Addiction is a disease

skeptigirl said:
You will have increased tolerance if you are a regular binge drinker. It is a physical change in the liver....
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However, later destruction of the liver leads to reduced tolerance because it takes longer to metabolize the alcohol. It takes less to keep you drunk.
 
Simone said:
Everyone is different in ways that our bodies process alcohol. I'm sure there can be studies of groups of people and the comparisons would be similiar, but how accurate can they really be?
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Very. The studies are more extensive than perhaps you are aware.

Simone said:
I have a friend that can drink 2 bottles of wine, she hardly eats, never gets a hangover, yes, alcoholism is in her family and she is fine the next day. She has an unrelated liver disease that is hereditary, that if not discovered early enough, the person can die and the diagnosis is often misdiagnosed as liver disease or cirrhosis of the liver. I, on the other hand, also have alcoholism in my family, have had an excess of alcohol at different times, which really isn't alot to some people, usually will be physically ill for 2 days. But I have been told that even tho I didn't appear intoxicated and I functioned pretty normal as one would say, my friend would be clearly drunk and would be staggering.
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I'm not sure what your point is here. You are only giving a tiny slice of details and it isn't enough to go on. Not everyone who has relatives with alcoholism will go on to be an alcoholic. And a person who can drink two bottles of wine in one night may not have yet crossed the threshold of becoming dependent, but they are at least at a very high risk of doing so.

Simone said:
Another example, I was in a class where individuals drank and were given field sobriety tests. After the tests were given, the individuals were given blood alcohol tests, where they blow into the machine to see what their levels were. The one female, who appeared to be intoxicated the most, who failed her field testing, ( standing on one foot, etc) did poorly on all accounts. Her alcohol level was not legal, but was one of the lowest. The male, who appeared to be the least drunk, passed the field tests, except the eye test that one has no control over. His blood alcohol was 3 times the others. Does this mean he is the seasoned alcoholic? Or just his body processed alcohol differently? Is he a functioning alcoholic?
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Depends on how much he drank but it sounds like he might be. And it is also true women seem to have lower tolerance for intoxication on average.

Simone said:
I know this is a bit off on the "is addiction a disease" track, but with alcoholism, with studies and tests, how can they really determine this unless every single human being is tested?
Addictions come in all forms, and no, it shouldn't be defined as a disease, can you say a sex addict has a disease? Sure, if they had alot of unprotected sex, they get the disease. Alcoholism can create liver disease and so forth, but it alone, no, its not a disease.
I think I am done now.
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Is compulsive-obsessive disorder a disease?

Diseases can have behavioral components. Many aspects of alcoholism fit well within the disease model. The most compelling on strictly an objective basis is that identical twins raised apart have similar rates of alcoholism and fraternal twins raised apart have dissimilar rates.
 
liver changes
Bradford BU; Rusyn I. Swift increase in alcohol metabolism (SIAM): Understanding the phenomenon of hypermetabolism in liver. Alcohol 35(1): 13-17, 2005. (35 refs.)
The swift increase in alcohol metabolism (SIAM) is a phenomenon defined as a rapid increase in hepatic respiration and alcohol metabolism after administration of a bolus dose of alcohol. Continuous exposure to alcohol is known to produce adaptive changes in liver alcohol and oxygen metabolism. A considerable burst of hepatic respiration can also occur after administration of a single large dose of alcohol and results in a near doubling of alcohol metabolism, a high demand for oxygen, and downstream or pericentral hypoxia. These dramatic changes in rates of alcohol metabolism and tissue concentrations of oxygen are not due to induced enzyme activity in liver. This phenomenon depends on activation of mitochondrial function, an increase in co-factor supply for nicotinamide adenine dinucleotide-dependent alcohol metabolism, depletion of glycogen reserves, liberation of fatty acids through activation of an adrenergic response to alcohol providing substrate for catalase, and activation of Kupffer cells, the hepatic resident macrophages responsible for production of cytokines and prostaglandins. An understanding of the mechanisms of hypermetabolism in liver can have vital ramifications for knowledge of both alcohol-related and alcohol-unrelated liver injury because hypoxia that is a result of hypermetabolism can compound effects of pharmaceuticals and environmental agents on the liver. Swift increase in alcohol metabolism is an excellent example of the complexity of cell-cell interactions in liver and extrahepatic regulation of biochemical and molecular events in this organ, and this important phenomenon shall be considered in studies of liver disease and biochemistry.

