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For many years, Human Growth Hormone (HGH) has been evaluated by the cardiovascular community with increasingly positive and beneficial findings. Despite these studies substantiating the possible beneficial effects of hormonal therapy in treating heart disease, it appears most cardiologists fail to recognize its importance (1). Data has shown HGH to be a very important endogenous substance in development of embryonic heart tissue(2). Much of the recent cardiovascular research has centered on its benefit with congestive heart failure (CHF). It has also gained significant media attention surrounding its use in cardiovascular performance enhancement and anti-aging efforts. The logical question remains, whether or not the reduction in HGH, either naturally with age or from cardiovascular disease states, and subsequent pharmacologic replenishment, might reduce cardiovascular deterioration or possibly extend quality of life.
There is clear reduction in the pulsatile secretion of growth hormone as measured by IGF-1, seen throughout the human life cycle, beginning in the 30's and 40's. This reduction in IGF-1 is important because HGH and other somatomedins under the effect of the hypothalamus are known to stimulate myocytes or the heart muscle cells. This myocyte stimulation causes an increase in cardiac contractility or heart strength. Additionally, IGF stimulation of nitric oxide causes increased coronary blood flow. These effects combined with the relaxation and increased performance of peripheral tissue cause IGF-1 to be a potent cardiovascular neuromodulator.
The traditional wisdom used to be that the cardiac tissue was end-differentiated thus, unable to regenerate new tissue. Now with the stem cells, cardiac tissue is being actively regenerated in clinical use. This growth potential of the heart is ushering a new era. The increase in endothelial factors and contractility based on calcium regulation seems to be regulated at least in part, by the IGF-1 axis after HGH pulsatile endogenous secretion. Subsequently, the increase in left ventricular mass and contractility as well as the ability to reduce peripheral arterial resistance causes clear cardiac improvement (3). The opposite situation with HGH is also true. Thus, in the absence of HGH, disease states such as Acromegaly, often shows cardiac deterioration and often contributes to mortality.
Currently, HGH supplementation is being researched as a cure for CHF, in the cardiovascular community. Naturally occurring hormones such as Testosterone, DHEA and IGF-1 are all shown to be reduced in significant CHF. The cause or effect of this is yet unknown. However, when blood levels of naturally occurring anabolic hormones (more when combined) are reduced, it becomes an independent risk factor for poor prognosis in CHF patients. In fact, cardiac cachexia is a state whereby full body muscle wasting is thought to occur due to the weakness of the cardiac muscle. HGH has been considered in many forms of cachexia, thus logical to consider its role in its most lethal form.
CHF has long been known to show distinct neurohormonal imbalances that work together to worsen a patient’s condition and prognosis. In fact, the renin-angiotensin system was described by many, including Starling, to begin a cascade of factors that led to worsening heart failure. This led to the basis of the first effective heart failure treatment with ACE inhibitors and Beta Blockers (4). However, of the 5.5 million people with significant heart failure, very few actually show significant improvement in their disease process. In spite of internal defibrillators, aggressive nursing home management, and other high tech tools, nothing has been shown to effectively reduce hospital readmission rates, or the progression of CHF. Only Heart Transplant, offered to approximately 2,200 patients per year, has shown to improve and not just slow the progression of CHF.
When HGH was studied and given to patients with CHF, it appears that most cardiac parameters improved an impressive 34 to 47% (5) including myocyte hypertrophy. Unfortunately, these studies are new and small but have caught the attention of many prominent investigators. Myocyte hypertrophy indirectly has been shown to improve scar tissue previously thought to be non-viable.
HGH supplementation demonstrated improvement in exercise capacity in CHF patients (6). and this improvement reversed 3 months after the HGH was removed. Actual survival benefits in rats were seen with HGH supplementation vs. placebo after having ischemic heart disease. An increase in capillary density was also seen thus, suggesting improved circulation with HGH. Thus, these smaller studies showing improvements in a variety of parameters, suggest combining all the data and into a met analysis to show that HGH might have very important benefits for heart health.
Finally, from an anecdotal perspective, I often treat patients with cardiomyopathy. After treatment with anabolic hormones (by doctor’s familiar with bio-identical hormone replacement) and careful monitoring, I have observed the CHF being completely resolved and the symptoms often completely abate. The root cause of the cardiomyopathy (usually hypertension or coronary artery disease) was then aggressively treated with conventional therapies. Other non-invasive novel therapies that improve nitric oxide, such as external counterpulsation (ECP) have been used either alone or in combination with bio-identical hormone replacement, with promising results in our clinical practice (7).
