Research on Progesterone and Multiple Sclerosis. For the sake of saving space and easier reading, I pasted just the gist of each article.
Dr. Ray Peat's post regarding MS and Progesterone initially got me on the PROG track and is a good overview, though I don't agree with all of his nutritional ideas. He also talks about other aspects of the disease/autoimmunity. http://raypeat.com/articles/articles/ms.shtml
Multiple Sclerosis / Pregnancy
Female hormones affect disease activity; 82% of women report worse symptoms before menses (Smith and Studd 1992). The progesterone/17-beta-estradiol ratio increases during the luteal phase of the menstrual cycle, and this corresponds to higher MRI activity (Pozzilli et al 1999). MRI activity increases during ovulation when estradiol is high and progesterone is low (Bansil et al 1999). Symptoms improve with aspirin, without affecting body temperature.http://www.medmerits.com/index.php/arti ... erosis/P12
Correlation between sex hormones and magnetic resonance imaging lesions in multiple sclerosis.
Patients with high estradiol and low progesterone levels had a significantly greater number of Gd enhancing lesions than those with low levels of both these hormones. Patients with a high estrogen to progesterone ratio had a significantly greater number of active MRI lesions than those with a low ratio.
Progesterone and Nestorone facilitate axon remyelination: a role for progesterone receptors.
We found that progesterone and the synthetic 19-norprogesterone derivative 16-methylene-17α-acetoxy-19-norpregn-4-ene-3,20-dione (Nestorone) promote the remyelination of axons by oligodendrocytes after lysolecithin-induced demyelination in organotypic cultures of cerebellar slices taken from postnatal rats or mice.
Progesterone attenuates neurological behavioral deficits of experimental autoimmune encephalomyelitis through remyelination with nucleus-sublocalized Olig1 protein.
Progesterone can promote the remyelination, but whether it exerts beneficial effect on treatment of MS still remains unclear. . . . The results indicate that the progesterone is beneficial to attenuating neurological behavioral deficits, for it can promote more successful remyelination of EAE with aid of the nucleus-sublocalized Olig1 protein.
Progesterone treatment reduces disease severity and increases IL-10 in experimental autoimmune encephalomyelitis.
Progesterone treated animals showed reduced peak disease scores and cumulative disease indices, and decreased inflammatory cytokine secretion (IL-2 and IL-17).http://www.ncbi.nlm.nih.gov/pubmed/20153059
Protective effects of progesterone administration on axonal pathology in mice with experimental autoimmune encephalomyelitis.
In conclusion, progesterone enhanced axonal density, decreased axonal damage and prevented GAP43 hyperexpression in the spinal cord of EAE mice.http://www.ncbi.nlm.nih.gov/pubmed/19497309
----- Progesterone in Spinal Cord Injury and Stroke -----
Progesterone up-regulates neuronal brain-derived neurotrophic factor expression in the injured spinal cord. [BDNF is responsible for plasticity - http://en.wikipedia.org/wiki/Neuroplasticity
Our findings suggest that PROG enhancement of endogenous neuronal BDNF could provide a trophic environment within the lesioned spinal cord and might be part of the PROG activated-pathways to provide neuroprotection.http://www.ncbi.nlm.nih.gov/pubmed/15099674
Progesterone neuroprotection in traumatic CNS injury and motoneuron degeneration.
In peripheral neuropathies, progesterone and reduced derivatives promote remyelination, axonal regeneration and the recovery of function. In traumatic brain injury (TBI), progesterone has the ability to reduce edema and inflammatory cytokines, prevent neuronal loss and improve functional outcomes. Clinical trials have shown that short-and long-term progesterone treatment induces a significant improvement in the level of disability among patients with brain injury. In experimental spinal cord injury (SCI), molecular markers of functional motoneurons become impaired, including brain-derived neurotrophic factor (BDNF) mRNA, Na,K-ATPase mRNA, microtubule-associated protein 2 and choline acetyltransferase (ChAT). . . . SCI also causes oligodendrocyte loss and demyelination. In this case, a short progesterone treatment enhances proliferation and differentiation of oligodendrocyte progenitors into mature myelin-producing cells, whereas prolonged treatment increases a transcription factor (Olig1) needed to repair injury-induced demyelination.http://www.ncbi.nlm.nih.gov/pubmed/19318112
Progesterone: therapeutic opportunities for neuroprotection and myelin repair.
A concept is emerging that progesterone may exert different actions and use different signaling mechanisms in normal and injured neural tissue. . . . Progesterone and its metabolites promote the viability of neurons in the brain and spinal cord. Their neuroprotective effects have been documented in different lesion models, including traumatic brain injury (TBI), experimentally induced ischemia, spinal cord lesions and a genetic model of motoneuron disease. Progesterone plays an important role in developmental myelination and in myelin repair, and the aging nervous system appears to remain sensitive to some of progesterone's beneficial effects. Thus, the hormone may promote neuroregeneration by several different actions by reducing inflammation, swelling and apoptosis, thereby increasing the survival of neurons, and by promoting the formation of new myelin sheaths. http://www.ncbi.nlm.nih.gov/pubmed/17659348
You get the idea.