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Johan G Eriksson

Publications and source records attributed to Johan G Eriksson.

30 records · Page 2Linked to original sources

Interactions between peroxisome proliferator-activated receptor-gamma 2 gene polymorphisms and size at birth on blood pressure and the use of antihypertensive medication.

OBJECTIVE: The combination of small birth size and the Pro12Pro variant of the peroxisome proliferator-activated receptor-gamma 2 (PPAR-gamma 2) gene has been shown to be associated with insulin resistance, which is linked to hypertension. We examined whether the association between small body size at birth and adult blood pressure is modulated by PPAR-gamma 2 gene polymorphism, and whether the use of any class of antihypertensive medication is related to birth size. DESIGN AND METHODS: A total of 500 subjects from an original epidemiological cohort of 7086 men and women aged 65-75 years attended a clinical study. Two hundred and eight of them (73 men and 135 women) were taking antihypertensive medication and are included in this study. The Pro12Ala polymorphism of the PPAR-gamma 2 gene was determined using the polymerase chain reaction single-strand conformation polymorphism method. RESULTS AND CONCLUSIONS: Hypertensive subjects with low birth weight or short length at birth and the Pro12Pro variant had raised systolic blood pressure. We suggest that insulin resistance enhances the regulatory responses of the renin-angiotensin system, leading to raised blood pressure levels. Those hypertensive subjects who had small birth size and the Pro12Pro variant tended to use angiotensin-converting enzyme inhibitors or angiotensin-receptor blockers (ACEI/ARB). This could be because insulin resistance interacts with the renin-angiotensin system in ways that make ACEI/ARB an effective therapy. Alternative explanations include more severe and treatment resistant hypertension, leading to application of ACEI/ARB, or co-morbid conditions, such as myocardial infarction and type 2 diabetes, known to be linked to low birth weight.

Aged↗

The association of the K121Q polymorphism of the plasma cell glycoprotein-1 gene with type 2 diabetes and hypertension depends on size at birth.

Birth weight and length serve as indicators of the intrauterine environment, and a small body size at birth is a predictor of type 2 diabetes and hypertension. Insulin is one of the growth factors regulating fetal growth. The plasma cell glycoprotein 1 (PC-1) gene impairs insulin signaling at the insulin receptor level. Therefore, we investigated whether the K121Q polymorphism of the PC-1 gene association with insulin sensitivity, insulin levels, and the prevalence of diabetes and hypertension in adult life depends on size at birth in 489 subjects born in Helsinki during 1924-1933. We found that the effect of the PC-1 gene polymorphism on insulin levels and insulin sensitivity, measured as the homeostasis model assessment for insulin resistance, depended on birth length because fasting insulin levels and insulin resistance were highest in subjects carrying the 121Q allele who were small at birth (P for interaction = 0.04 and 0.05). Additionally, in those whose birth length was up to 49 cm, the K121Q polymorphism of the PC-1 gene was associated with a 2-fold higher incidence of type 2 diabetes. Moreover, subjects who were short at birth and who had the 121Q allele had the highest incidence (31.6%) of type 2 diabetes together with hypertension. We conclude that the interaction between the K121Q polymorphism of the PC-1 gene and birth length affects insulin sensitivity and increases susceptibility to type 2 diabetes and hypertension in adulthood.

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Prevalence of the metabolic syndrome and its components: findings from a Finnish general population sample and the Diabetes Prevention Study cohort.

