The Scientific Method
- Define the problem.
- Propose a hypothesis (theory).
- Make predictions based on the assumption that the hypothesis is true.
- Do experiments to confirm the predictions.
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1. Define The Problem
Amyotropic Lateral Sclerosis (ALS) is thought to be a degenerative disease of motor neurons in the spinal cord, of unknown cause. Some cases are correlated with genetic factors (but correlation is not causation).
The problem I noticed right away is, “How is it that a specific cell type, widely spread throughout the body, is attacked so selectively, leaving other very similar cell types unharmed?”
2. Propose A Hypothesis (Theory)
The immune system is the only thing that I know of that is capable of attacking specific cell types anywhere in the body. Normally the immune system attacks foreign cells, like bacteria. This is necessary for survival. But sometimes, the immune system attacks cells that are part of the body, which is called “Autoimmunity.” My hypothesis is that the immune system attacks spinal motor neurons to cause the disease, ALS. Put more simply:
Hypothesis: ALS Is An Autoimmune Disease
3. Make predictions based on the assumption that the hypothesis is true.
I find it easiest to write a prediction as an “IF/THEN” computer programming statement:
IF (Hypothesis is true) THEN (Prediction)
IF (ALS is an autoimmune disease) THEN (ALS is treatable)
4. Do experiments to confirm the predictions.
The obvious experiment to test this hypothesis is to treat ALS as an autoimmune disease. This requires a test subject with ALS willing to take the risk of trying a new treatment.
I recently was diagnosed with ALS. By recently, I mean after my symptoms were pronounced and rapidly progressing. It took 6 weeks to make the first appointment, and another month to do a followup appointment for EMG’s.
The neurologist refused to prescribe the dexamethasone I needed, and I had to wait 10 days to get my own supply (I’m a psychiatrist and former emergency physician).
I decided to try the dexamethasone protocol for an acute exacerbation of Multiple Sclerosis (MS). This is 30mg daily for 7 days, then 4 to 12mg daily for one month (this dose turned out to be way too high). My only goal was to stop the progression of the disease. That is, rapid progression to total paralysis of all voluntary muscles, with certain death by suffocation, aspiration, or other equally unpleasant end.
I started the treatment on June 26, 2018. I noticed some improvement in my walking and hand dexterity in the first few days. But since then, I have had no further improvement. I did have a lot of trouble with steroid toxicity and withdrawal, with loss of balance, weakness and muscle atrophy. I was able to reduce the dosage all the way down to 0.1mg daily, but stiffness increased considerably while lowering the dose.
With the onset of cold weather this winter, I’ve had a lot of trouble walking because of stiffness and multiple falls. But the most important thing is that my eating, swallowing, breathing, talking, and typing haven’t deteriorated since June 26th.
Stopping ALS progression should be the only goal of this treatment. Dead nerve cells are dead. They never come back to life, so my ALS symptoms can never improve significantly either. But, by stopping the deadly progression of ALS, this experiment supports the hypothesis (now called a theory).
THEORY: ALS Is An Autoimmune Disease