20mcg each side. 30 each side in the quads. That's plenty. Now, you won't see major, immediate LBM increases, but THAT IS NOT WHAT IGF-1 IS FOR. That's what anabolic steroids are for. 40-50mcg total will let you get plenty of hyperplasia, not grow your intestines too much, and save you plenty of $. The newly added muscle cells will take months to grow, but they will, and you will use IGF-1 again because it gets reasonably inexpensive with such a protocol.
At the end of the day, when it comes to longevity, dietary fat seems to be the odd man out, as limiting it does not appear to extend lifespan.35 Interestingly, when the protein versus carbohydrate wars are being waged, there seems to be a mysterious void of any discussion including fat. So, while generally speaking, dietary carbohydrates most strongly stimulate insulin and protein most strongly stimulates IGF-1, fat remains the odd man out. Along these lines, when scientists create a strain of mice with a mutated insulin receptor and feed them a high-fat diet, they live significantly longer.36

Rhonda Patrick gives a succinct and powerful case for an IGF trade-off:  Better physical and mental performance vs shorter life span. She hints that you might be able to get the benefits without the costs with natural means of enhancing IGF:  physical exercise and saunas.  Physical Exercise is a safe bet, because we know there is a net benefit for longevity, as well as abundant health benefits in the here and now.  Saunas (“hyperthermic conditioning”) also boost the body’s own HGH without injecting anything.  Heat shock has a hormetic benefit for life span in rodents and especially in worms; but I know of no epidemiological evidence linking the result to either a longer or shorter life span in humans.

This entry was posted in Exercise, Personal System Biology and tagged aging, antioxidants, centenarians, dark chocolate, diet, EGCG, epigenetics, executive function, fitness, growth hormone, hormesis, IGF-1, insulin-like growth factor 1, longevity, neurogenesis, peak performance, polyphenols, Rhonda Patrick, sauna therapy, strength conditioning, turmeric, verbal memory, weight loss on September 4, 2013 by Rhonda Patrick, Ph.D.
"Rats that were given IGF-1 and did nothing were bigger and stronger than rats that weren’t given IGF-1 but exercised. And I’ll bet you guessed that rats that were given IGF-1 and exercised were the biggest, strongest rats in the house. The positive effects of IGF-1 on the rats continued for months after the rats stopped getting the supplemental hormone, whereas the exercising rats immediately lost size and strength as soon as they stopped exercising.”
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The intricate balance of leucine and protein is best exemplified by cachectic cancer patients. Cachexia, a state of severe muscle loss, weakness, fatigue, and anorexia, is often seen in cancer patients and is difficult, if not impossible, to combat. Even consuming massive amounts of calories often fails to offset the potentially lethal loss of muscle mass. As a result, leucine supplementation has been a potential target to offset this muscle loss. Yet, recent animal studies – limitations aside – have shown that leucine supplementation may fuel pancreatic cancer growth.84
During puberty, IGF is the most responsible for the natural muscle growth that occurs during these few years. There are many different things that IGF does in the human body; among the effects the most positive are increased amino acid transport to cells, increased glucose transport, increased protein synthesis, decreased protein degradation and increased RNA synthesis. 
Overall, it seems that restricting calories daily to a short window of time might be metabolically beneficial in the absence of significant calorie or protein restriction. In combination with a diet with adequate protein and resistance exercise, it seems to promote favorable changes in body composition and improve metabolic markers related to inflammation. The combination of IF and CR might be synergistic, while the effects of longer daily fasting periods with a shorter eating window is unknown.
The main way that circulating IGF-1 is believed to kick-start muscle growth is by binding to its receptor found on the membrane of muscle cells, where it sets off a cascade of events that leads to an increase in muscle protein synthe-growth. Binding IGF-1 to its receptor also decreases muscle protein breakdown. Muscle protein is constantly being shredded and built up. A decrease in muscle protein breakdown with a boost in its buildup (synthesis) leads to growth.[2]

