Accounting for the rise in pediatric nonalcoholic fatty liver disease


Suggested Citation: Garko, Michael (2018, July). Accounting for the rise in pediatric nonalcoholic fatty liver disease is on the rise. Retrieved from


Accounting for the rise in pediatric nonalcoholic fatty liver disease


Dr. Michael Garko, Ph.D.

Host & Producer Let’s Talk Nutrition – Health Talk Radio for the 21st Century

Epidemiologically, the prevalence of pediatric nonalcoholic fatty liver disease (NAFLD) has doubled globally during the past 20 years (Ranucci et al., 2007). It is widely recognized as the most prominent cause of chronic liver disease among children and adolescents in Western countries and the most prevalent pediatric liver disease worldwide (Berardis & Sokal, 2013; Utz-Melere et al., 2018).

Several primary and secondary risk factors have been identified in the literature as being associated with NAFLD. Primary factors include: Ethnicity, genetics, Type II diabetes, obesity, insulin resistance, dyslipidemia and metabolic syndrome (see Mishra & Younossi, 2012). Secondary risk factors include: Age, gender, family history, obstructive sleep apena, polycystic ovary syndrome, medications and environmental toxins (see Mishra & Younossi, 2012).

The July, 2018, edition of Health & Wellness Monthly focuses on the rise pediatric NAFLD and the multiple hit hypothesis to account for the increase of this disease in children and adolescents.

The pathogenesis of NAFLD is currently accounted for by the multiple hit hypothesis, whereby, obesity and other factors (e.g., genetics, epigenetics, environmental factors, insulin resistance) cause the accumulation of fat in the liver and the development of a fatty liver which then becomes susceptible to further hits including oxidative stress, mitochondrial dysfunction, an imbalance of proinflammatory cytokines and activation of stellate cells which result in necroinflammation and fibrosis (i.e., NASH) (see Berardis & Sokal, 2014).

Pediatric NAFLD is running linearly and in parallel with the pediatric obesity epidemic. Consequently, obesity is widely recognized as the primary risk factor associated with pediatric NAFLD to the extent that its prevalence in obese children is reported to run as high as 70%-80% (Berardis & Sokal, 2013; Mencin & Lavine, 2011).

Hence, taking together its prevalence worldwide, recognition as a primary risk factor, acceptance as being a pathogenic hit factor and simultaneous increase alongside obesity, it is contended here that obesity potentially accounts for a significant of amount of the variance in pediatric NAFLD and helps to explain the rise of NAFLD in children and adolescents. In sum, while it is not a sufficient condition, obesity is among the most important necessary conditions (if not the most important condition) accounting for the disturbing rise worldwide in pediatric NAFLD


Assuming that moderating the unrelenting rise in pediatric obesity would reduce the rise in pediatric NAFLD, investigators who recognize an association between obesity and pediatric NAFLD offer a number of dietary and lifestyle recommendations (e.g., reduced calorie intake, reduced consumption of fat, simple carbohydrates, sugar-loaded foods, especially processed and fast foods and sugary drinks, along with increased fiber intake physical activity) to help prevent obesity (e.g., Berardis & Sokal, 2014; Ranucci et al., 2017; Utz-Melere et al., 2018).

Sypher (2004) argues that some of the dietary recommendations in preventing obesity (e.g., eat less & move more) fall-short in preventing weight gain. Sypher (2004) contends that it is more effective to consider the glycemic-index of carbohydrate-containing foods. He recommends the consumption of low-glycemic-index starches constituted of whole grains and fiber (e.g., legumes, green vegetables) because they create better postprandial glucose and insulin responses. Sypher (2004) points to three mechanisms that help explain consuming high-glycemic index carbohydrate and obesity. First, high-glycemic carbohydrate results in postprandial hyperinsulinemia, leading to excessive weight-gain. Second, sugar-containing drinks fail to displace energy from other food sources, leading to an increase in energy consumption. Third, high-glycemic-index foods result in hyperphagia.

Sypher’s (2004) glycemic-index-related recommendations merit consideration in helping to prevent pediatric obesity and, thereby, help reduce the rise in pediatric NAFLD.


Berardis, S. & Sokal, E. (2013). Pediatric non-alcoholic fatty liver disease: An increasing public health issue. European Journal Pediatrics. 173, 131-139.

Mencin, A.A. & Lavine, J.E.(2011). Nonalcoholic fatty liver disease in children. Current Opinion in Clinical Nutrition and Metabolic Care. 14, 151-157.

Mishra, A. & Younossi, Z.M. (2012, June). Epidemiology and natural history of non-alcoholic fatty liver disease. Journal of Clinical and Experimental Hepatology. 2 (2), 135-144.

Ranucci, G., Immacolata, M. & Iorio, R. (2007). Obese children with fatty liver: Between reality and disease mongering. World Journal of Gastroenterology. 23 (24), 8277-8282.

Sypher, A. H. (2004). The pediatric obesity epidemic: Causes and controversies. The Journal of Clinical Endocrinology & Metabolism. 89 (6), 2540-2547.

Utz-Melere, M., Cristina, T.A., Lessa-Horta, B., Epifanio, M., Mouzaki, M. & Maitos, A. A. (2018). Non-alcoholic fatty liver disease in children and adolescents: Lifestyle change – a systematic review and meta-analysis. Annals of Hepatology. 17 (3),, 345-354.

Suggested Citation: Garko, Michael (2018, July). Accounting for the rise in pediatric nonalcoholic fatty liver disease is on the rise. Retrieved from