Does anyone know the research?
Member of SMART Recovery
Join Date: Mar 2010
Posts: 1,722
What the research actually shows is that a significant percentage of formerly alcohol dependent people do return to safe levels of drinking:
"More than one-third (35.9 percent) of U.S. adults with alcohol dependence (alcoholism) that began more than one year ago are now in full recovery, according to an article in the current issue of Addiction. The fully recovered individuals show symptoms of neither alcohol dependence nor alcohol abuse and either abstain or drink at levels below those known to increase relapse risk. They include roughly equal proportions of abstainers (18.2 percent) and low-risk drinkers (17.7 percent). The analysis is based on data from the 2001-2002 National Epidemiologic Survey on Alcohol and Related Conditions (NESARC), a project of the National Institutes of Health's National Institute on Alcohol Abuse and Alcoholism (NIAAA)."
2001-2002 Survey Finds that Many Recover from Alcoholism: Researchers Identify Factors Associated with Abstinent and Non-Abstinent Recovery
What the research CANNOT show is whether you, personally, are someone who can return to safe levels of drinking, or whether, like me, you are someone who will do better with complete abstinence. Unfortunately, that is something you must determine for yourself.
I know that in my own case, 25 years of drinking, with periodic unsuccessful attempts to cut down, lead me to the firm conclusion that I am not someone who can safely consume alcohol at any level. That being the case, abstinence was the only choice and abstinence saved my life. What is the answer for you? You might want to try using one of the SMART Recovery tools, called a CBA or "cost benefit analysis" to help you take a close look at your drinking and its real impact on your life.
OTT
"More than one-third (35.9 percent) of U.S. adults with alcohol dependence (alcoholism) that began more than one year ago are now in full recovery, according to an article in the current issue of Addiction. The fully recovered individuals show symptoms of neither alcohol dependence nor alcohol abuse and either abstain or drink at levels below those known to increase relapse risk. They include roughly equal proportions of abstainers (18.2 percent) and low-risk drinkers (17.7 percent). The analysis is based on data from the 2001-2002 National Epidemiologic Survey on Alcohol and Related Conditions (NESARC), a project of the National Institutes of Health's National Institute on Alcohol Abuse and Alcoholism (NIAAA)."
2001-2002 Survey Finds that Many Recover from Alcoholism: Researchers Identify Factors Associated with Abstinent and Non-Abstinent Recovery
What the research CANNOT show is whether you, personally, are someone who can return to safe levels of drinking, or whether, like me, you are someone who will do better with complete abstinence. Unfortunately, that is something you must determine for yourself.
I know that in my own case, 25 years of drinking, with periodic unsuccessful attempts to cut down, lead me to the firm conclusion that I am not someone who can safely consume alcohol at any level. That being the case, abstinence was the only choice and abstinence saved my life. What is the answer for you? You might want to try using one of the SMART Recovery tools, called a CBA or "cost benefit analysis" to help you take a close look at your drinking and its real impact on your life.
OTT
Member
Join Date: Dec 2008
Location: nj
Posts: 541
some research:
>> Alcohol also is metabolized in the liver by the enzyme cytochrome P450IIE1 (CYP2E1), which may be increased after chronic drinking. Lieber, C.S. Metabolic consequences of ethanol. The Endocrinologist 4(2):127-139, 1994.
>> Long-term alcohol abuse produces physiological changes in the brain such as tolerance and physical dependence. Such brain chemistry changes maintain the alcoholic's compulsive inability to stop drinking and result in alcohol withdrawal syndrome upon discontinuation of alcohol consumption. Hoffman, PL.; Tabakoff, B. (Jul 1996). "Alcohol dependence: a commentary on mechanisms." Alcohol 31 (4): 333-40. For an abstract of this article (published back in 1996, a long time ago) see: Alcohol dependence: a commentary on mechanisms. [Alcohol Alcohol. 1996] - PubMed result
The biochemistry is backed up by other types of studies:
>> For example, does "moderation management" work? Almost no alcoholic who tries this can continue to drink moderately for more than ten years without either (a) relapsing back into uncontrolled drinking or (c) stopping all drinking absolutely. See the study by George Vaillant at Harvard Medical School:
>> "A long-term (60 year) follow-up of two groups of alcoholic men concluded that 'return to controlled drinking rarely persisted for much more than a decade without relapse or evolution into abstinence.' Vaillant also noted that 'return-to-controlled drinking, as reported in short-term studies, is often a mirage.'" Vaillant, GE (2003). "A 60-year follow-up of alcoholic men". Addiction (Abingdon, England) 98 (8): 1043-51.
