Thank you Mr. Alkhawaja! I appreciate the link! You are most helpful!
Dear Tatiana,
These resources may interest you:
http://www.sfu.ca/~palys/321OralHistory-Ngo-AddictionAccordingToThreeModels.pdf
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3736117/
http://66.199.228.237/boundary/addiction/Theoryofaddictionfirsthalf.pdf
Wonderful resources Stephen! I especially liked the first one! Deeply appreciate the links.
We used another scale in this study, but you can have a look at it. You might find some useful refs inside it
http://bmchealthservres.biomedcentral.com/articles/10.1186/s12913-016-1306-9
The first question is why you would want to include the moral perspective? This is outmoded and not compatible with the science.
The science points to genetic and epigenetic components to addiction that require consideration for the concept of maladaptive behaviors. What learning theory and many views of addiction do not consider is that genetics influence the reinforcement potential of ingesting a substance. This can be do to genetic variation or epigenetic influences as documented by research. For example, those who smoke tobacco are likely to have epigenetic influences that would produce a more pronounced reaction to cocaine.
All theories or perspectives on addiction do not merit equal weight or credibility.
To everyone who answered: I would like to say thank you so much! As an undergraduate student this support is deeply appreciated.
Mr. Hoffmann,
That is an excellent point! We are debating the relevance of the moral perspective in class and I have found that it does not match up well with the science at all. Great point to bring up!
Tatiana James,
With I recommend reading the definition of addiction provided by the American Society of Addictions Medicine (ASAM).
Link:
http//www.asam.org/quality-practice/defenition-of-addiction
For studies supporting this, see Milner and Olds research on the rolling reward system (dopamine), Koob and LeMoal research on craving and the amygdala, Earnest P. Noble's research on the D2-dopamine-receptor gene and review the work of Dr. Michael S. Gazzagina and Dr. Roger Sperry on split brain patients.
The short answer is that it is a genetic defect in the reward and memory processing centers of the midbrain and the frontal lobe of the new brain. That creates a condition (if you prefer not to call it a disease) that is neurologic in nature (physiological) where stress triggers cravings to use drugs or alcohol in the survival circuitry in the midbrain.
There are other points of view, but these appear to be the most grounded in science.
The problem is that we have to admit that we do not know enough about it yet.
respectfully,
James Annand
We can surely all agree that addiction - like all human behaviour and however we define it - is a product of some combination of the personality, the environment and the brain (in no order of precedence). If there are other broad factors, perhaps someone can tell me. Whatever the importance of these 3 factors in an individual patient, addiction/abuse/excessive use is by definition a habit - a repeated and fairly predictable pattern of behaviour. If it weren't habitual (and even if the habit consists of damaging binges months apart) it would hardly be a problem.
The best techniques we know for changing habits involve the repeated practice of better (i.e. more appropriate and adaptive) alternatives. CBT management of phobic and compulsive behaviour gives many well-documented examples. All 'success' in addiction treatment (as with phobia treatment) is ultimately judged by the extent to which patients acquire, perfect and continue to practise these alternatives and the extent to which they abandon their previous habits.
'Success' may be instantaneous, as when patients realise they have a problem and decide, often without any treatment, to stop. Clinicians naturally don't see it very often, so they tend to discount it. It also poses problems for the 'brain disease' theory. Gradual improvement is commoner (as is refusal to engage in treatment) but the main mechanisms are changes in some aspect of 'personality. ('Those are the attitudes I used to have to alcohol/heroin/cocaine and the situations in which I consumed it but I now have different attitudes').
Brain mechanisms can make people more (or less) vulnerable to addiction than the average but - as several people have pointed out - fail to explain recovery, especially the instant and lasting kind. They also fail to explain the enormous changes in the demographics of addiction of the last half century. Finally, no medication supposedly acting primarily on those brain mechanisms has more than very modest effects on outcomes compared with placebo - and placebo effects are consistently underrated by pharmacologists, especially those employed by drug companies.
