I read with great interest the article by Das et al. 1 Although presence of nonalcoholic fatty liver (NAFL) in nonobese individuals is a fairly common observation in India, this is the first such scientific documentation for the same. However, I would like to make a few points in this regard.
First, NAFL constitutes a wide spectrum of liver disease with varied natural history extending from simple steatosis to more sinister variants, i.e., nonalcoholic steatohepatitis (NASH) and fibrosis/cirrhosis. Only a proportion of NAFL actually progresses to the more sinister end of this spectrum. Therefore, instead of a blanket focus on NAFL, it would be more appropriate to identify the subset of patients with NAFL who are more likely to progress to NASH. In this regard, the authors have defined ''potentially significant NAFL'' as ''subjects with definite NAFL who had persistently elevated ALT (>40 IU/L)''. However, even in this study only one-third of these subjects with ''potentially significant NAFL'' were found to have NASH on liver biopsy, which means elevated ALT alone is not a good enough marker of ''potentially significant'' NAFL. A full panel of noninvasive markers of liver fibrosis would be more appropriate to define this subset and save costly and/or potentially harmful procedures like liver biopsy or computed tomography scans for them.
Second, although the authors have claimed to have excluded people with alcohol consumption from this study, this population in context comes largely from a tribal background who indulges in many nonconventional forms of ethanol consumption, e.g., mahua flower (Madhuca longifolia). It would be interesting to know if the authors have ruled out those possibilities as well.
Third, risk of NAFL is undoubtedly associated with obesity and metabolic syndrome and has been traditionally associated with more affluent living standards. In the current study too, even nonobese subjects with NAFL had worse metabolic parameters and higher income than their age-matched and sex-matched counterparts who did not have NAFL. Nevertheless, coexistence of intrauterine and neonatal malnutrition and the development of obesity, type 2 diabetes, and related comorbidities have been confirmed in a number of studies in humans and animal models. 2 Moreover, it has been shown that, in humans, the intrahepatic lipid content increase following starvation also may be due to reduced apolipoprotein B-100 production and hepatic lipid export, and/or impaired mitochondrial function; this could have implications for exacerbations of steatohepatitis that is sometimes seen with rapid weight loss, anorexia nervosa, and parenteral nutrition. 3 Therefore, in contrast to the popular view, malnutrition rather than obesity at different stages of life may well be an explanation for pathogenesis of NAFL in this predominantly poor population.