Growth Hormone

[Dr Pangloss]

Yes - NOT steroids. It's GH that causes the jaw, brow, head, hands, feet, gut to grow. LARGE amounts.

like sallyanne says: Large amounts.

[tribal]

my nails got really strong, hair got even CURLIER! (if that is possible!), great recovery, crazy vivid dreams.

how much were you dosing, and what time of day?

Yes - NOT steroids. It's GH that causes the jaw, brow, head, hands, feet, gut to grow. LARGE amounts.

what type of amount are we talking about for this side effect?

[AndroGrrL]

Can someone go more in-depth on dosage and such? I've never even considered GH because...well I know for my ex-bf...it was SUPER expensive...but he was on quite a bit...so I just assumed I'd be poor if I took up GH...

[sassy69]

Can someone go more in-depth on dosage and such? I've never even considered GH because...well I know for my ex-bf...it was SUPER expensive...but he was on quite a bit...so I just assumed I'd be poor if I took up GH...

For women, you're talking normally 1-2iu ED. You hear about guys using a lot more , like on the order of 6-10 iu ED. I guess unless you're a very experienced top or pro FBB, there's no reason to go > 2 iu ED. You'll also find amounts on the order of 4 iu + cause the wrist pain that people equate w/ lots of growth.

By itself it produces very subtle effects, e.g. softer hair, skin, greater sense of well-being. It's not a 'miracle drug' and its not a steroid so its not going to be promoting massive muscle growth. The whole premise is to supplement dropping natural growth hormone levels as you get older. Where "more" isnt' necessarily better , but rather to approximate the peak of your youth when your body is running optimally in terms of promoting lean muscle / not promoting fat, etc.

Combined w/ AAS, it also works to promote recovery and support the cycle.

It does cause water retention for some people, also can be sensitive to the carbs you're eating.

[Tatyana]

There is also the school of thought you don't need to take it until you are 30 as you produce a considerable amount of your own GH until then.

Like insulin, I think it is possible to manipulate GH naturally. They are opposing hormones that have an interesting effect on each other.

[tribal]

For women, you're talking normally 1-2iu ED. You hear about guys using a lot more , like on the order of 6-10 iu ED. I guess unless you're a very experienced top or pro FBB, there's no reason to go > 2 iu ED. You'll also find amounts on the order of 4 iu + cause the wrist pain that people equate w/ lots of growth.

By itself it produces very subtle effects, e.g. softer hair, skin, greater sense of well-being. It's not a 'miracle drug' and its not a steroid so its not going to be promoting massive muscle growth. The whole premise is to supplement dropping natural growth hormone levels as you get older. Where "more" isnt' necessarily better , but rather to approximate the peak of your youth when your body is running optimally in terms of promoting lean muscle / not promoting fat, etc.

Combined w/ AAS, it also works to promote recovery and support the cycle.

It does cause water retention for some people, also can be sensitive to the carbs you're eating.

best time to take it? upon waking? if you go the the gym first thing in the morning, can you do half before an half after?

[Bob Smith Jr.]

upon waking, before cardio/breakfast.

[Johnny Phenomenon]

There is also the school of thought you don't need to take it until you are 30 as you produce a considerable amount of your own GH until then.

Like insulin, I think it is possible to manipulate GH naturally. They are opposing hormones that have an interesting effect on each other.

How would you do so?

[sassy69]

best time to take it? upon waking? if you go the the gym first thing in the morning, can you do half before an half after?

What's unique about your workout time that would make you split the dose?

At the risk of regurgitating the stuff I've seen on this topic from other boards, dose it in the morning because your natural GH production peaks at night. I have no idea why whether or not you train would make a difference.

[Tatyana]

How would you do so?

1. Being slightly hungry when lifting (typical with comp prep), serious exertion on lifting

2. Waiting 20-30 min post workout to eat, with the exception of supplementing with 4-6 g of lysine

3. Going to bed slightly hungry, again supplementing with 4-6 g of lysine

[tight booty]

gh almost instantly flattens out the belly.

I would love to use it for this and for the anti aging benefits.

[sassy69]

gh almost instantly flattens out the belly. i have not experienced the arm and leg fat, i stay pretty lean in those areas year round.

In combination w/ what? Tight diet & training? I have heard people say it "melts the fat off" for years... but w/ no diet or training or in the presence of something they changed from doing absolutely nothing to doing something?

[Johnny Phenomenon]

1. Being slightly hungry when lifting (typical with comp prep), serious exertion on lifting

2. Waiting 20-30 min post workout to eat, with the exception of supplementing with 4-6 g of lysine

3. Going to bed slightly hungry, again supplementing with 4-6 g of lysine

How significant would the manipulation be? Obviously not comparable to taking exogenous amounts, but would you notice it?

[Tatyana]

I would love to use it for this and for the anti aging benefits.

There is one issue with GH. It is pretty much established in the scientific community that the GH/insulin/IGF-1 pathways is defective in most cancers (just as the loss of p53 is lost in a high percentage of cancers).

Just to be clear, I am not saying GH or IGF-1 causes cancers, however, this is the irony of GH use.

It is safer to use when you are younger, and there is a greater potential for it to accelerate cancer as you get older when it is claimed that GH levels decrease (although as I mentioned earlier, I have issues with this belief).



Study protocol: Insulin and its role in cancer
BMC Endocrine Disorders 2007,

7:10 doi:10.1186/1472-6823-7-10


K Harish (drkhari@yahoo.com)
M Dharmalingam ([email protected])
M Himanshu ([email protected])


ISSN 1472-6823
Article type Study protocol
Submission date 16 July 2007
Acceptance date 22 October 2007
Publication date 22 October 2007
Article URL http://www.biomedcentral.com/1472-


Abstract
Background: Studies have shown that metabolic syndrome and its consequent biochemical derangements in the various phases of diabetes may contribute to carcinogenesis. A part of this carcinogenic effect could be attributed to hyperinsulinism. High levels of insulin decrease the production of IGF-1 binding proteins and hence increase levels of free IGF-1.