As the German OLITA studies have shown, the only drug that consistently improves psychosocial treatment outcomes is supervised disulfiram, which works not by any neuropharmacological process but by deterrence based on its extra-cerebral pharmacological effects, thus giving patients a better chance of staying dry for long enough to benefit from the other aspects and components of treatment. I maintain that this has important implications for 'brain disease' theories but this stance is not popular, especially with brain researchers. I have nothing against brains (my first addiction paper was about alcoholic brain damage) but I don't think brain research has produced much of practical benefit and it has led to some frankly disturbing papers from China about surgery on the amygdala for addicts.
In short, whatever the main etiological factors are in an individual case, treatment is essentially a matter of re-training and re-education. Some people learn more quickly than others.
Dear Tatiana,
It is not the same treatment for alcoholism and for gambling. It was tried out in Sweden to treat them together. Moral, Disease, Mal adaptive Behavior. Do you mean addicted to porn? Shame and guilt keeps the viscous cycle going.
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The moral model might be outdated, but I still find that patients blame themselves for having the illness with thoughts like: "I'm a weaker person that cannot control the use of alcohol/drugs". Thus, shame is still very much a relevant problem. Patients also feel that the society and significant others blame them; "Why do you not "pull yourself together" and stop using?". Thus, I'm sorry to say that the moral model is not "dead", and as professionals we should be very much aware of such thoughts in those having the illness and do our best to remediate it. I've experienced that patient education about brain mechanism may be one way to change such negative thoughts in patients (about being a weaker or less moral person). See enclosed slides we used in a previous study.
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Data Appendix S1
Use of the word “habit” like the word “abuse” should be eliminated from the discussion of addiction and substance use disorders. Both terms trivialize addictions and cause confusion among not only the public, but professionals as well.
A habit is putting your right shoe on first. An addiction is a biologically based condition that produces repetitive behaviors in response to a positive brain reaction. Addictions are not habits. The term habit suggests that the person should just stop taking the substance in question.
The same is true for the word “abuse” in that it trivializes addiction. The best definition of alcohol abuse is “pouring water into good Scotch.” At least one prestigious scientific journal has banned the use of the word “abuse” to refer to a substance use disorder. The editor’s argument is that you can abuse people or animals, but you cannot abuse an inanimate object such as alcohol.
The same linguistic issues relate to referring to a person with a substance use disorder as an “addict” or “alcoholic” in that one does not call a person who has cancer a “canceritic.” By naming an individual as essentially being the condition we are demeaning the person. This has profound impacts on attitudes and behaviors as determined by research conducted by John Kelly, Ph.D. at Harvard University.
Mr. Hoffmann this is a truly great answer. Thank you for contributing such wonderful thoughts!
The statement that disulfiram, or Antibuse, is the only medication to show improvements in treatment outcomes is no longer accurate. Naltrexone has been shown to be effective in the treatment of alcohol dependence, as have other medications such as buprenorphine for opioid dependence.
Medication assisted treatments are increasingly used and accepted by treatment providers because they do address some of the biological pressures to resume use. This gives that "talk therapies" the ability to work on the behavioral aspects for recovering from addictions.
I said that supervised disulfiram/Antabuse (not Antibuse please, though I've heard patients call it 'Antibooze') is the only drug that consistently improves treatment and I think that is evidence-based. There are several large but negative trials of naltrexone and acamprosate but patients taking an adequate dose of DSF usually don't continue to drink, for much the same reasons that Japanese who are homozygous for inefficient ALDH don't drink. If people do drink on DSF without much reaction, they generally stop if the dose is increased because they then get a reaction. That is not true for either NTX or ACP. Effect sizes for DSF at fixed doses are typically twice as large as those for NTX and ACP
As to 'habits', there are surely 'good' habits and 'bad' habits as well as neutral ones of the shoelace kind. Since both doctor and patient (and often the patient's family and employers as well) typically agree - and for good and generally obvious reasons - that excessive drinking is a 'bad' habit in this particular case, questions of 'moral judgement' are not very important.
Substance abusers get a raw deal from society and the failed and utterly disastrous US-led 'war on drugs' has demonised illicit drug users/abusers/addicts much more than alcoholics. However, I don't think that many of them decline to seek help because someone calls them by one term rather than another.
