Category : Injectable Growth Hormone

HGH A Natural Cure for Boomer Belly and Reversal of Somatopause – Fitcommerce

Stimulating the bodys own HGH production can reverse Somatopause, remove fat, add muscle, and take years off your appearance, and perhaps extend longevity because its natures way, its safe.

Capsule: For you boomers, imagine one day a drug that will make you look 20 years younger, remove 15 lbs. of body fat, add lean muscle mass, increase your cognitive functions including memory, give you a healthier heart, increase your bone density, and elevate both your mood and your libido. Well, actually that drug is here now and its called, human growth hormone (HGH). The injecting of HGH is popular among the Hollywood cognoscenti but its expensive and risky. However, there is a way tap into this amazing fountain of youth naturally

The Long Steady Decline

O.K., so youre 60-years old and have been sedentary your whole adult life, but you weigh only 15 pounds more than you did at age 30 so youre O.K. right? Wrong.

Meet HGH, a powerful hormone that keeps us lean, young and strong and keeps all our biomarkers in the healthy range. With enough of it you can stay young and vital long into your elder years.

Unfortunately theres a pivot point right around age 30 where there is a marked drop in your bodys natural production of HGH which, if unabated, will continue to decline for the rest of your life. This condition is called somatopause.

This precipitous drop in HGH leads to a severe drop in lean muscle mass and an increase in adipose tissue especially in the belly. On average, without proper exercise people will lose 10 lbs. of lean muscle mass per decade after the age of 30.

So, the aforementioned 60-year-old may only weigh 15 more pounds, but in actuality he/she lost 30 lbs. of muscle! Add that onto the gain of 15 lbs. and he/she actually has 45 lbs. more visceral fat not a healthy condition.

Dont be depressed, there are positive actions you can take to reverse this trend of HGH loss, read on.

From Hollywood to Main Street

If you want to know whats truly hot and fashionable, look to Hollywood. Many aging actors have been regularly taking human growth hormones for years to remain thin and attractive for their careers. This was originally made known in a March 2012 article in Vanity Fair.

Although far from being a mainstream phenomenon, it is estimated that about 30,000 Americans are shooting up with HGH, a rapid rise from the estimated 2,000 that were doing so in the mid-1990s.

One of the reasons is that HGH is more readily available now that biotech companies have learned to synthesize it through recombinant DNA technology; previously the only source was natural HGH from human cadavers, an obviously rare and expensive supply.

Somatopause The Boomer Belly

Older people face a double whammy. Although they work out at the gym regularly and seem to be constantly dieting, as they age they lose more muscle mass and gain more body fat especially around the middle. Those long cardio sessions cant seem to get the midriff reduced past a certain point.

This malady is called somatopause (So-MAT-a-pause). Somatopause is signified by energy decline, weight-gain (usually around the middle, and hips), loss of muscle, and wrinkled skin. Other symptoms include energy decline, a rise in LDL cholesterol and a lowering of the good HDL.

Somatopause is related directly to the decline of HGH being produced by the body by the pituitary gland as we age. It is an extrapolation of the term menopause and applies to both men and women whose natural production of HGH started a steady gradual decline since age 30 and continues to decline for the rest of their lives.

So, it begs the question, if somatopause is caused by the bodys natural decline of HGH, what if we were to increase the HGH in our system, would that reverse its effects? By most observations, the answer appears to be yes.

It All began With a 1990 Journal of Medicine Article

The late Dr. Daniel Rudman of Madison Wisconsin along with a team of researchers made a startling discovery in July 1990. They performed experiments on men age 61 to 81 to determine if HGH could cause a reversal in symptoms were succumb to during aging.

One group was given subcutaneous injections of HGH while the control group was not. HGH cannot be measured directly because it is detectable in the blood for only a few minutes; therefore they measured a byproduct called IGF-1 (Insulin Like Growth Factor). The more IGF-1 in the system, the more HGH is there as well.

At the start, both groups averaged less than 350 U per liter of IGF-1. After 6 months, the group given the HGH injections had levels of IGF-1 in the range of 500 to 1500 U per liter, a level found at a much youthful age, while the control group still remained at the original 350 level.

What was more astonishing was that with no other variables, there was: An 8.8% increase in lean body mass A 14.4% decrease in adipose tissue, aka body fat A 1.6% increase in vertebral bone density.

It was concluded that the drop in natural HGH levels is directly responsible for much of the observable effects we call aging. And furthermore, that agings effects could be reversed if the level of HGH could be maintained at a higher elevation. This is the finding that launched a thousand ships and explains why today you get all those spam e-mails trying to sell you HGH and HGH releasers over the web. Who doesnt want the fountain of youth?

The Vanity Medicine

There are roughly 74 million baby boomers in the U.S. alone and in contrast to previous generations that have reached older age, this generation is determined to remain young and vigorous. They seem to be looking for that magic bullet, or pill they can take to keep their looks and vitality. Should that magic pill be regular subcutaneous injections of HGH cost anywhere from $500 to $1,000 per month and carry unknown health risks?

Risks of Artificial HGH

If taking a pill, or in this case an injection, for prolonged youth seems too good to be true, well, youre probably right.

A respected source about anti-aging is Dr. Nicolas Perricone, a Yale affiliated dermatologist. In his book, The Perricone Prescription, he clarified the findings of the original Rudman studies as follows:

As exciting as these results were, there was a downside. Subsequent studies using injectable growth hormone at similar doses to the first study found unacceptable side effects . . . The studies were extended to a period of a year or longer and researchers realized that prolonged supplementation could induce diabetes, arthritis or carpal tunnel syndrome, making the results very disappointingSupplementation with injectable human growth hormone is still very experimental and we have not accumulated enough data to assure its safety.

He goes on to explain that HGH is basically good, its the means of injecting high doses of HGH that causes health risks, therefore, its best to mimic our own bodys production of HGH.

Dr. Perricone goes on to say: Another very new and exciting strategy for growth hormone supplementation is to use amino acids or small peptides to trigger the bodys own release of HGH from our pituitary. This is a much safer method because we have normal feedback mechanisms and controls over a hormone when it is being produced by our own bodies.

Read our post:

The Promise of Successful Aging An Interview with Superstar Dermatologist/Nutritionist Dr. Nicolas Perricone

Luckily, there are alternative ways of raising the HGH levels without costly injections and one of those is the neighborhood gym.

Look Younger and Lose Weight with HGH The Natural Way

It is widely believed that certain forms of exercise will stimulate the bodys natural production of HGH in older adults. Since the body seldom produces compounds that will be harmful to itself, what better way to enjoy the benefits of HGH invoked youth without the health risks?