IGF-1 and IGF-2 are regulated by a family of proteins known as the IGF-Binding Proteins. These proteins help to modulate IGF action in complex ways that involve both inhibiting IGF action by preventing binding to the IGF-1 receptor as well as promoting IGF action possibly through aiding in delivery to the receptor and increasing IGF half-life. Currently, there are six characterized IGF Binding Proteins (IGFBP-1 to IGFBP-6). There is currently significant data suggesting that IGFBPs play important roles in addition to their ability to regulate IGFs. IGF-1 and IGFBP-3 are GH dependent, whereas IGFBP-1 is insulin regulated. IGFBP-1 production from the liver is significantly elevated during insulinopenia while serum levels of bioactive IGF-1 is increased by insulin.
Jump up ^ Sorenson EJ, Windbank AJ, Mandrekar JN, Bamlet WR, Appel SH, Armon C, Barkhaus PE, Bosch P, Boylan K, David WS, Feldman E, Glass J, Gutmann L, Katz J, King W, Luciano CA, McCluskey LF, Nash S, Newman DS, Pascuzzi RM, Pioro E, Sams LJ, Scelsa S, Simpson EP, Subramony SH, Tiryaki E, Thornton CA (November 2008). "Subcutaneous IGF-1 is not beneficial in 2-year ALS trial". Neurology. 71 (22): 1770–5. doi:10.1212/01.wnl.0000335970.78664.36. PMC 2617770. PMID 19029516. Lay summary – newswise.com.
The Institute of Medicine (IOM), which is tasked with the nearly impossible job of creating the Dietary Reference Index recommends 0.8 g per kg body weight daily, or 0.36 g/lb. For a 185-pound male, this would be about 67 g of protein per day, which is much smaller than the amount eaten by your average American. The IOM must take politics, dogma, science, and political pressure, blend them all together, and somehow come up with dietary recommendations for everyone. Regardless, it’s the best we’ve got. Keep in mind, this is also recommended for the average American, of whom less than 20% actually achieve the daily recommended amount of exercise. While it is reasonable to consume between 0.8-1 g/kg of protein per day (0.36-0.59 g/lb),102 most of us eating a reasonable diet – especially if we are exercising and lifting weights – may not need to worry too much about protein.
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Specific IGF-binding proteins (IGF-BPs) that do not recognize insulin also regulate IGF-I activity. Chondrocytes at different stages of differentiation express IGF-I and IGF receptors and different arrays of IGF-BPs, providing a unique system by which IGF-I can exert different regulatory effects on these cells. IGF-BP-2 is a positive regulator that increases proteoglycan synthesis in chondrocytes, whereas binding of IGF-BP-3 to IGF-I negatively regulates the anabolic functions of IGF-I. IGF-BP-3 may also directly inhibit chondrocyte proliferation in an IGF-independent manner.
A typical IGF-1 cycle will last four weeks and will yield the best results when stacked with anabolic androgenic steroids which amplify its effects. The thing to remember with IGF-1 is you’re unlikely to see specular results; it’s the cherry on the cake for advanced trainers who are happy to see half a pound to a pound of quality muscle gained per week and expectation of long-term benefits.
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IGF-1 is produced by the liver and skeletal muscle as well as many other tissues in response to GH stimulation. IGF-1 mediates many of the actions of GH, stimulating the growth of bones and other tissues and promoting the production of lean muscle mass. Since GH is released into the blood in pulses throughout the day, it is difficult to interpret the results from a single GH test. IGF-1 mirrors GH excesses and deficiencies, but unlike GH, its level is stable throughout the day. This makes IGF-1 a useful indicator of average GH levels. The IGF-1 test is therefore often used to help evaluate for GH deficiency or GH excess.
Even if one assumes that the IF group was in significant calorie deficit, the degree of IGF-1 reduction in such a short time and with the amount of protein is remarkable. As mentioned in the other post, comparable reductions have only been observed after 3 cycles of a Fasting-Mimicking Diet(13%) or reducing protein from 1.67 g/kg to 0.95 g/kg for 3 weeks (22%), the latter being the most effective.
IGF-I was first described as somatomedin C, a serum factor controlling sulfate incorporation by articular cartilage in vitro, and it was later found to have the specific capacity to stimulate or maintain chondrocyte phenotype in vitro by promoting the synthesis of type II collagen and aggrecan. IGF-I is a competence factor for cell proliferation that is categorized more appropriately as a differentiation factor because its limited mitogenic activity seems to depend on the presence of other growth factors, such as FGF-2, a progression factor. IGF-I is considered an essential mediator of cartilage homeostasis through its capacity to stimulate proteoglycan synthesis, promote chondrocyte survival, and oppose the activities of catabolic cytokines in cooperation with other anabolic factors such as BMP-7. IGF-I and insulin can activate cell signaling via the IGF-I tyrosine kinase receptor or the type I insulin receptor at concentrations proportional to their binding affinities.67

IGF-1 is part of an ancient signaling system that promotes growth and depresses life span across many species.  The system includes insulin, a protein structurally very similar to IGF-1 (hence the name).  Insulin is a mediator of life span regulation through food, exercise and the energy metabolism.  Some proteins carry instructions in the blood; they attach to receptors on the surface of a cell and tell the cell what to do.  Others get inside the cell and play a more direct role in the chemistry.  IGF-1 does both.  It has “both endocrine and autocrine functions”.


