Description

The allure of IGF-1 LR3’s potential benefits has piqued scientific interest, but its use is heavily restricted due to potential risks. The delicate balance between the promise of muscle growth and the peril of adverse health effects makes IGF-1 LR3 a complex and intriguing substance in the scientific community. The path to fully understanding its potential and limitations is a journey that requires further exploration, highlighting the importance of continued research and ethical considerations in its use.

 The Science Behind IGF-1 LR3

The fascinating aspect of IGF-1 LR3 is its engineered structure, mirroring the natural human insulin-like growth factor 1 (IGF-1), but with nuanced modifications. The protein’s architecture is enhanced with an additional 13 amino acids at the N-terminus, while the third position sees a swap of Glutamic Acid for Arginine. These precise changes notably amplify the biological potency and stability of IGF-1 LR3. IGF-1 LR3, the synthetic variant of IGF-1, has drawn significant scientific attention due to its enhanced potency, longevity, and unique ability to induce hyperplasia (an increase in muscle cell numbers). This characteristic sets it apart from HGH, which primarily causes hypertrophy (the enlargement of existing muscle cells). Nevertheless, it’s crucial to underscore that the FDA does not sanction the use of synthetic IGF-1 variants like IGF-1 LR3, given their potential to trigger severe health issues.

IGF-1 LR3, or Long-R3 Insulin-like Growth Factor-1, is a marvel of biological engineering. This synthetic protein is designed to mirror the naturally occurring human insulin-like growth factor 1 (IGF-1), with carefully calibrated alterations. An additional 13 amino acids at the N-terminus and a swap of Glutamic Acid for Arginine at the third position enhance IGF-1 LR3’s biological potency and stability, making it a hot topic in scientific research.

IGF-1 LR3, the synthetic counterpart of IGF-1, has piqued scientific interest due to its enhanced potency, longevity, and unique ability to induce hyperplasia (an increase in the number of muscle cells). This differs from HGH, which mainly prompts hypertrophy (the enlargement of existing muscle cells). These precise modifications significantly enhance IGF-1 LR3’s biological potency and stability, making it a captivating subject in the realm of scientific research. Its impact is especially noteworthy in the development and growth of muscle and bone structures. The Enhanced Capabilities of Synthetic IGF-1 LR3 The man-made version of IGF-1, known as IGF-1 LR3, has captured the interest of the scientific community due to its amplified potency, longevity, and unique ability to induce hyperplasia (an increase in the number of muscle cells). In contrast, HGH primarily triggers hypertrophy (the enlargement of existing muscle cells). However, it’s crucial to emphasize that the FDA does not approve the use of synthetic IGF-1 variants such as IGF-1 LR3, due to potential health risks.

The Imperative Precaution with IGF-1 LR3 As per a study conducted in September 2021, IGF-1 LR3 is classified as a substance strictly for research purposes and is not intended for human use. Before considering the use of such substances, consultation with a competent healthcare professional is crucial. Misuse can lead to severe health complications, including an increased risk of cancer due to elevated rates of cellular growth and division. As per the latest research in September 2021, IGF-1 LR3 is classified as a substance intended strictly for research purposes and is not approved for human use. According to the latest research conducted in September 2021, IGF-1 LR3 is categorized strictly as a research substance, not approved for human use. It is essential, therefore, to consult a certified healthcare professional before considering such substances’ usage. Improper use can lead to severe health complications, including a heightened risk of cancer due to escalated rates of cellular growth and division. As per research conducted in September 2021, IGF-1 LR3 is classified as a substance strictly intended for research purposes and is not approved for human use.

