Relative glycaemic impact of customarily consumed portions of eighty-three foods measured by digesting in vitro and adjusting for food mass and apparent glucose disposal.

Practical values to guide food choices for control of postprandial glycaemia need to refer to entire foods in amounts customarily consumed. We tested an in vitro method for determining the relative glycaemic impact (RGI) of customarily consumed portions of foods. Sugars released during in vitro pancreatic digestion of eighty-three foods were measured as glucose equivalents (GE) per gram of food, adjusted by the glycaemic indexes of the sugars to obtain glycaemic GE (GGE) per gram and multiplied by food portion weight to obtain the GGE contribution of the food portion, its RGI. The results were compared with clinical GGE values from subjects who consumed the same food amounts. In vitro and in vivo GGE values were significantly correlated, but the slope of the regression equation was significantly less than one, meaning in vitro GGE values overestimated in vivo GGE values. Bland-Altman method comparison showed the in vitro-in vivo disparity to increase as mean GGE increased, suggesting the need to allow for different rates of homeostatic blood glucose disposal (GD) due to different GGE doses in the customarily consumed food portions. After GD correction, Bland-Altman method comparison showed that the bias in predicting in vivo GGE values from in vitro GGE values was almost completely removed (y = 0.071x - 0.89; R2 0.01). We conclude that in vitro food values for use in managing the glycaemic impact of customarily consumed food quantities require correction for blood GD that is dependent on the GGE content of the food portions involved.

Is population mixing associated with childhood type 1 diabetes in Canterbury, New Zealand?

There is growing evidence to support a role for infections in the aetiology of childhood type 1 diabetes. However, previous studies suggest that infections can either protect against or initiate type 1 diabetes onset, depending on the timing of exposure. Population mixing has recently been employed as a proxy measure for area-level infectious exposure in childhood diabetes research. Research has found that the incidence of type 1 diabetes tends to be higher in areas with low population mixing, suggesting that children with low infectious exposure in early life have increased susceptibility to the disease. Subsequent exposure to infection could act as the final trigger to type 1 diabetes development. We assess whether an increase in population mixing over a short time period is associated with a higher incidence of type 1 diabetes. We test this hypothesis using data on childhood type 1 diabetes from the Canterbury region in New Zealand for the period 1999-2004, and population mixing change measures derived from the 1996 and 2001 censuses. We found that the incidence of type 1 diabetes was higher in areas where population mixing had increased the most. This effect was small, but remained significant after adjustment for potential confounding variables. The findings suggest that large increases in population mixing, over short time periods, could act as a trigger for type 1 diabetes development in children.

The deleted in colorectal carcinoma (DCC) gene 201 R --> G polymorphism: no evidence for genetic association with autoimmune disease.

The product of the deleted in colorectal carcinoma (DCC) gene has a role in apoptosis and is a positional candidate for IDDM6, the putative chromosome 18q12-q23 autoimmune disease locus. We hypothesised that a nonconservative substitution (DCC 201 R --> G; nucleotide (nt) 601 C --> G), located in an extracellular immunoglobulin-like domain of DCC, is an aetiological determinant of autoimmunity. We tested this hypothesis by genetically testing the nt 601 C --> G polymorphism for association with three autoimmune phenotypes in a large population-based case-control study. There was no evidence for association of DCC nt 601 C --> G with autoimmune disease in cohorts comprising 2253 subjects with rheumatoid arthritis, type I diabetes and Graves' disease, and 2225 control subjects, from New Zealand and the United Kingdom. Furthermore, using the transmission disequilibrium test, there was no significant evidence for biased transmission of the nt 601 C --> G polymorphism to probands within a 382 family type I diabetes affected sibpair cohort from the United Kingdom. Thus, the DCC 201 R --> G polymorphism does not appreciably influence risk of developing the autoimmune diseases tested.

Seasonality of birth and onset of clinical disease in children and adolescents (0-19 years) with type 1 diabetes mellitus in Canterbury, New Zealand.

AIMS: To determine the seasonality of clinical disease onset and month of birth in type 1 diabetes mellitus (DM) in the southern hemisphere. PATIENTS: Two hundred and seventy-five children with type 1 DM in the South Island of New Zealand were studied. The total live births (91,394) of the same period were used as control data. METHODS: Seasonal rhythms were analyzed using the 12 month cosinor method. RESULTS: The month of birth pattern of the patients with DM showed a statistically significant peak (p < 0.01) in summer, whereas the disease onset had a significant peak in winter (p < 0.01), similar to that registered in countries of the northern hemisphere, but in different months of the year. The total live births had no significant rhythm. The different seasonality of birth of the children who subsequently developed type 1 DM from that of the total live births is suggestive of the initiation of the autoimmune process in utero or perinatally.

