Not sure why you think (and state in almost every thread) that ALS symptoms must go very quickly from nothing to full-time paralysis. This very rarely happens. Instead, initial symptoms are often subtle and/or intermittent in the beginning -- esp. any bulbar symptoms. Ask any neurologist, read any number of personal accounts from bulbar onset patients, or read a neurology text. People don't go from not choking at all to choking on everything overnight.
I hate to throw cold water on your little rant, but I've never said anything of that nature and I never will. Unlike your wild oversimplification of what you think I have said, I am careful to not make generalized statements like that.
ALS is a disease that kills motor neurons in the brain and spinal cord. Portions of a muscle (called fascicles, which are groups of muscle fibers) become denervated when their controlling motor neurons die. These fascicles can no longer contribute their share to the muscle's function, causing weakness and an accompanying loss of functionality proportionate to the percentage of total muscle fibers in the muscle that have been taken offline.
A denervated muscle fascicle stays in a state of paralysis unless and until it is reinnervated, which does occur in the earliest stages of ALS. This cycle of denervation and reinnervation causes changes in the "wiring" of the nerves and muscles -- fewer motor neurons controlling increasing percentages of the fibers in a given muscle (large MUPs, decreased recruitment, etc.) and it is these "wiring" changes that the EMG detects, even when the disease is still subclinical.
Eventually, the disease gets beyond the repair (reinnervation) capacity of the body and this is usually the stage when the clinical symptoms begin to appear. By the time ALS symptoms become clinically detectable, recognizable paralysis is occurring. The paralysis of the muscles is seen at the clinical level as clinical weakness, changes in muscle tone, altered responsiveness to reflex stimulation, and, eventually, muscle wasting. From that point forward, paralysis becomes greater and greater as more and more muscle fascicles are permanently denervated (paralyzed).
Furthermore, choking on liquids is initially caused by muscle coordination issues, not weakness. The windpipe fails to seal in proper timing with the swallow. Strength issues present in the form of trouble with swallowing solids.
Muscle coordination issues caused by what, exactly? What prevents the epiglottis from closing properly? What causes reduced laryngeal elevation or reduced pharyngeal contraction? Could it be denervated portions of muscles that can no longer play their assigned role in the action.
Early ALS does not equal paralysis. By the time a part of the body is paralyzed, ALS has been at work for quite some time. And by definition, anyone posting in this sub-forum is trying to assess whether he has early ALS -- not whether he has advanced ALS with rampant paralysis.
ALS, early or late, does equal paralysis. What differentiates the stages is simply the scale upon which the paralysis is detectable and measurable. Early ALS -- detectable by the EMG, subclinical. Intermediate (clinically detectable) ALS -- detectable by clinical examination as changes in the nature and quality of muscular contraction, muscle tone, and response to reflex stimulation. Late ALS -- total paralysis of a muscle and accompanying loss of bodily function, muscle wasting, easily seen by gross visual examination.
Don't know why you feel compelled to call me out, but setting fire to your own strawman really is only a Pyrrhic victory.