Robbie,
I wish I had answers for you on that, because I have experienced those drugs, too. I have to worry about what the long term effects of all of those drugs will be, too. I am including, here, a simple explanation of how LDN works for PWMS. Again, I am sorry it has not helped you. Bill
LDN- A Simple Explanation
Naltrexone (Low Dose Naltrexone)
The following explains Low Dose Naltrexone (also known as LDN) from a layperson's perspective that everyone should be able to understand.
Please note that we are not medical doctors, and that there is no formal proof of the following statements; they are merely informed hypotheses. You should always do your own research and consult with your doctor before undertaking any medical treatment.
The simple explanation:
Naltrexone is an FDA approved drug (1984) that was originally intended to treat people suffering from opium (e.g., heroin) addiction. It treated these addictions by blocking the "pleasant" effects from the drug, so addicts who took it did not get "high" anymore.
How does it block the "high?" There are receptors in our brain that an opioid like heroin would use to get into the cell and do its deed. Naltrexone blocks those receptors, so the heroin can't have an effect. Think about it like a puzzle piece-- some brain cells have a piece that accepts opium and its derivatives, and the Naltrexone simply matches that piece. When the heroin floats around, it has no where to go.
OK, that's all well and good, but what relevance is there to Multiple Sclerosis?
Well, those opiod receptors in our brains are not JUST for receiving drugs like heroin-- our bodies actually produce opiods every day, among other things, we produce a set of hormones called endorphins. So if you were to take Naltrexone, you would actually block the reception of something your body produces. These hormones, as it turns out, play a very important part in controlling the immune system. Keep this in mind for what we'll talk about below.
The FDA-approved dosage for heroin addicts was 50 milligrams per day. This ensured that those receptors were blocked all day and there was no chance that any heroin could connect with a cell and give the user a "high."
BUT a medical doctor named Dr. Bihari found that if you give someone a much lower dose, say THREE milligrams instead of 50, you would not block the receptors all day, but just for a couple of hours. After that, everything would function as normal.
But the human body is funny-- when you block something, it often responds by producing more. In other words, if you were to take Naltrexone at a low dose (Low Dose Naltrexone, even!) you would block the receptors for a couple hours. The body would notice that it was not receiving the endorphins it produced, so it would think "Since they're not getting though, I must not be producing enough-- turn it up!" The gland responsible for producing the endorphins, called the pituitary, would respond by producing significantly more. Not enough to cause any problems, but enough to make a difference.
So how can this all matter for Multiple Sclerosis? Remember how we discussed above that the endorphins actually regulate the immune system? Well, in Multiple Sclerosis, the immune system is malfunctioning-- it's attacking it's own body. Anything that helps regulate, control, and tame the immune system could potentially have a positive effect on MS. And that's exactly what some people who take LDN report-- a halt of the progression of the disease, and even some improvement in symptoms.
Adding some scientific validity are studies that show that in MS patients, the pituitary gland (which produces endorphins) shrinks as the disease progresses. This shrinkage can be assumed to correspond with less endorphin production, though the link is not concrete. The million dollar question is: is the pituitary gland shrinking BECAUSE of the MS, in which case fixing the pituitary is more like treating a symptom rather than the cause, OR is the pituitary smaller in people who have multiple sclerosis and could potentially be a, if not the, cause of the disease in the first place? In other words, is a shrunken pituitary a cause of MS or is it an effect? If it's a cause, making up for the lower endorphin output by taking something like LDN could have significant positive implications.
There is a catch to all of this-- there are no formal, clinical trials on taking low dose naltrexone for multiple sclerosis. All there is is speculation, a few doctors backing it, and most remarkably, many positive testimonials from patients.
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