Over the past 10 to 15 years, there has been a great deal of interest in medical research on Growth Hormone. It has been used extensively, of course, for children that are short in stature.
Research over 20 years has described benefit for adults for a variety of conditions.
As science shows, Growth Hormone is produced in the brain and is a master hormone. It controls cellular reproduction in all cells of the body. In the infant and child it allows maturation of all tissues and creates size and height. As teenage comes and goes, the growth plate of the bones closes and height is set.
But, even though height is determined, GH is needed daily to keep making new cells to replace older less functioning cells. With good levels of GH, our function and appearance is at its best. With decline, however, all areas of the body decline in ability.
In some cases GH levels drop in the late 20’s and changes begin. In most these occurrences start in the 30’s.
Some of these include:
- Increased body fat, higher cholesterol and lipids
- Decreased energy and activity levels
- Changes in skin, hair, nails
- Decrease in memory, focus and concentration
- Decrease in visual acuity, focus
- Decrease in deep REM and restful sleep
- Increase in blood pressure
- Decrease in sexual desire and function
- Decrease in muscle strength and ability
- Decrease in exercise endurance and stamina
- Increase in heart, diabetes and degenerative disease risk
Unfortunately, the traditional approach to these patients involves using medications to try to change symptoms. Soon, people are on a different medication for each of many ailments. The disease is never eradicated, only prolonged, and will progress.
However, if this scenario is really understood, and growth hormone therapy is applied under physician supervision, all of the above problems can be dramatically changed.
Please look at the following articles, and those on my website under the “Article ” section about growth hormone.
Dr. Chris Calapai
Cardiac Effects of Growth Hormone in Adults With Growth Hormone Deficiency
Background— Growth hormone (GH) treatment may improvemorphological and functional cardiac parameters in adults withGH deficiency (GHD). However, clinical trials reported to dateinvolved few patients and yielded variable effects.
Methods and Results— We systematically reviewed blinded,placebo-controlled, randomized clinical trials of GH treatmentin adults with GHD and open studies in patients with GHD beforeand after GH treatment, evaluating the effects of GH on cardiacparameters assessed by echocardiography. Sixteen trials (9 blindedand 7 open), involving a total of 468 patients, were identifiedin 3 bibliographic databases.
GH dosage, duration of treatment,and study populations varied among the studies. We conducteda combined analysis of effects on left ventricular mass (LVM),interventricular septum thickness (IVS), left ventricular posteriorwall (LVPW), left ventricular end-systolic (LVESD) and diastolic(LVEDD) diameters, stroke volume, E/A ratio, isovolumic relaxationtime (IRT), and fractional shortening.
Overall effect size wasused to evaluate significance, and weighted mean differencebetween GH and control was given to appreciate size of the effect.GH treatment was associated with a significant increase in LVM:+10.8 (SD: 9.3) g (P=0.02); IVS: +0.28 (0.38) mm (P<0.001),LVPW: 0.98 (0.22) mm (P=0.05), LVEDD: +1.34 (1.13) mm (P<0.001),and stroke volume: +10.3 (8.7) mL (P<0.001). A trend towarda difference in fractional shortening was observed: +1.1 (1.1)%(P=0.06). Overall effect sizes were not significant for LVESD,E/A, and IRT.
Conclusions— GH treatment is associated with a significantpositive effect on LVM, IVS, LVPW, LVEDD, and stroke volume,as assessed by echocardiography, in adults with GHD
Growth Hormone Increases Bone Mineral Content in Postmenopausal
Osteoporosis: A Randomized Placebo-Controlled Trial
Eighty osteoporotic, postmenopausal women, 50–70 years of age, with ongoing estrogen therapy (HRT), were randomized to recombinant human growth hormone (GH), 1.0 U or 2.5 U/day, subcutaneous, versus placebo. This study was double-blinded and lasted for 18 months. The placebo group then stopped the injections, but both GH groups continued for a total of 3 years with GH and followed for 5 years.
Calcium (750 mg) and vitamin D (400 U) were given to all patients. Bone mineral density and bone mineral content were measured with DXA. At 18 months, when the double-blind phase was terminated, total body bone mineral content was highest in the GH 2.5 U group (p _ 0.04 vs. placebo). At 3 years, when GH was discontinued, total body and femoral neck bone mineral content had increased in both GH-treated groups (NS between groups).
At 4-year follow-up, total body and lumbar spine bone mineral content increased 5% and 14%, respectively, for GH 2.5 U (p _ 0.01 and p _ 0.0006 vs. placebo). Femoral neck bone mineral density increased 5% and bone mineral content 13% for GH 2.5 U (p _ 0.01 vs. GH 1.0 U). At 5-year follow-up, no differences in bone mineral density or bone mineral content were seen between groups. Bone markers showed increased turnover. Three fractures occurred in the GH 1.0 U group.
No subjects dropped out. Side effects were rare. In conclusion, bone mineral content increased to 14% with GH treatment on top of HRT and calcium/vitamin D in postmenopausal women
with osteoporosis. There seems to be a delayed, extended, and dose-dependent effect of GH on bone. Thus, GH could be used as an anabolic agent in osteoporosis.