Stressing our muscles with weights leads to the anabolic process of muscle growth, and this hypertrophy follows increases in IGF-1 production within the exercised muscle.65 The key word is within the exercised muscle. Much like the increase in the “inflammatory” hormone IL-6 that accompanies exercise, systemic levels do not always correlate with local levels within the muscle. Even stretching our muscles increases in IGF-1 production within the stretched muscle.66
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Insulin-like growth factor-1 (IGF-1) and growth hormone are hormones that are vital for normal bone and tissue growth and development. GH is produced by the pituitary gland, a grape-sized gland located at the base of the brain behind the bridge of your nose. GH is secreted into the bloodstream in pulses throughout the day and night with peaks that occur mostly during the night. IGF-1 is produced by the liver and to a lesser degree by skeletal muscles, primarily in response to GH stimulation. It mediates many of the actions of GH, stimulating the growth of bones and other tissues and promoting the production of lean muscle mass. The blood level of IGF-1 mirrors GH levels. However, unlike GH the blood IGF-1 level is stable and does not fluctuate throughout the day. 
Now, the IGF-1 from insulin & gh - growth hormone (somatropin) - is not long R3 IGF-1, it's hIGF-1. It's different and possibly the effects are somewhat different than when using Long R3, especially with regards to IGF-1 losing effectiveness, which is likely much lesser with the liver-synthesized IGF-1 than with the Long R3. No studies proving this, it is theory at this point and such a study will possibly never be made, for many good reasons. One reason why hIGF-1 loses effectiveness less quickly is its half-life, or its very limited ability to run around the body and saturate all receptors everywhere. And here we join up with the EOD and E3D protocols which state that letting the body rest is extremely important to continued results. You get the same effect out of insulin & gh - growth hormone (somatropin) - because of IGFBP3 that mops up the IGF-1 within minutes of synthesis, which makes it impossible to saturate the receptors and lets them rest. Similar effect, completely different way of achieving it.
Function Important for growth/development in children and adults. Vital role in anabolic processes in general. Important functions in osteogenesis, axonal generation in nerves, nerve regeneration after ischemic insult, muscle repair and hypertrophy after trauma or exercise (Cheng et al., 2006). Although still under investigation, studies suggest that individual isotype/binding protein combinations manifest in response to specific environmental interactions or physiological demands. In addition, the binding proteins are critical for maintaining the bioavailability of the IGF-1. The unique IGF-1/IGF-1 receptor complex will then signal the protein cascade necessary for tissue metabolism or regeneration. Ischemic damage to the brain illustrates how this concept materializes. Cytotoxic edema and inflammatory markers induce the transcription of a specific isotype; which then binds to a tissue specific binding protein; protecting the integrity of the protein and preventing its renal clearance. The distinctive IGF-1/IGF-1R complex will then activate the protein kinase cascade necessary for axonal regeneration.
Adiponectin has also been reported to have antiatherogenic effects (Funahashi et al. 1999, Ouchi et al. 1999). In addition, adiponectin exhibits cardioprotective activity in ischemic heart disease through AMPK and cyclooxygenase 2 pathways (Shibata et al. 2005). (…) Adiponectin also has anti-inflammatory effects that contribute to its protective role against metabolic stress in obesity. Adiponectin suppresses TNFα production in obese mice (Xu et al. 2003a), and adiponectin-deficient mice have high levels of TNFα in adipose tissue (Maeda et al. 2002). Low levels of plasma adiponectin are associated with C-reactive protein in humans (Ouchi et al. 2003). Adiponectin enhances the clearance of apoptotic cells by facilitating their opsonization and uptake by macrophages (Takemura et al. 2007). Some of the anti-atherogenic effects of adiponectin are also mediated by its role in the suppression of inflammatory responses. Adiponectin inhibits nuclear factor-κB (NFκB) activity and its downstream adhesion molecules leading to reduced monocyte adhesion to endothelial cells (Ouchi et al. 1999, Okamoto et al. 2002). In addition, adiponectin confers vascular-protective activities by suppressing the apoptosis of endothelial cell (Kobayashi et al. 2004).
IGF-1 is a fantastic hormone, but it is truly not for everyone. This is not a hormone for a new individual to the world of performance enhancement. Such an individual may find it difficult to use, he may find body fat piles on quickly, and in reality he really shouldn’t need it. IGF-1 should not be used until a true benefit can be obtained, which will normally be when the individual has already seen a lot of advancement in his physique. At this stage, the individual is also strongly encouraged to include HGH with his use. Not only will this produce better results, but it will ensure his body fat does not get out of control. The only exception to this rule pertaining to when to use is if you suffer from an IGF-1 deficiency, which will be rare for most.
The ketogenic diet, or keto diet, has become one of the most popular diets in recent years for its ability to enhance fat loss, increase energy, improve athletic performance, and control appetite. But despite these benefits, research and decades of clinical experience have found the diet to increase the risk for multiple nutrient deficiencies. Read […]
Good to read this briefing on the effects of HGH & IGF…Bu I suggest that a lot more could be said. We know that a large number of individuals have been taking HGH on the recommendation of some anti-aging doctors since the early 1990’s. Surely by now there is some evidence of 1) whether HGH has anti-aging effects in these individuals and 2) whether substantial numbers of these individuals have been impacted by cancers as a result..AS for me it seems that creatine is the way to go.

