Nutrition is central to human existence from sustenance of cellular life to powering its myriad functions. Contrasting images of Haitian or Ugandan malnourished children and Westerner obese kids mirror not only the economic reality of a nation but also the propensity to diseases albeit of opposite polarity from Kwashiorkor/Marasmus to metabolic syndrome with equal implications for health outcomes. In addition to specific nutritional deficiency states such as scurvy and rickets, indirect effects of nutrition on human health are of greater importance.In this context, astute clinical observations in 1960s brought attention to a rather typical form of chronic pancreatitis (CP) in Kerala [1]. The picture of a young malnourished patient with chronic calcific pancreatitis and diabetes evoked much interest. Since one of its most peculiar features was malnutrition (undernutrition), it was soon implicated in its etiopathogenesis. At a time when the basic structure of DNA was just about making the headlines, genetic mutation as the cause of disease was not even on the agenda outside of Mendelian disorders. Malnutrition thus made the cut being the striking clinical feature. Since the disease was reported mainly from tropical countries, which ironically were much poorer and undernourished than their temperate counterparts, the term 'tropical pancreatitis' (TP) was coined for want of a more defining terminology.Protein deficient and high carbohydrate diet was thus implicated in the etiopathogenesis of the thus coined TP. Sandhyamani et al. [2] showed that high carbohydrate and low protein diet, either comprising of cornstarch or cassava, resulted in ductal changes with mucoid metaplasia and parenchymal atrophy in an animal model of bonnet monkey. However, pancreatic changes were rather different from those typically seen in CP and the animals predominantly developed vascular and cardiac changes-features not observed in CP patients. Furthermore, severe malnutrition has been shown to result in pancreatic atrophy and insufficiency and not CP thus disproving the nutritional hypothesis [3]. Since cassava was a staple diet in Kerala, it gained the status of a co-culprit as a logical extension of the nutritional hypothesis. The cassava hypothesis has also been discarded because: (i) cassava consumption was not found as a risk factor in case-control studies including one from Kerala [4], (ii) patients with the TP were reported from areas where cassava was not consumed [5], and (iii) long-term cassava consumption did not produce diabetes or pancreatitis in a rat model [6].Even though the association of malnutrition with CP was consistent, not many clinical studies examined the cause and effect relationship. Our group first showed that malnutrition was an effect and not a cause of CP. In a prospective study of 120 patients with idiopathic CP, only 20.6% were underweight before the onset of the disease while 67% lost weight following the disease suggesting that malnutrition was an effect and not a cause of CP [5]. A recent study by Sathi...