Copyright 2005, Elsevier Science

Chai YG; Oh DY; Chung EK; Kim GS; Kim L; Lee YS et al. Alcohol and aldehyde dehydrogenase polymorphisms in men with type I and type II alcoholism. American Journal of Psychiatry 162(5): 1003+, 2005. (7 refs.)
Objective: The authors examined the genetic polymorphisms of alcohol dehydrogenase 2 and 3 (ADH2 and ADH3) and aldehyde dehydrogenase (ALDH2) in patients diagnosed as having Cloninger's type I or type II alcoholism. Method: Seventy-two alcoholic men and 38 nonalcoholic, healthy men were tested for the distribution of genotypes and alleles of ADH2, ADH3, and ALDH2. Forty-eight of the alcoholic men had type I alcoholism, and 24 had type II alcoholism. Results: The frequencies of ADH2* 1 and ADH3* 2 alleles were significantly higher in men with type II alcoholism than in men with type I alcoholism and healthy men. The frequency of the ALDH2* 1 allele was significantly higher in men with alcohol dependence than in healthy men. Conclusions: The genetic characteristics of alcohol dehydrogenases in men with type I alcoholism were similar to those of healthy men, and the genetic characteristics of aldehyde dehydrogenase in men with type I alcoholism were similar to those of men with type II alcoholism. These findings suggest that the genetic characteristics of alcohol metabolism in type I alcoholism fall between nonalcoholism and type II alcoholism.

Copyright 2005, American Psychiatric Association. Used with permission

Lieber CS. The discovery of the microsomal ethanol oxidizing system and its physiologic and pathologic role. (review). Drug Metabolism Reviews 36(3-4): 511-529, 2004. (117 refs.)
Oxidation of ethanol via alcohol dehydrogenase (ADH) explains various metabolic effects of ethanol but does not account for the tolerance. This fact, as well as the discovery of the proliferation of the smooth endoplasmic reticulum (SER) after chronic alcohol consumption, suggested the existence of an additional pathway which was then described by Lieber and DeCarli, namely the microsomal ethanol oxidizing system (MEOS), involving cytochrome P450. The existence of this system was initially challenged but the effect of ethanol on liver microsomes was confirmed by Remmer and his group. After chronic ethanol consumption, the activity of the MEOS increases, with an associated rise in cytochrome P450, especially CYP2E1, most conclusively shown in alcohol dehydrogenase negative deer mice. There is also cross-induction of the metabolism of other drugs, resulting in drug tolerance. Furthermore, the conversion of hepatotoxic agents to toxic metabolites increases, which explains the enhanced susceptibility of alcoholics to the adverse effects of various xenobiotics, including industrial solvents. CYP2E1 also activates some commonly used drugs (such as acetaminophen) to their toxic metabolites, and promotes carcinogenesis. In addition, catabolism of retinol is accelerated resulting in its depletion. Contrasting with the stimulating effects of chronic consumption, acute ethanol intake inhibits the metabolism of other drugs. Moreover, metabolism by CYP2E1 results in a significant release of free radicals which, in turn, diminishes reduced glutathione (GSH) and other defense systems against oxidative stress which plays a major pathogenic role in alcoholic liver disease. CYP1A2 and CYP3A4, two other perivenular P450s, also sustain the metabolism of ethanol, thereby contributing to MEOS activity and possibly liver injury. CYP2E1 has also a physiologic role which comprises gluconeogenesis from ketones, oxidation of fatty acids, and detoxification of xenobiotics other than ethanol. Excess of these physiological substrates (such as seen in obesity and diabetes) also leads to CYP2E1 induction and nonalcoholic fatty liver disease (NAFLD), which includes nonalcoholic fatty liver and nonalcoholic steatohepatitis (NASH), with pathological lesions similar to those observed in alcoholic steatohepatitis. Increases of CYP2E1 and its mRNA prevail in the perivenular zone, the area of maximal liver damage. CYP2E1 up-regulation was also demonstrated in obese patients as well as in rat models of obesity and NASH. Furthermore, NASH is increasingly recognized as a precursor to more severe liver disease, sometimes evolving into "cryptogenic" cirrhosis. The prevalence of NAFLD averages 20% and that of NASH 2% to 3% in the general population, making these conditions the most common liver diseases in the United States. Considering the pathogenic role that up-regulation of CYP2E1 also plays in alcoholic liver disease (vide supra), it is apparent that a major therapeutic challenge is now to find a way to control this toxic process. CYP2E1 inhibitors oppose alcohol-induced liver damage, but heretofore available compounds are too toxic for clinical use. Recently, however, polyenylphosphatidylcholine (PPC), an innocuous mixture of polyunsaturated phosphatidylcholines extracted from soybeans (and its active component dilinoleoylphosphatidylcholine), were discovered to decrease CYP2E1 activity. PPC also opposes hepatic oxidative stress and fibrosis. It is now being tested clinically.

