Baclofen is an analog of the inhibitory neurotransmitter GABA. What it does is open a pore in the cells in your spinal nerves that allows potassium to enter the cell and switch off the signaling that makes your muscles contract. The problem is Baclofen loves fat. Taken orally, you need to digest it and then pass it through your liver. Very little of what you take arrives at that pore. Hence the oral doses are quite large. Some people have a pump inserted that delivers about 1% of the dose you would swallow directly into a space between the meninges of your spine, called the intrathecal space. That takes it straight to the CSF. Your weakness is due to the ability of Baclofen to stop muscle contraction.
Maybe you could change the timing of your dose or reduce it and add more magnesium to your regimen. The magnesium will go directly to a receptor on the muscle called the ryanadine receptor. It won't make any difference to your spine. The Baclofen works in the central nervous system but the magnesium works on the muscle. Lower the Baclofen but increase the magnesium and see what happens.
Neuro-Mag Magnesium L-Threonate
Chelated Magnesium Glycinate
Absorption Magnesium Glycinate Lysinate
And there are others. Which do you suggest?
Magnesium threonate is supposed to be preferentially taken up by the brain. It's been found to increase synaptic density. I suggest that if you take it, you use it as an add-on to other magnesium supplements.
viewtopic.php?f=27&t=28183&p=243547&hil ... te#p243428
Magnesium oxide is difficult to absorb and has laxative effects.
Magnesium citrate may be better than the oxide form.
Magnesium glycinate is well absorbed. Both forms listed are amino acid chelates.
The one I take is predominately diglycinate as a chelated product. I think just means the magnesium is bonded to glycine and that makes it more easily absorbed. (happy to be corrected)
The tablet form I take is this one https://www.ethicalnutrients.com.au/pro ... -tablets-1
If you scroll down the page you can see the ingredients listed. It's a bit like a horse tablet but does work for me.
I take one morning and night. Sometimes, but not often, I take an extra one in the middle of the day. It does seem to make a difference.
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I take magnesium bisglycinate...have for several years. Helps me with my bowels, relaxes me and helps me sleep at night. If I miss a day or 2, I might get a cramp in a lower leg from a spasm. Magnesium Chloride gel also helps if I have burning heels at night. I sometimes put it on my hands at night too.
The Baclofen is centrally acting so it would make alcohol seem stronger (that's dose dependent). There is a receptor in your muscles called the ryanodine receptor that controls the release of calcium in your muscle cells. Alcohol has a high affinity for that receptor. If it blocks the receptor so calcium can't be released then you feel more relaxed. In that example it's working at the muscle level not at the nerve level. The Baclofen is working at the nerve level. I don't use Baclofen, but I wouldn't combine it with alcohol.
I'm unsure about the caffeine. It's molecule looks very similar to adenosine and can bind to its receptors (which is probably why it sometimes seems to perk you up). I don't think it's going to change spasticity outcomes but that's hard to predict at an individual level.
Limiting salt and added sugar is good for everyone.
Scott1 wrote: ↑Wed Aug 19, 2020 4:43 pmI'm unsure about the caffeine. It's molecule looks very similar to adenosine and can bind to its receptors (which is probably why it sometimes seems to perk you up). I don't think it's going to change spasticity outcomes but that's hard to predict at an individual level.
Caffeine and the central nervous system: mechanisms of action, biochemical, metabolic and psychostimulant effects
Brain Res Brain Res Rev. May-Aug 1992;17(2):139-70.
Caffeine is the most widely consumed central-nervous-system stimulant. Three main mechanisms of action of caffeine on the central nervous system have been described. Mobilization of intracellular calcium and inhibition of specific phosphodiesterases only occur at high non-physiological concentrations of caffeine. The only likely mechanism of action of the methylxanthine is the antagonism at the level of adenosine receptors. Caffeine increases energy metabolism throughout the brain but decreases at the same time cerebral blood flow, inducing a relative brain hypoperfusion. Caffeine activates noradrenaline neurons and seems to affect the local release of dopamine. Many of the alerting effects of caffeine may be related to the action of the methylxanthine on serotonin neurons. The methylxanthine induces dose-response increases in locomotor activity in animals. Its psychostimulant action on man is, however, often subtle and not very easy to detect. The effects of caffeine on learning, memory, performance and coordination are rather related to the methylxanthine action on arousal, vigilance and fatigue. Caffeine exerts obvious effects on anxiety and sleep which vary according to individual sensitivity to the methylxanthine. However, children in general do not appear more sensitive to methylxanthine effects than adults. The central nervous system does not seem to develop a great tolerance to the effects of caffeine although dependence and withdrawal symptoms are reported.