* Desensitization seems to occur after about 4 weeks of chronic usage, at which point the individual has the option of either discontinuing the peptide for a 2-4 week period (after which the individual can resume use), or the individual can elect to increase the dosage further, in order to over-ride the desensitization and continue experiencing its benefits. However, the process of desensitization will continue to occur at each ascending dosage.


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.
(References: Buyukkayhan et al (2003). Int J Vitam Nutr Res, 73:343-6; Giovannucci et al (2003). Cancer Epidemiol Biomarkers Prev, 2:84-9; Gunnel et al (2003). Br J Cancer, 88:1682-6; Heald et al (2001). Diabetologia, 44:333-9; Heald et al (2003). Public Health Nutr, 6:175-80; Hoppe et al (2004). Eur J Clin Nutr, 58: 1211-6; Hoppe et al (2004). Am J Clin Nutr, 80:447-52; Howarth (2003). J Nutr, 133:2109-12; Krause's Food, Nutrition & Diet Therapy (2000). Edited by Mahan & Escott-Stump, Chapter 17, p380; Larsson et al (2005), Am J Clin Nutr, 81:1163-7; Lonnerdal (2003). Am J Clin Nutr, 77:1537S-1543S; Moorman & Terry (2004). Am J Clin Nutr, 80:5-14; Norat & Riboli (2003). Eur J Clin Nutr, 57:1-17; Sandhu et al (2002), Lancet, 359:1740-5).
But the IER protocol is more similar to the 5:2 diet than to a 16/8 IF protocol (and it involves less overall fasting period). Nevertheless, it shows that 6 months of 25% CR that produced significant changes in body weight and fat loss didn’t reduce IGF-1 levels. Similar results have been observed by the same authors: no change in IGF-1 with 25% daily or intermittent energy restriction despite significant weight/fat loss.
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.

There is a considerable amount of hype surrounding IGF1. Every one is blaming the distended bellies of modern Bodybuilders on it. Also the freaky proportions that old bodybuilders that have been around for years are starting to attain. Anti-aging proponents are touting it as the miracle cure for every thing from Parkinson's disease to Alzheimer's. And the medical community has published numerous articles on it for its ability to cause cancer, diabetes and gigantism. While at the same time performing documented experiments on thousands of patients of muscle wasting diseases. And reporting significant turnabouts in there conditions. So what is a guy to think about IGF1 as far as athletic enhancement is concerned? Well first of all you need to know that most experiments conducted with IGF1 do not list the type of IGF used. I have written Dr. Robert Saline of the Swedish rejuvenation institute on several occasions and we have had in-depth discussions on the subject of IGF1 for physical appearance enhancement. He feels it would be unethical to prescribe IGF1 to a bodybuilder to increase muscle mass simply due to the fact that IGF1 has valid applications in the medical community, (Like I could give a rats ass about "ethical"). He can not argue that it is extremely effective as a promoter of muscle growth far beyond what androgens (steroids) alone can offer. Well fortunately in America IGF1 is not a drug (yet) and the FDA has no control over it as of now. This will change in the very near future however, Im absolutely sure of it.
A knowledge of the physicochemical properties of inclusion bodies is important for the rational design of potential recovery processes such as flotation and precipitation. In this study, measurement of the size and electrophoretic mobility of protein inclusion bodies and cell debris was undertaken. SDS-PAGE analysis of protein inclusion bodies subjected to different cleaning regimes suggested that electrophoretic mobility provides a qualitative measure of protein inclusion body purity. Electrophoretic mobility as a function of electrolyte type and ionic strength was investigated. The presence of divalent ions produced a stronger effect on electrophoretic mobility compared with monovalent ions. The isoelectric point of cell debris was significantly lower than that for the inclusion bodies. Hence, the contaminating cell debris may be separated from inclusion bodies using flotation by exploiting this difference in isoelectric points. Separation by this method is simple, convenient, and a possible alternative to the conventional route of centrifugation.
