Type 1 diabetes
The acute onset of type 1 diabetes and the fact that almost all cases rapidly reach medical attention means that registers of new cases can be relatively easily established. Provided ascertainment can be verified, these data can be combined with population denominator data to give age-specific and sex-specific rates.
1. Geographical variation
There is a marked geographical variation in the incidence of type 1 diabetes.In Finland, the age-standardized incidence in children aged 14 years and under is 36.8/100,000/year. A high rate is also observed in Sardinia (36.5/100,000/year) that is notably discordant with the incidence in Italy as a whole. These two countries have incidences 350-fold greater than those in Zunyi, China and Caracas, Venezuela, where the incidence is 0.1/100,000/year. In general, countries in Europe and North America have either high or intermediate incidences. The incidence in Africa is generally intermediate, and that in
Asia is low. Variation in incidence by age and sex – in the UK, wellestablished registers with high ascertainment (98.6%) (e.g. in Scotland) show an incidence of 15.3/100,000/year in children aged 0–4 years, rising to 24.4/100,000/year at 5–9 years and 31.9/100,000/year at 10–14 years. Overall, the incidence is slightly higher in boys than in girls (ratio 1.08:1). The peak incidence in boys is at 12–13 years,whereas in girls the peak occurs at 9–12 years.
2. Temporal variation
In the Scottish register, a steady increase in the incidence of type 1 diabetes of about 2% per annum was described during the period 1984–1993. This increase is seen in other studies worldwide in both low incidence and high-incidence areas. The overall pooled increase in 37 countries was 3.0% per year; the increase was relatively greater in populations with the lowest incidence. The incidence of type 1 diabetes also varies with season, being highest in autumn and winter.
3. Aetiological factors
genetic susceptibility is necessary but not sufficient as a cause of type 1 diabetes. The nature of the environmental factors that impact on this genetic predisposition are unclear. Studies have concentrated on the ecological correlation between incidence and geographical variation in environmental factors. These have includedsocial factors such as population density, household overcrowding and population mixing. These studies are ecological because the data on the risk of outcome (diabetes) is not collected from the same individuals as that on exposure (social factors). Inferences about causality from such data are weaker than evidence from studies based on the association between individual exposure and risk. However, prospective cohort studies are difficult to conduct in type 1 diabetes because of the relatively low incidence – many individuals would have to be recruited and assessed and only a few would progress to disease.The case-control approach is efficient, but is subject to recall bias because exposure is assessed by proxy from parents after the diagnosis has been made. Case-control studies havedemonstrated associations with early social mixing, viral infections, toxins and dietary factors such as exclusive breastfeeding and delayed introduction of cows’ milk.
Type 2 diabetes
1. geographical variation
The slow onset of type 2 diabetes, and its presentation without the acute metabolic disturbance seen in type 1 diabetes, means that the true time of onset is difficult to determine. Thus, the distinction between abnormality and normality is more blurred, there is a long pre-detection period, and as many as one-half of cases in the population at any one time are undiagnosed. Data on the prevalence of clinically detected type 2 diabetes provide information that is useful for health service planning, but cannot provide any insight into the true prevalence unless the prevalence of undetected diabetes is also known. Because the ratio of detected to undetected cases may vary over time and between places, epidemiological research aimed at defining the true prevalence of type 2 diabetes has had to rely on special studies in which the presence and absence of disease is defined by the oral glucose tolerance test (OGTT). However, the distinction between normality and abnormality is unclear, and debate continues about how it should be defined. The WHO currently recommends use of the 75-g OGTT, with diabetes defined by fasting glucose 7.0 mmol/litre or more and/or 2-hour post-challenge glucose 11.1 mmol/litre or more. Geographical variation – Figure 2 shows the agestandardized and sex-standardized prevalence of type 2 diabetes and impaired glucose tolerance as defined by the 75-g OGTT in various countries. As in type 1 diabetes, there is marked geographical variation, but the pattern is different. The prevalence is lowest in rural areas of developing countries, is generally intermediate in developed countries, and is highest in certain ethnic groups who have adopted Western lifestyle patterns. The populations with the highest prevalences (Pima Indians in Arizona and Nauruans in Micronesia) have a high prevalence of obesity. It is hypothesized that genetic susceptibility to obesity in these populations would be disadvantageous in times of food abundance, but would be advantageous when food is scarce, giving rise to maintenance of the gene by natural selection. This ‘thrifty genotype’ hypothesis is supported by evidence of gene–environment interaction – individuals who migrate from low prevalence areas (e.g. Japan) to the West are at increased risk of type 2 diabetes.
