Loosening the Grip: a handbook of Alcohol Information 9th



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Parekh RS; Klag MJ. Alcohol: Role in the development of hypertension and end-stage renal disease. (review). Current Opinion in Nephrology and Hypertension 10(3): 385-390, 2001. (96 refs.)


Alcohol is a common risk factor in the general population for a variety of health outcomes. In the present review, we discuss the recent literature on alcohol, hypertension, and renal disease. The regular consumption of more than two drinks per day is associated with both hypertension and renal disease. The mechanisms by which consumption of alcohol leads to hypertension and perhaps renal disease are unknown. Copyright 2001, Lippincott, Williams & Wilkins

Poschl G; Seitz HK. Alcohol and cancer. (review) Alcohol and Alcoholism 39(3) 155-165, 2004. (139 refs)


Epidemiological data have identified chronic alcohol consumption as a significant risk factor for upper alimentary tract cancer, including cancer of the oropharynx, larynx and the oesophagus and of the liver. The increased risk attributable to alcohol consumption of cancer in the large intestine and in the breast is much smaller. However, although the risk is lower, carcinogenesis can be enhanced with relatively low daily doses of ethanol. Considering the high prevalence of these tumours, even a small increase in cancer risk is of great importance, especially in those individuals who exhibit a higher risk for other reasons. The epidemiological data on alcohol and other organ cancers is controversial and there is at present not enough evidence for a significant association. Although the exact mechanisms by which chronic alcohol ingestion stimulates carcinogenesis are not known, experimental studies in animals support the concept that ethanol is not a carcinogen but under certain experimental conditions is a cocarcinogen and/or tumour promoter. The metabolism of ethanol leads to the generation of acetaldehyde (AA) and free radicals. Evidence has accumulated that acetaldehyde is predominantly responsible for alcohol associated carcinogenesis. Acetaldehyde is carcinogenic and mutagenic, binds to DNA and proteins, destructs folate and results in secondary hyperproliferation. Acetaldehyde is produced by tissue alcohol hydrogenases, cytochrome P 4502E1 and through bacterial oxidative metabolism in the upper and lower gastrointestinal tract. Its generation or its degradation is modulated due to functional polymorphisms of the genes coding for the enzymes. Acetaldehyde can also be produced by oral and faecal bacteria. Smoking, which changes the oral bacterial flora, and poor oral hygiene also increase acetaldehyde. In addition, cigarette smoking and some alcoholic beverages such as calvados contain acetaldehyde. Other mechanisms by which alcohol stimulates carcinogenesis include the induction of cytochrome P-4502E1, which is associated with an enhanced production of free radicals and enhanced activation of various procarcinogens present in alcoholic beverages; in association with tobacco smoke and in diets, a change in the metabolism and distribution of carcinogens; alterations in cell cycle behaviour such as cell cycle duration leading to hyperproliferation; nutritional deficiencies, such as methyl-, vitamin E-, folate-, pyridoxal phosphate-, zinc- and selenium deficiencies and alterations of the immune system eventually resulting in an increased susceptibility to certain virus infections such as hepatitis B virus and hepatitis C virus. In addition, local mechanisms may be of particular importance. Such mechanisms lead to tissue injury such as cirrhosis of the liver, a major prerequisite for hepatocellular carcinoma. Also, an alcohol-mediated increase in oestradiols may be at least in part responsible for breast cancer risk. Thus, all these mechanisms functioning in concert actively modulate carcinogenesis leading to its stimulation. Copyright 2004, Medical Council on Alcoholism. Used with permission

Regev A; Jeffers LJ. Hepatitis C and alcohol. Alcoholism: Clinical and Experimental Research 23(9): 1543-1551, 1999. (63 refs.)


Background: Alcohol abuse and hepatitis C virus (HCV) infection frequently coexist in patients with chronic liver disease. It is widely believed that alcohol and HCV act synergistically in these patients to promote the development and progression of liver damage. Methods: A review of the relevant medical literature, identified by computer assisted literature search, was conducted. Results: It has been established that alcohol consumption is associated with the accelerated progression of liver injury, higher frequency of cirrhosis, and higher incidence of hepatocellular carcinoma. Alcohol abuse is also associated with decreased response to interferon treatment, and there are reports to suggest that patients with HCV cirrhosis, who abuse alcohol, have higher mortality than those who do not. Abstinence may reverse some of these deleterious effects of alcohol, and may even improve the ultimate response to treatment. The mechanism for the synergistic effect of alcohol and HCV is not fully understood, but has been attributed to alcohol's effect on viral replication, or to its effect on the immune system, hepatic iron content, or hepatic regeneration. Conclusions: Alcohol has a deleterious effect on HCV associated liver disease. It is recommended that patients with HCV infection abstain from alcohol consumption. Copyright 1999, Research Society on Alcoholism

Rehm J; Gmel G; Sempos CT; Trevisan M. Alcohol-related morbidity and mortality. Alcohol Research & Health 27(1): 39-51, 2003. (106 refs)