Copyright 2004, Marcel Dekker Inc.
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I know these might not be of interest to many folks but I was looking for something which described the mechanisms which alter alcohol metabolism in heavy drinkers. So this is just an example of where the research is on this.
 
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ponderingturtle said:
So you are not an alcoholic if you say have regular binge drinking with out these issues?
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I am not drawing a hard line, it is a spectrum thingee.

In binge drinking the other questions may be answered yes, and the defintion of binging is a vauge one. Does the person have blackouts? Are there negative consequences to thier use and most importantly do the people close to them feel it is a problem.

By binging usualy the idea is that someone consumes large amounts of alcohol over a short period of time, in that they drink six beers in a half hour and the like. Or they drink a case of beer in a very short period, say two hours.

There are many people who consume large amounts of alcohol and are not alcoholics.
 
athon said:
*sigh*

I'm going to state this one last time, as the argument is either more convenient when my points are ignored, or people are just plain ignorant.

Give a strict definition for disease, then make your point on whether alcoholism or drug addiction can be described that way.

All well and good to not like the idea, or prefer your own set of definitions that you make up as you go along, but unfortunately language doesn't work that way.

Athon
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Thanks Athon, i respect you but you need to loosen up, i have stated my case and I am not a strident one on this thread.

When I want you to tell me how to use language and it's proper defintion i will ask , Thanks!

If you wish to argue then i suggest you argue withsome one else. i have helped plenty of addicted people without having to argue the nature of the 'disease' of behavioral issues. If you wish to say it is disease then please do so, if I say it is a behavioral problem with a biological basis and vulnerabilities then I will continue to do so. The nomenclature thing is a real detraction to the job of helping people, and when people argue the words rather than the how, it is a waste of time.

If you think I have argued that addiction is not a disease then feel free to feel that way. Please read my posts and decide what it is that you are in disagreement with.
 
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Jeff Corey said:
However, later destruction of the liver leads to reduced tolerance because it takes longer to metabolize the alcohol. It takes less to keep you drunk.
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Wow, that is like the red flag of progressed alcoholic behavior. And it is like the last stage before they enter the pearly gates. I had not thought to mention that.
 
Dancing David said:
Thanks Athon, i respect you but you need to loosen up, i have stated my case and I am not a strident one on this thread.
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Mate, I'm hardly heated over this, but it is frustrating having people make claims with their own variations on a definition. Arguments, which could otherwise be productive, become nothing more than battles of semantics.

When I want you to tell me how to use language and it's proper defintion i will ask , Thanks!
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A truly arrogant statement if ever there was one. I point out that definitions need to be clear if you are to argue a term, and you state that you don't need to be told how to use language? Well, could have fooled me.

If you wish to argue then i suggest you argue withsome one else. i have helped plenty of addicted people without having to argue the nature of the 'disease' of behavioral issues. If you wish to say it is disease then please do so, if I say it is a behavioral problem with a biological basis and vulnerabilities then I will continue to do so. The nomenclature thing is a real detraction to the job of helping people, and when people argue the words rather than the how, it is a waste of time.
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No, a waste of time is when people make bold statements without defining what they mean by them. It's like somebody stating they are gay because they once kissed their uncle on the cheek. Sure, they might have their own definition of gay, but if it doesn't suit everybody else's, confusion arises.

As here. You state clearly that it isn't a disease. Fine. Define disease. If you're really are more concerned about the 'how' rather than the definition, then why are you so adamant that it isn't a disease?

If you think I have argued that addiction is not a disease then feel free to feel that way. Please read my posts and decide what it is that you are in disagreement with.
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Dancing David said:
I agree, alcoholism and addiction are not a diaease, they are behaviors which can have a biological vulnerability and a biological basis.
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Short memory?

