CureOrBust wrote:The documentary, "Eat, Fast and Live Longer" and a lot of the articles appear to attempt to reduce IGF-1 (Insulin like Growth Factor). One of the things that is hard to reconcile, is that I am sure
I have read numerous articles that say IGF-1 is good for MS. How do you reconcile this contradiction?
eg:
The insulin-like growth factor system in multiple sclerosis.
Abstract wrote:Multiple sclerosis (MS) is a chronic disorder of the central nervous system characterized by inflammation, demyelination, and axonal degeneration. Present therapeutic strategies for MS reduce inflammation and its destructive consequences, but are not effective in the progressive phase of the disease. There is a need for neuroprotective and restorative therapies in MS. Insulin-like growth factor-1 (IGF-1) is of considerable interest because it is not only a potent neuroprotective trophic factor but also a survival factor for cells of the oligodendrocyte lineage and possesses a potent myelinogenic capacity. However, the IGF system is complex and includes not only IGF-1 and IGF-2 and their receptors but also modulating IGF-binding proteins (IGFBPs), of which six have been identified. This chapter provides an overview of the role of the IGF system in the pathophysiology of MS, relevant findings in preclinical models, and discusses the possible use of IGF-1 as a therapeutic agent for MS.
IGF-1 May Give Hope to MS
Recent laboratory experiments on IGF-1 have demonstrated a stimulation of the protective sheath around nerves known as the myelin sheath. In degenerative diseases like multiple sclerosis and ALS or Lou Gehrig’s disease, damage around the sheath stops signals from being transmitted between the brain and nerves.
IGF-1 has been found to regrow these sheaths according to the University of Michigan scientists. Although several growth factors are currently being studied, IGF-1 appears to be most effective at inducing the growth of the sheath and preventing neuronal cell death according to chief researcher Hsin-Lin Cheng. Michigan scientists presented the first results from their experiments with IGF-1 at a conference in New Orleans. The scientists said they removed nerve cells called dorsal root nerves from newborn rats and grew them in a dish. They found that if they stimulated the conditions of diabetes in the dish and then applied the IGF-1 it helped the nerves remain normal.
Tests with IGF-1 are now underway on 40 people with neuropathy at the Mayo Clinic in Rochester, Minnesota. According to these researchers, IGF-1 may provide a new treatment for a whole group of diseases that have not heretofore been treatable.
Sure, the last one is from a whole website promoting IGF-1
I cannot reconcile the contradiction, but I can't discount this article in
Momentum magazine (NMSS application). It belongs here for its mention that IGF-1 actually worsened MS:
This idea was expressed (page 67) in the Winter 08-09 issue of the MS Society publication named
Momentum; it does refer to earlier "success in promoting myelin formation." Of course, that poor mouse! BUT which abstract fits people?…
The growth factor IGF-1 had shown some success in promoting myelin formation, so a Society-funded team led by Stephane Genoud, PhD (The Salk Institute, La Jolla, Calif.), injected it into mice with EAE. The injections actually worsened the disease. (Journal of Neuroimmunology 2005; 168:40-5) Such failures are important to pinpoint before they affect people with MS in clinical trials.
Here is the abstract of the work mentioned:
1: J Neuroimmunol. 2005 Nov;168(1-2):40-5. Epub 2005 Aug 24. Links
Targeted expression of IGF-1 in the central nervous system fails to protect mice from experimental autoimmune encephalomyelitis.Genoud S, Maricic I, Kumar V, Gage FH.
Laboratory of Genetics, The Salk Institute, 10010 N Torrey Pines Rd, La Jolla, CA 92037, USA.
Insulin-like growth factor 1 (IGF-1) has been identified as a critical molecule in the induction of myelination in the central nervous system (CNS). Systemic injection of IGF-1 has been shown to have a varied and transiently protective effect on the clinical course of experimental autoimmune encephalomyelitis (EAE). Since systemic IGF-1 can also modulate peripheral immune lymphocytes, we examined whether a sustained and local delivery of IGF-1 into the spinal cord would have any influence on the chronic course of EAE in C57/BL6 mice. The capability of adeno-associated virus (AAV) to be retrogradely transported efficiently from muscle to motor neurons of the spinal cord was used to overcome the difficulty routinely encountered when attempting chronic delivery of molecules into the CNS. We demonstrate that AAV-mediated delivery of IGF-1 in CNS did not have any beneficial effect on the clinical course of EAE. Injection of AAV-IGF1 after induction of the disease
worsened the clinical symptoms. Furthermore, CNS expression of IGF-1 did not affect the pathogenic anti-MOG T cell response, as examined by proliferation and cytokine secretion. Thus, enhanced expression of IGF-1 in the CNS during inflammation does not have a significant effect on myelination. These data have important implications for the potential use of IGF-1 in the treatment of multiple sclerosis.
PMID: 16120466 [PubMed - indexed for MEDLINE]
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Fundamentally, I think the IGF-1 IS worsening people's MS. Does anyone have the results of the Mayo Clinic test of IGF-1 mentioned above: "Tests with IGF-1 are now underway on 40 people with neuropathy at the Mayo Clinic in Rochester, Minnesota."?