____________________________________________
AT SLIGHTLY GREATER LENGTH, SEE:
Alcohol Metabolism
Alcohol Metabolism
An informational bulletin from the NIAAA (National Institute of Alcohol Abuse and Alcoholism)
(This government agency, which is part of the U.S. government's National Institutes of Health, was originally put into its present form as part of the process of passing the Hughes Act. Nancy Olson, the founder of the AAHistoryLovers, was the principal senatorial aide in charge of the passage and implementation of the Hughes Act.)
Metabolism is the body's process of converting ingested substances to other compounds. Metabolism results in some substances becoming more, and some less, toxic than those originally ingested. Metabolism involves a number of processes, one of which is referred to as oxidation.
Through oxidation, alcohol is detoxified and removed from the blood, preventing the alcohol from accumulating and destroying cells and organs. A minute amount of alcohol escapes metabolism and is excreted unchanged in the breath and in urine. Until all the alcohol consumed has been metabolized, it is distributed throughout the body, affecting the brain and other tissues.
When alcohol is consumed, it passes from the stomach and intestines into the blood, a process referred to as absorption. Alcohol is then metabolized by enzymes, which are body chemicals that break down other chemicals. In the liver, an enzyme called alcohol dehydrogenase (ADH) mediates the conversion of alcohol to acetaldehyde. Acetaldehyde is rapidly converted to acetate by other enzymes and is eventually metabolized to carbon dioxide and water. Alcohol also is metabolized in the liver by the enzyme cytochrome P450IIE1 (CYP2E1), which may be increased after chronic drinking.* Most of the alcohol consumed is metabolized in the liver, but the small quantity that remains unmetabolized permits alcohol concentration to be measured in breath and urine.
*Lieber, C.S. Metabolic consequences of ethanol. The Endocrinologist
4(2):127-139, 1994.
Alcohol Metabolism--A Commentary by NIAAA Director Enoch Gordis, M.D.
With respect to its broader scientific application, metabolism, which has long been studied, is emerging with new implications for the study of alcoholism and its medical consequences. For instance, how is metabolism related to the resistance of some individuals to alcoholism? We know that some inherited abnormalities in metabolism (e.g., flushing reaction among some persons of Asian descent) promote resistance to alcoholism. Recent data from two large-scale NIAAA-supported genetics studies suggest that alcohol dehydrogenase genes may be associated with differential resistance and vulnerability to alcohol. These findings are important to the study of why some people develop alcoholism and others do not. Studies of metabolism also can identify alternate paths of alcohol metabolism, which may help explain how alcohol speeds up the elimination of some substances (e.g., barbiturates) and increases the toxicity of others (e.g., acetaminophen). This information will help health care providers in advising patients on alcohol-drug interactions that may decrease the effectiveness of some therapeutic medications or render others harmful.
FOR MORE DETAILS SEE this NIAAA publication:
NIAAA Publications
- - - -
Alcoholism
http://en.wikipedia.org/wiki/Alcoholism
Long-term alcohol abuse produces physiological changes in the brain such as tolerance and physical dependence. Such brain chemistry changes maintain the alcoholic's compulsive inability to stop drinking and result in alcohol withdrawal syndrome upon discontinuation of alcohol consumption.**
Alcohol's primary effect is the increase in stimulation of the GABAA receptor, promoting central nervous system depression. With repeated heavy consumption of alcohol, these receptors are desensitized and reduced in number, resulting in tolerance and physical dependence. When alcohol consumption is stopped too abruptly, the person's nervous system suffers from uncontrolled synapse firing.
