Growing on gh

Cog

Well-known member
Trusted Member
Childhood friend of mine got the treatment.Six inch growth over the summer.
 

resilient1

Well-known member
Trusted Member
I'm average height, 5'10, but I would have gladly had a slightly demented parent throw me on Gh for a few months. I can believe a parent could do something like that. There's all sorts out there.
 
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Bagua

Moderator
Growth Hormone Deficiency in Adults Treatment & Management


Medical Care

Growth hormone (GH) replacement therapy is provided in the form of human recombinant GH. This is available in subcutaneous injection form. The starting dose of GH depends on the age and clinical condition of the patient. A dose regimen that is based on age along with dose titration has been associated with less adverse effects compared with a weight-based regimen. [16] The following regimen is suggested [7] :

  • Age younger than 30 years: 0.4-0.5 mg/day (may be higher for patients transitioning from pediatric treatment)
  • Age 30-60 years: 0.2-0.3 mg/day
  • Age >60 years or those with diabetes mellitus or prediabetes: 0.1-0.2 mg/day

For patients with adherence issues, a less frequent dose regimen such as alternate days or 3 times per week using the same total weekly dosage can be used. [7]

Follow-up is usually planned at intervals of 1-2 months when the dose of GH can be adjusted by increments of 0.1-0.2 mg/day based on the clinical response, serum insulin-like growth factor-1 (IGF-1) levels, and side effects. Longer time intervals and smaller dose increments are suggested for older patients.



Serum IGF-1 levels are the main determinant for adjusting the dose of GH. No studies are available to guide this decision. A commonly used target is the upper half of the normal range appropriate for age and sex, unless significant side effects develop. [5]

Once maintenance doses of GH are achieved, follow-up is provided at intervals of 6 months. Monitoring includes clinical evaluation, assessment of side effects, and measurement of serum IGF-1, fasting glucose, and lipid profile. Quality of life (QOL) is also assessed using standardized questionnaires. If the initial bone mineral density findings, measured by dual-energy x-ray absorptiometry (DXA) scanning, are abnormal, repeat testing at intervals of 2-3 years is recommended. [5]

No studies are available regarding the optimal length of GH replacement therapy. Patients with childhood GH deficiency who attained adult height and had persistent deficiency on retesting should continue to receive GH therapy. [5]

GH therapy can also be continued indefinitely if benefits such as significant improvement in QOL and objective improvements in biochemistry and body composition are observed. If no objective or subjective benefits are seen after 1 year of treatment, discontinuation of GH therapy should be considered. [7]
 

Bagua

Moderator
Complications

Growth hormone (GH) deficiency has been associated with cardiovascular disease, osteopenia/osteoporosis, alteration in body composition, decreased life expectancy, psychological disturbances, and insulin resistance.


Cardiovascular disease

Early epidemiologic data showed that patients with hypopituitarism who were on hormone replacement therapy, not including GH, had increased cardiac events, suggesting an association of GH deficiency with cardiovascular disease. [14, 28, 29, 30, 31] Patients with GH deficiency have increased rates of the presence of markers of cardiovascular disease, such as greater intima-media thickness of the carotid arteries, reduced left ventricular mass, decreased ejection fraction, high levels of serum low-density lipoprotein (LDL) cholesterol (LDL-C) and triglycerides, low levels of high-density lipoprotein (HDL) cholesterol (HDL-C), and high coronary calcium scores. [14, 29, 30, 32] GH therapy improves certain markers of cardiovascular disease, such as serum lipids (reduction of LDL-C levels and increase in HDL-C levels), systolic function, intima-media thickness of the carotid arteries, endothelial function, left ventricular mass, and cardiac output. [29, 33, 34, 35] However, evidence is limited regarding the effect of GH replacement therapy on cardiovascular morbidity and mortality. [28, 29, 36]



A study that evaluated the prevalence of metabolic syndrome and associated cardiovascular complications in adult-onset GH deficiency during GH replacement therapy found an essentially unchanged prevalence of metabolic syndrome in these patients during 1 year of GH therapy. [37] However, there was a significant reduction in abnormal waist circumference (P< 0.001), a significant increase in impaired glucose metabolism (P < 0.001), and a decrease in HDL-C (P = 0.011). Moreover, over a 7-year period of GH therapy, those with metabolic syndrome had a 66% higher risk of developing a new coronary disease compared to those without metabolic syndrome (P = 0.0016). [37]


Osteopenia/osteoporosis

Patients with GH deficiency have reduced bone mineral density and increased rates of fractures. [38, 39] A gender difference in the response to GH treatment has been hypothesized, as bone mineral density has been show to improve with this therapy more in men than in women. [40, 41, 42] The effect of GH therapy on fracture rate was less pronounced, with stabilization of the incidence of clinical fracture after GH treatment. [40]