According to Phil Campbell, author of a fitness book, Ready, Set, GO! Synergy Fitness, natural HGH production can indeed be stimulated to produce outstanding physical results. He cites 160 biomedical research studies in his book.

Read our post on how to boost HGH naturally:

Stay Youthful by Biohacking Your HGH through Sprinting

His presents a new regimen which focuses on high-intensity training (HIIT). Such training, combined with proper sleep and diet, can spur the pituitary glands pulsing output of HGH. Campbell calls such HGH goosing a natural anti-aging regimen. And he stresses natural.

Anaerobic Exercise Should Be a Part of Every Fitness Routine

The focus is not on endless hours of aerobic exercise, but on the incredible benefits of anaerobic exercise on the bodys hormone release system.

Short bursts lasting 10 to 30 seconds of intense activity can induce your body to naturally release HGH growth hormone by 530%, which is the substance that keeps you looking and feeling young.

The reason older professional athletes keep playing beyond their time, is due to the anaerobic exercise that they perform during practice. Anaerobic exercise the hard and fast, sprinting types of exercise is shown by medical researchers to make the body produce significant amounts anti-aging growth hormone, says Campbell, and this keeps older players strong, lean and muscular.

Growth hormone is given to children with clinical stature growth problems to help them grow normally, says Campbell, however, it does not make adults grow taller, but it does reverse several measurable clinical factors of the middle-age spread, which has been named the somatopause by researchers.

Anaerobic exercise should be a part of every fitness routine, However, he cautions that physician clearance and a progressive build-up of the high-intensity exercise is necessary to prevent injury.


Youth and fitness are an associated pair. Conversely, pharmacology is closely associated with disease. Nature should always be preferred over drugs. Mankinds quest for the fountain of youth may lie not in a bottle or in a syringe, but in the grunts and groans of intense exercise.

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HGH A Natural Cure for Boomer Belly and Reversal of Somatopause - Fitcommerce

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National Organization for Rare Disorders Gives Batten Disease Community a Voice in Washington – Batten Disease News

Even by the standards of rare illnesses, Batten disease is extremely uncommon, affecting only two to four of every 100,000 births in the United States. That translates into 20 or so American babies born each year with the hereditary illness.

Yet no disease is too insignificant for the National Organization for Rare Disorders, or NORD, which represents those with 7,000 rare conditions that together affect an estimated 30 million Americans.

In April, the U.S. Food and Drug Administration approved Brineura (cerliponase alfa) as a treatment for children 3 and older with a Batten disease.BioMarin Pharmaceuticalsenzyme replacement therapy is for a version of the disease known aslate infantile neuronal ceroid lipofuscinosis type 2 (CLN2). Another name for the condition is tripeptidyl peptidase-1 (TPP1) deficiency.

We were excited to learn of the FDAs approval of the very first treatment for Batten disease, Paul Melmeyer, the National Organization for Rare Disorders director of federal policy, said in an interview in Washington. Yet as we understand it, it will be effective in only a small portion of those with Batten a specific genetic subset of 150 or so patients.

BioMarin said its therapy costs $27,000 per biweekly infusion, or just over $700,000 a year, to treat each of the few children born with the condition. This makes Brineura one of the worlds most expensive drugs.

While Brineura doesnt cure the condition, clinical trials have shown that it delays major symptoms. Those treated with it are able to continue walking and talking until around 6 years of age.

Now that theres an innovative treatment for a genetic subtype, we also want to be sure that the rest of the population with Batten disease will have access to therapies which may be coming down the pipeline over the next couple of years, Melmeyer said.

The suggested dose of Brineura is 300 mg, administered once every other week by intraventricular infusion into the cerebrospinal fluid, followed by an infusion of electrolytes. The whole process lasts about four and a half hours. The FDA recommends pre-treatment of patients with antihistamines with our without antipyretics [to prevent fever] or corticosteroids 30 to 60 minutes before starting the infusion.

Orphan therapies [those for rare diseases] do run the gamut of medical technologies and routes of administration, Melmeyer said. Many therapies are infused, many are blood products delivered through plasma, many are standard pills, and many are medical foods. Theres a whole lot of innovative ways to get effective treatment to individuals with rare diseases. Theyre unique and complex and the developers of these therapies have to get very creative.

The patient organizations and advocates who lobbied for passage of the Orphan Drug Act founded the National Organization for Rare Disorders in 1983. The law facilitates the development of treatments for rare diseases.

Ever since then, our role has been to support the rare disease patient organizations and act as a union of those associations, Melmeyer told Batten Disease News.

The organization operates from the fifth floor of a Dupont Circle office building that also houses the Pulitzer Center, the Carnegie Endowment for International Peace and the Embassy of Papua New Guinea.

Its 260 or so member organizations include the Batten Disease Support and Research Association.The voluntary nonprofit group, based in Columbus, Ohio, promotes the civil and human rights of people with Batten disease.

Established in 1987, the association offers referral services so that families with Batten disease can secure benefits available by law. It also maintains a database of people with Batten disease by state, nationally and internationally. And it functions as a national registry for researchers worldwide who are studying the disease.

We did a survey showing that 70 percent of our member organizations have fewer than five full-time employees, Melmeyer said. Many of them may have only one or two staffers or volunteers. Thats indicative of the level of resources, that only a handful of people are paying attention to them.

On the wall of his office are posters marking The Orphan Drug Hall of Fame drugs that has become successful therapies against rare diseases. One is for Norditropin, an injectable growth hormone that the FDA approved in August 2006. Another is for Revlimid, a multiple myeloma therapy approved in December 2005. And still another for Cystadane, an oral powder to treat homocystinuria that was approved in May 1994.

BioMarin, which is based in San Rafael, California, said most patients with CLN2 are on federal medical assistance programs such as Medicaid. The mandatory discounts the government demands drop the price by about a third, from $700,000 a year to $486,000, it said.

Weve been hearing from a lot of patients who are frustrated by the cost of these therapies, and also a lot from advocates who want us to focus more on ensuring innovation and less on what the end-stage cost is, Melmeyer told us. We see both sides of those arguments.

He added: We have been very public in our advocacy [for rare diseases insurance coverage] over the last couple of months, ever since efforts to repeal and replace the Affordable Care Act started last year. We understood it was going to take a very large effort on our part to protect our patients.

Tiny organizations such as the Batten association pay $50 a year to belong to the National Organization for Rare Disorders, while larger ones pay a few hundred dollars. The rare disease organization sometimes offers research grants, partnering with a specific disease community.

We are seeing patient organizations starting to get more and more into investing in companies, Melmeyer said. Organizations also take stakes in compounds that are being developed in return for a portion of the compounds sales when theyre approved.

For example, the Cystic Fibrosis Foundation invested from start to finish in Vertexs development of Kalydeco and Orkambi.

