different theories about alcoholism

Posted on 06 Янв 201815

THEORIES OF ACCIDENT CAUSATION - Cleveland State …

THEORIES OF ACCIDENT CAUSATION - Cleveland State …
Cleveland State University Work Zone Safety and Efficiency Transportation Center Section 3 Accident Theories THEORIES OF ACCIDENT CAUSATION

Leventhal and Cleary (1980) have pointed out how inexact the regulation of nicotine intake is in Schachter's studies: Schachter (1977) found that a 77 percent reduction in nicotine level produced only a 17 to 25 percent increase in cigarette consumption. It is impossible to explain—as Smith attempts to do—how innate, predetermined reactions could cause the same person to become excessively involved with substances as disparate as cocaine, alcohol, and Valium. Another Schachter student and his colleague recorded Schachter's (1982) finding but dismissed its significance by indicating it was probably only those obese subjects who were above their set-points who had been able to lose weight in this study (Polivy and Herman 1983: 195-96). For Siegel and others who have analyzed the Vietnam remission data in conditioning terms, the crucial variable is simply situational change. Zinberg 1984), they provided little in the way of basic mechanisms to account for the dynamics of addiction.

Addiction to pleasure: A biological and social-psychological theory of addiction. As with alcohol and narcotic use (see below), there is no prima facie reason why destructive eating and smoking habits need necessarily be dictated by separate classes of factors. If the behavior of laboratory animals is not locked in by drug action, how is it possible for human beings to become addicted and lose the possibility of choice? One proposal to account for the feverish pursuit of drugs and other human involvements has been that these experiences bring in ordinate pleasure, or euphoria. Social-learning theorists have been especially active in alcoholism, where they have analyzed how alcoholics' expectations and beliefs about what alcohol will do for them influence the rewards and behaviors associated with drinking (Marlatt 1978; Wilson 1981). Lastly, theories must be able to describe addiction as it occurs through human experience.

However, his model left open the question of the source of this insensitivity to somatic cues, suggesting the probability that this was an inherited trait. Such social-psychological theories addressed the function of drug use in adolescent and postadolescent life stages as a way of preserving childhood and avoiding adult conflicts (Chein et al. It was only a matter of time, however, before pharmacological and biological theorists began to hypothesize inherited mechanisms to account for differences in addictive susceptibility. Vaillant (1983) found that self-reports by AA members that they immediately succumbed to alcoholism the first time they drank were false and that severe drinking problems developed over periods of years and decades. Polivy and Herman's (1983) description of their outlook did not reflect this understanding about set-point and obesity. As we have seen, neither the positive feelings it posits from narcotics use nor the traumatic withdrawal it imagines can account for human drug taking. The most prominent name in metabolic research and theory, Maurice Seevers, characterized efforts during the first sixty-five years of this century to create a model of addictive narcotic metabolism to be "exercises in semantics, or plain flights of imagination" (cited in Keller 1969: 5). Yet further nongenetic influences remain to be partialed out of Vaillant's results. Bejerot 1980; Dole 1972; Goldstein 1976a; McAuliffe and Gordon 1974; Wikler 1973). In recent years theorizing of this sort has become broader: less wedded to specific child-rearing deficits, more accepting of a range of psychological functions for drug use, and including other substances besides narcotics (cf.

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Another Schachter student and his colleague recorded Schachter's (1982) finding but dismissed its significance by indicating it was probably only those obese subjects who were above their set-points who had been able to lose weight in this study (Polivy and Herman 1983: 195-96). Their work signaled a burst of addiction theorizing in areas other than substance abuse, the bulk of which—paradoxically—sought to analyze these phenomena at a biological level. This last requirement may seem the most difficult of all. The longer parents and their children live together (even when the children are age 40) the more they resemble each other in fatness. Whereas his formulation of nicotine addiction had emphasized the ineluctable, overwhelming nature of withdrawal from cigarettes, he now found the ability to overcome such withdrawal "to be relatively common" (p.

Such people would then especially welcome—and might even require—the elevation of their pain threshold brought on by narcotics. However, the appearance of withdrawal in alcoholism is itself variable and subject to drinkers' subjective constructions. Since a large proportion of the alcohol available is drunk by those at the extreme end of this skewed curve, increases or decreases in alcohol availability are believed to push many drinkers above or below what might be considered a heavy and dangerous drinking level. As a result, the social-psychological literature exists in almost total isolation from the pharmacological and learning literature on addiction. It must account for regional and cultural variation, interpersonal preferences as well as hold true for the variety of addictions.

Harold Kalant (1982), a distinguished neuroscientist, was more conclusive in his rejection of the idea that alcohol and narcotics could act according to the same neurological principles. The enormity of the implications of the genetic transmission of addictive impulses is driven home by several theories claiming that people are compelled by chemical imbalances to form unhealthy, compulsive, and self-destructive interpersonal relationships. Polivy and Herman based this calculation on the estimate that from 60 to 70 percent of obese people were not obese in childhood. Furthermore, the apparent uniformity in the addictive use of cigarettes that Schachter's model suggests is illusory. Yet this new theoretical synthesis is less than meets the eye: It mainly recycles discredited notions while including piecemeal modifications that make the theories marginally more realistic in their descriptions of addictive behavior. Morphine titration in positive laparotomy patients using patient-controlled analgesia. Addicted running—defined by inflexibility and insensitivity to internal and external conditions, running until the point of harming oneself, and being unable to quit without experiencing withdrawal—is no better explained by endorphin levels than is the self-destructiveness of the heroin addict (Peele 1981). In the language of behavior theory the substance acts as a powerful reinforcer: behaviors instrumental in obtaining the substance become more frequent, vigorous, or persistent. In his influential internal-external model of obesity, Schachter (1968) proposed that fat people had a different style of eating, one that depended on external cues to tell them when to eat or not. Yet it has also been social-learning theorists who have launched the alcohol-dependence syndrome and who seem to feel subjective interpretation is far less important than the pharmacological effects of alcohol in causing drinking problems (Hodgson et al.

Disease theory of alcoholism - Wikipedia

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