In the UK, the prevalence of known diabetes is about 2% and the age-standardized prevalence of undiagnosed diabetes is 2% in the over-40s. The true incidence of the disease is difficult to determine because this requires repeated glucose tolerance testing. However, such studies have been undertaken and the incidence found to be about 6/1000 personyears of follow-up. The incidence in individuals known to have impaired glucose tolerance is about eight times greater than in those with normal glucose tolerance; the absolute cumulative incidence is 10% over 5 years in Caucasians, but may be higher in high-risk populations. The risk of future progression to diabetes is also greater in those with other hyperglycaemic states, including gestational diabetes mellitus.
2. Temporal variation
data from studies such as the National Health and Nutrition Examination Survey (NHANES III) demonstrate that the prevalence of type 2 diabetes in the USA increased by 33%, from 4.9% in 1990 to 6.5% in 1998. This increase mirrors the increasing prevalence of obesity. Repeated surveys in developing countries show even more marked increases, particularly in areas where populations are rapidly adopting Western lifestyles . The increase in the prevalence of obesity in childhood has led to the appearance of type 2 diabetes in children and young adults, particularly those in highly susceptible ethnic groups.
3. Aetiological factors
Prospective population-based cohort studies suggest that the main pathophysiological defects leading to type 2 diabetes are insulin resistance and a relative insulin secretory defect. The main aetiological risk factors for type 2 diabetes are age, obesity, family history, physical inactivity and dietary factors such as a high proportion of energy consumed as saturated fat and low intake of fruit and vegetables. The observation of an association between low birth weight and risk of diabetes in later life has led to the development of an alternative to the thrifty genotype hypothesis. In this ‘thrifty phenotype’ hypothesis, the risk of diabetes and other adult disorders is programmed by fetal nutrition and the pattern of early growth. The causal nature of these associations is strengthened by data from studies in which the incidence of diabetes is reduced by interventions aimed at reducing weight, increasing activity and improving diet.
The acute onset of type 1 diabetes and the fact that almost all cases rapidly reach medical attention means that registers of new cases can be relatively easily established. Provided ascertainment can be verified, these data can be combined with population denominator data to give age-specific and sex-specific rates.
1. Geographical variation
There is a marked geographical variation in the incidence of type 1 diabetes.In Finland, the age-standardized incidence in children aged 14 years and under is 36.8/100,000/year. A high rate is also observed in Sardinia (36.5/100,000/year) that is notably discordant with the incidence in Italy as a whole. These two countries have incidences 350-fold greater than those in Zunyi, China and Caracas, Venezuela, where the incidence is 0.1/100,000/year. In general, countries in Europe and North America have either high or intermediate incidences. The incidence in Africa is generally intermediate, and that in
Asia is low. Variation in incidence by age and sex – in the UK, wellestablished registers with high ascertainment (98.6%) (e.g. in Scotland) show an incidence of 15.3/100,000/year in children aged 0–4 years, rising to 24.4/100,000/year at 5–9 years and 31.9/100,000/year at 10–14 years. Overall, the incidence is slightly higher in boys than in girls (ratio 1.08:1). The peak incidence in boys is at 12–13 years,whereas in girls the peak occurs at 9–12 years.
2. Temporal variation
In the Scottish register, a steady increase in the incidence of type 1 diabetes of about 2% per annum was described during the period 1984–1993. This increase is seen in other studies worldwide in both low incidence and high-incidence areas. The overall pooled increase in 37 countries was 3.0% per year; the increase was relatively greater in populations with the lowest incidence. The incidence of type 1 diabetes also varies with season, being highest in autumn and winter.
3. Aetiological factors
genetic susceptibility is necessary but not sufficient as a cause of type 1 diabetes. The nature of the environmental factors that impact on this genetic predisposition are unclear. Studies have concentrated on the ecological correlation between incidence and geographical variation in environmental factors. These have includedsocial factors such as population density, household overcrowding and population mixing. These studies are ecological because the data on the risk of outcome (diabetes) is not collected from the same individuals as that on exposure (social factors). Inferences about causality from such data are weaker than evidence from studies based on the association between individual exposure and risk. However, prospective cohort studies are difficult to conduct in type 1 diabetes because of the relatively low incidence – many individuals would have to be recruited and assessed and only a few would progress to disease.The case-control approach is efficient, but is subject to recall bias because exposure is assessed by proxy from parents after the diagnosis has been made. Case-control studies havedemonstrated associations with early social mixing, viral infections, toxins and dietary factors such as exclusive breastfeeding and delayed introduction of cows’ milk.
