What is known? |
Chemicals with endocrine-disrupting activity increase the risk of diabetes, independently of obesity |
Prenatal exposure to environmental chemicals increase the risk of obesity, especially in early life |
Dysbiosis increases the risk of obesity |
Prenatal exposure to environmental chemicals is associated with low birth weight |
Emerging evidence |
Adipocyte precursors may be more susceptible that mature adipocytes to environmental chemicals |
Central obesity in early life may predispose to insulin resistance regardless of body mass index |
Speculation |
The immunological and metabolic consequences of the pattern of dysbiosis seen in adults with obesity or type II diabetes are likely to have life-long effects, especially if encountered during fetal development or in early life |
The pattern of dysbiosis that is detrimental in obesity/type II diabetes is also detrimental to respiratory health |