Nonalcoholic fatty liver disease (NAFLD), a common and progressive disease, is on track to become the leading cause of liver transplants among adults. Childhood intervention is essential for mitigating serious disease in future generations, but the nutritional mechanisms contributing to NAFLD have remained unclear. Researchers at Children’s Hospital Colorado recently published findings that illuminate how both the severity of this disease — and its reversal — depend on a surprisingly simple ingredient: sugar.
Rising NAFLD and risk of non-alcoholic steatohepatitis
NAFLD, a disease characterized by fat accumulation in the liver, is an obesity-related complication that can increase the risk of high blood pressure, cardiovascular disease and Type 2 diabetes, among other comorbidities. In the United States, this disease now affects 10% of all children and 38% of children with obesity, with Hispanic youth experiencing disproportionately higher rates of NAFLD.
At Children’s Colorado’s Liver Center, director Shikha Sundaram, MD, sees patients with this disease daily. That first-hand experience is exactly why her recent research explores the role of dietary interventions in curbing rates of NAFLD.
“We think that by 2030, NAFLD will take over as the number one indication for adult liver transplant,” Dr. Sundaram says. “We’ve got huge cohorts of kids with NAFLD that are 10, 11, 12 or 13. What does this mean for patients when they’re 40 or 50?"
Without intervention, NAFLD can worsen into non-alcoholic steatohepatitis, or NASH, which results in both liver damage and inflammation in addition to fat buildup. Treatment for NAFLD and NASH typically includes general lifestyle interventions, such a healthier diet and increased physical activity, but rising cases among both children and adults stress the importance of more specific dietary guidance.
Shikha Sundaram, MD
Gastroenterology and Transplant Hepatology
Children’s Hospital Colorado
Liver Transplant Program
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The role of sugar in NAFLD
Dr. Sundaram and her team recently published findings that illuminate the nutritional mechanisms underpinning this disease. The study compared 28 adolescents with NAFLD to 15 control subjects with neither NAFLD nor obesity. Participants logged their daily food and beverage intake using the Harvard Food Frequency Questionnaire over a six-month period. The study looked at consumption of both micronutrients (such as vitamins and minerals) and macronutrients (such carbohydrates, fats and proteins).
“Our study suggested that kids with NASH probably take in about 10 more spoons of sugar than kids without the disease,” Dr. Sundaram says.
Specifically, among patients with NASH, a bigger proportion of their energy intake came from simple sugars — such as those found in sweetened beverages, rather than those found in fruit.
“When we speak to families, we talk about sugar, sweetened beverages, juice, Gatorade, sweet tea and soda, and it’s not unusual for us to hear that a child is taking in two to three of those beverages per day,” Dr. Sundaram says.
This study is the first to show that sweeteners can directly contribute to the onset and progression of NAFLD, but that’s not all. Their research also proved that in children, reducing dietary intake of added sugars can reverse — and even eliminate — severe instances of disease (and its complications).
“Our study suggested that kids with NASH probably take in about 10 more spoons of sugar than kids without the disease.”
SHIKHA SUNDARAM, MD, MSCI
Disproving misconceptions about NAFLD
While her research focuses on obesity-related liver disease, it also helps clarify a major misconception around obesity at large: It cannot be cured by simply eating less.
“Our data shows that, when comparing the lean kids to those with NAFLD, their total caloric intake is actually very similar,” Dr. Sundaram says. “That speaks, physiologically and biologically, to what’s happening.”
Specifically, the research shows that the onset of NAFLD isn’t about how much a child eats; rather, it’s about how a child’s digestive system absorbs and metabolizes sugar differently than kids without the disease. This understanding sheds light on how NAFLD could be better detected and assessed through biopsies.
“These results hinted at not just what their enzymes might look like, which is the easiest way to theoretically assess disease, but also what their biopsies would look like,” Dr. Sundaram says. “We still consider biopsy to be the gold standard for assessing disease severity.”
Her findings have set a precedent, guiding future NAFLD research toward understanding the biological origins of obesity-related liver disease — and why the disease is more prevalent among Hispanic youth.
For now, Dr. Sundaram’s team will use these results to guide NAFLD patients and their families toward achievable, effective dietary changes that reduce sweetened foods.
“When we’re taking care of these patients clinically, we try to emphasize that we’re looking for them to change their lifestyle and their relationship with food — we’re not trying to put them on a diet,” Dr. Sundaram says. “Rather, we’re trying to cultivate a lifelong commitment to eating healthy.”