Genetic differences exist between different racial groups which affect the risk of developing alcohol dependence. For example, there are differences between African, East Asian and Indo-racial groups in how they metabolize alcohol. These genetic factors are believed to, in part, explain the differing rates of alcohol dependence among racial groups.
**Hoffman, PL.; Tabakoff, B. (Jul 1996). "Alcohol dependence: a commentary on mechanisms.". Alcohol Alcohol 31 (4): 333-40. For an abstract of this article (published back in 1996, a long time ago) see: Alcohol dependence: a commentary on mechanisms. [Alcohol Alcohol. 1996] - PubMed result 1996 Jul;31(4):333-40.
Alcohol dependence: a commentary on mechanisms. Hoffman PL, Tabakoff B. Department of Pharmacology, University of Colorado Health Sciences Center, Denver 80262, USA.
Abstract: The alcohol dependence syndrome includes the presence of alcohol tolerance, physical dependence and an inability to control one's alcohol intake. Studies are reviewed that implicate the mesolimbic dopaminergic systems, and the gamma-aminobutyric acid-A (GABAA) and N-methyl-D-aspartate (NMDA) receptors as mediators of various aspects of the alcohol dependence syndrome. It is suggested that alcohol-induced changes in the GABAA receptor may play a role in certain aspects of tolerance to alcohol and in altered abilities of an individual to terminate alcohol intake. Chronic alcohol-induced increases in the activity of NMDA receptors may contribute to the withdrawal signs that are the defining feature of physical dependence on alcohol. It is hypothesized that decreased mesolimbic dopaminergic function, which occurs during alcohol withdrawal, may be involved in the compulsion to initiate and maintain alcohol drinking, another aspect of the alcohol dependence syndrome. Furthermore, evidence is presented that this decreased dopaminergic function could occur secondarily to the increase in NMDA receptor function, such that the alcohol-induced increase in NMDA receptor function could underlie both the overt withdrawal signs and the compulsion to drink alcohol in the alcohol-dependent individual.
Does "moderation management" work? Almost no alcoholic who tries this can continue to drink moderately for more than ten years without either (a) relapsing back into uncontrolled drinking or (c) stopping all drinking absolutely. See the study by George Vaillant at Harvard Medical School:
"A long-term (60 year) follow-up of two groups of alcoholic men concluded that 'return to controlled drinking rarely persisted for much more than a decade without relapse or evolution into abstinence.' Vaillant also noted that 'return-to-controlled drinking, as reported in short-term studies, is often a mirage.'"***
***Vaillant, GE (2003). "A 60-year follow-up of alcoholic men". Addiction (Abingdon, England) 98 (8): 1043-51.
- - - -
Ethanol metabolism - Wikipedia, the free encyclopedia
Acetyl coenzyme A or acetyl-CoA is an important molecule in metabolism, used in many biochemical reactions. Its main function is to convey the carbon atoms within the acetyl group to the citric acid cycle to be oxidized for energy production.
The reaction from ethanol to carbon dioxide and water is a complex one that proceeds in three steps. Complete Reaction: C2H6O(Ethanol)?C2H4O(Acetaldehyde)?C2H4O2(acetic Acid) ?Acetyl-CoA?3H2O+2CO2.
Ethanol is oxidized to acetaldehyde via the enzyme alcohol dehydrogenase IB (class I), beta polypeptide (ADH1B). The gene coding for this enzyme is 1.1.1.1 on chromosome 4, locus 4q21-q23.
Acetaldehyde is a highly unstable compound and quickly forms free radical structures which are highly toxic if not quenched by antioxidants such as ascorbic acid (Vitamin C) and Vitamin B1 (thiamine). These free radicals can result in damage to embryonic neural crest cells and can lead to severe birth defects. Prolonged exposure of the kidney and liver to these compounds in chronic alcoholics can lead to severe damage. The literature also suggests that these toxins may have a hand in causing some of the ill effects associated with hang-overs.