Type 2 diabetes
1. geographical variation
The slow onset of type 2 diabetes, and its presentation without the acute metabolic disturbance seen in type 1 diabetes, means that the true time of onset is difficult to determine. Thus, the distinction between abnormality and normality is more blurred, there is a long pre-detection period, and as many as one-half of cases in the population at any one time are undiagnosed. Data on the prevalence of clinically detected type 2 diabetes provide information that is useful for health service planning, but cannot provide any insight into the true prevalence unless the prevalence of undetected diabetes is also known. Because the ratio of detected to undetected cases may vary over time and between places, epidemiological research aimed at defining the true prevalence of type 2 diabetes has had to rely on special studies in which the presence and absence of disease is defined by the oral glucose tolerance test (OGTT). However, the distinction between normality and abnormality is unclear, and debate continues about how it should be defined. The WHO currently recommends use of the 75-g OGTT, with diabetes defined by fasting glucose 7.0 mmol/litre or more and/or 2-hour post-challenge glucose 11.1 mmol/litre or more. Geographical variation – Figure 2 shows the agestandardized and sex-standardized prevalence of type 2 diabetes and impaired glucose tolerance as defined by the 75-g OGTT in various countries. As in type 1 diabetes, there is marked geographical variation, but the pattern is different. The prevalence is lowest in rural areas of developing countries, is generally intermediate in developed countries, and is highest in certain ethnic groups who have adopted Western lifestyle patterns. The populations with the highest prevalences (Pima Indians in Arizona and Nauruans in Micronesia) have a high prevalence of obesity. It is hypothesized that genetic susceptibility to obesity in these populations would be disadvantageous in times of food abundance, but would be advantageous when food is scarce, giving rise to maintenance of the gene by natural selection. This ‘thrifty genotype’ hypothesis is supported by evidence of gene–environment interaction – individuals who migrate from low prevalence areas (e.g. Japan) to the West are at increased risk of type 2 diabetes.
In the UK, the prevalence of known diabetes is about 2% and the age-standardized prevalence of undiagnosed diabetes is 2% in the over-40s. The true incidence of the disease is difficult to determine because this requires repeated glucose tolerance testing. However, such studies have been undertaken and the incidence found to be about 6/1000 personyears of follow-up. The incidence in individuals known to have impaired glucose tolerance is about eight times greater than in those with normal glucose tolerance; the absolute cumulative incidence is 10% over 5 years in Caucasians, but may be higher in high-risk populations. The risk of future progression to diabetes is also greater in those with other hyperglycaemic states, including gestational diabetes mellitus.
2. Temporal variation
data from studies such as the National Health and Nutrition Examination Survey (NHANES III) demonstrate that the prevalence of type 2 diabetes in the USA increased by 33%, from 4.9% in 1990 to 6.5% in 1998. This increase mirrors the increasing prevalence of obesity. Repeated surveys in developing countries show even more marked increases, particularly in areas where populations are rapidly adopting Western lifestyles . The increase in the prevalence of obesity in childhood has led to the appearance of type 2 diabetes in children and young adults, particularly those in highly susceptible ethnic groups.
3. Aetiological factors
Prospective population-based cohort studies suggest that the main pathophysiological defects leading to type 2 diabetes are insulin resistance and a relative insulin secretory defect. The main aetiological risk factors for type 2 diabetes are age, obesity, family history, physical inactivity and dietary factors such as a high proportion of energy consumed as saturated fat and low intake of fruit and vegetables. The observation of an association between low birth weight and risk of diabetes in later life has led to the development of an alternative to the thrifty genotype hypothesis. In this ‘thrifty phenotype’ hypothesis, the risk of diabetes and other adult disorders is programmed by fetal nutrition and the pattern of early growth. The causal nature of these associations is strengthened by data from studies in which the incidence of diabetes is reduced by interventions aimed at reducing weight, increasing activity and improving diet.
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