It is well established that bioactivity of free insulin growth factor 1 (IGF-1) increases tumor turnover rate.

The objective is to investigate the role of insulin resistance/sensitivity in carcinogenesis by studying the relation between insulin resistance/sensitivity and IGF-1 levels in cancer patients. We postulate that hyperinsulinaemia which prevails during initial phases of insulin resistance (condition prior to overt diabetes) increases bioactivity of free IGF-1, which may contribute to process of carcinogenesis.


Methods / Design: Based on our pilot study results and power analysis of the same, we have designed a two group case-control study. 800 proven untreated cancer patients (solid epithelial cell tumors) under age of 50 shall be recruited with 200 healthy subjects serving as controls. Insulin resistance/sensitivity and free IGF-1 levels shall be determined in all subjects. Association between the two parameters shall be tested using suitable statistical methods.


Discussion: Well controlled studies in humans are essential to study the link
between insulin resistance, hyperinsulinaemia, IGF-1 and carcinogenesis. This study could provide insights to the role of insulin, insulin resistance, IGF-1 in
carcinogenesis although a precise role and the extent of influence cannot be determined. In future, cancer prevention and treatment strategies could revolve around insulin and insulin resistance.

Background

The association of diabetes mellitus and cancer has been reported more than 100 years ago [1]. Population studies have shown increased evidence of this
association.

Diabetes has been recognized as a risk factor for development of
breast, endometrial, colorectal and pancreatic carcinomas [2]. Breast, endometrial, colorectal and pancreatic carcinomas are best studied with regard to their association with diabetes/insulin resistance. Population studies have shown that the effects of diabetes mellitus on colorectal cancer may be mediated through mechanisms ranging from increased colonic transit time to hyperinsulinaemia.

In relation to the latter, at least in the early phase of development, type 2 diabetes mellitus is associated with increased circulating insulin concentrations [3, 4]. A large cohort study concluded that diabetes is associated with a modestly increased risk for endometrial cancer among women [5]. Future research, particularly prospective studies with biological samples, could be very helpful in answering questions aimed at clarifying these mechanisms [5]. Data suggest that type 2 diabetes might be associated with up to 10–20% excess risk for breast cancer and that it could also have detrimental effects on the natural history, diagnosis, and treatment of breast cancer [1, 6].

In the past few years both laboratory investigations and population studies have provided some circumstantial evidence that insulin growth factor biochemical derangements may contribute to carcinogenesis.

Several studies implicate hyperinsulinism, a condition that prevails prior to the onset of diabetes (part of metabolic syndrome) as candidate mediator in carcinogenesis [10].

Studies have revealed that high levels of circulating insulin decreases levels of insulin like growth factor binding protein 1 and 3 (IGFBP 1,3). Thus free IGF-1 levels increase in circulation [11, 12].


Another aspect of IGF physiology is the IGF signaling. In this signaling process, IGF-1 receptor is a predominant factor and is crucial for tumor
transformation and survival of malignant cell. It has comparatively less role in normal cell growth [13].

Thus role of IGF-1 in promoting carcinogenesis and its prognosis is
well established. Over the recent years, IGF-1 physiology has been widely studied.

The IGF system, comprises of insulin-like IGF-I, IGF-II, and IGFBPs. IGF-1 as a
growth factor plays a dominant role over IGF-2 and hence is widely studied.

Until recently, growth hormone was the only known stimulant of IGF-1 production.

Different lines of evidence suggest that the IGF/IGFBP system may be regulated by factors other than growth hormones. States of nutritional deprivation, such as starvation and protein caloric under-nutrition and type 1 diabetes mellitus, in animal models have long been known to influence the production of IGFs [14-16].

Various studies have shown that resistance to insulin action, as found in diabetic patients, has been associated with an increase IGFBP-3 protease activity, there by reducing IGFBP-3 levels [17]. Also, Insulin increases IGF-I bioavailability through IGFBP-1 suppression [14, 18, 19]. Thus there is ample evidence to suggest that insulin resistant states increase free IGF-1 levels.

Medical literature suggests that well controlled biochemical and genetic studies are required to establish the link between insulin, IGF-1, diabetes and cancer. We propose to investigate the role of hyperinsulinemia in carcinogenesis.

The primary objective of the study is to investigate the role of insulin resistance or sensitivity in carcinogenesis.

This is done by studying the relation between insulin resistance/sensitivity and IGF-1 levels in cancer patients. The secondary objective is to study the above mentioned association with organ specific cancers if possible.

Carcinogenesis is multi-factorial.


The metabolic and genetic derangements that take place during carcinogenesis may be induced by carcinogens and inherited genetic
factors. The role of either could be variable in a given case. We hypothesize that people with insulin resistance are at risk of developing cancer due to high levels of circulating IGF-1.

Such a risk would increase if other such factors are prevalent / acquired. A person with high levels of IGF-1 may be predisposed to cancer and his/her risk of developing cancer would increase with the presence of other such factors. Cancer being a non-communicable disease, with multiple risk factors,
modifiable risk factors are very few.

Controlling hyperinsulinaemia would modify one major risk factor. IGF-1 levels in body change with age. In addition, risk IGF-1 has high bioactivity on epithelial cells. Thus their role in carcinomas is of significance rather than other types of malignancies. Hence we limit our study to carcinomas of breast, GIT, liver, prostate, uterus, cervix and ovaries.
__________________

[tight booty]

Thanks for that interesting info Tatyana.