Acetaldehyde to acetic acid: Aldehyde dehydrogenase is the second enzyme of the major oxidative pathway of alcohol metabolism. Two major liver isoforms of this enzyme, cytosolic and mitochondrial, can be distinguished by their electrophoretic mobilities, kinetic properties, and subcellular localizations. Most Caucasians have two major isozymes, while approximately 50% of Asians have only the cytosolic isozyme, missing the mitochondrial isozyme. A remarkably higher frequency of acute alcohol intoxication among Asians than among Caucasians could be related to the absence of the mitochondrial isozyme.
>> Alcohol also is metabolized in the liver by the enzyme cytochrome P450IIE1 (CYP2E1), which may be increased after chronic drinking. Lieber, C.S. Metabolic consequences of ethanol. The Endocrinologist 4(2):127-139, 1994.
>> Long-term alcohol abuse produces physiological changes in the brain such as tolerance and physical dependence. Such brain chemistry changes maintain the alcoholic's compulsive inability to stop drinking and result in alcohol withdrawal syndrome upon discontinuation of alcohol consumption. Hoffman, PL.; Tabakoff, B. (Jul 1996). "Alcohol dependence: a commentary on mechanisms." Alcohol 31 (4): 333-40. For an abstract of this article (published back in 1996, a long time ago) see: Alcohol dependence: a commentary on mechanisms. [Alcohol Alcohol. 1996] - PubMed result
The biochemistry is backed up by other types of studies:
>> For example, does "moderation management" work? Almost no alcoholic who tries this can continue to drink moderately for more than ten years without either (a) relapsing back into uncontrolled drinking or (c) stopping all drinking absolutely. See the study by George Vaillant at Harvard Medical School:
>> "A long-term (60 year) follow-up of two groups of alcoholic men concluded that 'return to controlled drinking rarely persisted for much more than a decade without relapse or evolution into abstinence.' Vaillant also noted that 'return-to-controlled drinking, as reported in short-term studies, is often a mirage.'" Vaillant, GE (2003). "A 60-year follow-up of alcoholic men". Addiction (Abingdon, England) 98 (8): 1043-51.
____________________________________________
AT SLIGHTLY GREATER LENGTH, SEE:
Alcohol Metabolism
Alcohol Metabolism
An informational bulletin from the NIAAA (National Institute of Alcohol Abuse and Alcoholism)
(This government agency, which is part of the U.S. government's National Institutes of Health, was originally put into its present form as part of the process of passing the Hughes Act. Nancy Olson, the founder of the AAHistoryLovers, was the principal senatorial aide in charge of the passage and implementation of the Hughes Act.)
Metabolism is the body's process of converting ingested substances to other compounds. Metabolism results in some substances becoming more, and some less, toxic than those originally ingested. Metabolism involves a number of processes, one of which is referred to as oxidation.
Through oxidation, alcohol is detoxified and removed from the blood, preventing the alcohol from accumulating and destroying cells and organs. A minute amount of alcohol escapes metabolism and is excreted unchanged in the breath and in urine. Until all the alcohol consumed has been metabolized, it is distributed throughout the body, affecting the brain and other tissues.
When alcohol is consumed, it passes from the stomach and intestines into the blood, a process referred to as absorption. Alcohol is then metabolized by enzymes, which are body chemicals that break down other chemicals. In the liver, an enzyme called alcohol dehydrogenase (ADH) mediates the conversion of alcohol to acetaldehyde. Acetaldehyde is rapidly converted to acetate by other enzymes and is eventually metabolized to carbon dioxide and water. Alcohol also is metabolized in the liver by the enzyme cytochrome P450IIE1 (CYP2E1), which may be increased after chronic drinking.* Most of the alcohol consumed is metabolized in the liver, but the small quantity that remains unmetabolized permits alcohol concentration to be measured in breath and urine.
*Lieber, C.S. Metabolic consequences of ethanol. The Endocrinologist
4(2):127-139, 1994.
Alcohol Metabolism--A Commentary by NIAAA Director Enoch Gordis, M.D.
