PLT Test Blog

Azosemide  C 12 H 11 ClN 6 O 2 S 2    Source: https://pubchem.ncbi.nlm.nih.gov/compound/azosemide Today’s post may be of interest to those already using bumetanide for autism and for those considering doing so .  It does go into the details, because they really do matter and does assume some prior knowledge from earlier posts. There has been a very thorough new paper published by a group at Johns Hopkins:- Off-Label Use of Bumetanide for Brain Disorders: An Overview It does cover all the usual issues and raises some points that have not been covered yet in this blog.   One point is treating autism prenatally. This issue was studied twice in rats, and the recent study was sent to me by Dr Ben Ari.   Short term treatment during pregnancy produced a permanent benefit. Maternal bumetanide treatment prevents the overgrowth in the VPA condition              Brief maternal administration of bumetanide before birth restores low ...

Today’s post is a little complicated, but should be relevant to parents already using bumetanide to reduce the severity of autism. Tuning neurons via Cl-sensitive WNK The science behind today’s post only started to evolve twenty years ago when it became understood how chloride enters and exits the neurons in your brain. Nonetheless there is now a vast amount of research and there are parts that have not yet been covered in this blog.   A moving target The first thing to realize is that trying to reduce the elevated level of chloride found in much autism is very much an ongoing battle. Chloride is flowing in too fast via NKCC1 and exiting too slowing via KCC2. If you want to reduce the entry via NKCC1, or increase the exit via KCC2, either of these two strategies should lower the equilibrium level of chloride.   Most strategies in this blog target NKCC1, but in another disease (neuropathic pain) the target has been KCC2. Whichever you target, the risk is that the body’s feedbac...