Alcohol use is related to a wide variety of negative health outcomes including morbidity, mortality, and disability. Research on alcohol-related morbidity and mortality takes into account the varying effects of overall alcohol consumption and drinking patterns. The results from this epidemiological research indicate that alcohol use increases the risk for many chronic health consequences (e.g., diseases) and acute consequences (e.g., traffic crashes), but a certain pattern of regular light-to-moderate drinking may have beneficial effects on coronary heart disease. Several issues are relevant to the methodology of studies of alcohol-related morbidity and mortality, including the measurement of both alcohol consumption and the outcomes studied as well as study design. Broad summary measures that reflect alcohol's possible effects on morbidity, mortality, and disability may be more useful than measures of any one outcome alone. Public Domain

Schuckit MA. Comorbidity between substance use disorders and psychiatric conditions. Addiction 101(Supplement1): 76-88, 2006. (138 refs.)


Aims: To review information relevant to the question of whether substance-induced mental disorders exist and their implications. Design and method: This paper utilized a systematic review of manuscripts published in the English language since approximately 1970 dealing with comorbid psychiatric and substance use disorders. Findings: The results of any specific study depended on the definitions of comorbidity, the methods of operationalizing diagnostic criteria, the interview and protocol invoked several additional methodological issues. The results generally support the conclusion that substance use mental disorders exist, especially regarding stimulant or cannabinoid-induced psychoses, substance-induced mood disorders, as well as substance-induced anxiety conditions. Conclusions: The material reviewed indicates that induced disorders are prevalent enough to contribute significantly to rates of comorbidity between substance use disorders and psychiatric conditions, and that their recognition has important treatment implications. The current literature review underscores the heterogeneous nature of comorbidity. Copyright 2006, Society for the Study of Addiction to Alcohol and Other Drugs

Standridge JB; Zylstra RG; Adams SM. Alcohol consumption: An overview of benefits and risks. (review) Southern Medical Journal 97(7): 664-672, 2004. (73 refs)


Published health benefits of regular light-to-moderate alcohol consumption include lower myocardial infarction rates, reduced heart failure rates, reduced risk of ischemic stroke, lower risk for dementia, decreased risk of diabetes and reduced risk of osteoporosis. Numerous complimentary biochemical changes have been identified that explain the beneficial effects of moderate alcohol consumption. Heavy alcohol consumption, however, can negatively affect neurologic, cardiac, gastrointestinal, hematologic, immune, psychiatric and musculoskeletal organ systems. Binge drinking is a significant problem even among moderate drinkers and is associated with particularly high social and economic costs. A cautious approach should be emphasized for those individuals who drink even small amounts of alcohol. Physicians can apply the research evidence describing the known risks and benefits of alcohol consumption when counseling their patients regarding alcohol consumption. Copyright 2004, Southern Medical Association

Streissguth A, Kanter J, eds: The Challenge of Fetal Alcohol Syndrome: Overcoming Secondary Disabilities, Seattle WA: University of Washington Press, 1997. (208 refs.)


This book is the proceedings of a symposium held in 1996 at the University of Washington, with over 62 professionals from 8 countries and 39 States convened to commemorate 25 years of research on Fetal Alcohol Syndrome conducted at that institution. The volume contains 22 selected papers. These papers provide a summary of the research to date as well as the most innovative approaches to assessment and treatment by health care professionals and community-based agencies. Individual chapters address neurobehavioral and neuroanatomical effects of heavy prenatal exposure to alcohol; primary and secondary disabilities of fetal alcohol syndrome and fetal alcohol effects; assessment of adults with FAS; stimulant medication with FAS children; case management and advocacy approaches; legal issues and judicial perspectives; and public health implications. The volume is rich with practical suggestions and clinical approaches, addressing important issues that are often under- or undiscussed, e.g. serving mothers who themselves have FAS/FAE; guidelines for parents to cope with inapprorpriate sexual touching to reduce the likelihood of criminal conduct; and the techniques used in a demonstration classroom for preadolescents with FAS. Copyright 1998, Project Cork

White AM. What happened? Alcohol memory blackouts, and the brain. Alcohol Research & Health 27(2): 186-196, 2003. (80 refs.)


Alcohol primarily interferes with the ability to form new long-term memories, leaving intact previously established long-term memories and the ability to keep new information active in memory for brief periods. As the amount of alcohol consumed increases, so does the magnitude of the memory impairments. Large amounts of alcohol, particularly if consumed rapidly, can produce partial (i.e., fragmentary) or complete (i.e., en bloc) blackouts, which are periods of memory loss for events that transpired while a person was drinking. Blackouts are much more common among social drinkers -- including college drinkers -- than was previously assumed, and have been found to encompass events ranging from conversations to intercourse. Mechanisms underlying alcohol-induced memory impairments include disruption of activity in the hippocampus, a brain region that plays a central role in the formation of new autobiographical memories. Public Domain
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