With respect to its broader scientific application, metabolism, which has long been studied, is emerging with new implications for the study of alcoholism and its medical consequences. For instance, how is metabolism related to the resistance of some individuals to alcoholism? We know that some inherited abnormalities in metabolism (e.g., flushing reaction among some persons of Asian descent) promote resistance to alcoholism. Recent data from two large-scale NIAAA-supported genetics studies suggest that alcohol dehydrogenase genes may be associated with differential resistance and vulnerability to alcohol. These findings are important to the study of why some people develop alcoholism and others do not. Studies of metabolism also can identify alternate paths of alcohol metabolism, which may help explain how alcohol speeds up the elimination of some substances (e.g., barbiturates) and increases the toxicity of others (e.g., acetaminophen). This information will help health care providers in advising patients on alcohol-drug interactions that may decrease the effectiveness of some therapeutic medications or render others harmful.
FOR MORE DETAILS SEE this NIAAA publication:
NIAAA Publications
- - - -
Alcoholism
http://en.wikipedia.org/wiki/Alcoholism
Long-term alcohol abuse produces physiological changes in the brain such as tolerance and physical dependence. Such brain chemistry changes maintain the alcoholic's compulsive inability to stop drinking and result in alcohol withdrawal syndrome upon discontinuation of alcohol consumption.**
Alcohol's primary effect is the increase in stimulation of the GABAA receptor, promoting central nervous system depression. With repeated heavy consumption of alcohol, these receptors are desensitized and reduced in number, resulting in tolerance and physical dependence. When alcohol consumption is stopped too abruptly, the person's nervous system suffers from uncontrolled synapse firing.
Genetic differences exist between different racial groups which affect the risk of developing alcohol dependence. For example, there are differences between African, East Asian and Indo-racial groups in how they metabolize alcohol. These genetic factors are believed to, in part, explain the differing rates of alcohol dependence among racial groups.
**Hoffman, PL.; Tabakoff, B. (Jul 1996). "Alcohol dependence: a commentary on mechanisms.". Alcohol Alcohol 31 (4): 333-40. For an abstract of this article (published back in 1996, a long time ago) see: Alcohol dependence: a commentary on mechanisms. [Alcohol Alcohol. 1996] - PubMed result 1996 Jul;31(4):333-40.
Alcohol dependence: a commentary on mechanisms. Hoffman PL, Tabakoff B. Department of Pharmacology, University of Colorado Health Sciences Center, Denver 80262, USA.
Abstract: The alcohol dependence syndrome includes the presence of alcohol tolerance, physical dependence and an inability to control one's alcohol intake. Studies are reviewed that implicate the mesolimbic dopaminergic systems, and the gamma-aminobutyric acid-A (GABAA) and N-methyl-D-aspartate (NMDA) receptors as mediators of various aspects of the alcohol dependence syndrome. It is suggested that alcohol-induced changes in the GABAA receptor may play a role in certain aspects of tolerance to alcohol and in altered abilities of an individual to terminate alcohol intake. Chronic alcohol-induced increases in the activity of NMDA receptors may contribute to the withdrawal signs that are the defining feature of physical dependence on alcohol. It is hypothesized that decreased mesolimbic dopaminergic function, which occurs during alcohol withdrawal, may be involved in the compulsion to initiate and maintain alcohol drinking, another aspect of the alcohol dependence syndrome. Furthermore, evidence is presented that this decreased dopaminergic function could occur secondarily to the increase in NMDA receptor function, such that the alcohol-induced increase in NMDA receptor function could underlie both the overt withdrawal signs and the compulsion to drink alcohol in the alcohol-dependent individual.
Does "moderation management" work? Almost no alcoholic who tries this can continue to drink moderately for more than ten years without either (a) relapsing back into uncontrolled drinking or (c) stopping all drinking absolutely. See the study by George Vaillant at Harvard Medical School:
"A long-term (60 year) follow-up of two groups of alcoholic men concluded that 'return to controlled drinking rarely persisted for much more than a decade without relapse or evolution into abstinence.' Vaillant also noted that 'return-to-controlled drinking, as reported in short-term studies, is often a mirage.'"***
***Vaillant, GE (2003). "A 60-year follow-up of alcoholic men". Addiction (Abingdon, England) 98 (8): 1043-51.
- - - -
Ethanol metabolism - Wikipedia, the free encyclopedia
Acetyl coenzyme A or acetyl-CoA is an important molecule in metabolism, used in many biochemical reactions. Its main function is to convey the carbon atoms within the acetyl group to the citric acid cycle to be oxidized for energy production.
