynamics.

Ideally, all exogenous insulin Lantus should be stopped by regular meals, without the feeling of hypoglycemia.

Lantus is quite acceptable for growth hormone doses of 2-5 IU. Accordingly, at higher doses, it will also provide the necessary help to the pancreas and avoid malfunction of this important organ.

Human growth hormone without using insulin

Let's look at another option of growth hormone use with no insulin.

In this case, the human growth hormone is used together with 2,4-dinitrophenol (DNP). This substance not only burns fat but also lowers the blood glucose level in the case of type 2 diabetes (insulin-dependent), just like in the case when insulin is taken together with growth hormone. The usual dosage in such a case is 100-200 mg of dinitrophenol.

It is desirable to use such a scheme during "drying out" period because fat mass is perfectly lost during it. Gaining muscle mass in this case is difficult due to metabolic changes in the body. The use of 2,4-dinitrophenol is a topic for a separate article in which the myth of this terrible and deadly drug will be debunked.

Introductory theory on FT3 and FT4

There are different views on the use of thyroxine (T4) and triiodothyronine (T3) together with growth hormone.

The thyroid gland produces thyroxine (T4) and triiodothyronine (T3). T3 is the physiologically active hormone that provides thyroid effects. On the other hand, the inactive hormone T4 is converted into T3 in the peripheral tissues by enzymes from the deiodinase group. There are three types of these. The majority of active T3 in the body (about 80%) is obtained through this conversion with the first two types of deiodinases, while inactivation is achieved with the third type.

Human growth hormone activates the conversion of T4 to T3, which influences the work of somatotropin through its effect on the IGF-1 hormone. At the same time, the action of somatotropin slows down in the presence of an excessive amount of T3.

T4 is synthesized in the body under the control of thyroid-stimulating hormone (TSH), which is secreted by the pituitary gland. TSH is controlled by thyrotropin-releasing hormone, which is produced in the hypothalamus. TSH levels are controlled by a negative feedback mechanism, similar to testosterone. That is, an increase in T3 leads to a decrease in TSH levels. Naturally (similar to testosterone), the administration of exogenous T3 also leads to a decrease in TSH. There is also a decrease in the level of endogenous T3. TSH stimulation of thyroid function also requires insulin or insulin-like growth factor.

Use of exogenous growth hormone suppresses endogenous growth hormone secretion by increasing somatostatin levels, which in turn suppresses TSH secretion. T4 levels also decrease. This type of connection works in the opposite direction. If T3 levels in the body are higher than normal, the hypothalamus increases the secretion of somatostatin, which inhibits its own growth hormone secretion and minimizes the stimulating effect that T3 produces on growth hormone secretion at their normal physiological levels.

T3 enhances most of the effects of growth hormone, including growth hormone IGF1 levels and growth hormone gene control. Some cases of stunting in children are very revealing. When growth hormone levels are normal, low levels of T3 have been observed.

Numerous experiments have shown that administration of exogenous growth hormone enhances the conversion of T4 to T3 and increases T3 levels / decreases T4 levels. The result is a decrease in T3 (via TTH feedback) and a decrease in the anabolic effect of hgh.

Using growth hormone to stimulate the full range of possible effects requires an additional dose of T3 in the body. Accordingly, the most reasonable solution seems to be additional use of T3 on the background of growth hormone therapy.

Unfortunately, this is wrong.

An excess of T3 in the body leads to the decrease of the synthesis of type I and type II deiodinases, while the synthesis of type III deiodinase increases, which not only inhibits the conversion of T4 to T3, but also reduces the effects of triiodothyronine itself.

The correct regimen

The best solution to the problem is to take not T3 but T4. In this case we will get all positive effects of high T3 level, optimal activity of deiodinases of the first and second types and quite physiological T4 level. 

Taking 0.5-1.0 mcg of thyroxine per 1 kg of an athlete's weight against the background of growth hormone supplementation is a fully acceptable and justified dose. Probably, it will seem high or, on the contrary, too low to some people. In this case, it is better to choose the dose according to the state of health and, better yet, based on the results of blood tests.