Activity impairment also increased as BMI increased, with normal weight (vs all OCs) respondents reporting significantly less activity impairment.
20 30 Manninen et al 31 found that increasing from normal weight to overweight during adult life might slightly increase the risk of developing knee OA leading to arthroplasty compared with being constantly overweight during adult life.
For women, clear weight-based patterns in the data are apparent as BMI classification increases beyond normal weight.
There is an apparent profile of cardiometabolic and inflammatory biomarkers that emerges as BMI increases from normal weight to obesity.
In conclusion, we observed a distinctive profile of metabolic phenotypes – including cardiometabolic disease markers and inflammatory biomarkers – that emerges as BMI increases from normal weight to obesity.
The number of clinical items and of weight-related clinical items increased with increasing BMI category (normal weight, overweight, obese), particularly among the obese (7.1 ± 0.3, 7.2 ± 0.3, and 8.2 ± 0.2 respectively for all clinical items, p < 0.0001; 1.5 ± 0.1, 1.9 ± 0.1, and 2.8 ± 0.15 respectively for weight-related items, p < 0.0001).
Studies in type 2 diabetes report both increased mortality for normal weight and no evidence of an obesity paradox.
There was no mortality risk for obese participants and an increased risk among normal weight compared with overweight participants (HR 1.72 [95% CI 1.12 2.64]).
In obese type 1 diabetic women, the adjusted OR of major malformations (1.77 (95% CI 1.18 to 2.65)) and PE (1.74 (95% CI 1.35 to 2.25)) were significantly increased compared with normal weight type 1 diabetic women.
While GI and glycaemic load (GL) were not found to be associated with GWG in two previous studies that did not stratify on pre-pregnancy BMI, 7 9 a recent study from the DNBC showed that GL increased GWG in normal weight and overweight women.
