It is forced sobriety but hey, I will take it any way I can get it.
And the next time your head starts to think that a drink is a good idea all you have to do is stop the antabuse again. Relapses are not spur of the moment instantaneous things that pop up out of the blue, every person that I know that has relapsed once they start to get thier head back on straight see that the relapse really began long before they actually drank. Kind of like getting to lazy to take the antabuse.
Why do I drink? I really am a pretty happy person. I have a great life. I think I drink because I am happy.
Have you evey met anyone who drank because they are happy? I need to start a new thread on the roots of our drinking.
Well I had and still have a good life, the reason I drank for the last 20 years I drank was because I am an alcoholic!
I drank when life was grand, I drank when life sucked! I drank because the sun rose! I drank because I breathed, in the end I drank to exist.
You may want to speak to your doctor about how long you can safely take antabuse, here are some of the possible side effects which I would imagine with prolonged use the chances of at least one happening increase.
Side Effects of Antabuse - for the Consumer
Antabuse
All medicines may cause side effects, but many people have no, or minor, side effects. Check with your doctor if any of these most COMMON side effects persist or become bothersome when using Antabuse:
Drowsiness; headache; metallic or garlic taste in mouth.
Seek medical attention right away if any of these SEVERE side effects occur when using Antabuse:
Severe allergic reactions (rash; hives; difficulty breathing; tightness in the chest; swelling of the mouth, face, lips, or tongue); blurred vision; changes in color vision; dark urine; loss of appetite; mental or mood problems; nausea; numbness or tingling of the arms or legs; seizures; tiredness; vomiting; weakness; yellowing of the eyes or skin.
Antabuse Side Effects - for the Professional
Antabuse
OPTIC NEURITIS, PERIPHERAL NEURITIS, POLYNEURITIS, AND PERIPHERAL NEUROPATHY MAY OCCUR FOLLOWING ADMINISTRATION OF DISULFIRAM.
Multiple cases of hepatitis, including both cholestatic and fulminant hepatitis, as well as hepatic failure resulting in transplantation or death, have been reported with administration of disulfiram.
Occasional skin eruptions are, as a rule, readily controlled by concomitant administration of an antihistaminic drug.
In a small number of patients, a transient mild drowsiness, fatigability, impotence, headache, acneform eruptions, allergic dermatitis, or a metallic or garlic-like aftertaste may be experienced during the first two weeks of therapy. These complaints usually disappear spontaneously with the continuation of therapy, or with reduced dosage.
Psychotic reactions have been noted, attributable in most cases to high dosage, combined toxicity (with metronidazole or isoniazid), or to the unmasking of underlying psychoses in patients stressed by the withdrawal of alcohol.
Side Effects by Body System
Other
Disulfiram inhibits the metabolism of acetaldehyde, a breakdown product of alcohol. Acetaldehyde formation is at least partially responsible for the reaction. The "disulfiram reaction" generally occurs within 15 minutes of ingestion of alcohol and persists as long as alcohol is present in the system. Death has rarely been reported, generally when higher dosages are given. Patients should not receive disulfiram until 12 hours after any alcohol ingestion. Disulfiram reactions may occur up to two weeks after disulfiram has been discontinued.
The ingestion of alcohol in patients pretreated with disulfiram generally results in an unpleasant reaction referred to as a "disulfiram reaction". Elements of this reaction may include any of the following: flushing, throbbing in the head and neck, headache, nausea, vomiting, sweating, thirst, chest pain, palpitations, dyspnea, hyperventilation, tachycardia, confusion, arrhythmias, and convulsions.
Hepatic
Disulfiram-induced hepatitis has been confirmed by rechallenge in several cases. The development of hepatitis has been reported to occur within 2 weeks to several months of beginning disulfiram. Liver biopsy frequently demonstrates fibrosis, liver cell necrosis, eosinophilic infiltrates, and portal inflammation. Disulfiram-induced hepatitis appears to be due to hypersensitivity, although extrahepatic signs of hypersensitivity are not always apparent. Baseline liver function tests should be obtained and monitored periodically during the first several months of therapy. In addition, patients should be educated about the symptoms of hepatitis. Disulfiram therapy should be discontinued promptly if liver function deteriorates.
Hepatic side effects have included cases of acute hepatitis accompanied by fatigue, malaise, anorexia, nausea, abdominal pain, and jaundice. Although hepatic function has returned to normal over several weeks in some patients, liver failure and death has also been reported.
Subcutaneous deposits of carotene which simulate jaundice has been reported in a 55-year-old man who presented with yellow palms of the hands and the sole of the feet within 2 months of the start of disulfiram.
Nervous system
Nervous system side effects have included lethargy, confusion, personality changes, disorientation, and memory impairment. These effects may develop after weeks or months of disulfiram therapy. This has progressed to seizures (in the absence of a disulfiram-alcohol reaction), psychosis, catatonia and encephalopathy.
Neuropathy, generally affecting the lower extremities, occurs rarely in patients. The upper body extremities may become involved if neuropathy progresses. Optic neuritis has also been reported. Development appears to occur earlier with higher dosages. Neuropathy generally resolves over several weeks after discontinuation of disulfiram, and full recovery may require several months.
Reports of seizures, psychosis, catatonia, and encephalopathy usually follow several weeks of higher doses of disulfiram. The incidence appears to be lower with decreased maintenance dosages. Disulfiram is an inhibitor of dopamine-beta-hydroxylase which converts dopamine to norepinephrine. Therefore disulfiram effectively lowers levels of norepinephrine and increases concentrations of dopamine which may facilitate encephalopathy and other adverse effects on the nervous system.
Neuropathy associated with disulfiram is similar in appearance to that associated with alcohol abuse. Neuropathy primarily involves axonal degeneration and affects both sensory and motor nerves. It appears to develop somewhat faster than alcohol-induced neuropathy and develops in the absence of ongoing alcohol use. A metabolite of disulfiram, carbon disulfide, has been shown to be neurotoxic and may be involved in the development of neuropathy.
Dermatologic
Dermatologic side effects have include maculopapular rashes. Patients with a sensitivity to tetramethylthiuram disulfide, present in rubber products, may show cross-sensitivity to disulfiram.
Gastrointestinal
Gastrointestinal side effects have included an unpleasant metallic or garlic-like taste in the mouth and bad breath.
Ocular
Ocular side effects have included optic neuritis. It appears to occur earlier with higher dosages and generally resolves over several weeks after discontinuation of disulfiram. Full recovery may require several months.
Eventually you will have to stop taking it, whether by choice or due to side effects, what then?