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@Otter I was going to mention this documentary earlier when you mentioned cue's. If you aren't in Canada, you'd need to use a VPN to watch it some other method. There are CT scans and MRI's taken of cue's and a discussion about Naltrexone. Even if you cannot watch the video the summary is there and some images.
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@cheeto Otter is correct in saying that you don't have to quit drinking before or while taking Baclofen. However Gabapentin may work differently. There are Baclofen users who had terrible side effects until their dose was over 100mg, then it got better. @Ne1 comes to mind. I eventually found my drinking decreasing after a period of time, but then going back up again until I reached indifference. Even at that point I still had to decide to put down the bottle because of habit and just being emotionally dependent on the stuff.
Well naltrexone wasn't for me.Constantly felt unwell even after 3 weeks and everything tasted bad all day and everyday .Was in a constant bad mood and felt vey very depressed.Wasnt sure if was the naltrexone but after being off it for a while I'm sure it was.
So I'm returning to baclofen in desperation.Currently drinking 1.5 bottles of wine a day and just had liver function test that shows high protein and albumin so hoping bac works soon.On 75mg at the mo
Yeah the study is with 1800 - I saw a psych who was going to put me on 2400-2800 or something like that, and I've taken up to 3600mg a day on my own. But like I've said here and elsewhere, gabapentin really seems to have no effect on me whatsoever. So I don't want to present my experience with it as typical, just possible.
Also, dopamine imbalance is a cause of other problems.
"Several important diseases of the nervous system are associated with dysfunctions of the dopamine system, and some of the key medications used to treat them work by altering the effects of dopamine. Parkinson's disease, a degenerative condition causing tremor and motor impairment, is caused by a loss of dopamine-secreting neurons in an area of the midbrain called the substantia nigra. Its metabolic precursor L-DOPA can be manufactured, and in its pure form marketed as Levodopa is the most widely used treatment for the condition. There is evidence that schizophreniainvolves altered levels of dopamine activity, and most antipsychotic drugs used to treat this are dopamine antagonists which reduce dopamine activity. Similar dopamine antagonist drugs are also some of the most effective anti-nausea agents. Restless legs syndrome and attention deficit hyperactivity disorder (ADHD) are associated with decreased dopamine activity." Wikipedia
What we are seeing are a lot of new treatments for conditions like Parkinson's Disease using baclofen, for instance, You will need register or log in to read this content
Arbaclofen was developed to treat autism. When doctors treat alcoholism, they tend to think that they need to get the patient first to stop drinking (just like that) and then treat the underlying mental illness. But, the underlying illness and "alcoholism" are likely to be one and the same thing. Alcohol comsumption is just a way of self-medicating. Because we a haven't seen the association of both alcoholism and things like autism and ADHD with dopamine, we talk about alcoholics who say they are only self-medicating with alcohol as being irresponsible when, in fact, they are right. Alcohol does medicate this dysphoria. It's an anxiolytic, but it isn't specific to the illness in its effect. It affects the whole body and causes behaviours which people don't like, which are anti-social and unpleasant. Baclofen is specific to the GABAB receptors so it is a better, more effective "treatment" than alcohol.
My beef with people who downplay baclofen is that they overlook the science behind it but you can't blame them because even the scientists and doctors involved in baclofen research and treatment haven't even got to grips with isolating and identifying the illness and just call it alcoholism, which allows detractors to ignore the science. If we could get proper diagnosis of a clearly defined, identifiable disorder of the neurological system it would make it easier to explain and treat, without all the misinformation and antagonism between supporters of this research and others who are committed to AA or some other method. We could look at each form of treatment and measure it in terms of whether it works for this neurological condition and we could say whether or not the patient actually has the illness or drink for social reasons. I used to drink every day and I had anxiety, but not to the extent that I couldn't chocoose to have a coke rather than a glass of wine. I don't drink at all now and I don't have overwhelming anxiety so I don't have the illness. My alcohol consumption when I was in a stressful job did cause me to have worse anxiety, particularly Sunday night job anxiety so I'd always drink on a Sunday night to calm my pre-Monday, back to work anxiety. But, that's not "alcohollism". I didn't have an organic disorder. although continued alcohol consumption and stress may, I suppose, have pushed me towards having a bit of a problem and I found it hard to quit.
@Otter, like my GP. Its easy to dismiss effects in sobriety as being caused by alcohol use and not why alcohol use was initiated in the first place. Or even if something happened during the course of normal drinking that caused a major spike in consumption. The concept that once you have your first drink at 16 you opened a door doesn't nearly work in that situation as possibly you had a fall, a stroke, a car accident and alcohol or substance use spikes and becomes the fill in gap measure. So much assumption made by AA and the gen pop. Many may have been normal drinkers before something happened.