What is the difference between type I and type II alcoholics?
The pursuit of categorizing subtypes of alcoholics has been an ongoing one for at least the past 200 years. Jellinek was the first physician to subdivide alcoholism into four distinct phases: the prepathogenic period con sisting of occasional symptoms of alcohol abuse, a pathogenic period consisting of a prodromal phase, a crucial phase, and a chronic phase. The prodromal phase was notable for the onset of blackouts, the crucial phase by the onset of loss of control, and the chronic phase by prolonged intoxication. The rate at which individuals pass through these phases appeared to follow two distinct patterns and was associated with distinguishable personality characteristics that are now referred to as type I or type A alcoholics and type II or type B alcoholics.
Studies suggested the following distinguishing features between type I and type II alcoholics: Type I characteristics include an onset later in adulthood; drinking to relieve anxiety; the development of psychological but not physical dependence; and finally, although it may be inherited, usually an environmental trigger. Type II characteristics include an association with criminal behavior (sociopathy); an onset in teen or early adult years; drinking specifically to get high; and finally, more likely inherited. Sons of type II alcoholic persons are seven times more likely to develop type II alcoholism compared with the general population. A recent Korean study published in 2005 demonstrated that a link exists between the gene coding for the enzyme known as alcohol dehydrogenase that breaks down alcohol into acetaldehyde and type II alcoholics. The theories from these studies remain controversial; however, recent evidence of varying responses to particular psychotropic medications based on one's particular subtype adds further support. These medications are discussed in detail in Question 52. Data on daughters of persons with alcohol problems are less clear. Daughters might be at an increased risk if the biological mother is alcoholic, but these studies do not delineate between subtypes. A recent twin study in women found higher concordance in identical twins than in fraternal twins.
Like any other theory, the distinction between type I and type II alcoholism is not as simple as it may seem, and Ben is an example. Although his history indicates type II alcoholism, he has never demonstrated violence or sociopathic behavior; however, the notion of different "types" does provide some guidelines that more people should be aware of. Too many type I alcoholics mistake type II alcoholics as the only type. In that way, they can stay in denial regarding their own consumption because they can function most of the time.
Are there any biological tests that aid in the diagnosis of alcoholism?
No biological test is available that alerts a patient or physician about whether an individual is at risk of becoming an alcoholic if he or she drinks regularly.
Biological tests for alcoholism measure both the direct and indirect effects of chronic alcohol use on one's body.
GGT (Gamma Glutamyl Transpeptidase) a liver enzyme that when elevated is associated with alcoholic liver disease (among other diseases).
The science of alcoholism is still far away from discovering specific genetic markers to identify those at risk; however, some biological tests help to identify those patients who have developed medical consequences of repeated heavy drinking. These tests are not specific for alcoholism per se. The fact that one has biological findings suggestive of alcoholism, therefore, is not a definitive test of one being an alcoholic. Nor is it the case that the absence of such biological findings rules out any possibility that one is an alcoholic. Many alcoholics never develop any laboratory abnormalities as a result of their drinking. To reiterate why there is this phenomenon, recall that the diagnostic criteria for alcohol dependence and alcohol abuse discussed earlier in Questions 13 and 14 do not require such evidence to establish the diagnosis.
However, the biological effects of chronic heavy alcohol use result in laboratory findings that demonstrate a consistent and reliable pattern. For this reason, anyone presenting to a physician's office with this pattern will be asked in detail about his or her pattern of drinking and, in all likelihood, will be told to stop all drinking no matter how much or little alcohol is consumed. This is because — even if the laboratory abnormalities are not a result of alcohol — alcohol may be contributing to the problem irrespective of whether someone is an alcoholic. People with hepatitis should not drink for any reason. Biological tests for alcoholism measure both the direct and indirect effects of chronic alcohol use on one's body. Alcohol's most direct impact is on the liver, leading to hepatitis, with a characteristic increase in various chemistries, most notably GGT (gamma-glutamyl transpeptidase), but also AST (aspartate aminotransferase) and ALT (alanine aminotransferase). GGT is the most sensitive in detecting alcohol consumption and therefore monitoring relapse, but false negatives and false positives do exist. Carbohydrate-deficient transferrin is another biomarker; though less sensitive, it is more specific for alcoholism. AST and ALT are elevated in all forms of hepatitis and are not particularly sensitive but are more specific in detecting the affects of alcohol consumption. They are also late-stage indicators that may normalize after maintaining about 6 weeks of sobriety. Because the liver is involved in the production of clotting factors, these can be affected by alcohol's effect on the liver, leading to increased bleeding times.
Chronic alcoholism also affects the hematological system. Alcohol has both direct and indirect effects on this system. First, most alcoholics use alcohol as their primary source of calories. This inevitably leads to severe vitamin deficiencies, notably the B vitamins, thiamine, and folate. These, in turn, lead to anemia that is known as macrocytic, meaning that the red blood cells are enlarged. This causes a low hemoglobin and hematocrit associated with an elevated mean corpuscular volume. Direct effects of alcohol, however, can affect the entire hematological system, including the white blood cells, which are a part of the body's immune system, the red blood cells, which carry oxygen throughout the body, and finally the platelets, which are involved in the clotting process. Alcohol suppresses all of these, leading to anemia, immunosuppression, and thrombocytopenia, or a lowering of the platelets, which leads to prolonged bleeding and easy bruising. Additionally, potassium, phosphate, calcium, and magnesium levels can be affected in chronic alcoholism. Other effects of alcoholism on the body will be further detailed in questions 61 and 62.
AST (Aspartate Aminotransferase) an indicator of acute liver disease. See ALT.
ALT (Alanine Aminotransferase) an indicator of acute liver disease. See AST.
Carbohydrate-deficient transferring a protein found in blood involved in transferring iron to cell tissues.
Clotting factors a group of proteins specifically designed to interact together to cause blood to clot and stop bleeding.
Thiamine vitamin B1.
Macrocytic from "macro" for large and "cytic" for cell. Primarily in reference to large red blood cells from thiamine deficiency (pernicious anemia) that is common in chronic alcoholics whose nutrition is poor.
Hematocrit measures of the proportion of blood volume that is occupied by red blood cells.
Mean corpuscular volume a measure of the size of the red blood cells.
Anemia a deficiency of red blood cells.
Immuno suppression involves an act that reduces the activation or effectiveness of the immune system.
Thrombocytopenia the presence of relatively few platelets in blood.
Platelets also known as thrombocytes. A type of blood cell involved in the cellular mechanisms of the formation of blood clots.