The studies on transgenic and knockout mice have shown that it can control its development and growth. It plays an important role as regulator in the G1 to S phase of the cell cycle. When applied to cardiomyocyte cultures, R3 have shown a large increase in proliferating cell nuclear antigen expression and in several cyclins involved in cell progression as well as in bromodeoxyuridien (BrdU) labeling (Kajstura et al. 1994). Other effects it has on cell lines are increased cell survival, inhibition of the apoptotic pathways, culture longevity and increased recombination of protein production (Fang et al. 1997). In another study, the application of the LR3 IGF-1 has led to an increase in the myocyte bromodeoxyuridine uptake by three to fivefold. But it has also shown that IGF-1 LR3 actions have been blocked by the ERK and P13K labeling which completely abolished the BrdU uptake. Furthermore, ut has been shown that in mycocytes, IGF-1 R3 stimulates the cardiomyocyte division in vivo (Sundgren et al. 2003). It has also been suggested that IGF-1-Long 3R is more potent than the IGF-1 because of its low binding capacity with all known IGF binding proteins (Tomas et al. 1995). In another investigation, feeding of LR3-IGF-1 in different amounts to investigate the effects on somatotropic axis (plasma levels of IGF-1 and 2, IGFBPs) was done. They have reported that plasma Long-R3 increased when administered subcutaneously but with no such behavior when administered orally. Furthermore, LR3 lowered the levels of native IGF-1 in rbGH-injected in calves, but L-R3 increased the amounts of IGF-II concentrations when administered with L-R3 subcutaneously. The parenteral administration of the Long R3 IGF-1 decreased the growth hormone concentration but did not affect the secretory system. It was also reported that the somatotrophic acis is basically functioning in neonatal calves and can be influenced by nutrition, growth hormone and Long-R3-IGF-1 (IGF1-LR3). (Hammon and Blum 1997).
There is a considerable amount of hype surrounding IGF1. Every one is blaming the distended bellies of modern Bodybuilders on it. Also the freaky proportions that old bodybuilders that have been around for years are starting to attain. Anti-aging proponents are touting it as the miracle cure for every thing from Parkinson's disease to Alzheimer's. And the medical community has published numerous articles on it for its ability to cause cancer, diabetes and gigantism. While at the same time performing documented experiments on thousands of patients of muscle wasting diseases. And reporting significant turnabouts in there conditions. So what is a guy to think about IGF1 as far as athletic enhancement is concerned? Well first of all you need to know that most experiments conducted with IGF1 do not list the type of IGF used. I have written Dr. Robert Saline of the Swedish rejuvenation institute on several occasions and we have had in-depth discussions on the subject of IGF1 for physical appearance enhancement. He feels it would be unethical to prescribe IGF1 to a bodybuilder to increase muscle mass simply due to the fact that IGF1 has valid applications in the medical community, (Like I could give a rats ass about "ethical"). He can not argue that it is extremely effective as a promoter of muscle growth far beyond what androgens (steroids) alone can offer. Well fortunately in America IGF1 is not a drug (yet) and the FDA has no control over it as of now. This will change in the very near future however, Im absolutely sure of it.
IGF-1 deficiencies early in life, usually the result of GH deficiency, can inhibit bone growth and overall development and can result in a child with a shorter than normal stature. In adults, decreased production can lead to low bone density, less muscle mass, and altered lipid levels. However, testing for IGF-1 deficiency, or GH deficiency, is not routine in adults who have decreased bone density and/or muscle strength or increased lipids. GH deficiency and consequent IGF-1 deficiency is a very rare cause of these disorders.
Great questions. I'll start with some background on the peptides from back before IGF-1 was commonly used. gh - growth hormone (somatropin) - was the first peptide to be used in Bodybuilding. We pretty much know what GH does and doesn't do and all that, so I'll skip this part. Then came along insulin. It quickly became apparent that insulin on its own doesn't do much for muscle. It does make you fat but not much bigger. With anabolic steroids and tons of food, it's better. Later it became extremely clear that Slin & GH was the winner combo, the most synergistic combination around.
The final effects of IGF-1 surround recovery. The hormone will improve overall recovery from training and strenuous activity, but it doesn’t end there. IGF-1 actually carries direct healing properties, not masking like a painkiller but true therapeutic healing. The use of IGF-1 can greatly reduce the total time for healing joint injuries. It has even been shown to significantly aid in the healing of tendons and ligaments. As all these areas of the body take a beating by most athletes, IGF-1 becomes extremely valuable.
You may notice that one macronutrient is often, and ironically, left out of the discussion. Fat, the demonized macronutrient that provides the largest calories per gram, aids in the absorption of fat-soluble vitamins, provides essential fatty acids that support our brain and our body cannot make, is used as the building block of our cell walls, and supports hormonal function and production. Many more benefits of this vital nutrient exist, but surprisingly, fat’s ability to directly affect the insulin/IGF-1 pathway pales in comparison to carbohydrates and protein, the infamous macronutrients over which present day health experts are waging an insulin/IGF-1-based war. This seems to have been lost somewhere in the shuffle.