Melmeyer said 80 percent of rare diseases are genetic, like Batten disease, and that half the patients who have them are children.

Those who donate to the National Association for Rare Disorders are mostly individuals and foundations, with some money coming from pharmaceutical companies. The organization has a grant from the FDA to work on family history registries.

Last year, over 40 percent of the therapies the FDA approved were orphan drugs. Were very happy that is the case, Melmeyer said. Back in the 80s, wed see one, two, maybe three approved each year. In the 90s, that increased very slightly, but it didnt get to over 10 a year. Really, its only within the last 10 years or so that weve seen a substantial increase in the development and approval of rare drugs for diseases.

Melmeyer said his organization doesnt take positions on drug pricing, including what an appropriate price should be for Brineura or any other therapy.

When we look at the drug pricing debate, we are constantly weighing the two sides, he said. On one side, we need to encourage innovations for individuals with rare diseases, while, on the other, ensuring these same therapies are accessible. Its such a delicate balancing act.

He added: We have drawn a line in the sand for ourselves to not get involved. Once we do, in the interest of consistency, wed have to do that for any drug.

Melmeyer, a native of Pittsburgh, did an internship with the office of Pennsylvania Democratic Sen. Bob Casey before working on health policy issues at the Center for American Progress. He took the National Association for Rare Disorders in February 2013 as associate director of public policy. Hes been in the directors job for five months.

We believe pharmaceutical companies want to ensure that patients with the disease can access their therapy, he said. There are publicity benefits for doing so, especially for kids with a very serious disease. It looks good. But we want it because our patients dont have any other options. Many of these orphan drugs will substantially improve the quality of their lives, which is why we hope the insurance companies will see the value of these therapies.

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National Organization for Rare Disorders Gives Batten Disease Community a Voice in Washington - Batten Disease News

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Growth Hormone IGF-1 Cancer – Trans-D Tropin

Growth Hormone IGF-1 cancer

Rashid A Buttar D.O. Visiting Scientist, North Carolina State University As published in "Anti-Aging Medical Therapies, Volume 5"


The benefits of growth hormone (GH, also known as human growth hormone or hGH) have received increasing attention from not only the media but the medical profession as well, as a result of studies indicating GH may have the ability to restore a more youthful physiology and enhance the quality of life. However, there is controversy centered on the possibility that maintaining youthful GH levels may actually be harmful in the long run and may result in shortening life span by inducing cancer.

The first foundational objective essential to gaining an insight into these issues is to clearly understand the hypothalamic-pituitary axis. More often than not, we forget the physiological safety mechanisms designed within our systems to protect us. In this case, we refer to the negative inhibitory feedback loop designed to decrease or stop the release of endogenous GH when levels exceed the physiological range. This inhibitory feed back loop plays a significant role in the hypothalamic-pituitary axis and realizing its significance is vital to understanding the advantages of using growth hormone releasing hormone (GHRH) to increase endogenous GH as opposed to using exogenous GH.

This will lead to the discussion of why assessing increases in insulin-like growth factor type1 (IGF-1) as a marker of GH efficacy may not only be unreliable, but a compelling argument will be presented that the practice may be nothing more than the perpetuation of a medical myth. In fact, conclusive data from multiple sources showing that increases in IGF-1 are conducive to the propagation of oncogenesis will be presented and then supported by general physiological concepts, scientific observation and published research.

Finally, the inter-relationship of GH, GHRH, and IGF-1, as well as how each individual component correlates with incidence of cancer, will be thoroughly explained.

Keywords: Growth Hormo ne ; IGF-1; Cancer; Trans-D Tropin; Geref; GHRH analog


The benefits of growth hormone (GH, also known as human growth hormone or hGH) have received increasing attention from not only the media but the medical profession as well, as a result of studies indicating GH may have the ability to restore a more youthful physiology and enhance the quality of life. However, there is controversy centered on the possibility that maintaining youthful GH levels may actually be harmful in the long run and may result in shortening life span by inducing cancer.

Intuitively, it is obvious that naturally occurring endogenous GH released within physiological parameters itself could not possibly cause cancer. The reasoning for this statement is actually quite simple because all mammalian species achieve the maximum level of GH levels when reaching late adolescence and young adulthood. If endogenous GH were actually a cause of cancer, then all mammalian species including man would have the highest incidence of cancer during late adolescence and young adulthood. However, as we all know, this is not what occurs.

So, what then causes cancer? The answer unfortunately, is more than a little involved. We know that a minimum of 75% of all cancers have been shown to have environmental etiologies. In addition, there are certain factors that predispose individuals to have a higher propensity to develop uncontrolled cellular proliferation and induce the suppression of apoptosis, leading to oncogenesis or the formation of cancer. In addition, we know that the incidence of cancer generally occurs later in life as opposed to late adolescence and young adulthood when we have the highest levels of GH.

The first foundational objective essential to gaining an insight into these issues is to clearly understand the hypothalamic-pituitary axis. More often than not, we forget the physiological safety mechanisms designed within our systems to protect us. In this case, we refer to the negative inhibitory feedback loop designed to decrease or stop the release of endogenous GH when levels exceed the physiological range. This inhibitory feed back loop plays a significant role in the hypothalamic-pituitary axis and realizing its significance is vital to understanding the advantages of using growth hormone releasing hormone (GHRH) to increase endogenous GH as opposed to using exogenous GH.

This will lead to the discussion of why assessing increases in insulin-like growth factor type1 (IGF-1) as a marker of GH efficacy may not only be unreliable, but a compelling argument will be presented that the practice may be nothing more than the perpetuation of a medical myth. In fact, conclusive data from multiple sources showing that increases in IGF-1 are conducive to the propagation of oncogenesis will be presented and then supported by published research. This conclusion is very well supported by scientific observation, clinical data, and published research, as well as being supported by general physiological concepts - all of which will be presented later in this chapter.

Finally, the inter-relationship between GH, GHRH, and IGF-1, as well as how each individual component correlates with incidence of cancer, will be thoroughly explained. It is important however, to first discuss the common characteristics of cancer and the various treatment options available so that all readers have the same foundational knowledge essential to understanding and conceptually comprehending the material being presented.


The vast majority of cancers exhibit certain common characteristics including, but not limited to, uncontrolled cellular proliferation, suppression of apoptosis, and anaerobic metabolism. They also require a specific environmental state within the biological system. Cancer is also characterized as being an opportunistic process, inflammatory in nature, an obligate glucose feeder, and is associated at least in the early stages with a hyperinsulinemic state.

