170220_TSF_BlogHero_02Incidence of non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH) are increasing.

NAFLD is the build-up of excess fat in liver cells and often associated with insulin resistance, overweight and high blood triglycerides.1

NASH can be considered the more extreme end of the NAFLD spectrum, where severe inflammation can lead to irreversible damage, fibrosis and cirrhosis of the liver.2-3

Liver fat accumulation impacts effective liver function.

Why does this matter?

Well! Among a myriad of other roles, the liver is one of the major detoxifying organs of the body, processing various compounds from the internal and external environment to be either expelled or recycled for future use.

Historically, fatty liver is usually a result of too much booze. Now, we are seeing people who are not large consumers of alcohol with fatty livers and it is the fastest growing cause of liver disease in the Western world. Even in kids.4

A new study from Italy has shared some pretty startling results on the independent link between obese children and adolescents with NAFLD, and fructose consumption, uric acids levels, and incidence of NASH.5

The study comprised of 271 participants, with the average age of 12.5years. Diet records were taken from which fructose intake was calculated. The researchers found the greatest source was sugar-sweetened beverages, and 90% consumed soft drink or a sweetened drink at least once per week.

Then they measured for the incidence of NASH.

37.6% of patients had NASH. Of those with NASH, 47% had high uric acid, compared to only 29.7% of non-NASH participants.

After adjusting for multiple confounding factors, uric acid level and fructose consumption were each independently associated with NASH, and the researchers also found the only independent dietary risk factor for increased uric acid in the blood was fructose consumption.

“In this study, we show for the first time that uric acid concentrations and dietary fructose consumption are independently and positively associated with NASH,” said study author Valerio Nobili. “The development of NASH may markedly affect life expectancy and quality of life in affected individuals and therefore it is crucial to understand the risk factors for NASH in children and adolescents in order to design effective interventions which can be used safely to treat this young group of patients.”

Uric acid, chemically an antioxidant, in high concentrations can crystallise, causing pain and the condition known as gout.

“In the intestine, fructose intake alters the gut microbiome and enhances endotoxin translocation into the portal circulation via increased permeability of tight junctions. In the liver, fructose is rapidly metabolized, consuming adenosine triphosphate, which may result in increased adenosine monophosphate and inosine monophosphate (IMP) and conversion of IMP to uric acid,” the researchers wrote.

It is important to remember that refined and added sugars are the issue for high fructose intake – not the fructose naturally occurring in whole foods like fruit. Sugar in fruit is packaged and delivered to the body alongside fibre, minerals, vitamins, and phytonutrients, altering the way it is digested, absorbed and impacts in the body.

Pediatric Endocrinologist Prof. Robert Lustig published an article several years back, likening the effects of ethanol (alcohol) and excess free fructose (and it is not limited to the liver).6

170120_TSF_OH and Fructose Affects on Body

Studies like this highlight the importance of taking care of what our kids and teens have access to. Education is critical for them to understand the short and long-term implications of consuming too much discretionary food in place of the real stuff, and how to identify the added sugars in seemingly healthy foods.

So, love your liver and go easy on the sweet stuff.

By Angela Johnson (BHSc Nut. Med.)

 

References:

  1. Better Health Channel 2012, Liver- fatty liver disease, viewed 15 February 2017, <https://www.betterhealth.vic.gov.au/health/conditionsandtreatments/liver-fatty-liver-disease>.
  2. Cleveland Clinic 2013, Nonalcoholic fatty liver disease, viewed 15 February 2017, <http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/hepatology/nonalcoholic-fatty-liver-disease/>.
  3. Dyson, JK, Anstee, QM, & McPherson, S 2014, ‘Non-alcoholic fatty liver disease: a practical approach to diagnosis and staging’, Frontline Gastroenterology, vol. 5, no. 3, pp. 211-218.
  4. Bellentani, S, Scaglioni, F, Marino, M, & Bedogni, G 2010, ‘Epidemiology of non-alcoholic fatty liver disease’, Digestive Diseases (Basel, Switzerland), vol. 28, no. 1, pp. 155-161.
  5. Mosca, A et al. 2017, ‘Serum uric acid concentrations and fructose consumption are independently associated with NASH in children and adolescents’, Journal of Hepatology, [ePub ahead of print].
  6. Lustig, RH 2010, ‘Fructose: Metabolic, Hedonic, and Societal Parallels with Ethanol’, Journal of the American Dietetic Association, no. 9, p. 1307.