Multiple Sclerosis Fix?!!!
- Holly Haag
- Jul 1
- 5 min read
Two articles for people with MS on the possible protective influence Ivermectin has on those diagnosed with Multiple Sclerosis.
While this looks promising, let’s take a deeper look into a few connections driving this disease. Modern thinking is that MS is not only a “myelin disease”, but also damage to the axon itself is a major driver of lasting disability. It appears axonal damage, oligodendrocyte degeneration, and an exacerbated microglial response are all part of this disease causing a cascading ripple of neuro inflammation in the affected. Plus the added APOE4 genetic connection to its carriers and a possible MS diagnosis.
Let us start with axon destruction (axonal damage) means the nerve fiber itself is injured or lost. An axon is the long “wire” part of a nerve cell that carries electrical signals from one neuron to another (or from the brain/spinal cord to the body). This matters because myelin (the insulation around the axon) can sometimes be repaired, but once the axon is permanently damaged, the nerve signal pathway may be impaired. It can contribute to symptoms like weakness, numbness, poor coordination, vision problems, or fatigue depending on where it occurs.
Oligodendrocytes are specialized support cells in the brain and spinal cord that make myelin the protective coating around axons. Degeneration means these cells are damaged, die, or stop functioning properly. When oligodendrocytes are lost, myelin can break down (demyelination), which slows or blocks nerve signals.
Taking a look into why microglial cells play a critical role in this disease process. An exacerbated microglial response means the brain’s immune cells called microglia become overly activated or stay activated longer than they should. Microglia are like the brain’s resident cleanup and security cells. They normally, remove damaged cells and debris, fight infections, help repair tissue, support healthy neurons. The problem is when they shift into a prolonged “alarm mode.” They can start releasing inflammatory signals(like cytokines), reactive oxygen species, and enzymes that can contribute to damage if the response becomes excessive. Common reasons microglia can become overactivated include:
•Autoimmune inflammation in conditions like Multiple Sclerosis, immune activity can activate microglia around areas of myelin injury.
•Persistent infections or immune triggers. Certain infections, gut immune signals, or repeated inflammatory exposures may keep immune pathways stimulated.
•Blood-brain barrier disruption. If the barrier that normally protects the brain becomes more permeable, more immune signaling molecules and immune cells can interact with brain tissue.
•Oxidative stress/mitochondrial stress. When cells generate too much oxidative damage, microglia can interpret it as a danger signal.
•Aging and chronic inflammation with older microglia can become “primed,” meaning they react more strongly to smaller triggers.
•Metabolic factors such as poor glucose regulation, high inflammatory signaling, and certain lipid imbalances can influence microglial behavior.
•The Gut–brain immune signaling through the gut microbiome can influence immune tone through molecules like short-chain fatty acids(such as butyrate), intestinal barrier integrity, and immune messengers.
A key idea in newer neuroscience is that microglia are not simply “bad.” They have different states, repair/support states, clearing debris, and helping healing. They also have pro-inflammatory states that can worsen tissue injury if sustained long term.
Things that influence microglial behavior include:
•sleep quality
•infections
•stress hormones
•metabolic health (glucose/insulin signaling)
•exercise
•omega-3 fatty acids
•gut microbiome signals
•smoking and some environmental exposures
More neurodegenerative patterns linked to this volume of chronic inflammation include brain volume loss(atrophy) over time, slowly expanding lesions often discussed in MS research), and higher inflammatory signaling markers researches have focused on such as:
•TNF-a
•IL-1B
•IL-6
•complement proteins
•markers of oxidative stress
Now getting into the dreaded 4 alleles of APOE4. People carrying the APOE4 genetic variant are more likely to experience damage and are urged to follow a lower saturated fat type diet. APOE4 is involved in lipid transport meaning they:
•Absorb dietary cholesterol more efficiently
•Have stronger LDL rises with certain high saturated-fat diets
•Have different lipid responses than non-carriers
However, research also suggests APOE4 carriers are going to be more able to repair myelin when consuming the proper fats such as mono-saturated fats and Omega 3 DHA/EPA. Due to genetic factors not working in isolation, the individuals tolerance to glucose metabolism and dietary fat intake may vary.
APOE4 appears to be a strong factor in those who carry it getting a MS outcome with improper fat consumption, but it also appears to be what helps repair the disease with proper fat intake.
The two best suggested diets to follow are a low saturated fat keto diet such as The Swank diet or mediterranean diet. Although my favorite diet still to this day to recommend is The Plant Paradox diet which somewhat follows both of the above diets suggested ideals. I do believe there is enough research into the possible effect lectins have on an overly active immune system to take the added precautionary during the healing process. These style diets are especially helpful if glucose metabolism is impaired.
It would appear that the very things I did such as dietary changes and regular fasting putting the body into its clean up mode Autophagy is what helped contribute to my positive outcome.
While MS is not simply a cholesterol disease,
MS is primarily an immune-mediated disease involving the microglia cells and T-cells having damaging effects on the Myelin Sheath(fatty tissue cover nerves), Oligodendrocytes(lost axon underneath becomes injured), Axonal loss(nerve fiber can thin or break).
The big question I ask myself here is, “How do you shift immune cells from chronic alarm mode toward repair mode?”
I think we have some of those answers for some of us:
Diet, fasting, ketones, exercise, possibly Ivermectin, and supplements effects on the microglia. I could be wrong here or I could be right. My body shifted to a positive outcome following these simple yet complex biological strategies. What are your next moves?
1)Suppressing a bodies biological processes as managed care life long program with Disease Modifying Drugs(that simply modify) or
2) Using that biology to benefit the repair processes through biofeedback. Positive feedback with lifestyle changes.
It is your choice ultimately. I made mine and that is why I got results. I often get asked what I did to improve my outcome, but few that hear me truly follow me.
I simply want to leave you with this thought. One single piece of candy or gluten maybe a small drop in the bucket to the human body, but we now know we feed microscopic bugs that drive our health. How many bugs do you think that one small(to you) piece of candy will feed in your system? This one choice will feed just how many of the trillions of microbial beings? What scale is tipping here, will the good microbes rise or the “bad” ones? Every single choice made in a single day shifts your overall outcome. What health outcome do you truly want to build? It is a choice, it is your choice!
Note: I personally do not believe in “bad” microbes. They serve a purpose and are suppose to be part of a BALANCED microbiome.
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