Thanks for sharing this facinating work. I just wanted to add, for those who only read the headline, that these findings are based on inpatient care before the invention of RUTF, where rates of weight gain were a lot faster. This means that the slower weight gain we now have in CMAM programmes is likely preferrable for long term health.

But should we be trying to make rehabilitation even slower? Whilst balancing the need for rapid stabilisation and protection from death and disease as soon as possible? This could tie in with the arguement for reduced dosages of RUTF which have been explored over the past few years.  

Hi Tash,

Thanks for the comments and interesting discussion. We looked at weight gain in children 6-59 months treated for SAM with RUTF in an outpatient setting with a particular focus on those who recruited by MUAC, have stunting and may be at risk of becoming overweight with treatment. We used overweight and obesity as markers for metabolic syndrome and increased risk of non-communicable disease in later life. It is worth noting that metabolic syndrome is not defined for children aged less than 6 years - but all other age groups include obesity as one of the several risk factors. 

This paper https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6292002/ argues that children with SAM (even stunted ones) do not become overweight or deposit excess fat following treatment with RUTF at standard doses in the outpatient setting. It also discusses the work of Madeira et al. and Bartz et al.:  "Studies using other markers of metabolic syndrome such as leptin have demonstrated that after 4–10 weeks of treatment with RUTF, leptin levels are lower than those of normally nourished children and approximately 7 times lower than the threshold for predicting metabolic syndrome"

We argue that exposure to SAM and other factors in later life are likely to be greater risk factors and that early recruitment and treatment with RUTF may serve to mitgate them. We did not investigate rate of weight gain.

I would concede that the use of 'markers' of metabolic syndrome based on weight or obesity, particularly in this age group should be viewed cautiously, and would agree with Thompson's conclusion that investigating a wider metabolic profile in these children would be useful. 

Hi Paul, 

I completely agree, and I too have done a study in Kenya showing no increase in fat mass acretion vs lean mass when treated with RUTF vs RUSF. That was after a few weeks. 

Thompson's study looked at NCD risk in survivors after after several decades. 

I think its a luxury to be able to consider optimising treatment for the health of the individual several decades down the line; we need to prioritise immediate survival, healthy growth and development.  And you're right to point on that the insult of SAM, and greater severity of SAM maybe be worse than the rapid weight gain. We havent been able to unpick that yet. Especially since those with the fastest weight gain tend to be those who were most wasted to begin with - a major confounder in the analyses. 

But, if we COULD acheive early treatment, survival, healthy growth and development, on a slightly slower weight gain so that there is lower risk of later life NCDs, that might be the best of all worlds! Still lots more work to be done on this topic though. 

 Tash