The reaction from ethanol to carbon dioxide and water is a complex one that proceeds in three steps. Complete Reaction: C2H6O(Ethanol)?C2H4O(Acetaldehyde)?C2H4O2(acetic Acid) ?Acetyl-CoA?3H2O+2CO2.
Ethanol is oxidized to acetaldehyde via the enzyme alcohol dehydrogenase IB (class I), beta polypeptide (ADH1B). The gene coding for this enzyme is 1.1.1.1 on chromosome 4, locus 4q21-q23.
Acetaldehyde is a highly unstable compound and quickly forms free radical structures which are highly toxic if not quenched by antioxidants such as ascorbic acid (Vitamin C) and Vitamin B1 (thiamine). These free radicals can result in damage to embryonic neural crest cells and can lead to severe birth defects. Prolonged exposure of the kidney and liver to these compounds in chronic alcoholics can lead to severe damage. The literature also suggests that these toxins may have a hand in causing some of the ill effects associated with hang-overs.
Acetaldehyde to acetic acid: Aldehyde dehydrogenase is the second enzyme of the major oxidative pathway of alcohol metabolism. Two major liver isoforms of this enzyme, cytosolic and mitochondrial, can be distinguished by their electrophoretic mobilities, kinetic properties, and subcellular localizations. Most Caucasians have two major isozymes, while approximately 50% of Asians have only the cytosolic isozyme, missing the mitochondrial isozyme. A remarkably higher frequency of acute alcohol intoxication among Asians than among Caucasians could be related to the absence of the mitochondrial isozyme.
Member
Join Date: Jun 2009
Location: New Jersey
Posts: 232
Originally Posted by SSIL75 
I and a lot of others have found that the 'stigma' is a figment of your alcoholic imagination. In reality nobody cares if you drink or not. Just your alcoholic self 
That is so true. Normal drinkers don't even notice such things. Or care. We're the only ones who obsess about it. Even been around someone trying to quit smoking? They seem to know who all the smokers in the room are, what brand they smoke and their smoking schedule. It's amazing.
Member
Join Date: Jun 2010
Location: NC
Posts: 1,737
AM,
I highly suggest you read Under the Influence - its an $8 paperback with a ton of info - its a little dated, but its more than enough to get you started if you want really in depth &/or recent medical research data later.
I highly suggest you read Under the Influence - its an $8 paperback with a ton of info - its a little dated, but its more than enough to get you started if you want really in depth &/or recent medical research data later.
Member
Join Date: Jul 2010
Location: New England
Posts: 5,285
Member
Join Date: Feb 2009
Location: SoCal
Posts: 222
Everyone is different. I believe I can have a "drink or two" and be alright, because for me that isnt really enough to feel anything/turn that "switch" on.
IS it a good idea to tempt fate like that though? NO!
IS it a good idea to tempt fate like that though? NO!
Member
Join Date: Mar 2011
Location: New York
Posts: 8
Hey April - I am also 25, also drank pretty heavily for the past 7-8 years, and recently have been at my all-time worst (past 6 months). Like you, I would LOVE to just be able to have like 2 (maybe 3?) drinks in a setting and be content. I wish nothing more than to be able to do that. It is almost impossible. I'm not preaching against you, I am on your side. I am not yet sober in my life and still attempt to have those evenings with friends (two, three drinks) and it just never pans out. I'm considering attending an AA meeting also. The fact of the matter is, I can be out with my friends..we'll all drink the same amount roughly (way too much) but it is almsot always just ME that it affects so much worse, both that evening and the next day. That is how I view it. Many people drink about the same amount as an alcohol abuser does but it's how they act and how it affects them that splits the crowd..at least in my experience. Hope that helps you.
Nick
Nick
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