Year : 2019 | Volume
: 8 | Issue : 8 | Page : 2558--2560
Personal or family history of metabolic traits predispose to higher hepatotoxic effects of alcohol
Ajeet Singh Bhadoria1, Surabhi Mishra2, Kanchan Gawande1, Raman Kumar3,
1 Department of Community and Family Medicine, All India Institute of Medical Sciences (AIIMS), Rishikesh, Uttarakhand, India
2 Department of Community Medicine, Himalayan Institute of Medical Sciences (HIMS), Dehradun, Uttarakhand, India
3 President Academy of Family Physicians of India, India
Dr. Ajeet Singh Bhadoria
Department of Community and Family Medicine, All India Institute of Medical Sciences, Rishikesh - 249 203, Uttarakhand
World Health Organization Global Status 2018 Report on alcohol and health states that global total alcohol per capita consumption has drastically risen from 2005 to 2016. Presence of inherited metabolic traits (MTs) such as diabetes, hypertension, and obesity predisposes to early and more severe liver damage, even with smaller quantity and shorter duration of exposure to alcohol. This editorial highlights the need for screening of individuals with either addiction of alcohol or alcoholic liver disease for personal and family history of diabetes, hypertension, obesity, and other MTs for risk stratification and specific interventions. Health education and awareness regarding deleterious effects of alcohol among those who have a personal or family history of MTs should be ensured.
|How to cite this article:|
Bhadoria AS, Mishra S, Gawande K, Kumar R. Personal or family history of metabolic traits predispose to higher hepatotoxic effects of alcohol.J Family Med Prim Care 2019;8:2558-2560
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Bhadoria AS, Mishra S, Gawande K, Kumar R. Personal or family history of metabolic traits predispose to higher hepatotoxic effects of alcohol. J Family Med Prim Care [serial online] 2019 [cited 2019 Sep 19 ];8:2558-2560
Available from: http://www.jfmpc.com/text.asp?2019/8/8/2558/265589
In an alarming revelation, the World Health Organization (WHO) Global Status 2018 Report on Alcohol and Health states that globally, total alcohol per capita consumption (APC) has drastically risen from 5.5 L in 2005 to 6.L in 2016. This worldwide rise is primarily contributed by its two of the most populous countries, namely, China and India.
In India alone, the APC almost doubled since 2005 (2.4 L in 2005 to 5.7 L in 2016) among population age 15 years and above. More than 90% of recorded APC (92%) was in the form of spirits (Indian-made foreign liquor: a type of alcohol beverage), followed by beer (8%), and least common is wine (<1%). Around 44% of Indian population reportedly indulges in heavy episodic or binge-drinking (defined as ≥60 g of pure alcohol on at least one occasion at least once per month), which is much above the global average (18.2%). Indian states with high prevalence of alcohol use are Chhattisgarh (35.6%), Tripura (34.7%), Punjab (28.5%), Arunachal Pradesh (28%), and Goa (28%). On the scale of alcohol-attributable “Years of Life Lost” between 1 and 5, India has been rated 4, implying alcohol consuming Indian population loses most years of their life because of drinking and its related consequences. In India, noncommunicable diseases (NCDs) including metabolic traits (MTs) [cumulatively includes diabetes mellitus (DM), hypertension, coronary artery disease, dyslipidemia, and obesity] also account for 60% of total deaths and 44% of disability-adjusted life-years lost in 2013 and 40% of all hospital admissions and 35% of all outpatient visits happening in 2004., The Global Burden of Disease Study 2013 estimates showed that India has witnessed a relative increase in absolute number of NCD-related deaths by 42% between 1990 [27.0 million (95% confidence interval (CI) 26.3–27.6)] and 2013 [38.3 million (95% CI 37·2–39·4)]. Needless to say that most underlying risk factors of these lifestyle alteration diseases are overlapping; for instance, a proportion of burden caused due to DM (44%) and cardiovascular diseases (23%) in India can be altogether attributed to overweight and obesity alone. In addition to commonly known NCDs, these MTs were also found associated with increased risk of nonalcoholic steatohepatitis (NASH) and advanced hepatic fibrosis. This led to generation of a new hypothesis that nonalcoholic fatty liver disease (NAFLD) is a hepatic manifestation of MTs.
Supporting the above hypothesis, Loomba et al. also showed in their seminal study that the presence of personal and family history of DM was independently associated with increased risk of NASH and advanced hepatic fibrosis. In the same direction, Bhadoria et al. carried out another cross-sectional study among 1,133 NASH-related cirrhosis patients at a tertiary health center from northern India. The authors reported high odds of cirrhosis with familial and personal history of MTs in the presence of certain identified poor hepatic-related prognostic factors compared with those who had negative familial and personal history. The identified poor hepatic-related prognostic factors were high severity scores such as Child–Turcotte–Pugh score and model for end-stage liver disease score, with ≥1 features of decompensation such as ascites, jaundice, hepatic encephalopathy, and variceal bleeding. Another recent study has documented presence of ≥1 components of metabolic syndrome among patients with NAFLD with significant steatosis and fibrosis as identified by transient elastography.
As per Center for Disease Control and Prevention (CDC) 2012 survey, 55% of alcohol-related deaths are due to alcoholic liver disease (ALD). In a study carried out at a tertiary healthcare institute of northeastern part of India, alcohol consumption was held responsible for 72% of total cirrhosis cases. However, recent studies have identified obesity as an additional risk factor; suggesting that among obese NASH patients, alcohol has much higher hepatotoxic effects compared with nonobese NASH individuals. An abstract published in a conference proceeding documented family history of MTs among two-third of patients with alcoholic cirrhosis. About one-fourth of subjects had both parents either DM or/and hypertensive and 17% had only one parent either DM or/and hypertensive. Presence of 1–2, 2–5, or >5 MTs among parents was observed in 22%, 30%, and 11% of cases, respectively. Reportedly, 26% cases had parental history of alcoholism. The similar group published data of 1,084 male alcoholic cirrhotics and documented younger age at diagnosis, increased incidence of jaundice, ascites, variceal bleed, and hepatic encephalopathy with consequently higher MELD and CTP score among those with family and personal history of MTs. These individuals developed cirrhosis despite shorter median duration and lesser amount of alcohol consumption. These findings very well support more hepatotoxic effect of alcohol with history of MTs.
Presence of inherited MTs predisposes to early and more severe alcoholic cirrhosis, with even a shorter duration of exposure to alcohol. Studies are needed to understand the molecular and metabolic pathways related to this association. Health education regarding deleterious effects of alcohol among those who have a family history of MTs should be ensured. There also exists growing evidence regarding gut microbiome playing potential exemplary role in causing liver cirrhosis and liver cancer. It well explains about the biological plausibility of familial clustering because of genetics and environment combination that might influence intestinal flora.
Primary care physicians regularly see patients with alcohol addiction, diabetes, hypertension, and fatty liver. This editorial highlights the need for screening of individuals with either addiction of alcohol or ALD for personal and family history of diabetes, hypertension, obesity, and other MTs for risk stratification and specific interventions. This raises a pertinent scope of involving primary care physicians for screening of alcohol addicts at community level for potential high risk of liver damage using already available health infrastructure.
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