Drinking Before BFS?

[melyssa221]

How many of you all were drinkers before BFS?

lite
moderate
heavy


just wondering (liver therory)

Anybody with BfS know what their exact liver test numbers are??
ALT? AST?

i heard alot of people with BFS have slightly elevated ALT and AST...or if it was normal it was in the high normal

optimal ALT and AST range is 21

I was a moderate drinker...weekend warroir..my liver ALT averages Around 58 high normal and My AST around 40-80 again slightly elevated

again your doctor might have told you your blood work was normal....but it might be in the high normal range..Just pursuing the liver theory...would love to know about the rest of us

aaron

 

[dylan.dibber1]

a severe hangover preceded my first twitches back in january, 2000. my liver tests have all been normal, even better than normal, though, so i don't think alcohol or liver function is involved. haven't had a biopsy, mind you, but with all the other numbers looking good i don't see much point.

 

[Nimbus899]

I am fascinated by the theoretical connection, as alcohol is indisputably toxic to the CNS, and alcoholic neuropathies/myopothies are well known.

What I do know is that a hangover tends to exacerbate the fasciculations -- the mechanism is unknown to me, but it intuitively makes sense. Of course, it could just be another feature of thw withdrawal syndrome that "we" BFS-types just happen to suffer in addition to the unpleasant constellation of miserable stuff you endure from over indulging.

I do not believe that alcohol, however, is a "trigger," as it were for ALS or other MNDs. There is absolutely no evidence for that proposition, and I have put the question to a few good neurologists, and they concur that it's bunk.

 

[Mike1980]

Nope. Sorry. Drinks are few and far between and when I have had them it has been one or two. For a guy my size (6'4" 230 lbs.) one beer makes the world spin. I figure it is best to avoid it.

My problems started after a back,neck, shoulder, arm injury jumping off a telephone pole on a ropes course.

 

[Ezecon75]

Lets take the guess work out and replace it with facts. Nerve transmission is based on flow of ions in/out of the cell components of the CNS. The flow of these ions (ions are charged particles thus we have electrical activity at work) is regulated by pores in the wall of the cell, referred to as the cellular membrane.

When the brain initiates a signal to move a muscle, a chain of chemical reactions occur along the nerve by the flow of these ions that changing the voltage potential from positive to negative and so on until it reaches the synapse-the junction between the nerve and muscle. At the synapse, neurotransmitters (there are many in the body) are released that bind to the neuro-receptor at the muscle that ultimately creates a muscle contraction.

On the flip side, inhibitors are also released (GABA is the main one) that stops or inhibits the neurotransmitter from having a prolonged effect (e.g. continued muscle contraction). Alcohol or more specifically ethanol, is a chemical that changes the cell membrane potential by allowing more flux of Chlorine ions in/out of the cell. Ethanol binds to the protein on the cell membrane and ultimately increases the effect of the “inhibitory” response to a neurotransmitter.

In contrast a muscle twitch is a spontaneous and involuntary muscle contraction which involves the flux of potassium ions related to an “excitatory” state not an “inhibitory” one. That’s why neurologists call it bunk (and so do anesthesiologists).

If there was any relation to alcohol and muscle twitching the alcohol should reduce it because it in directly increases the inhibitory effect in a muscle contraction. That’s why our great-great-great grand daddies were given a bottle of J/D whiskey when the doctor pulled the bullet of their guts. Alcohol is an anesthetic!

Further evidenced by Isaac in 1961 who observed that application of a local anesthetic to the nerve did not make muscle twitching stop in patients presenting with BFS type symptoms. This led to him to use curare to block the neurotransmission chemical at the neuromuscular junction (synapse) where upon the twitching ceased. Therefore, benign muscle twitching has root in the hyper excitability state of the peripheral nerves.

More specifically, recent research has accumulating and mounting evidence that our muscle twitching is caused by changes in the cell membrane that controls the flux of potassium ions. Potassium ions are responsible for controlling the cells membrane potential at the neuro-receptor. At this hyper excited state, neurotransmitters are released to elicit an involuntary muscle contraction-has not relation to the loss of neurons in a motor neuron disease like ALS.

Nice theories, but bio-chemistry rules in this case!