Interleukin‐6 (IL‐6), interleukin 1b (IL‐1b) and tumour necrosis factor α (TNFα) are the principal pro‐atherogenic cytokines,1 which are also produced in tissues other than the vascular wall and immune system, such as adipose tissue, myocardium, intestine, etc.1 They upregulate the expression of adhesion molecules on vascular endothelium, depress nitric oxide synthesis and promote the subendothelial migration of leucocytes. Further to their local regulatory role at a vascular level, these cytokines induce the liver‐derived synthesis of acute phase proteins, such as fibrinogen, plasminogen, C‐reactive protein (CRP) and serum amyloid α (SAA), which amplify inflammatory and pro‐coagulant responses.
But a closer look at the biology of IGF-1 makes support for the AP theory more dubious.  The details of where and when IGF-1 is expressed don’t fit the convenient story of AP.  There is a lot of IGF-1 early in life, but no sign of deleterious effects.  Later in life when the piper is to be paid, IGF-1 is expressed at very low levels.  It is not easy to relate high levels of IGF-1 in our teens to the cancer and heart risk in our 70’s.  
If IGF-1 is still elevated after the surgical removal of a pituitary tumor, then the surgery may not have been fully effective. Decreasing IGF-1 levels during subsequent drug and/or radiation therapies indicate that the treatment is lowering GH production. If levels of IGF-1 become "normalized," then the person is no longer producing excess amounts of GH. When someone is undergoing long-term monitoring, an increase in IGF-1 levels may indicate a recurrence of the pituitary tumor.

Giovannucci and coworkers (2003) say, "IGF may play opposing roles in health and disease. The age-related declines in growth hormone and IGF-1 may be associated with potentially deleterious changes in body composition and functioning, but recent studies suggest that IGF-1 levels may be related to risk of prostate, colorectal, premenopausal breast and possibly other cancers."


I would follow the authors suggestion and get your level tested. Have you read the website mastattack, she is a scientist with MCAD, I would ask her. Also, have you tried butyrate? It is helping my daughter slowly who has chronic daily migraine which arrived with food allergies (true IgE reactions) and also now has a plethora of food intolerances like you describe gluten, dairy, eggs, almost anything including veg with high histamine, and at one point all animal protein. It was awful. I feel your pain. She was completely vegan less high histamine ones like avacado and spinach. Butyrate can help heal the lining of the gut, promotes mucin cells to make mucous, and promotes Tregs which are important in promoting immune tolerance. More foods being tolerated. Good write up on this site, read it. Tolerating more foods now. I am add colostrum next to see if this helps gut further. But it definately has IGF-1 in it.
So insulin & gh - growth hormone (somatropin) - are synergistic. Then the next question: what about insulin & IGF or Gh & IGF? IGF is synergistic with both. MOST of the effects of GH are mediated through IGF-1 but not ALL of them. Among the good effects of gh - growth hormone (somatropin) - that IGF-1 does not exert is anabolism to ligaments, for example. This is just an example to show that there is a benefit to using gh - growth hormone (somatropin) - & IGF-1 at the same time. There is evidence that ED dosing of LR3 reduces gh - growth hormone (somatropin) - release in the body, so it makes plenty of sense to use both at the same time.
Gains out of IGF-1 are difficult to account for. Firstly, it is much more a recomposition compound than a mass or fatloss compound. On anabolic steroids, the gains are "this many lbs of LBM". On Clenbuterol/Thyroid, gains are "so many lbs of flab". On IGF-1 the gains are "some fatloss, some muscle gain/retention, and this many new cells that I will grow in the coming months".
Rare diseases characterized by inability to make or respond to IGF-1 produce a distinctive type of growth failure. One such disorder, termed Laron dwarfism does not respond at all to growth hormone treatment due to a lack of GH receptors. The FDA has grouped these diseases into a disorder called severe primary IGF deficiency. Patients with severe primary IGFD typically present with normal to high GH levels, height below 3 standard deviations (SD), and IGF-1 levels below 3 SD. Severe primary IGFD includes patients with mutations in the GH receptor, post-receptor mutations or IGF mutations, as previously described. As a result, these patients cannot be expected to respond to GH treatment.
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