Abstract

The association between severe acute malnutrition (SAM) in early childhood and liver fat in adults is unknown. We hypothesized that exposure to SAM, especially severe wasting, is associated with fatty liver later in life. In this observational study, abdominal CT was used to quantify mean liver attenuation (MLA) and liver:spleen attenuation ratio (L/S). Birth weight (BW), serum lipids, insulin resistance (homeostatic model assessment), anthropometry and intrabdominal fat were collected. Mean differences between diagnostic groups were tested and hierarchical regression analysis determined the best predictors of liver fat. We studied 88 adult SAM survivors and 84 community participants (CPs); age 29.0 ± 8.4 years, BMI 23.5 ± 5.0 kg/m2 (mean ± SDs). SAM survivors had less liver fat than CPs (using L/S) (p = 0.025). Severe wasting survivors (SWs) had lower BW (-0.51 kg; p = 0.02), were younger, thinner and had smaller waist circumference than oedematous malnutrition survivors (OMs). In the final regression model adjusting for age, sex, birth weight and SAM phenotype (i.e., oedematous malnutrition or severe wasting), SWs had more liver fat than OMs (using MLA) (B = 2.6 ± 1.3; p = 0.04) but similar liver fat using L/S (p = 0.07) and lower BW infants had less liver fat (MLA) (B = -1.8 ± 0.8; p = 0.03). Greater liver fat in SWs than OMs, despite having less body fat, supports our hypothesis of greater cardiometabolic risk in SWs. Other postnatal factors might influence greater liver fat in survivors of severe wasting, suggesting the need to monitor infants exposed to SAM beyond the acute episode.

Highlights

  • The association between severe acute malnutrition (SAM) in early childhood and liver fat in adults is unknown

  • We have previously reported worse beta cell function, greater glucose intolerance and a tendency towards greater insulin resistance among adult survivors of severe wasting compared to survivors of oedematous ­malnutrition[12]

  • Data for 172 participants (88 adult SAM survivors and 84 community participants) were analyzed after 7 participants were excluded; 5 as they had no liver image on CT scan and 2 as their CT scans were delayed by more than 3 months after body composition was assessed by DEXA

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Summary

Introduction

The association between severe acute malnutrition (SAM) in early childhood and liver fat in adults is unknown. Despite a benign clinical presentation, FLD is a significant public health concern and the most significant hepatic disorder in high-resource s­ ettings[2] It is considered an independent risk factor for cardiovascular ­disease[3] and has established associations with o­ besity[4] and insulin ­resistance[5]. Individuals from the Helsinki Birth Cohort who were small during early childhood had a higher risk of developing FLD, but this risk was higher in those who were obese as ­adults[10] It is unclear whether there is an association between severe acute malnutrition in early life and fatty liver in adults that is independent of adult overweight/obesity. We hypothesized that adults who were exposed to severe malnutrition in early life would have more liver fat than participants from their communities who were not previously exposed to SAM. These hypotheses were tested in a unique cohort of Afro-Caribbean adult survivors of severe acute malnutrition and community participants

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