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Articles by A Pouta
Total Records ( 3 ) for A Pouta
  R. M Freathy , A. J Bennett , S. M Ring , B Shields , C. J Groves , N. J Timpson , M. N Weedon , E Zeggini , C. M Lindgren , H Lango , J. R.B Perry , A Pouta , A Ruokonen , E Hypponen , C Power , P Elliott , D. P Strachan , M. R Jarvelin , G. D Smith , M. I McCarthy , T. M Frayling and A. T. Hattersley

Low birth weight is associated with an increased risk of type 2 diabetes. The mechanisms underlying this association are unknown and may represent intrauterine programming or two phenotypes of one genotype. The fetal insulin hypothesis proposes that common genetic variants that reduce insulin secretion or action may predispose to type 2 diabetes and also reduce birth weight, since insulin is a key fetal growth factor. We tested whether common genetic variants that predispose to type 2 diabetes also reduce birth weight.


We genotyped single-nucleotide polymorphisms (SNPs) at five recently identified type 2 diabetes loci (CDKAL1, CDKN2A/B, HHEX-IDE, IGF2BP2, and SLC30A8) in 7,986 mothers and 19,200 offspring from four studies of white Europeans. We tested the association between maternal or fetal genotype at each locus and birth weight of the offspring.


We found that type 2 diabetes risk alleles at the CDKAL1 and HHEX-IDE loci were associated with reduced birth weight when inherited by the fetus (21 g [95% CI 11–31], P = 2 x 10–5, and 14 g [4–23], P = 0.004, lower birth weight per risk allele, respectively). The 4% of offspring carrying four risk alleles at these two loci were 80 g (95% CI 39–120) lighter at birth than the 8% carrying none (Ptrend = 5 x 10–7). There were no associations between birth weight and fetal genotypes at the three other loci or maternal genotypes at any locus.


Our results are in keeping with the fetal insulin hypothesis and provide robust evidence that common disease-associated variants can alter size at birth directly through the fetal genotype.

  D Canoy , A Pouta , A Ruokonen , A. L Hartikainen , P Saikku and M. R. Jarvelin

Context: Impaired fetal growth is associated with increased risk for coronary heart disease and diabetes in adulthood, but the underlying mechanism is unclear.

Objective: The objective of the study was to examine the relation between early growth (weight at birth and first year) and adult total leukocyte count, the primary cell effectors of inflammation.

Design: This was a birth cohort study (Northern Finland Birth Cohort 1966) with participants prospectively and longitudinally followed up from birth to age 31 yr.

Setting: This was a general population-based cohort in Finland.

Participants: A total of 5619 offspring of expectant mothers who attended a clinical examination and blood draw at 31-yr follow-up (4486 with complete data on weight at 1 yr) participated in the study.

Main Exposure Variables: Weight at birth and at 1 year.

Main Outcome Measure: Absolute leukocyte count was measured.

Results: Total leukocyte count was lower at higher birth weight categories with or without adjustments for adult systolic blood pressure, total cholesterol, fasting insulin, body mass index, cigarette smoking, sex, gestational age, and other life course factors. The covariate-adjusted regression coefficient for log-transformed total leukocyte count (x 109 cells/liter) per 1 sd (525 g) increase in birth weight was –0.012 (95% confidence interval –0.021 to –0.004). The association persisted, even when limiting our analyses among healthy and nonsmoking individuals, and the inversely linear relation was steepest among those with lower weight attained at 1 yr (P for interaction = 0.027).

Conclusion: Poorer growth in early life was associated with systemic low-grade inflammation in adulthood. This relation suggests a plausible inflammatory mechanism linking early growth impairment with risk of coronary heart disease and diabetes later in life.

  J Lahti , K Raikkonen , U Sovio , J Miettunen , A. L Hartikainen , A Pouta , A Taanila , M Joukamaa , M. R Jarvelin and J. Veijola


Although schizotypal traits, such as anhedonia and aberrant perceptions, may increase the risk for schizophrenia-spectrum disorders, little is known about early-life characteristics that predict more pronounced schizotypal traits.


To examine whether birth size or several other early-life factors that have been previously linked with schizophrenia predict schizotypal traits in adulthood.


Participants of the Northern Finland 1966 Birth Cohort Study (n = 4976) completed a questionnaire on positive and negative schizotypal traits at the age of 31 years.


Lower placental weight, lower birth weight and smaller head circumference at 12 months predicted elevated positive schizotypal traits in women after adjusting for several confounders (P<0.02). Moreover, higher gestational age, lower childhood family socioeconomic status, undesirability of pregnancy, winter/autumn birth, higher birth order and maternal smoking during pregnancy predicted some augmented schizotypal traits in women, some in men and some in both genders.


The results point to similarities in the aetiology of schitzotypal traits and schizophrenia-spectrum disorders.

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