Despite the traditional methods of fighting cancer which include surgery, chemotherapy, and radiation, as well as the non-traditional treatments including nutrition, supplementation, herbs, lifestyle changes, detoxification, metabolism optimization, IV treatments, hyperthermia, immune modulation using peptides, insulin potentiation techniques, and the hundreds of other methods which can not be listed due to space constraints, the best defensive strategy against cancer remains maintaining a good offensive stance. What exactly do we mean by this statement? Remember, the process of oncogenesis begins not weeks or months before it manifests itself as cancer, but actually starts years before the cancer reaches a point where it can be diagnosed.

What this means is that it is essential to be proactive earlier in the game prior to the cancer being diagnosed. This strategy is most evident in the cardiovascular model where physicians intervene prior to the manifestation of heart disease, by managing hypertension and hypertriglyceridemia while encouraging life style changes such as reducing body fat, increasing exercise, and facilitating smoking cessation. Despite the trillions of dollars spent in the war against cancer, the mortality rate from cancer is secondary only to cardiac disease, with the incidence steadily rising. Therefore, the key to solving the issue of cancer, just as in cardiovascular disease, is prevention.


Extensive research to further the understanding of the aging process is currently being conducted at a number of leading institutions. Some of the findings from these studies show that as we age, GH levels steadily decline. The numerous potential benefits associated with GH treatments to stem this decline have generated an incredible plethora of products claiming to increase GH and IGF-1 levels. The studies necessary to validate these various anti-aging treatments as a result of this marketing surge unfortunately have not followed suit.

The answer that we seek as clinicians is how to effectively inhibit, or at least slow down the aging process and thus prevent the associated debilitating limitations, which are accepted by society as being inevitable as we grow older. The benefits of GH have increasingly received attention as a result of the ability of GH to restore a more youthful physiology and enhance the quality of life. However, controversy has centered on the possibility that maintaining youthful growth hormone levels may actually be harmful in the long run, actually shortening life span by promoting cancer. The topic of GH and cancer will be discussed in detail later but it is now becoming clear that in the quest for a longer life, we may possibly be hurting our patients by contributing to the increased incidence of cancer. We must be ever vigilant of the first rule of medicine as epitomized by Hippocrates, to Do No Harm.

Currently, there are only two clinically documented methods of increasing GH. The first method is by injecting recombinant, synthetic GH (a 198 amino acid peptide with a terminal end). There are a number of choices available to physicians who choose to pursue this method of increasing GH in their patients. The pitfalls of this choice will be clearly delineated. Tosimply summarize, the physiological safety mechanism, namely the negative, inhibitory feedback loop between the hypothalamus and pituitary is violated, leading to many potentially serious consequences.

The increased attention to the benefits attributed to GH has also given rise to hundreds of products that reportedly claim to increase GH levels. This second method of increasing GH levels is achieved by stimulating the pituitary to increase endogenous levels of GH. This technique of simulating the action of growth hormone releasing hormone (GHRH) has rapidly become a popular method, although the vast majority of products claiming to achieve these results have no scientific validity, having failed medical scrutiny.

The first foundational objective is to clearly understand the hypothalamic-pituitary axis (Figure 1). More often than not, we forget the physiological safety mechanisms designed within the biological system to protect us. In the case of GH, the reference is being made to the negative inhibitory feedback loop designed to decrease or stop the release of GH if the levels being released are beyond physiological range. This inhibitory feedback loop plays a significant role in the hypothalamic-pituitary axis and realizing its significance is vital to understanding the advantages of using GHRH manipulation to increase endogenous GH as opposed to simply injecting exogenous GH.

Although the GH injections and secretagogues (substances that cause the release of GH, including GHRH and other substances like GHRH) do offer many benefits to counteract the limitations associated with aging, the need for a safer and more effective modality of therapy has long been warranted. The necessity for a therapy offering a greater spectrum of results while providing an accelerated and rapid onset of subjective and objectively measurable efficacy, with a safer profile, a more efficient delivery mechanism, and an ease of administration leading to better patient compliance has led to the advent of many innovative and promising therapeutics. One among these has been uni que due to having created some interesting controversy as a result of going against the current fundamental understanding of the relationship between GH and IGF-1.

Figure 1. The hypothalamic-pituitary axis.

To date, there are only two GHRH analog products that have been clinically validated and scientifically studied. Both are available only via prescription. The first is Geref (NDC # 44087- 4010-1), which is marketed by Serono Laboratories, one of the largest producers of injectable growth hormone. Their product, Geref, is a 22 amino acid analog of GHRH, administered via subcutaneous injection. The second GHRH analog on the market is Trans-D Tropin (NDC # 65448-2115-1) marketed by a European company named Balance Dermaceuticals. Compared to Geref, Trans-D Tropin has the uniqueness of being the first and only GHRH analog that is administered transdermally (TD-GHRH-A). Trans-D Tropin is a polypeptide combinant, consisting of four different naturally conjugated amino acid sequences that are not recombinant in nature. Although not animal derived, these peptide combinants are also not synthetically sequenced. Rather, they are sequenced in a natural proprietary manner most easily explained as being as close to the in vivo process as we currently understand.

In an editorial review appearing in the Journal of Clinical Endocrinology (1999;50:547-556) Scott Chappel, PhD of Serono Laboratories wrote:

"Long-term stimulation of pituitary cells with GHRH will shift the GHRH/somatostatin tone by exogenous [injection] therapy to increase GHRH responsivity and pituitary GH stores. It is predicted that this therapy will reverse the chronic inhibitory state induced by long-term somatostatin domination and create an environment now responsive to the endogenous GHRH toneand allow for the normal [physiological] pulsatile GH release to reappear. This would produce a greater therapeutic benefit and a better safety profile compared with once daily injections of a bolus of recombinant GH...[the need for] repeated stimulation of GHRH receptors is required in a patient friendly formatefforts are ongoing"

From a long-term efficacy, safety, physiological, functional, and compliance standpoint, Trans-D Tropin (henceforth referred to as the trans-dermal GHRH analog or TD-GHRH-A in this chapter), appears to accomplish the goals that Chappel delineates. But some further interesting additional observations were noted during the clinical studies conducted on this TD-GHRH-A by the author, shedding light on a subject that is of great importance to any physician considering manipulation of their patient's hypothalamic-pituitary axis and vital for any patient who may be considering GH therapy as a treatment option.

It was during the initial clinical testing of this TD-GHRH-A, while undergoing the characteristic rigid scrutiny used for medical therapeutics, where the observation was made of IGF-1 deviating from the expected trend. Later, during subsequent clinical studies, the same observations were reproduced with findings being confirmed not only by other independently conducted studies but also found to be well documented within the published medical literature.

At the same time, other clinicians and researchers studying IGF-1 independent of the author, began observing and documenting similar findings. When these scientists began to report their findings starting in 1999, they enabled a greater understanding of the actual nature of IGF-1.