Future of IGF-1 LR3 Research

The potential benefits of IGF-1 LR3 have sparked scientific interest. However, its use is heavily regulated due to potential health risks. Balancing the promise of muscle growth with the danger of adverse health effects makes IGF-1 LR3 a complex subject in the scientific community. Further research and ethical considerations are required to fully understand its potential and limitations. The intriguing benefits of IGF-1 LR3 have drawn scientific interest, although its use remains tightly regulated due to its potential health risks. Striking a balance between the promising aspects of muscle growth and the lurking danger of adverse health effects renders IGF-1 LR3 a complex entity in the realm of scientific research. To fully comprehend its potential and constraints, continuous research, coupled with ethical considerations, remains a necessity. IGF-1 LR3, with its potential benefits, has attracted considerable scientific interest.  Comprehensive understanding of its potential and limitations necessitates continued research and ethical considerations in its usage.

Below are some findings from a number of past researches been done by renowned peptides researchers on IGF1-LR3:

Cell Division

Like IGF-1, IGF1-LR3 is a potent stimulus for cell division and proliferation. Its primary effects are on connective tissues like muscle and bone, but it also promotes cell division in liver, kidney, nerve, skin, lung, and blood tissues. IGF-1 is best thought of as a maturation hormone because it not only promotes cell proliferation, but differentiation as well. IGF-1 causes cells to mature, in other words, so that they can carry out their specialized functions. Unlike IGF-1, IGF1-LR3 remains in the bloodstream for long periods of time. This property makes IGF1-LR3 a much more potent molecule. A dose of IGF1-LR3 provides approximately three times as much cell activation as a similar dose of IGF-1. Note that IGF1-LR3 and all IGF- 1 derivatives do not promote cell enlargement (hypertrophy), but rather promote cell division and proliferation (hyperplasia). In the case of muscle, for instance, IGF1-LR3 does not cause muscle cells to get larger, but it does increase total numbers of muscle cells.

IGF1-LR3 boosts fat metabolism in an indirect manner by binding to both the IGF-1R receptor and the insulin receptor. These actions increase glucose uptake from the blood by muscle, nerve, and liver cells. This results in an overall decrease in blood sugar levels, which then triggers adipose tissue as well as the liver to begin breaking down glycogen and triglycerides. Overall, this produces a net decrease in adipose tissue and a net energy consumption (i.e. net catabolism).

Given its role in reducing blood sugar levels, it should come as no surprise that IGF1-LR3 reduces insulin levels as well as the need for exogenous insulin in diabetes. In most cases, this translates into a 10% decrease in insulin requirements to maintain the same blood sugar levels. This fact may help scientists understand how to decrease insulin doses in individuals who have decreased insulin sensitivity and may even offer insight into preventing type 2 diabetes in the first place.

Impairs Myostatin

Myostatin (a.k.a. growth differentiation factor 8) is a muscle protein that primarily inhibits the growth and differentiation of muscle cells. While this function is important to prevent unregulated hypertrophy and ensure proper healing following injury, there are times when inhibiting myostatin could be of benefit. The ability to stop myostatin from functioning could be useful in conditions like Duchenne muscle dystrophy (DMD) or in people who suffer muscle loss during prolonged immobility. In these cases, inhibiting this natural enzyme could help to slow muscle breakdown, maintain strength, and stave off morbidity.

In mouse models of DMD, it has been found that IGF1-LR3 and other IGF-1 derivatives can counteract the negative effects of myostatin to protect muscle cells and prevent apoptosis. IGF1-LR3, thanks to its long half-life, is highly effective in counteracting myostatin and appears to work by activating a muscle protein called MyoD[1], [2]. MyoD is the protein normally activated by exercise (e.g. weight lifting) or tissue damage and is responsible for muscle hypertrophy.

IGF1-LR3 Longevity Research

IGF1-LR3 promotes tissue repair and maintenance throughout the body, making it a protective molecule against cell damage and the effects of aging. Research in cows and pigs indicates that IGF1-LR3 administration may be an effective solution for offsetting the effects of cellular aging. Ongoing research in mice seeks to determine if IGF1- LR3 might be useful in preventing progression of a wide range of conditions such as dementia, muscle atrophy, and kidney disease. This research reveals that IGF-1 administration can prolong life and reduce disability[3], [4], [5, p. 1].