Effect on body composition

Patients with GH deficiency tend to have a relative increase in fat mass with a preferential increase in visceral fat and a relative decrease in muscle mass. [43, 44] GH therapy decreases total body fat and increases muscle mass. [43, 45] Some, but not all, studies have shown increased muscle strength along with improved exercise capacity and physical performance after GH therapy. [45, 46, 47]



In an observational retrospective monocentric study of 47 patients with GH deficiency who were treated with GH during childhood, investigators evaluated changes in pediatric growth parameters relative to an increase of insulin-like growth factor-1 (IGF-I) z-score as well as other indexes of GH response, such as body composition and lipid profile, after 1 year of treatment in adulthood. [48] The investigators noted the following [48] :

  • Positive correlation between final growth velocity in the last year of childhood GH treatment and an increase in IGF-I z-score in GH-treated adults ( P<  0.01), but no significant positive correlation between the main parameters that evaluate response to GH treatment in children and adults
  • No correlation between growth-promoting effects of GH as child and metabolic changes induced by GH as adult
  • Negative correlation between weight at the end of childhood GH treatment and the IGF-I response during first year of treatment in adults ( P < 0.05)
  • Potential predictive response of the final growth velocity in children to GH treatment in adulthood


Decreased life expectancy

Patients with hypopituitarism have decreased life expectancy compared with age- and gender-matched healthy people despite replacement with adrenal, thyroid, and gonadal hormones, primarily owing to cardiovascular and cerebrovascular disease. [7, 49, 50, 51] Therefore, it has been speculated that GH deficiency in patients with hypopituitarism is associated with premature mortality. [7] However, other factors potentially contribute to the increased mortality in these patients, including the following [7] :

  • Administration of cranial radiation to treat the pituitary disease
  • Use of different thyroid, gonadal, and glucocorticoid replacement regimens, including what is currently considered high doses of glucocorticoids
  • Unavailability of effective treatments for hyperlipidemia and hypertension during the survey periods



There are no published studies on the effect of GH therapy on mortality. Observational data suggest a lower mortality in those who receive GH therapy compared to those who remain untreated, but these findings may be a result of selection bias. [36]
 

Sorbate

Beta Male
Trusted Member
Growth Hormone Deficiency in Adults Treatment & Management


Medical Care

Growth hormone (GH) replacement therapy is provided in the form of human recombinant GH. This is available in subcutaneous injection form. The starting dose of GH depends on the age and clinical condition of the patient. A dose regimen that is based on age along with dose titration has been associated with less adverse effects compared with a weight-based regimen. [16] The following regimen is suggested [7] :

  • Age younger than 30 years: 0.4-0.5 mg/day (may be higher for patients transitioning from pediatric treatment)
  • Age 30-60 years: 0.2-0.3 mg/day
  • Age >60 years or those with diabetes mellitus or prediabetes: 0.1-0.2 mg/day

For patients with adherence issues, a less frequent dose regimen such as alternate days or 3 times per week using the same total weekly dosage can be used. [7]

Follow-up is usually planned at intervals of 1-2 months when the dose of GH can be adjusted by increments of 0.1-0.2 mg/day based on the clinical response, serum insulin-like growth factor-1 (IGF-1) levels, and side effects. Longer time intervals and smaller dose increments are suggested for older patients.



Serum IGF-1 levels are the main determinant for adjusting the dose of GH. No studies are available to guide this decision. A commonly used target is the upper half of the normal range appropriate for age and sex, unless significant side effects develop. [5]

Once maintenance doses of GH are achieved, follow-up is provided at intervals of 6 months. Monitoring includes clinical evaluation, assessment of side effects, and measurement of serum IGF-1, fasting glucose, and lipid profile. Quality of life (QOL) is also assessed using standardized questionnaires. If the initial bone mineral density findings, measured by dual-energy x-ray absorptiometry (DXA) scanning, are abnormal, repeat testing at intervals of 2-3 years is recommended. [5]

No studies are available regarding the optimal length of GH replacement therapy. Patients with childhood GH deficiency who attained adult height and had persistent deficiency on retesting should continue to receive GH therapy. [5]

GH therapy can also be continued indefinitely if benefits such as significant improvement in QOL and objective improvements in biochemistry and body composition are observed. If no objective or subjective benefits are seen after 1 year of treatment, discontinuation of GH therapy should be considered. [7]

How does one convert mg to iu?
 

Bagua

Moderator
Practice Essentials

The somatotroph cells of the anterior pituitary gland produce growth hormone (GH), which is stimulated by GH-releasing hormone (GHRH) and inhibited by somatostatin, both of which are produced by the hypothalamus.

