Although this information was discussed here about a year ago (April 28, 2013), I can't shake the feeling that IGF-1 is important. However, I have focused on the "growth factor" or growth hormone aspect; but now I think the key lies in the "insulin-like" part.
This idea was expressed (page 67) in the Winter 08-09 issue of the MS Society publication, Momentum
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]
This seems to indict insulin again: on March 5, 2014 Dr. Oz spoke with oncologist Marleen I. Meyers, M.D., who thinks that no dairy with artificial hormones should be consumed (rbGH-recombinant bovine growth hormone is given to increase a cow’s milk output, but it also increases IGF-1 in milk, which is linked to breast, prostaste, colon cancer – cancers have increased numbers of insulin receptors on the cells) [Could this be the reason that elimination of dairy often improves MS symptoms?]http://www.doctoroz.com/episode/everyda ... wont-touch
The slideshow explains this again: http://www.doctoroz.com/slideshow/foods ... llery=true
My hypothesis: excess insulin (hyperinsulinemia) plays a major role in MS, as developed in my initial post: http://www.thisisms.com/forum/general-discussion-f1/topic1878.html "Insulin – Could This Be the Key?"