In 1998, we conducted a subjective study based upon the SF-36 patient outcome based research model, evaluating 30 patients taking the TD-GHRH-A. The study, which was published in published in the Journal of Integrative Medicine (2000;4:51-61), measured 22 subjective life style criteria and 5 objective criteria including overall strength, endurance, and IGF-1. Although every patient reported significant improvement in most criteria being monitored, a departure from the expected trend of IGF-1 was noted.

The observation of decreasing levels of IGF-1 prompted a second small study, this time to evaluate endogenous GH by drawing serum GH radioimmunoassays and comparing the response to changes measured in IGF-1. A total of 53 sets of serum GH levels were drawn before and after treatment, and analyzed using radioimmunoassays. IGF-1 levels were also collected at baseline and again at three weeks post treatment with the TD-GHRH-A.

Endogenous GH levels measured 90 minutes post treatment showed a 631.46% increase compared to baseline levels (Figure 2). The data was then re-evaluated using the first set of blood drawn and compared to the second set of blood drawn two weeks later in order to assess if changes in GH levels were only dose dependent or if the response were transitory in nature (Figure 3). There was also a concern that the response measured in GH would decrease after a few weeks due to desensitization or acclimatization to the TD-GHRH-A. The results were again diametrically opposed to what was expected. There was actually an improvement in GH release measured after two weeks of treatment with the TD-GHRH-A compared to first time usage. The results indicated an actual increase in sensitization or improvement in pituitary responsivity with continuous usage. This subject will be addressed in greater detail later in this chapter.

Figure 2. Effect of TD-GHRH treatment on endogenous growth hormone levels.

One of the criticisms when this data was presented was regarding the amount of change that was measured in GH levels. The increases in GH levels were felt to be insignificant since they were less than 5 ng/ml. However, the opposing argument questioned how an increase of greater than 600% within a two-week period could be considered insignificant. This argument can only be settled by defining what level of GH increase is necessary in order to achieve therapeutic benefit.

Endocrinology and physiology textbooks indicate that an absolute level of GH above 5 ng/ml is needed before efficacy can be attained. However, the "efficacy" being referred to is a "diagnostic" response (for purposes of diagnosis), not a "therapeutic" response. The "diagnostic" response would be defined as a change to elicit a response far beyond the normal physiological range by taxing and overloading the system. An example of this would be seen in the insulin and dopamine challenges done by endocrinologists to determine GH deficiency.

Figure 3. Comparison of growth hormone levels after initial treatment and after two weeks of treatment.

However, a "therapeutic" response would simply elicit a subtle response well within the normal physiological range in order to achieve a "therapeutic" effect. Although the average range of GH levels measured during this study was well below the 5 ng/ml level defining the diagnostic criteria, an increase in endogenous GH levels greater than 600% compared to baseline measurements is clinically and statistically significant. Furthermore, by keeping the levels of GH below 5 ng/ml, we experience a more physiological increase in endogenous GH as opposed to exceeding the physiological parameters achieved by exogenous, recombinant, injectable GH.

The interesting component of this study was the relationship of "increasing endogenous GH' to a concomitant measurable "decrease in IGF-1 levels' (ng/ml) on a consistent basis. TD-GHRH- A caused not only an increase in endogenous GH but also a decrease in IGF-1. If IGF-1 is an active metabolite of GH and is known to be converted in the liver from GH to one of the many growth factors responsible for normal growth, then why would IGF-1 levels decrease when the GH levels are increasing? Before discussing this important question, let's first discuss the data.

Figure 4. Serum IGF-1 levels at baseline and at three weeks post treatment with TD-GHRH-A

The IGF-1 levels reported in Figure 4 were drawn at baseline and three weeks post treatment with the TD-GHRH-A. There was over a 14% drop measured in IGF-1 levels in the males participating in the study. The female participants showed a greater drop in IGF-1 exceeding a 26% drop. The overall drop in IGF-1 was over a 20% decline in IGF-1 levels compared to baseline measurements over the three-week period. The evidence based on this study seemed to show an inverse correlation between IGF-1 and GH levels. Upon reviewing the published literature, it became clearly evident that IGF-1 and GH have at best, an unreliable correlation.


Eventually, the above mentioned data showing the increase in endogenous GH and decrease in IGF-1 became the pilot for a larger, more definitive study to determine not only the correlation between GH and IGF-1 but also to evaluate the effect the TD-GHRH-A had on cortisol, glucose, chemistry, and lipid parameters. The preliminary results of this multi-centered, double blind, placebo controlled, crossover study evaluating endogenous GH levels with serial GH radioimmunoassay levels after TD-GHRH-A administration showed some very interesting results and reinforced the earlier findings of the smaller previous studies.

The requirements for this study were stringent due to the transitory nature of serum GH so all data collection was tightly regulated in order to insure accuracy of the information collected. Patient selection criteria was simple, with age over 30 and non-gravid state being the only absolute exclusion criteria. The primary end point was eight weeks post treatment when the placebo group was scheduled to crossover into the treated group with the secondary endpoint being 16 weeks after the initiation of either treatment or placebo. The placebo (control) was completely indistinguishable from the TD-GHRH-A (treatment) with both utilizing the exact same carrier, with the same consistency, smell, color, and appearance, and with the packaging kept identical.

All control and treatment bottles were labeled with a numerical code and randomly distributed among the patient population selected for the study. The numerical codes facilitated the double blind component with supervising physicians unaware of which patients received placebo versus treatment . Study participants were scheduled for blood draws at very specific time intervals. If a study patient did not present as scheduled for blood draws, the patient was eliminated from the study. Out of 25 centers selected for participation, only eight centers completed the study, with 117 patients out of 317 patients reaching the stated endpoints without deviances from the testing schedule.

All study patients had blood drawn at specified intervals, starting with baseline GH radio- immunoassay levels as well as IGF-1, cortisol, lipid panels, and basic chemistry panels, followed immediately by administration of either the placebo in the control group or the TD-GHRH-A in the treated group. All study patients then had to have repeat blood draws at 30, 60, and 90 minutes after treatment administration. Each of these subsequent blood draws consisted of all the above mentioned serum parameters, with each set of blood draws obtained at a very specific weekly interval. If a study participant did not present at the specified time for a scheduled blood draw, they were eliminated from the study. This was the primary reason why only 117 patients completed the study.

The blood specimen analysis schedule for the treated group (on the TD-GHRH-A) was at the onset of the study, followed up again at the end of the second week, the fifth week and finally on the eighth week after study initiation. The blood specimen analysis schedule for the control group (on placebo) was at the onset of the study and then repeated at eight weeks after the initiation of the study. The blood specimens obtained during the second and fifth week blood draws in the placebo group were discarded, primarily due to the study's financial constraints but also because no significant change was anticipated in the placebo group. Only the start and the endpoint specimens, prior to the crossover point, were analyzed in the control (placebo) group. However, the blood had to be drawn in both placebo and treatment groups at the same time in order to preserve the double blind component of the study.