Lifespan of male and female mice is correlated with IGF-1 levels. Glucocorticoid Signaling. Glucocorticoids, secreted primarily by the adrenal glands, are important clinical drugs used to control pain and reduce inflammation in autoimmune diseases, neurological injury,  cancer, and more. Unfortunately, glucocorticoids have a number of undesirable side effects such as muscle wasting, fat gain, and deterioration of bone density. There is some interest in using IGF1-LR3 to reduce the side effects of glucocorticoids and thus allow for more effective therapy[6].

Article Author

The above literature was researched, edited and organized by Dr. E. Logan, M.D. Dr. E. Logan holds a doctorate degree from Case Western Reserve University School of Medicine and a B.S. in molecular biology.

Scientific Journal Author

Dr. Anastasios Philippou, Ph.D. focused on Experimental Physiology at the National & Kapodistrian University of Athens Medical School. He is now a National Center Manager and Assistant Professor, however his extensive studying and documented research pertaining to the effects of muscle regeneration, the role of IGF-1 in skeletal muscle physiology, the expression of IGF-1 isoforms after exercise induced muscle damage in humans, characterization of the MGF E peptide actions in vitro, and epigenetic regulation on gene expression induced by physical exercise are most impressive.

Dr. Anastasios Philippou, Ph.D. is being referenced as one of the leading scientists involved in the research and development of IGF1-LR3. In no way is this doctor/scientist endorsing or advocating the purchase, sale, or use of this product for any reason. There is no affiliation or relationship, implied or otherwise, between Peptidesforsale.com and this doctor. The purpose of citing the doctor is to acknowledge, recognize, and credit the exhaustive research and development efforts conducted by the scientists studying this peptide. Dr. Anastasios Philippou, Ph.D. is listed in [7] and [8] under the referenced citations.

References and Citations

[1] “Adipose Tissue-Derived Stem Cell Secreted IGF-1 Protects Myoblasts from the Negative Effect of Myostatin.” [Online]. Available: https://www.hindawi.com/journals/bmri/2014/129048/. [Accessed: 16-May-2019].

[2] N. Li, Q. Yang, R. G. Walker, T. B. Thompson, M. Du, and B. D. Rodgers, “Myostatin Attenuation In Vivo Reduces Adiposity, but Activates Adipogenesis,” Endocrinology, vol. 157, 1, pp. 282–291, Jan. 2016.

[3] E. Corpas, S. M. Harman, and M. R. Blackman, “Human growth hormone and human aging,” Endocr. Rev., vol. 14, no. 1, pp. 20–39, Feb. 1993.

[4] W. E. Sonntag, A. Csiszar, R. deCabo, L. Ferrucci, and Z. Ungvari, “Diverse roles of growth hormone and insulin-like growth factor-1 in mammalian aging: progress and controversies,” J. Gerontol. A. Biol. Sci. Med. Sci., vol. 67, no. 6, pp. 587–598, Jun. 2012.

[5] “IGF-I/IGFBP system: metabolism outline and physical exercise. – PubMed – NCBI.” [Online]. Available: https://www.ncbi.nlm.nih.gov/pubmed/22714057. [Accessed: 16-May-2019].

[6] B. Y. Hanaoka, C. A. Peterson, C. Horbinski, and L. J. Crofford, “Implications of glucocorticoid therapy in idiopathic inflammatory myopathies,” Nat. Rev. Rheumatol., vol. 8,8, pp. 448–457, Aug. 2012.

[7] A Philippou, A Halapas, M Maridaki, M Koutsilieris – J Musculoskelet Neuronal Interact, 2007 [Semantic Scholar]

[8] A Philippou, E Papageorgiou, G Bogdanis, A Halapas… – In vivo, 2009 [Iiar Journals]