Growth hormone inhibits signal transducer and activator of transcription 3 activation and reduces disease activity in murine colitis.BACKGROUND & AIMS: Constitutive signal transducer and activator of transcription (STAT) 3 activation promotes chronic inflammation and epithelial proliferation in murine colitis and human inflammatory bowel disease. SHP-2, through binding to the glycoprotein 130 signaling receptor, negatively regulates STAT3 activation. Growth hormone reduces disease activity and promotes mucosal healing in colitis and can activate SHP-2.
METHODS: We hypothesized that growth hormone administration would reduce disease activity in experimental colitis and that this would involve modulation of SHP-2/glycoprotein 130 association and STAT3 activation.
RESULTS: Growth hormone administration improved weight gain and colon histology in interleukin 10-null mice with colitis. Growth hormone reduced apoptosis and increased proliferation of crypt epithelial cells while increasing apoptosis of lamina propria mononuclear cells.
Growth hormone increased SHP-2/glycoprotein 130 association and reduced colonic STAT3 activation in interleukin 10-null mice and in biopsy samples from patients with Crohn’s colitis. Expression of the antiapoptotic protein bcl-2 was increased in crypt epithelial cells after growth hormone treatment. Growth hormone increased SHP-2/glycoprotein 130 binding and reduced interleukin 6-dependent STAT3 activation in the T84 human colon carcinoma and Jurkat human T-cell leukemia lines.
CONCLUSIONS: Growth hormone administration improves weight gain and reduces disease activity in interleukin 10-null mice with colitis. The improvement in disease activity is associated with increased SHP-2/glycoprotein 130 binding and reduced STAT3 activation in both murine and Crohn’s colitis. Growth hormone may be a useful therapy in inflammatory bowel disease, in terms of both improving anabolic metabolism and enhancing mucosal healing.
Truncal Adiposity, Relative Growth Hormone Deficiency, and Cardiovascular Risk
We hypothesized that endogenous GH would be reduced in healthywomen with relative truncal adiposity despite lack of generalizedobesity and that decreased GH would be associated with increasedcardiovascular risk markers. Fifteen healthy female volunteerswere divided into two groups, low truncal fat and high truncalfat, of comparable body mass index (BMI).
Age and BMI (23.7± 2.1 vs. 25.8 ± 2.8 kg/m2) were similar in thetwo groups. Trunk fat was higher in the high-truncal-fat group,as designed. Twenty-four-hour mean GH, amplitude, and basalGH concentration were 41, 32, and 36% lower, respectively, inthe high-truncal-fat group, but GH pulse frequency and IGF-Ilevels did not differ. In a stepwise regression model, trunkfat accounted for 38% of the variation of mean GH levels (P= 0.02), but neither total body fat nor BMI were significantdeterminants of mean GH in the model.
There was a strong inverseassociation between mean 24-h GH and both truncal fat and cardiovascularrisk markers, including high-sensitivity C-reactive protein.Our data suggest that visceral adiposity may be associated withreduced endogenous GH in healthy women, even in the absenceof generalized obesity, and that decreased GH secretion maybe associated with increased cardiovascular risk markers inthis population.
Growth hormone as a neuronal rescue factor during recovery from CNS injury.There is growing evidence to suggest that growth hormone plays a role in the growth and development of the CNS. Specifically, growth hormone has been implicated in promoting brain growth, myelination, neuronal arborisation, glial differentiation and cognitive function. Here we investigate if growth hormone has a role in the recovery from an unilateral hypoxic-ischaemic brain injury.
Using moderate (15 min hypoxia) and severe (60 min hypoxia) models of hypoxic-ischaemia in juvenile rats and standard immunohistochemical techniques, we found intense growth hormone-like immunoreactivity present within regions of cell loss by 3 days (P<0.05). Growth hormone-like immunoreactivity was observed on injured neurones, myelinated axons, glial cells within and surrounding infarcted tissue and on the choroid plexus plus ependymal cells within the injured hemisphere.
The pattern of immunoreactivity suggests that (a) growth hormone (or a growth hormone-like substance) is transported via the cerebrospinal fluid and (b) that growth hormone (or a growth hormone-like substance) is acting in a neurotrophic manner specifically targeted to injured neurones and glia.To test this hypothesis we treated a moderate hypoxic-ischaemic brain injury with 20 microg of rat growth hormone by intracerebroventricular infusion starting 2 h after injury (n=12/group).
After 3 days the animals were killed and the extent of neuronal loss quantified. Growth hormone treatment reduced neuronal loss in the frontoparietal cortex (P<0.001), hippocampus (P<0.01) and dorsolateral thalamus (P<0.01) but not in the striatum. This spatial distribution of the neuroprotection conveyed by growth hormone correlates with the spatial distribution of the constitutive neural growth hormone receptor, but not with the neuroprotection offered by insulin-like growth factor-I treatment in this model.
These results suggest that some of the neuroprotective effects of growth hormone are mediated directly through the growth hormone receptor and do not involve insulin-like growth factor-I induction.In summary, we have found that a growth hormone-like factor increased in the brain in the days after injury. In addition, treatment with growth hormone soon after an hypoxic-ischaemic injury reduced the extent of neuronal loss. These results further suggest that a neural growth hormone axis is activated during recovery from injury and that this may act to restrict the extent of neuronal death.