The percent change measured in endogenous GH levels as measured by GH radioimmunoassay in the 117 patients that completed the study were statistically significant. The change from the baseline blood draw to the blood drawn 90 minutes after the TD-GHRH-A treatment showed a 462.39% increase upon first time usage. At the end of two weeks after using the TD-GHRH-A, an increase of 815.59% in endogenous GH levels was noted, compared to baseline base line levels drawn 90 minutes earlier. By the fifth week, an increase of 1754.22% in endogenous GH was measured from baseline to 90 minutes post treatment with the TD-GHRH-A. However, by the eighth week, there was actually a drop in GH levels when compared to the fifth week, but overall, endogenous GH levels still increased over 609% over a 90 minute period compared to baseline.

The statistical analysis of the data was conducted by an independent source, showing a baseline mean of 0.295918367 with a 90-minute mean of 2.213636364 and a P value < 0.001. The baseline standard deviation was 0.464112 with the 90-minute standard deviation being 2.673173, establishing that the increase s in endogenous GH levels observed in this study were statistically significant. The most dramatic increases in endogenous GH release were measured between the 60 and 90 minute time periods post treatment, regardless of what weekly interval in the study the serum GH samples were drawn. All four time periods (initial baseline, second week, fifth week, and eighth week) clearly showed the time interval between 60 and 90 minutes as the most significant for endogenous GH release.

Figure 5. The change in endogenous growth hormone levels from baseline to 90 minutes after TD-GHRH-A treatment over an eight week period.

Although an increase in endogenous GH levels was clearly established, the decrease in GH levels at week eight compared to week five (Figure 5) was initially confusing. However, referring back to basic physiological principals, it became evident that there were only two possible postulates explaining the reason for a decrease in GH levels during the eight week of usage of the TD-GHRH-A.

The first possibility revolved around somatostatin. An increase of over 1750% in endogenous GH levels by the fifth week is a very significant increase. It would therefore logically follow that with such a tremendous increase in GH from baseline in such a short period, the negative inhibitory feedback loops would be initiated, causing the release of somatostatin from the hypothalamus in order to inhibit the release of GH by the pituitary. An increase in somatostatin (GH antagonist) would result in decreased levels of endogenous GH being released. This hypothesis based on clinical observation will be confirmed or refuted in future studies. The second postulate involves the issue of pituitary reserves. The pituitary gland holds only a limited amount of GH in store, releasing it in a pulsatile manner. Due to the effectiveness of the TD- GHRH-A, the pituitary reserves of GH may have been rapidly depleted and by the eight week, required additional time necessary for the pituitary to replenish its GH stores.

Figure 6. Serum cortisol levels obtained at baseline and 90-minutes after TD-GHRH-A administration.

As the possibilities were being entertained regarding the drop in GH observed at the eighth week compared to the fifth week in the TD-GHRH-A treated group, the placebo data was also being analyzed. The increase in GH in the treated group was measured at 1754 % at the fifth week interval but in the placebo group, although the blood was drawn, the samples were not analyzed as previously mentioned because the placebo group had the second and fifth weeks blood draws discarded. Therefore, a comparison of the fifth week data in the treated versus the placebo group could not be made. However, the data for the eighth week for both the treated group (on the TD-GHRH-A) and the control group (on placebo) were analyzed. Although this comparison did not allow for an explanation for the relative drop in GH from the fifth week to the eighth week in the treated group, it did give additional confirmation to previously conducted research unrelated to this study, further intriguing the study investigators.

The eighth week data for the treated group on the TD-GHRH-A showed 609.04 % increase in endogenous GH. However, surprisingly, the placebo group showed an increase of endogenous GH of 118.13% during the same time period. Although initially unexpected, this increase in GH in the placebo group validated previous research regarding the effect of diet and exercise on GH release. Life style modifications that all study patients were instructed to follow while participating in the study included a specific combination of aerobic and resistance exercise, as well as a high protein, low carbohydrate diet.

These findings validate some earlier independent studies showing that even without medical intervention, one can significantly increase endogenous GH levels by simple lifestyle modifications in diet and exercise. All patients in this study were crossed over into the treated group at the eighth week and subjectively followed for another eight weeks. Subjective improvements reported by patients were recorded in the form of a detailed questionnaire based upon the SF-36 patient outcome based research model, answered every two weeks by all study participants. Results correlated well with the objective data collected.

The most significant changes noted were in renal function, with bilirubin dropping 34.56% and creatinine dropping 22.23%. In addition, significant decreases were noted in serum glucose, serum cortisol and IGF-1 levels.

Figure 7. Percentage drop in serum cortisol levels over the 8-week study period.

Serum cortisol levels dropped significantly within a 90-minute interval on each consecutive blood draw (Figure 6). With the exception of a slight increase in baseline cortisol measured during the second week, all cortisol levels drawn decreased in a consistent manner. As depicted in Figure 7, cortisol levels not only dropped from baseline blood draw to the 90-minute blood draw during every occasion, but were also observed to consistently decrease throughout the study period as well. These changes in cortisol were significant for a number of reasons.

First, subjective improvements in attitude, depression, anxiety, sense of well being, ability to focus, concentration and ability to handle periods of stress were reported by a large number of patients participating in this study. These changes were reported later in the course of treatment, usually experienced by the third or fourth month of therapy. The steadily decreasing levels of cortisol correlate with the subjective response reported by patients in their patient self-assessment forms. Second, cortisol, being commonly referred to as the stress hormone, is known to have a significant inflammatory component and contributes to increased rate of aging. Reduction in any inflammatory component may have a substantial effect by reducing oxidative stress on the physiology and improving the "peak and trough" nature of cortisol, as opposed to chronically elevated levels. Reduction in serum cortisol levels was pronounced and consistent.

In addition, IGF-1 and serum Glucose levels were also noted to consistently drop (Figure 8).

Figure 8. Effect of TD-GHRH-A on serum IGF-1 and glucose levels.

The TD-GHRH-A appears to have a distinct "euglycemic" effect on serum glucose. Glucose level modulation was evidenced by glucose levels below 75 mg/dl trending up to approximately the 100 mg/dl levels while the levels above 150 mg/dl trending down to approximately the 110 mg/dl levels. Patients with Insulin-dependent diabetes mellitus (IDDM) experienced 50 to 70 mg/dl drops in serum glucose levels within 90 minutes after using the TD-GHRH-A. The IGF-1 levels were expected to drop based upon the earlier pilot study results, and were observed to drop on a consistent basis as expected.

Figure 9. Response in serum IGF-1 levels to TD-GHRH-A treatment.