GH deficiency in adults usually manifests as reduced physical performance and impaired psychological well-being. It results in alterations in the physiology of different systems of the body, manifesting as altered lipid metabolism, increased subcutaneous and visceral fat, decreased muscle mass, decreased bone density, low exercise performance, and reduced quality of life. [1]

Adult GH deficiency can be a transition from childhood-onset GH deficiency or it can be acquired during adulthood. The majority of cases are caused by pituitary tumors or by their treatment with surgery, radiation therapy, or both. Traumatic brain injury is another important cause. [2, 3, 4]

The goals of GH therapy in adults are to improve conditioning, strength, body composition, and quality of life, as well as reduce the burden of associated medical conditions such as cardiovascular disease and decreased bone mineral density.



Patients should be educated about the technique of subcutaneous injection of GH.

For patient education resources, see Thyroid and Metabolism Center as well as Growth Hormone Deficiency, Growth Hormone Deficiency Medications, and Growth Hormone Deficiency FAQs.






Etiology

The main cause of growth hormone (GH) deficiency is a pituitary tumor or the consequences of treatment of the tumor, including surgery and/or radiation therapy. Traumatic brain injury is increasingly recognized as an important cause of GH deficiency, both during the acute stage of the injury and during the rehabilitation stage. [2, 3, 4]



Causes of GH deficiency can be divided into three categories: congenital, acquired, and idiopathic. [5]



Congenital conditions are caused by genetic abnormalities or structural brain defects. Genetic abnormalities include transcription factor defects (PIT-1, PROP-1, LHX3/4, HESX-1, PITX-2), GH-releasing hormone (GHRH) receptor gene defects, GH gene defects, and GH-receptor or post-receptor defects. Structural defects include agenesis of the corpus callosum, septo-optic dysplasia, empty sella syndrome, encephalocele, hydrocephalus, and arachnoid cyst. GH deficiency can occur in association with midline facial defects such as single central incisor, cleft lip, and cleft palate.



Acquired conditions of GH deficiency include tumors of the pituitary gland or the hypothalamus and metastatic disease; surgery or radiation therapy of the pituitary or hypothalamus; infiltrative diseases such as sarcoidosis, tuberculosis, histiocytosis X, hemochromatosis, and lymphocytic hypophysitis; infarction of the pituitary or hypothalamus (which can be spontaneous or result from Sheehan syndrome); and head trauma.



In some cases, no clear etiology can be determined.










Epidemiology

An estimated 6,000 adults are diagnosed with growth hormone (GH) deficiency every year in the United States. [2] Adult GH deficiency has been estimated to affect 1 in 100,000 people annually, whereas its incidence is approximately 2 cases per 100,000 population when childhood-onset GH deficiency patients are considered. About 15%-20% of the cases represent the transition of childhood GH deficiency into adulthood. [6]



The age of presentation of acquired GH deficiency in adults often coincides with the discovery of pituitary tumors, usually between the fourth and fifth decades of life.
 

Bagua

Moderator
The last time I went for med training I was told to drop IU for a simple Unit. That was just five years ago.
If you take a look at your Insulin Syringe it will only have Unit on it.
 

DerekD

Active member
Trusted Member
Of course it would work. As far as how much that would depend on way to many factors. I think the safer alternative would be using a growth hormone secretagogue such as Ibutamoren.
 

Furius_Saturninus_Plautia

Well-known member
Trusted Member
I grew a full 3 inches from 14-15 on fucking kraft dinner and hot dogs and I was natural lol! That growth spurt was the MOST pain I've ever experienced and it lasted a full god damn year! Shorter people have no idea 😬
 

Neverwas

New member
Better question what fucking parent would put their kid on GH - script from a doctor was it - because 6 feet is really short?
Maybe he bought script GH and stuck it in his kid but ask yourself why? I will stop there as I’m getting really angry at the irresponsibility.
If you've got hoop dreams 6' is short...likely too short.

I'm not saying what he did was right but I am sure it happens a lot more than you would think.
 

Cog

Well-known member
Trusted Member
My son grew 5 inches in just under 18 months. Between 14 and 16 he grew from 5’11 to 6’4. And I don’t think he is done yet.

He also went from 145-180 lbs

No GH but he goes through a ton of steak, salmon and pizza lol

With their natural test levels at that age, if they are active and have a caloric surplus of quality protein they can grow like crazy.


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Did he get any taller?Would assume he is done.
 

Oldguyjiujitsu

OAF
Trusted Member
Did he get any taller?Would assume he is done.
Yes he appears to have stopped growing taller at 6'4. He just turned 17. He is now getting thicker by the day....he is right around 190lbs and that has been on a stead increase for the past year or so. He lifts 3 days per week on an upper/lower split. Still eating us out of house and home LOL
 
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