In summary, increasingly, scientific data exists suggesting that bio-identical hormone replacement might be crucial in maintaining adequate heart health and improving the lives of people already suffering from cardiovascular disease. Many cardiologists have seen the futility of existing therapies in this disorder that is killing hundreds of millions of people worldwide. Therefore, cautious use of bio-identical hormones in select patients under careful physician guidance, might benefit patients and our society, as studies are further developed to confirm these hypotheses. For many patients, the time required for the medical establishment to have enough studies and enough momentum for general consensus might be too long to delay such treatment. Clearly, in many cases of CHF, with limited treatment options, HGH might be an innovative and effective solution.
There is clear reduction in the pulsatile secretion of growth hormone as measured by IGF-1, seen throughout the human life cycle, beginning in the 30's and 40's. This reduction in IGF-1 is important because HGH and other somatomedins under the effect of the hypothalamus are known to stimulate myocytes or the heart muscle cells. This myocyte stimulation causes an increase in cardiac contractility or heart strength. Additionally, IGF stimulation of nitric oxide causes increased coronary blood flow. These effects combined with the relaxation and increased performance of peripheral tissue cause IGF-1 to be a potent cardiovascular neuromodulator.
The traditional wisdom used to be that the cardiac tissue was end-differentiated thus, unable to regenerate new tissue. Now with the stem cells, cardiac tissue is being actively regenerated in clinical use. This growth potential of the heart is ushering a new era. The increase in endothelial factors and contractility based on calcium regulation seems to be regulated at least in part, by the IGF-1 axis after HGH pulsatile endogenous secretion. Subsequently, the increase in left ventricular mass and contractility as well as the ability to reduce peripheral arterial resistance causes clear cardiac improvement (3). The opposite situation with HGH is also true. Thus, in the absence of HGH, disease states such as Acromegaly, often shows cardiac deterioration and often contributes to mortality.
Currently, HGH supplementation is being researched as a cure for CHF, in the cardiovascular community. Naturally occurring hormones such as Testosterone, DHEA and IGF-1 are all shown to be reduced in significant CHF. The cause or effect of this is yet unknown. However, when blood levels of naturally occurring anabolic hormones (more when combined) are reduced, it becomes an independent risk factor for poor prognosis in CHF patients. In fact, cardiac cachexia is a state whereby full body muscle wasting is thought to occur due to the weakness of the cardiac muscle. HGH has been considered in many forms of cachexia, thus logical to consider its role in its most lethal form.
CHF has long been known to show distinct neurohormonal imbalances that work together to worsen a patient’s condition and prognosis. In fact, the renin-angiotensin system was described by many, including Starling, to begin a cascade of factors that led to worsening heart failure. This led to the basis of the first effective heart failure treatment with ACE inhibitors and Beta Blockers (4). However, of the 5.5 million people with significant heart failure, very few actually show significant improvement in their disease process. In spite of internal defibrillators, aggressive nursing home management, and other high tech tools, nothing has been shown to effectively reduce hospital readmission rates, or the progression of CHF. Only Heart Transplant, offered to approximately 2,200 patients per year, has shown to improve and not just slow the progression of CHF.
When HGH was studied and given to patients with CHF, it appears that most cardiac parameters improved an impressive 34 to 47% (5) including myocyte hypertrophy. Unfortunately, these studies are new and small but have caught the attention of many prominent investigators. Myocyte hypertrophy indirectly has been shown to improve scar tissue previously thought to be non-viable.
HGH supplementation demonstrated improvement in exercise capacity in CHF patients (6). and this improvement reversed 3 months after the HGH was removed. Actual survival benefits in rats were seen with HGH supplementation vs. placebo after having ischemic heart disease. An increase in capillary density was also seen thus, suggesting improved circulation with HGH. Thus, these smaller studies showing improvements in a variety of parameters, suggest combining all the data and into a met analysis to show that HGH might have very important benefits for heart health.
Finally, from an anecdotal perspective, I often treat patients with cardiomyopathy. After treatment with anabolic hormones (by doctor’s familiar with bio-identical hormone replacement) and careful monitoring, I have observed the CHF being completely resolved and the symptoms often completely abate. The root cause of the cardiomyopathy (usually hypertension or coronary artery disease) was then aggressively treated with conventional therapies. Other non-invasive novel therapies that improve nitric oxide, such as external counterpulsation (ECP) have been used either alone or in combination with bio-identical hormone replacement, with promising results in our clinical practice (7).
In summary, increasingly, scientific data exists suggesting that bio-identical hormone replacement might be crucial in maintaining adequate heart health and improving the lives of people already suffering from cardiovascular disease. Many cardiologists have seen the futility of existing therapies in this disorder that is killing hundreds of millions of people worldwide. Therefore, cautious use of bio-identical hormones in select patients under careful physician guidance, might benefit patients and our society, as studies are further developed to confirm these hypotheses. For many patients, the time required for the medical establishment to have enough studies and enough momentum for general consensus might be too long to delay such treatment. Clearly, in many cases of CHF, with limited treatment options, HGH might be an innovative and effective solution.
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