This study looked at the effect of nutrients (or lack thereof) on inflammation, insulin resistance and obesity in pre-pubescent and pubescent children. Here’s a summary of the findings.
— Inflammation is the route through which obesity results in insulin resistance
— Insulin resistance is also affected by genetic (now thought to be a cluster of genes in the FTO region of our chromosomes – click here for this recent study) and environmental factors (such as sedentary lifestyles and poor diet). The latter affects the expression of the former; that is, exercise, diet, thoughts and more can affect whether certain genes are switched on or off.
— Diets in excess of energy and/or too much saturated fat or refined carbohydrate have been implicated in the risk of insulin resistance  but there are other risk factors.
— These risk factors include diets deficient nutrients such as the anti-inflammatory calcium, magnesium, vitamin D, and possibly omega-3 polyunsaturated fatty acids.
— Refined carbohydrates, mainly from soft drinks, increase the risk of weight gain, fatty liver, and the metabolic syndrome ; all these are pathological conditions linked to insulin resistance.
— Probably refined carbohydrates help cause insulin resistance by increasing the visceral (inside the abdomen) de novo lipogenesis; that is, these carbs cause fat to be made inside the body.
— Carbohydrates intake is related to waist circumference; it makes one’s waist larger by building up visceral fat, and this is not good for your health.
— Saturated fat affects negatively the concentration of circulating adiponectin, which can also increase insulin resistance.
They concluded that, independently of central obesity, puberty, and other nutrients deficiencies or excess, magnesium-deficient diets predict inflammation and that refined carbohydrates predict insulin resistance.
The upshot is, eat fewer carbs, especially refined ones, and make sure you have enough magnesium through diet and/or supplements.
Excessive refined carbohydrates and scarce micronutrients intakes increase inflammatory mediators and insulin resistance in prepubertal and pubertal obese children independently of obesity.
Low-grade inflammation is the link between obesity and insulin resistance. Because physiologic insulin resistance occurs at puberty, obese pubertal children are at higher risk for insulin resistance. Excessive diets in refined carbohydrates and saturated fats are risk factors for insulin resistance, but calcium, magnesium, vitamin-D, and the omega-3 fatty acids likely protect against inflammation and insulin resistance.
To analyze interactions among dietary saturated fat, refined carbohydrates, calcium, magnesium, vitamin D, and omega-3 fatty acids on the risk of inflammation and insulin resistance in a sample of prepubertal and pubertal children.
A sample of 229 children from Mexico City was analyzed in a cross-sectional design. Anthropometric measurements, 24 h recall questionnaires, and blood samples were obtained. Serum insulin, glucose, calcium, magnesium, 25-OHD3, C-reactive protein, leptin, adiponectin, and erythrocytes fatty acids were measured. Parametric and nonparametric statistics were used for analysis.
While mean macronutrients intake was excessive, micronutrients intake was deficient (P < 0.01). Inflammation determinants were central obesity and magnesium-deficient diets. Determinants of insulin resistance were carbohydrates intake and circulating magnesium and adiponectin.
Magnesium-deficient diets are determinants of inflammation, while high intake of refined carbohydrates is a risk factor for insulin resistance, independently of central adiposity.