Athon
 
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Dancing David said:
I am not drawing a hard line, it is a spectrum thingee.

In binge drinking the other questions may be answered yes, and the defintion of binging is a vauge one. Does the person have blackouts? Are there negative consequences to thier use and most importantly do the people close to them feel it is a problem.

By binging usualy the idea is that someone consumes large amounts of alcohol over a short period of time, in that they drink six beers in a half hour and the like. Or they drink a case of beer in a very short period, say two hours.

There are many people who consume large amounts of alcohol and are not alcoholics.
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If you are 21 getting too drunk at a frat party more often than you should but when the time comes to be serious you grow out of it then I agree with you. Youthful indiscretion as they say, there's a learning curve involved. But when I was that age there were still some people who enjoyed getting drunk more than they enjoyed the party. Some of them stood out. Of those a good number of them were alcoholics in the making.

I'm not sure of the stats and don't want to hunt down a reliable source but I recall the rate of alcoholism is about 10% of the adult population if you use a low threshold definition. By all means if someone knows the correct %, post it for us. I'd guess in college or around that age, a lot of people drank more than later in their lives, and more than a few got drunk once or twice. But I would bet not a lot more than 10% got 'really drunk once a week or more'. And of those that did get really drunk often most of them did indeed have a problem. How many of those people self arrested their drinking when the social climate changed from party time to work/family time or how many went on to develop full blown alcoholism I have no statistics on. I can say people who drink a lot over estimate how many other people drink as much as they do.

So when you say, "many people consume large amounts of alcohol and are not alcoholics", you really have to quantify the time frame this goes on for. The majority of people in this culture (USA) who drink, do not do so to the point of intoxication very often throughout their lives. Maybe during that age of enlightenment, but certainly not much after that. For one, the partying stops at some point and other people do not enjoy being around a drunk. Right then you have a problem.
 
Dustin said:
How many of you still hold the belief that addiction is a "disease"?
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Appeal to popularity? Surely you're not serious...

Looking back through all of these posts, I cannot see anybody else having offered up even a hint at what constitutes a disease, and what does not. And still there's the pretense of a discussion on the subject.

If you're asking if a cat is a species of dog, then you need to say what exactly a dog is, and why a cat is not that. By asking 'who here still believes a cat is a dog?' is merely an appeal to the popular vote.

Athon
 
Dustin said:
In order for it to be an "appeal to popularity" it would need to be an argument. It was not an argument, just a question.
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Do you have a point then? Or are you contending Tai Chi's 'interesting' posts for 'pointless statement of the year award'?

Athon
 
So you do have a position then? And when you said, "It was not an argument, just a question," you were merely curious about the result but weren't using it to defend your position?

I'm with athon, unless we are all using the same definition of the word, "disease", there's no point arguing whether or not something is or isn't one.
 
chris epic said:
So SCIENCE is saying that addiction is a disease, thanks to phychologists. Frankly this is absolute rubbish.
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It's primarily psychological, the other being genetics. Certain people have lower 'set' moods which make substance abuse, particularly opioids/opiates and drugs which affect serotonin, very likely. Some of these people are easy to spot - you see them at the gym for two hours or more a day, and if you ask them why they exercise, they say "It's the greatest sensation in the world..". What they are actually describing is natural endorphins released from tearing their muscles. They are also at a loss often to understand why everyone else considers it, despite clear health and aesthetic benefits, a burdensome uphill climb. Alcohol, being a neurotoxic chemical, mostly appeals to people who want an escape, whether it be from inhibitions, or a depth of hang ups. As far as I know there is nothing to suggest alcohol addiction is anything but psychological, despite the horrible physical dependence and damage that develops.
 
skeptigirl said:
liver changesI know these might not be of interest to many folks but I was looking for something which described the mechanisms which alter alcohol metabolism in heavy drinkers. So this is just an example of where the research is on this.
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Fascinating, but is it really a scientific mystery why people drink too much, day after day?
 
SirPhilip said:
Fascinating, but is it really a scientific mystery why people drink too much, day after day?
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I don't understand this post but as to your one above, the brain is an organ and can malfunction. If a virus infects your brain or you have a fever and hallucinate, there is no question it is a disease. Alcoholism has some qualities we characterize as behavioral and some we characterize as disease. Read the previous posts.
 
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