OBJECTIVE: To assess the prevalence of the metabolic syndrome (MetS) in two independent Finnish study cohorts. RESEARCH DESIGN AND METHODS: The prevalence of the MetS by modified World Health Organization criteria was analyzed in different categories of glucose tolerance in a cross-sectional, population-based sample of 2,049 individuals (FINRISK) aged 45-64 years and in 522 participants of the Finnish Diabetes Prevention Study (DPS) with impaired glucose tolerance (IGT). RESULTS: In the FINRISK cohort, the MetS was present in 38.8% of the men and 22.2% of the women. The prevalence was 14.4 and 10.1% in subjects with normal glucose tolerance, 74.0 and 52.2% in subjects with impaired fasting glucose, 84.8 and 65.4% in subjects with IGT, and 91.5 and 82.7% in subjects with type 2 diabetes in men and women, respectively. Among women, the prevalence of the MetS increased with increasing age. In the DPS cohort, the MetS was present in 78.4% of the men and 72.2% of the women with IGT. CONCLUSIONS: The MetS was extremely common in middle-aged subjects The high prevalence in men was mostly due to their high waist-to-hip ratio. The prevalence of the MetS increased in both sexes with deterioration in glucose regulation. Approximately 75% of the subjects with IGT had the MetS. Because the syndrome includes the major risk factors for atherosclerotic vascular diseases and is the major antecedent for type 2 diabetes, concerted preventive action should be targeted to control all the features of the MetS.

Body Mass Index↗

Quality of life and metabolic status in mildly depressed women with type 2 diabetes treated with paroxetine: a single-blind randomised placebo controlled trial.

BACKGROUND: Depression is prevalent in people with type 2 diabetes and affects both glycemic control and overall quality of life. The aim of this trial was to evaluate the effect of the antidepressant paroxetine on metabolic control, quality of life and mental well-being in mildly depressed women with type 2 diabetes. METHODS: We randomised 15 mildly depressed women with non-optimally controlled type 2 diabetes to a 10-week single-blind treatment with either paroxetine 20 mg per day or placebo. Primary efficacy measurements were glycemic control and quality of life. Glycosylated hemoglobin A1c (GHbA1c) was used as a measure of glycemic control. Quality of life was evaluated using RAND-36. Mental state was assessed using two clinician-rated scoring instruments, Hamilton's Anxiety Scale (HAM-A) and Montgomery-Asberg's Depression Rating Scale (MADRS), and a patient-rated scoring instrument, Beck's Depression Inventory (BDI). RESULTS: At the end of the study no significant difference between groups in improvement of quality of life was found. A trend towards a superior improvement in glycemic control was found in the paroxetine group (p = 0.08). A superior increase in sex-hormone-binding-globuline (SHBG) levels was evidenced in the paroxetine group (p = 0.01) as a sign of improved insulin sensitivity. There was also a trend for superior efficacy of paroxetine in investigator-rated anxiety and depression. This notion was supported by a trend for superior decrease of serum cortisol levels in the paroxetine group (p = 0.06). CONCLUSION: Paroxetine has a beneficial effect on measures of insulin sensitivity and may improve glycemic control. Larger studies of longer duration are needed to verify the benefits of paroxetine in type 2 diabetes. While waiting for more conclusive evidence it seems sensible to augment standard care of type 2 diabetes with paroxetine even in patients who do not fulfil routine psychiatric criteria for initiation of antidepressant drug treatment.

Adult↗

Self-perpetuating effects of birth size on blood pressure levels in elderly people.

It has been suggested that essential hypertension is determined by 2 separate mechanisms: a growth-promoting process in childhood and a self-perpetuating mechanism in adult life. We report a clinical study of 500 people taken from a cohort of 7086 men and women who were born in Helsinki from 1924 to 1933, and whose body size at birth was recorded. As expected, blood pressure levels were inversely related to birthweight and birth length. These associations, however, were confined to the 213 people who had previously been diagnosed as having hypertension. In them, a 1-kg increase in birthweight was associated with a 6.4-mm Hg (95% confidence interval, 1.0 to 11.9) decrease in systolic blood pressure recorded at the clinic, and with a 9.3-mm Hg (95% confidence interval, 2.1 to 16.5) decrease recorded by ambulatory measurement. We conclude that pathological processes initiated in utero become self-perpetuating in adult life and lead to hypertension. Among elderly people with established hypertension, these processes have a strong effect on blood pressure levels, because they are processes that do not respond well to treatment.

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Prevention of diabetes mellitus in subjects with impaired glucose tolerance in the Finnish Diabetes Prevention Study: results from a randomized clinical trial.