The response in serum IGF-1 levels in the treated group showed a consistent and significant drop while on the TD-GHRH-A, dropping acutely within 90 minutes of administration of the TD- GHRH-A compared to baseline levels, and overall throughout the study period intervals as well. Despite endogenous GH levels increasing over 1750% by the 5 week, the mean serum IGF-1 t h levels dropped over 60 ng/ml in the treated group on the TD-GHRH-A. Figure 9 shows the consistently decreasing IGF-1 levels as the study progressed. This was the final indication that an increase in IGF-1 levels was not an appropriate method of monitoring efficacy of GH therapy.

In fact, an inverse correlation between IGF-1 and GH efficacy seemed to be established based on this data, which upon further review was well supported in published literature, current research, and in clinical observation. But further investigation revealed another component of IGF-1 that seemed to have been ignored despite extensive documentation in the medical literature. It was during this study and resulting subsequent inquiry into the IGF-1 controversy that led to the following observations, conclusions, and discovery regarding the correlation between IGF-1 and cancer. The evidence of this correlation is overwhelmingly clear and well supported.


IGF-1 insulin-like growth factor type is regarded as the most important metabolite of growth hormone, an anabolic hormone that promotes tissue growth. IGF-1 has a structure highly similar in morphology and function to that of insulin, while the receptor site of IGF-1 is indistinguishable from the insulin receptor site. Many of the effects attributed to IGF-1 are also attributable to, and overlap with, those of insulin.

Figure 10. Molecular Structure of IGF-1

The traditional view is that growth hormone is "translated" in the liver into IGF-1, and expresses its activity through IGF-1, even though it has been documented that low levels of IGF-1 are not a reliable indicator of growth hormone deficiency. Yet, many clinicians continue to use IGF-1 as a monitor of efficacy for GH treatment. The problem however is that numerous studies have shown IGF-1 to be modulated by factors completely independent from GH levels.

Many in the research arena have long felt that the chief culprits responsible for reducing life expectancy are likely to be excessive levels of insulin as well as IGF-1. In fact, excessive insulin and IGF-1 are precisely the type of pathological endocrine profiles that are observed in sedentary, obese patients. This has been reported in a number of studies, and recently confirmed in a massive National Institute of Aging study, which singled out low insulin as the best predictor of longevity in men.

All physicians treating patients with any modality used to manipulate growth hormone levels should make themselves familiar with the research on the extraordinary longevity of dwarf mice, which are deficient in IGF-1. Dr A Bartke, one of the chief investigators involved in the dwarf mouse research, was interviewed by Ivy Greenwell for the consumer oriented periodical LifeExtention Magazine (February 2001). When questioned regarding his opinion on the controversy of IGF-1, Bartke expressed that it is high IGF-1 that is likely to be harmful. Low IGF-1 correlates with longevity and is "virtually absent" from the serum of the long-lived dwarf mice according to Bartke. He stated that aiming at high IGF-1 levels might not be desirable not only in terms of life expectancy but also in those of cancer susceptibility as well. However, Bartke points out that the confusion regarding this issue is in great part, due to the difficulty and trouble with separating the effects of GH itself from those of its metabolites, specifically IGF-1. There is growing consensus that IGF-1 levels are indeed not related to GH levels. In a study published in the Journal of Metabolism Research (1999;10:576-579) , Inuki et al found that thyroid hormone modulates IGF-1 and IGF-BP3, without mediation by GH. Just a few months later, Janssen et al, published a study in the Journal of Clinical Endocrinology and Metabolism (2000:85:464-466), where the authors reported finding a direct relationship between serum levels of estradiol and IGF-1 levels, completely independent of GH levels.

Both these studies have set precedence in developing new strategies in treating cancer patients, which will be discussed in detail later in this chapter. However, before delving into the topic of IGF-1 and its relationship to cancer, it is important to review a few fundamental physiological concepts that may enhance the understanding of the nature of IGF-1.

Review of General Physiological Principals

When considering basic science physiological principals, the nature of IGF-1 becomes easier to understand and the controversy surrounding IGF-1 is removed. In order to accomplish this goal, the reader is asked to consider the following two questions and answer them before continuing to read. By answering these two questions, a logical explanation for the decrease in IGF-1 levels witnessed in the aforementioned studies will become self-evident.

Question 1: EXERCISE AND INSULIN SENSITIVITY Do sedentary people or athletes have lower glucose levels?

Exercise leads to an increase in insulin sensitivity. In other words, an increase in exercise leads to the body becoming more "sensitive" to the effects of insulin, thus requiring less insulin to accomplish the same task. The function of insulin is to drive glucose into the cell. Since exercise sensitizes the cells of the body to the effects of insulin, the body needs less insulin to drive the same amount of glucose into the cell. Thus, exercise leads to lower insulin levels by increasing insulin sensitivity.

There is also a higher efficiency in the use of glucose in individuals who exercise. This is due to a number of reasons. First, individuals who exercise have a higher metabolism because they have a greater lean body mass compared to sedentary individuals. Since it takes more energy (glucose) to maintain a greater lean body mass, i ndividuals who exercise have lower levels of circulating gl ucose. This is due to higher fuel consumption as a result of higher levels of activity, as well as a higher requirement to maintain an increased resting metabolism. The higher lean body mass plus higher levels of activity lead to more glucose usage.

Using a car as an analogy, an individual who exercises (exerciser) is like a racecar. The racecar (exerciser) has a larger engine (more lean body mass) and travels greater distances in a shorter period of time (more activity due to exercise), which leads to lower fuel levels due to increased consumption (lower glucose levels due to increased utilization). This in turn, reduces the need for a fuel injector that pushes fuel into the engine (insulin). A decrease in insulin requirements is referred to as becoming insulin sensitive.

This basic physiological concept is evidenced in clinical medicine every day. Individuals who exercise regularly have lower circulating glucose levels, and as a result require less insulin. The sedentary, obese, non-exercising patients have higher glucose levels, eventually having to increase their insulin requirements due to becoming insulin resistant. Insulin resistance is more commonly referred to as non insulin-dependent diabetes (NIDDM). Our obvious goal as clinicians should be to drive the physiology of our patients towards that of the exercising, athletic patient with lower insulin levels.

Question 2: EXERCISE AND YOUNGER PHYSIOLOGY Are people who exercise, biologically (physiologically) younger or older?

Exercise has always been considered a natural form of anti-aging or longevity therapy. From the study on the TD-GHRH-A, we know the placebo group was able to increase GH levels simply by lifestyle modifications including exercise. Other studies have also shown that exercise will increase GH. However, exercise will increase other hormones as well, including testosterone. In fact, exercise has been shown to improve the overall hormonal response within the entire biological system.

