The thrifty genotype hypothesis.
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Diabetes Mellitus, Type 2↗
Biomedical subjects
J C Brand Miller
Publications and source records attributed to J C Brand Miller.
The metabolic syndrome: from inherited survival trait to a health care problem.
A critical role is proposed for the quantity and quality of dietary carbohydrate in the pathogenesis of the insulin resistance and hyperinsulinaemia which characterise the Metabolic Syndrome. We propose that an insulin-resistant genotype evolved to provide survival and reproductive advantages for the cold-climate, large game hunters of the last Ice Age who consumed a low carbohydrate, high protein diet with periodic starvation. Insulin resistance would have minimised glucose utilisation by muscles thereby facilitating the preferential utilisation of glucose by the brain, foetus and mammary gland. But beginning about 10,000 years ago following the end of the last Ice Age and the development of agriculture, dietary carbohydrate increased and the selection pressure for insulin resistance decreased in some groups. Agriculture began in the Middle East and spread throughout Europe long before it was developed elsewhere. Hence the prevalence of the insulin-resistant genotype decreased in Europeans and other groups exposed to a high carbohydrate intake for sufficiently long. Some geographically isolated groups such as the Pima Indians and Nauruans experienced conditions which further diminished the gene pool diversity and resulted in particularly insulin resistant populations. Traditional carbohydrate foods have a low glycaemic index and produce only modest increases in plasma insulin. However, the constant supply of highly refined high glycaemic index carbohydrate in modern diets, results in postprandial hyperinsulinaemia. The insulin-resistant genotype is now disadvantageous and predisposes to the development of the Metabolic Syndrome.
Blood Glucose↗
Sialic acid content of infant saliva: comparison of breast fed with formula fed infants.
Sialic acid is found in especially high concentrations in brain gangliosides, and supplementary sialic acid is associated with increased learning behaviour in animals. It was hypothesised that breast fed infants may have higher concentrations of sialic acid in body fluids and tissues because human milk is a rich source of sialylated oligosaccharides, while formulas contain very little. The aim therefore was to compare the sialic acid content of saliva collected from full term infants who were either solely breast fed or formula fed until weaning at 3-5 months of age. Thirty three infants, 18 breast fed and 15 formula fed, were studied at a mean (SD) age of 5 (2) months. The breast fed infants, when compared with formula fed infants, were found to have almost two times more free sialic acid in saliva (mean (SE) 16.0 (2.7) v 8.2 (2.1) mg/l, p < 0.036) and nearly 50% more total sialic acid (47.3 (3.9) v 32.2 (4.4) mg/l, p < 0.014). The findings provide a preliminary indication that an exogenous source of sialic acids derived from human milk may contribute to higher concentrations of sialic acid in body fluids. There are important implications for the formulation of human milk substitutes.
Adult↗
Development of insulin resistance in the rat is dependent on the rate of glucose absorption from the diet.
The effect of long-term consumption of diets of different carbohydrate composition was investigated be feeding rats for up to 52 wk on diets in which the carbohydrate was either glucose, amylose or amylopectin. A glucose-based diet was included to examine the relationship between the rate of carbohydrate absorption from the diet and the development of insulin resistance. Insulin sensitivity was assessed by subjecting animals to an intravenous glucose tolerance test (IVGTT). Amylopectin-fed animals became progressively insulin resistant from 12 to 26 wk of feeding. The area under the plasma insulin curves in response to a glucose load (IVGTT) for these animals rose progressively from 15.1 +/- 2.5 nmol/L.30 min at 8 wk to 45.8 +/- 3.5 nmol/L.30 min (P < 0.001) at 26 wk of feeding. Amylose-fed animals did not exhibit insulin resistance until 26 wk of feeding when insulin secretion in response to a glucose load was 28.3 +/- 0.9 vs. 14.6 +/- 3.2 nmol/L.30 min at 16 wk of feeding (P < 0.005). Glucose-fed animals displayed insulin resistance after only 8 wk of feeding. At this time, the area under their plasma insulin curves was almost double that for amylose- or amylopectin-fed animals (P < 0.001). We conclude that long-term consumption of a diet in which available carbohydrate is rapidly absorbed causes insulin resistance in rats. The more rapidly glucose is absorbed from the diet, the faster the insulin resistance develops.
Absorption↗
Interrelationships among postprandial satiety, glucose and insulin responses and changes in subsequent food intake.
OBJECTIVE: The aim of this study was to investigate whether postprandial glucose and insulin responses were related to concurrent changes in satiety. DESIGN: Thirty-eight common foods, grouped into six food categories, were tested in total. Each food category was fed to a separate group of subjects. A within-subjects repeated-measures design was used such that within each food category each subject consumed all of the test foods in random order. SETTING: The study was conducted at the Human Nutrition Research Unit, Sydney University. SUBJECTS: Separate groups of 11-13 healthy young subjects, who were unrestrained eaters, were recruited for each of the six food categories. INTERVENTIONS: Isoenergetic 1000 kJ (240 kcal) portions of the test foods were fed to fasting subjects. Fingerprick blood samples and satiety ratings were obtained every 15 min over 120 min after which a standard meal was presented and ad libitum food intake was recorded. A glycaemic score, insulin index and satiety index score was calculated for each food by dividing the area under the 120 min response curve (AUC) for the test food by the AUC for white bread and multiplying by 100. Expressing the results of the test foods relative to those for white bread minimised the confounding influence of inherent differences between the subjects. RESULTS: Among the 38 test foods, there were no significant relationships between satiety and plasma glucose or insulin responses. However, a negative correlation was found between insulin AUC responses and ad libitum food intake at 120 min which suggests that test foods producing a higher insulin response within 120 min were associated with less food intake and thus indirectly greater satiety. This result is consistent with previous findings that carbohydrate-rich foods are more satiating than fat-rich foods. Thus, total carbohydrate content appears to have been a stronger determinant of short-term satiety, in conjunction with the foods structural characteristics, than the foods glycaemic impact. CONCLUSIONS: The total amount of carbohydrate consumed at a meal and subsequent insulinaemia may partly determine the degree of hunger arising within the next 2 h.
Adult↗