Finally - though I know this space is supposed to be about answers rather than questions or argument - I'd still like to know how the 'brain disease' hypothesis primarily explains instant recovery or demographic phenomena such as the vast increase in women alcoholics/alcohol abusers/consumers or what have you in the last half century. Have women's brains undergone major anatomical or biochemical changes in that period? When I was a student, the M:F alcoholism ratio was about 5:1. The difference now is very much less.
Actually, there are some promising studies on Vivitrol in addition to the experience of a large treatment provider that have not been published.
As to the “war on drugs” this was a ploy used by the Nixon administration to target African-Americans and hippies – two groups who Nixon want to decimate via incarceration. That is why cannabis was classified as a class one drug and crack cocaine was targeted for greater sanctions than the powdered form. Unfortunately, this Machiavellian ploy as dominated US policy for decades. What started as a malevolent undertaking was then adopted by those addressing a problem for which they had little understanding not unlike the some psychologists in the UK that persisted in trying to teach alcohol dependent people how to drink in moderation based on learning theory that completely ignored biology.
The point about semantics and the use of words such as “habit” and “abuse” is that they trivialize true addictions. As I pointed out, Dr. Kelly has found that the terms affect what people would do based on semantic differences. Kelly is scheduled to conduct a webinar on the topic of word usage soon.
Finally, the “brain disease” construct is compatible with the observed increase in addictions among women. The science suggests that the younger one begins regular use of alcohol, for example, the greater the probability of addiction. In more recent years girls have been rivaling boys in terms of age and prevalence of use onset. The biology plus societal trends comport to the observed narrowing of the male to female ration of alcoholism.
For an off-line discussion I can be reached at [email protected]
For an off-line discussion I can be reached at [email protected]
There is no good and comprehesive theory on addiction. All existing theories are low-level viewpoints from different perspectives.
I have discussed this and reviewed various theoretical viewpoints in my book Perfect drinking and its enemies. Available from amazon and www.perfectdrinking.com.
Dear Tatiana. As you can see, there are more questions than answers in this field but addiction can still be a very satisfying specialty. Most younger patients will largely grow out of it by the time they hit 30, just as most people grow out of juvenile delinquency and excess. Placebo and non-specific responses to any intervention are usually much larger than specific pharmacological or psychological effects but drug companies and researchers don't like to hear that. In any case, we're not really allowed to exploit them these days, even with beneficial and honest intentions and in essentially salaried services like the British NHS, where the corrupting effects of fee-per-item systems hardly apply. I hope you enjoy your medical career, as most of us do despite the bureaucrats. My medical school's motto translated as: 'of all the arts, medicine is the most brilliant' and I quite often agreed.
Hello Colin,
Thank you for your response. I am finding the same conclusion that there are not many definite answers when it comes to addiction. I am looking forward to doing research on the complexities of addiction.
I infer from your examples of three “perspectives” you seem to include the moral “perspective”, which has been totally debunked.
The science clearly indicates that we are not dealing with a single diagnostic entity of “addiction” but rather a family of conditions resulting in some common behaviors but with different genetic, biological, and social underpinnings. The most impressive neuroscience indicates that some “addictions” are based on genetic and neurological foundations. These are the conditions that are typically chronic conditions not associated with the capacity to “grow out” of it. Individuals with these conditions are also less likely to be capable of moderating use of substances – be it alcohol or cannabis.
On the other hand, there are those who misuse substances, but do not manifest the aforementioned genetic or neurological aspects. These are those who through apparently largely social circumstances misuse substances and who are able to successfully moderate use if desired. They are also those most likely to “grow out of it”.
Previous diagnostic criteria were unable to allow for discrimination between those with a more serious and chronic condition vs. those with a more transient or situational one. The DSM-5 may facilitate the prospect of such discrimination if clinicians and researchers document findings at the individual criterion level. Our research has indicated that some of the 11 DSM-5 criteria are found predominantly among those with a severe diagnosis while others are scattered among the three diagnostic levels. Such criterion level investigations might facilitate discrimination between the more chronic vs. transient conditions.
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