Obesity Diet & Nutrition

Microbiota under 3 years old fluctuates substantially and is more impressionable to environmental factors than the adult microbiota. Lifestyle, sanitization, caesarean sections, antibiotic usage, immunizations. It has been studied that there is a “critical window” early in life during which the microbiota can be disrupted in a way that may favour the development of disease later in life and there is and increasing evidence concerning role of microbiota changes during early life impacting the development of intestinal and extra- intestinal diseases. Many factors determine the establishment and composition of microbial communities in all mucosa, including the gut. The most important occurs at birth and shortly afterwards. Early life changes in microbiota composition can alter susceptibility to developing obesity later in life. Many studies shown presence/absence of specific microbes can modulate and program life-long changes in immunity and further clinical study might help understand exact paths on metabolic disease progression. A critical early window exists in a child’s life where its environmental exposures (diet, microbes exposure) can shift the immune-metabolism-microbiota interaction to pathophysiological states which lead to alterations in host growth rates, metabolism, immunity and result in diseases relating to obesity and malnutrition (diabetes 2). Research showed that impact of diet and environmental change stresses on the host can be passed on maternally to children through epigenetic modulation of the DNA by methylation. Thus maternal dietary and microbial exposures are also crucial to the development of the microbiota early in life as children may inherit genes with differing potential for predisposition for malnutrition or obesity, based on the diet of their mother.There is a need to focus on early life therapeutic approach to promote improved intestinal health to combat obesity and malnutrition but also on maternal health and therapeutic interventions in mothers and further clinical data would help to bring insightful value. A study showed that treatment of obese mice with Akkermansia muciniphila reduced high fat diet induced metabolic disorders, including fat mass gain, metabolic endotoxemia, adipose tissue inflammation and insulin resistance. Microbiota derived metabolites signal to distant organs in the body where they activate cellular receptors. Thus diet microbiota interactions may regulate host metabolism at several levels. Based on preclinical studies diabetes associated microbiota appears to metabolize amino acids differently leading to a unique suite of metabolites that can contribute to insulin resistance. Early life stress induces type 2 diabetes - like symptoms at adulthood in mice associated with defect of intestinal IL17 and IL22 secretion. By understanding the differing energy harvest and metabolic capabilities of each child’s gut microbiota, there might be support for crafting microbiota based interventions (supported already by preclinical data and research) to reverse susceptibility to obesity diabetes early in life and clinical data might support research evidence. A critical window exists early in life where interventions could have more of profound, long lasting impact on health. Understanding the microbiota changes during this window will be of great importance.