Type 2 diabetes mellitus is increasing worldwide largely as a result from increasing obesity and sedentary lifestyle. The Finnish Diabetes Prevention Study (DPS) is the first individually randomized controlled clinical trial to test the feasibility and efficacy of lifestyle modification in high-risk subjects. We randomly assigned 522 (172 men, 350 women) middle-aged (mean age 55 yr), overweight (mean body mass index 31 kg/m(2)) subjects with impaired glucose tolerance either to the lifestyle intervention or control group. Each subject in the intervention group received individualized counseling aimed at reducing weight and intake of total and saturated fat, and increasing intake of fiber and physical activity. An oral glucose tolerance test was performed annually to detect incident cases of diabetes and to measure changes in metabolic parameters. The mean (+/- SD) weight reduction from baseline to year 1 and to year 2, respectively, was 4.2 +/- 5.1 kg and 3.5 +/- 5.5 in the intervention group and 0.8 +/- 3.7 kg and 0.8 +/- 4.4 in the control group (P < 0.001 between the groups). At the time of first analysis of the outcome data the mean duration of follow-up was 3.2 yr. The risk of diabetes was reduced by 58% (P < 0.001) in the intervention group compared with the control group. The reduction in the incidence of diabetes was directly associated with number and magnitude of lifestyle changes made. In conclusion, the DPS is the first controlled trial demonstrating that type 2 diabetes can be prevented by changes in lifestyle in high-risk subjects.

Adult↗

Pathways of infant and childhood growth that lead to type 2 diabetes.

OBJECTIVE: Although a link between small body size at birth and later type 2 diabetes has been repeatedly documented, less is known about the associations between the disease and growth during infancy. The aim of this study was to explore the pathways of infant and early growth that lead to type 2 diabetes in adult life. RESEARCH DESIGN AND METHODS: We carried out a longitudinal study of 8760 subjects born in Helsinki from 1934 to 1944. On average, they had 8 measurements of height and weight between birth and 1 year of age and another 10 measurements between 1 and 12 years of age. We identified people with type 2 diabetes using a national register. RESULTS: Among babies whose birth weights were 3.5 kg, slow growth in length between birth and 3 months of age predicted later disease. Rapid gain in BMI after age 2 years increased the risk of later disease in both groups of babies, but this effect was greatest among children who had slow growth in length between birth and 3 months of age. In children whose Z-scores for length decreased, an SD increase in BMI at age 12 years was associated with an odds ratio (OR) for type 2 diabetes of 1.77 (95% CI 1.50-2.09). The corresponding OR in subjects whose Z-scores for length increased was 1.42 (95% CI 1.20-1.69). Rapid gain in childhood BMI was associated with high maternal BMI and socioeconomic factors (fewer people in the home and lower social class). CONCLUSIONS: Babies with above-average birth weights may develop type 2 diabetes later in life if poor living conditions lead to faltering growth in length in the first few months after birth. We speculate that growth faltering at this time is associated with lifelong impairment of insulin metabolism and inability to meet the challenge of rapid childhood increase in BMI.

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Growth and living conditions in childhood and hypertension in adult life: a longitudinal study.

OBJECTIVES: To examine the interplay between childhood growth and living conditions in the development of hypertension. DESIGN: A longitudinal study of people whose growth between birth and 12 years, and social circumstances during childhood and adult life, were recorded. SETTING: Helsinki, Finland. PARTICIPANTS: Eight thousand seven hundred and sixty men and women born in Helsinki University Central Hospital during 1934-44, who attended child welfare clinics in the city and were still resident in Finland in 1971. MAIN OUTCOME MEASURES: Incidence of hypertension defined by prescription of medication. RESULTS: The 1404 children who later developed hypertension grew differently to other children. Low birthweight and shortness or thinness at birth were followed by rapid compensatory growth in weight and height, and an above-average body mass index (BMI, kg/m(2)) from the age of 8 years onwards. Some 25% of children with low birthweight but high BMI at 12 years subsequently developed hypertension, compared to 9% of those with high birthweight but low BMI. Growth had large effects on the risk of later hypertension in children living in poor social conditions, but only small effects in children in good living conditions. Living conditions in adult life did not affect the risk of hypertension. CONCLUSIONS: Hypertension originates in slow fetal growth followed by rapid compensatory growth in childhood. This path of growth has a greater effect on the risk of disease among children who live in poor social conditions. Living conditions in adult life do not seem to be important.

