High rates of fructose malabsorption are associated with reduced liver fat in obese African Americans

Calorie Control Council Response

Walker RW, Le KA, Davis J, Alderete TL, Cherry R, Lebel S, Goran MI. J Am Coll Nutr 2012;31:369-74.

The aim of this study was to investigate the frequency of fructose malabsorption between obese Hispanic and African American young adults.  The authors hypothesized that fructose malabsorption would be negatively associated with liver fat accumulation and that this relationship may explain some of the difference in liver fat between Hispanics and African Americans. However, the conclusions made by the authors may be confounded by issues with references and research protocol.

First, the reference cited in support of elevated fructose intake is the 10y old AJCN commentary by Bray, Nielsen & Popkin that kicked off the HFCS furor.  Contemporary data do not support this contention.  Though correlation is not causation, the fructose-obesity correlation is the lead justification used by the authors. Additionally, references cited in support of fructose-enhanced liver fat and NAFLD include hyper-fructose dosing (+35% E as fructose) and NAFLD population prevalence studies.

Second, fructose malabsorption was measured by the standard breath-hydrogen test.  In principal, unabsorbed fructose from a bolus challenge dose passes to the large intestine where it is fermented by native microbes to short-chain fatty acids and hydrogen.  These compounds are absorbed into the bloodstream; the hydrogen measured in expired air is only a crude measure of the amount of undigested fructose reaching the colon.  The biggest problem with the test is that large fractions of the population absorb a 50g dose of fructose (like that used in this study) poorly.  However, when glucose is co-administered at levels ≥50% of the amount of fructose, malabsorption symptoms largely disappear (see Riby et al.,AJCN, 1993;58:748S).  Thus, the breath hydrogen test overestimates fructose malabsorption.

Third, Figure 1a shows a striking difference in breath hydrogen production between the two ethnic groups.  However, the data correlating liver fat with breath hydrogen in Figures 1b and 1c is quite scattered.  The authors based their ethnicity-wide conclusions on trend lines through data points, but the data are so scattered as to be poorly predictive for individuals.

In conclusion, the authors’ hypothesis that fructose malabsorption is protective against fructose-induced fatty liver disease was not generally supported by the data:  it worked for African Americans, but not Hispanics.


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