You are right, the number is a guesstimate and I have removed it from this version of my thread for the reason that it was getting misunderstood as an absolute rather than an indicator. From talking with other users, 40mcg is a dose at which, when injected immediately postworkout, good long-term gains are experienced with slowly diminishing effect.
The other pathway, the one that is rarely discussed, is the autocrine pathway. This is where a cell will produce its own IGF-1, different peptides than the systemic, for its own internal use. These are called IGF-1Ea and IGF-1Ec or MGF. They are produced inside the cell, and act on receptors within the cell and just outside of the cell, on the myoblasts. These peptides don't go anywhere. When they leave the cell, they stay close to the surface. This is the pathway that anabolic androgenic steroids will greatly upregulate.

Since general calorie restriction has thus far failed to reduce IGF-1, attempts have turned to intermittent fasting. Unfortunately, fasting has also been relatively unsuccessful in reducing IGF-1 in the real-world setting (including reasonable fasts). Fasting, however, greatly decreases insulin (which will increase IGFBP-1), increases ketones, and downregulates the insulin/IGF-1 pathway.60 This can even be accomplished in more reasonable fasts, like 15 hour periods.


Good to read this briefing on the effects of HGH & IGF…Bu I suggest that a lot more could be said. We know that a large number of individuals have been taking HGH on the recommendation of some anti-aging doctors since the early 1990’s. Surely by now there is some evidence of 1) whether HGH has anti-aging effects in these individuals and 2) whether substantial numbers of these individuals have been impacted by cancers as a result..AS for me it seems that creatine is the way to go.

While the connection between IGF-1 and cancer is concerning, it’s worth reminding that IGF-1 serves many vital purposes that antagonize its villainous side. IGF-1 helps to build muscle and reduce adipose (fat) tissue, which provides many anticancer effects. As we have already discussed, muscles – and specifically contracting those muscles – secrete anti-inflammatory hormones that sensitize our cells to insulin, decreasing cancer-promoting inflammation, blood sugar, and insulin. Adipose tissue also increases inflammation, dysregulates our blood sugar control, and secretes several hormones that can aid in cancer initiation and  growth. However, like most aspects of our health, there are two sides to the coin.


Finally, attempts to lower IGF-1 with a lower fat and higher carbohydrate diet have, not surprisingly, failed. In fact, when postmenopausal women were randomized to a low-fat, high-fat, or low-fat diet with omega-3 fats, the low-fat diet increased both IGF-1 and the IGF-1/IGFBP ratio.64 Decreasing fat in the diet and instead relying on carbohydrates to minimize either insulin or the IGF-1 pathway makes little sense.

Several companies have evaluated IGF-1 in clinical trials for a variety of indications, including type 1 diabetes, type 2 diabetes, amyotrophic lateral sclerosis (ALS aka "Lou Gehrig's Disease"),[31] severe burn injury and myotonic muscular dystrophy (MMD). Results of clinical trials evaluating the efficacy of IGF-1 in type 1 diabetes and type 2 diabetes showed great promise in reducing hemoglobin A1C levels, as well as daily insulin consumption.[medical citation needed] However, the sponsor, Genentech, discontinued the program due to an exacerbation of diabetic retinopathy[32] in patients coupled with a shift in corporate focus towards oncology. Cephalon and Chiron conducted two pivotal clinical studies of IGF-1 for ALS, and although one study demonstrated efficacy, the second was equivocal,[medical citation needed] and the product has never been approved by the FDA.
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