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common knowledge that growth hormone (GH) and insulin-like growth factor-1 (IGF-1)
are some of the agents used by bodybuilders and athletes. These agents are banned
from being used by athletes in most international sport federations, including
the International Olympic Committee (IOC). Since about 1990, the use of these
agents has increased tremendously because of their potential use in anti-aging
therapies. Reports of gains in lean body mass and strength with concurrent loses
in fat mass have created even more interest in the general public. Supplement
companies, sensing the public demand for GH and IGF-1, have released all kinds
of supplements that allegedly elevate these anabolic hormones. Unfortunately in
most cases the claims are made while drawing the reader’s attention to studies
on GH instead of research that involves the GH releasing products directly. In
most cases supplements that are alleged to elevate GH and IGF-1 do not hold up
to scientific scrutiny. Growth Hormone and Insulin-Like
Growth Factor-1 Human growth hormone (hGH) is a protein hormone secreted
into the blood by the anterior pituitary gland. It is the major hormone responsible
for growth in humans after birth. It acts on a variety of tissues including bone,
cartilage and muscle. While most people know of its anabolic actions, many don’t
know that it is also involved in carbohydrate and lipid metabolism through interactions
with other hormones [1]. Primarily two hormones produced in the hypothalamus modulate
the secretion of GH: Somatostatin, and growth hormone releasing hormone (GHRH).
GH, in turn, stimulates the liver to produce IGF-1. This is referred to as the
GH/IGF-1 Axis. The diagram below illustrates this process. --------Hypothalamus-----------
---------I----------------I------------ Somatostatin---GHRH-------- ---------I
(-)-------------I (+)------- --------Anterior Pituitary------- ----------------
GH ---------------- ------------------ I (+) ------------- ----------------Liver---------------
------------------ I ------------------ --------------- IGF-1-------------- What
is not evident from the diagram is that GH and IGF-1 exert a negative feedback
on their own future production. This means that as GH and/or IGF-1 levels increase,
GHRH levels will decrease, resulting in less GH/IGF-1 being produced. This makes
it very important to accurately measure GH/IGF-1 levels and use the appropriate
diagnosing criteria to determine if GH/IGF-1 therapy is appropriate. Giving exogenous
GH or IGF-1 to people with normal levels of these hormones will result in decreased
endogenous production of these hormones. A number of factors can stimulate
GH, including exercise, deep sleep, hypoglycemia, fasting, a high protein meal,
and the infusion of amino acids. Growth hormone was originally used in the treatment
of growth hormone- deficient children. It was prepared by extraction from cadaver
pituitaries and/or rhesus monkeys. High demand placed the agent in extremely short
supply, so pharmaceutical companies searched out alternative methods of producing
GH. Growth hormone is now produced by recombinant DNA techniques and referred
to as recombinant human growth hormone (rhGH). IGF-1 is a protein hormone
produced by the liver in response to GH. Once produced it travels in the blood
and can exert anabolic actions on a variety of tissues. It is also produced by
various cells in the body and acts locally. At the local level, IGF-1 secreted
by muscle cells (or other cells) can act on adjacent cells or on the cell secreting
the IGF-1. It can stimulate protein synthesis resulting in an increase in cell
size and/or cell number. Like GH, it can also be produced by recombinant techniques. Anti-Aging
Protocols More and more physicians are now jumping on the longevity
bandwagon. It provides a nice source of income for them (especially if they sell
the GH) and allows them to work with higher functioning patients in an outpatient
setting. This is still a relatively young area of medicine and unfortunately there
are lots of inexperienced physicians practicing in this area. If you are searching
for a longevity physician, find out how long the doc has been practicing and ask
for references. Standardized guidelines for determining proper function of the
GH/IGF-1 Axis should be followed, and hormone levels should be obtained prior
to initiation of GH therapy. Ideally, GHRH levels should also be obtained. If
GHRH is low, ask your physician to try GHRH, GHRP-6, and/or hexarelin first. These
agents will stimulate endogenous GH and IGF-1 levels in some people, but not all.
If these agents don’t work after 2-3 months of treatment, your physician
should be able to determine their ineffectiveness and then will most likely proceed
to using GH. Lift weights and follow a healthy diet, which includes 5 or more
servings of fruits and vegetables each day. Follow-up visits should include assessment
of body composition, blood glucose levels, and insulin levels to verify that insulin
sensitivity is not declining. Glycerylphosphorylcholine
(GPC) GPC is used in the treatment of amnesia and cognitive disorders.
A 1000-milligram (mg) injection of GPC elevated plasma choline levels for 15-30
minutes [2]. The plasma levels of choline remained elevated for up to 6 hours.
From experiments on rats, researchers have shown that GPC increases acetylcholine
levels in the brain. An increase in this neurotransmitter serves to inhibit somatostatin.
Somatostatin lowers GH levels. By decreasing somatostatin, GPC could indirectly
elevate GH. Another interesting property of GPC is that it serves as a precursor
for the synthesis of phosphatidylcholine. This has been speculated to lead to
changes in the cell membranes of anterior pituitary cells that enhance the stimulatory
effect of growth hormone releasing hormone (GHRH) on GH release. In 1992,
the effects of GPC on younger and older subjects were studied [3]. Alpha-glycerylphosphorylcholine
stimulated GH in both groups. GHRH also increased GH levels in both groups. However,
when GPC and GHRH were combined, the resulting increase in GH levels was even
greater than either agent alone. Given this evidence, GPC looks like a viable
supplement to try. There are a few problem areas, though. The first is that the
1000 mg of GPC was injected. By itself, GPC did not increase GH levels very much.
While injectable GPC enhanced the effect of GHRH on stimulating GH, there are
no published studies on oral GPC and GH release. However, my lab was recently
contracted to test a GH releasing product called Ageless Growth from a company
called Ageless Options. This product contains GPC along with some other supplements.
The results were submitted at an upcoming scientific conference. While the rest
of the world waits to find out about the study, I was asked to share my results
with the readers of Natural Muscle magazine. Below is a graph of the effects of
Ageless Growth on the GH levels of one of our research subjects. His growth hormone
levels increased 80 times after taking the supplement. These are the most impressive
results I have seen so far for a GH-releasing supplement. If you are serious about
wanting to increase your growth hormone levels this is the only product I would
recommend at this point in time.

About the Author: Tom is a
scientist, nutritionist, writer, and athlete. He is currently the Director of
Performance Research and Nutrition at Athletes’ Performance – a world
class training facility for athletes. Contact him via: www.thomasincledon.com
References 1. Adamson, U. and E. Cerasi, Acute effects of exogenous growth
hormone in man: time- and dose-bound modification of glucose tolerance and glucose-induced
insulin release. Acta Endocrinologica, 1975. 80(2): p. 247-261. 2. Gatti,
G., et al., A comparative study of free plasma choline levels following intramuscular
administration of L-alpha-glycerylphosphoryl-choline and citicoline in normal
volunteers. International Journal of Clinical Pharmacology, Therapy, & Toxicology,
1992. 30(9): p. 331-335. 3. Ceda, G., et al., alpha-Glycerylphosphorylcholine
administration increases the GH responses to GHRH of young and elderly subjects.
Hormone & Metabolic Research, 1992. 24(3): p. 119-121.
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