Here we go. This all may well be apropos of nothing, but I think there is something in this.
All this AMN/ALD differences. If I am any expert (and I am), I put it all down to age at onset, then speed of progression.
The later in life you start noticing symptoms, the easier ride you’ll have. Feel free to shoot me down with that rather oversimplified theory.
I often think about myself and my brother. Pretty much identical in every way. Character, good looks, intelligence, both loud-mouthed, arrogant idiots. But I moved away when I was 16, lived in the South of England, he in the North. Different cultures, climates, lifestyles, diets. I was a dope smoking vegetarian, he a carnivore that only drank at weekends.
Then I traveled the world. My life abroad was like Alice in Wonderland compared to him. Everywhere , Europe, Africa, Asia.
OK, almost everywhere.
I restarted eating meat in Asia, and I stopped smoking that damn dope. It was then that my symptoms started firing up.
My brother carried on with the same old, same old. And his symptoms are (according to him) – nothing. But his wife and I see his limping, his fatigue. I can see how every step is forced and he has to concentrate to balance. That was me 10 years ago.
Still, he is 3 years older and doing better than me. Throw in how I visit a neurologist every three months and have an MRI every six. He never, ever goes to the doctor for anything. I am constantly told I am sick. He never even thinks of AMN unless I mention it, and the conversation doesn’t usually last long.
Why the difference in onset and progression? Who knows? But I’ll have a stab. Apart from the lifestyle/environment factors I threw in, there are variants of AMN. A lot of us that have had genetic tests, they were simply looking for a mutation in the ABCD1 gene. It is either mutated, or it isn’t.
Take a look at the ABCD1 Variant Database.
adrenoleukodystrophy.info/m...
There are like 1000 different variants of the disease, all based on the chromosome pattern and factors I cannot get my head around. Not all the variants are significant, some are more likely to lean towards adrenal insufficiency, AMN, ALD. But the sample sizes are really small, one case here, ten cases there. Statistically, these numbers cannot prove anything, except for the fact that the ABCD1 mutation is the root cause of our woes. Your ABCD1 variant has no predictive value.
But there are plenty of other genes that can mutate in a myriad of ways as well, and study of the human genome is in it’s infancy.
Here is where I go off the reservation (as usual). I was drawn to this article about MS:
Genetic variant identified that may increase multiple sclerosis severity
theguardian.com/society/202...
That’s the beauty of having a much more common disease. 12000 people screened for this one, yielding results good enough to invest money in future treatments.
And this one:
Common viral antibodies could trigger MS, research reveals
theguardian.com/society/202...
This one I’d heard before, a usually harmless virus, your antibodies to it can consign you to a future life of MS misery.
And that one was from a 20 year, 10 million person study, here is the report:
science.org/doi/10.1126/sci...
And this article about the chemicals used to manufacture some clothes being potentially harmful to human health:
Are your clothes making you sick? The opaque world of chemicals in fashion
theguardian.com/fashion/202...
It reminded me of this report I read years ago about the (possible) link between dry cleaning chemicals and Parkinson’s Disease:
journals.lww.com/neurotoday...
And there you have it. Plainly, I don’t have a clue, current AMN science isn’t that much further ahead either. Or is it?
Seborrheic dermatitis with AMN
Possible AMN , I’m in the process of finding out