Exercise causes a decrease in blood pressure, heart rate, respiratory rate, and peripheral vascular resistance, making the system more efficient and allowing the "engine" to idle at a lower threshold. Exercise increases endorphin release, lean body mass, immunity, range of motion, endurance, stamina, libido, etc. These physiological changes induced by exercise are well established and extensively documented in the medical literature. All these responses are evidence of a younger physiology and are characteristics of younger individuals. Therefore, exercise leads to the physiology of a younger state. This is one of the primary reasons that exercise has long been recommended for better health.


The answers to our two questions at this point should be clear. The answer to the first question is that athletes have lower serum glucose levels secondary to an increase in insulin sensitivity. The answer to the second question is that exercise leads to a younger physiological age, i.e., increase in lean body mass, increase in insulin sensitivity (decrease in insulin levels), increase in GH, etc.

Now lets look at IGF-1 versus insulin. First, why is the molecule commonly referred to as IGF-1, named "Insulin-like growth factor type 1?" Insulin-like growth factor type 1 is just one of many growth factors. The polypeptide sequence of the general class of molecules referred to as IGF overall are very similar to the insulin molecule. The fact that IGF-1 is an acronym for "insulin-like growth factor type 1" should be the first indication that insulin and IGF-1 may be highly similar molecules. In fact, insulin and IGF-1 are extremely similar and have many of the same morphological characteristics, appearing to share many of the same properties and traits as one another much more so than the other insulin like growth factors

Figure 11. The Insulin-like growth factors, their receptors, and their binding proteins. SOURCE: The International Society for IGF Research website,

In Figure 11, note that the receptor site for insulin and the receptor site for IGF-1 are morphologically identical. Also note the significant difference in IGF-1 and insulin receptor sites compared to that of the IGF-2 receptor site. IGF-1 and insulin receptors appear to be completely interchangeable. Therefore, any molecule that binds to these receptor sites could also be interchangeable, indicating that insulin and IGF-1 should be able to interchangeably bind to either receptor site. All evidence indicates this theory to be correct with the findings appearing to be well confirmed on a clinical basis as well as confirmed within the didactic and research communities.


Based upon the answers to the two questions asked earlier, we can now support the conclusion that athletes have lower insulin levels and are biologically younger compared to their counterparts who do not exercise. As an example, a 79 year-old patient who exercises regularly is biologically younger than his 79 year-old sedentary counterparts. Based on this supposition, we can now logically conclude that exercise equates to a slowing down of the aging process or, a form of "anti-aging" therapy. Put another way, exercise promotes longevity.

Recognizing that exercise creates a physiological situation that results in an increase in lean body mass, an increase in GH levels, an overall increase in hormonal levels, an increase in insulin sensitivity, a decrease in physiological age and a decrease in insulin levels, we can now understand why exercise equals "anti-aging". These physiological changes represent the goal all physicians desire to achieve in all their patients. These biological parameters are what doctors strive to accomplish, regardless of a patient seeking to simply optimize their health and live a longer life or facing a life threatening chronic illness such as diabetes, heart disease, or cancer.

If we recognize that all the above-mentioned desired physiological parameters are a consequence of exercise, then it would follow that as physicians, we would want to embrace any treatment modality for our patients that would recreate the same physiological parameters achieved by exercising, i.e., creating lower glucose levels, leading to insulin sensitivity and resulting in lower insulin levels as observed in young athletes. Conversely, we would want to refrain from any treatment modality that would oppose the effects of exercise, i.e., creating higher glucose levels, leading to insulin resistance and resulting in higher insulin levels as observed in sedentary, obese, diabetic patients. As previously discussed, the problem is that IGF-1 and insulin are very similar to one another morphologically. Even more importantly, IGF-1 and insulin receptor sites are virtually identical and interchangeable.

If lower insulin levels, such as those found in young athletes, are desirable from a longevity standpoint, then wouldn't we expect IGF-1 to also be lower in young athletes? The answer of course is "yes'. This is due to one simple reason that as a result of IGF-1 and insulin being morphologically identical, these two substances generally cannot be opposed in a normally functioning biological system. If IGF-1 is high, then the insulin levels will also be high.

IGF-1 should be lower in young athletes, just as insulin levels are lower in athletes. And in fact, this is exactly what is clinically observed! The same observation is noted when insulin begins to drop in individuals who begin to exercise. We tested this basic physiological principal and applied it clinically. The above conclusions were easily verified in a small clinical study, demonstrating IGF-1 to be demonstratively lower in athletes.


In a small, outcome based study to assess IGF-1 levels in un-manipulated patients (patients who had no hormonal manipulation), the true nature of IGF-1 was clearly elucidated (Figure 12). The aged, inactive, obese subjects (sedentary group) had very high levels of IGF-1 when compared to the younger, active subjects (athletic group) who had levels as low as 88 ng/ml.

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Growth Hormone IGF-1 Cancer - Trans-D Tropin

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Retarding Aging: Injectable Growth Hormone (HGH)

Since Dr. Rudmans initial findings, a number of studies have supported the fact that HGH will retard aging, but also reverses the process as well.

Even though called Growth Hormone, the effects are not that it causes you to grow after the age of 20, but to repair and heal.

Despite comments made, Growth hormone is not used to make people muscular, but to cause a lean appearance as well as to provide recovery and healing.

Also there is a tremendous amount of confusion that Growth Hormone is a steroid. It is not a steroid, but is a chain of 191 amino acids.

And because those amino acids are readily available and can cause a secretogogue response (something that allows and encourages more growth hormone to be produced in the pituitary) we have excellent alternatives to increase growth hormone production versus using actual growth hormone therapy.

Benefits of increasing Growth hormone levels include consistent increase in lean muscle mass, loss of the belly fat, improved cardiovascular risk profile, more energy, improved memory, improved sleep and just feeling good. HGH affects almost every cell in our body and it helps to regenerate skin, bones, heart, lungs, liver and kidneys to their more youthful function.

Because HGH reduces inflammation and improves lipid profiles, the heart attack and stroke factors are diminished.

I believe that healing and repairing is the main function of HGH after the age of 20 and with aging when the HGH levels drop to critically low and dangerous values bringing those levels of IGF-1 ( best way of monitoring HGH levels and production) down to below 200, we move into a programmed annihilation mode.

And that doesnt sound very good!

Increasing HGH levels to more healthy levels will begin to restore, recover and heal our aging body. With healthy HGH levels, osteoporosis is blocked, hair growth is increased, and, and skin integrity, once healthy and now injured resulting in the aging appearance of skin with wrinkling and loss of texture, is restored to a healthy appearance.

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Retarding Aging: Injectable Growth Hormone (HGH)

Recommendation and review posted by Alexandra Lee Anderson