Incidence of type 1 diabetes mellitus diagnosed before age 20 years in Canterbury, New Zealand over the last 30 years.

This study examined the epidemiological characteristics of type 1 diabetes mellitus (DM) presenting in Canterbury, New Zealand, between 1970 and 1999. All patients with type 1 DM aged 0-19 years at diagnosis within the Canterbury geographical region were either admitted to the regional hospital or seen acutely as outpatients in clinics at the same institution. Primary ascertainment of incident cases, through notification by the attending physician or paediatrician, began prospectively in 1982. Incident cases between 1970 and 1982 were ascertained retrospectively from clinic and hospital records. For the years 1970-99, there were 474 incident cases (256 males, 218 females). Incidence rates determined from 5-yearly census population denominators ranged from 2.40 to 26.59 patients/100,000 person years. The mean for 5-year periods, starting from 1970, increased from 6.79 to 22.79 patients/100,000 person years, i.e. a 3.4-fold increase over 30 years. The increase in incidence based on linear regression of these data is 0.59 patients/100,000 per year, or an annual increase of 5% derived from regression of the natural logarithms of the incidence data. These observations are consistent with the increasing attack rates for type 1 DM reported worldwide.

Urban-rural variation in childhood type 1 diabetes incidence in Canterbury, New Zealand, 1980-2004.

Geographical variation in the incidence of childhood type 1 diabetes is well documented. Such patterns are thought to give clues to the potential causes of this complex disease. This study examined the urban-rural differences in childhood type 1 diabetes in the Canterbury region of New Zealand between 1980 and 2004. We found significantly higher incidence of childhood type 1 diabetes in satellite urban communities, which could not be explained by the ethnic composition, neighbourhood deprivation, population density or household overcrowding in these areas. Varying levels of immigration and or/commuting in different urban-rural settings could explain this finding. This study highlights the value of geographical investigations for aetiological hypothesis generation.

Variability in measurements of blood glucose response to foods in human subjects is not reduced after a standard breakfast.

Measurements of blood glucose response to food are highly variable. We determined whether within-individual variability in data for blood glucose responses were reduced if individuals consumed a standard meal 2 hours before testing and investigated the effect of serving size. Blood glucose responses to muesli and macaroni cheese were determined in 13 individuals by taking 2 fasting capillary blood samples. Food was then consumed, and capillary blood samples were taken every 15 minutes for the first hour and every 30 minutes for the second hour. The incremental area under the blood glucose response curve was determined, and glycemic glucose equivalents (GGEs) were calculated. The GGE values were not significantly different whether the muesli and macaroni cheese were fed fasting or after a standard breakfast (29.2 vs 34.5 g for muesli and 11.0 vs 14.6 g for macaroni cheese). Within-individual coefficients of variation were not significantly different whether the food was consumed fasting or after a standard breakfast (24.9% and 32.5% for muesli and 38.1% and 59.4% for macaroni cheese). Differences in GGE between measured and estimated half serving size for macaroni cheese were 0.8 g (P = .6) and for muesli, 3 g (P = .2); for the double serving size for macaroni cheese, 1.7 g (P = .7); and for muesli, 6.7 g (P = .06). The GGE values for foods and variability in blood glucose response within individuals were not significantly different whether individuals fasted or consumed a standard breakfast before testing. However, blood glucose levels tended to differ significantly after consumption of the double serving size of muesli compared with other serving sizes.

Considerable temporal variability in glucose reference curves in humans for a year period.

Glycemic glucose equivalent (GGE) is a measure of the blood glucose response to a defined portion of food. Their calculation requires the measurement of a standard glucose-response curve, with beverages containing 0, 12.5, 25, 50, and 75 g of glucose measured twice each. This study was designed to determine the stability of an individual's glucose-response curve measured every 3 months for a year and of their GGE estimates for 10 foods for that period. The blood glucose response to beverages containing 0, 12.5, 25, 50, and 75 g glucose and to 10 foods was measured for 16 healthy individuals. Capillary blood samples were collected fasting, then every 15 minutes for 1 hour, and every 30 minutes for at least 2 hours. The slopes and intercepts of the 4 glucose curves and the GGE of the 10 foods calculated using the available curves for each food was compared. The results showed considerable temporal variability in the slope (intraindividual coefficient of variation (CV) = 30%) and intercept (intraindividual CV = 40%) of the glucose curves. However, if GGE values were categorized into 3 groups (low GGE, < or = 10; medium GGE, 10.01-19.99; and high GGE, > or = 20), all but one food was consistently classified in the same category across the 4 glucose curves. In conclusion, it appears that if the exact GGE value is required, glucose curves should be repeated at least once every 3 months, but if foods are classed into general GGE categories, it may be possible to use the same glucose curve for a longer period.