Birth Weight↗

The effects of the Pro12Ala polymorphism of the peroxisome proliferator-activated receptor-gamma2 gene on insulin sensitivity and insulin metabolism interact with size at birth.

Type 2 diabetes is known to be associated with a small body size at birth. Body size at birth is an indicator of the intrauterine environment. There is also a well-established association between the peroxisome proliferator-activated receptor (PPAR)-gamma2 gene and type 2 diabetes. We therefore assessed whether the effects of the Pro12Ala polymorphism of the PPAR-gamma2 gene on insulin sensitivity and insulin concentrations in adult life are modified by size at birth. We found that the effects of the Pro12Pro and Pro12Ala polymorphisms of the PPAR-gamma2 gene in elderly people depended on their body size at birth. The well-known association between small body size at birth and insulin resistance was seen only in individuals with the high-risk Pro12Pro allele. In those who had low birth weight, the Pro12Pro polymorphism of the PPAR-gamma2 gene was associated with increased insulin resistance (P < 0.002) and elevated insulin concentrations (P < 0.003). These interactions between the effects of the Pro12Ala polymorphisms of the PPAR-gamma2 gene on adult traits and the effects of birth weight link two previously unknown associations together within the context of type 2 diabetes. We suggest that these findings reflect gene-environment interaction.

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Association of the Pro12Ala polymorphism in the PPAR-gamma2 gene with 3-year incidence of type 2 diabetes and body weight change in the Finnish Diabetes Prevention Study.

The association of the Pro12Ala polymorphism of the PPAR-gamma2 gene with the incidence of type 2 diabetes was investigated in 522 subjects with impaired glucose tolerance (IGT) participating in the Finnish Diabetes Prevention Study. Subjects were randomized to either an intensive diet and exercise group or a control group. By 3 years of intervention, the odds ratio of the development of type 2 diabetes for subjects with the Ala12 allele was 2.11-fold compared with that for subjects with the Pro12Pro genotype (95% CI 1.20-3.72). The risk for type 2 diabetes increased also in subjects who gained weight or belonged to the control group. In the intervention group, subjects with the Ala12Ala genotype lost more weight during the follow-up than subjects with other genotypes (Pro12Pro vs. Ala12Ala P = 0.043), and none of subjects with the Ala12Ala genotype developed type 2 diabetes in this group. In conclusion, the Ala12 allele may predispose to the development of type 2 diabetes in obese subjects with IGT. However, beneficial changes in diet, increases in physical activity, and weight loss may reverse, to some extent, the diabetogenic impact of the Ala12 allele, possibly due to an improved insulin sensitivity.

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Childhood growth and coronary heart disease in later life.

Coronary heart disease (CHD) originates early in life and numerous studies have shown inverse associations between body size at birth and CHD in adult life. Recently it has been shown that the increased risk for CHD associated with a small body size at birth is modified by growth during childhood. The greatest risk for CHD is noted in individuals with small body size at birth and who 'catch-up' in weight and body size during childhood. An increase in body weight and body mass index during the first year of life is however associated with a reduced risk of CHD. These recent findings add to the evidence that optimizing early growth is an important area in primary prevention of CHD. There are several potential mechanisms explaining the association between a non-optimal early growth and CHD. Behavioral, physiological, hormonal and genetic factors influence growth. Although socio-economic factors influence the risk of CHD, the association between slow fetal growth and CHD is not caused by confounding socio-economic factors. Biological programming - the process whereby a stimulus during critical periods of development has long lasting or lifelong effects on metabolism - is proposed to mediate the effects between early growth and adult diseases.

Adult↗