Spontaneous Hypothyroidism in Adult Women Is Predicted by Small Body Size at Birth and during Childhood

Kajantie, Eero; Phillips, David I. W.; Osmond, Clive; Barker, D. J. P.; Forsén, Tom; Eriksson, Johan G.

doi:10.1210/jc.2006-1093

Cited by 44 publications

(32 citation statements)

References 16 publications

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“…For example, it has recently been reported that hypothyroidism in adult women is predicted by size at birth [19]. Many of the women in this study developed autoimmune thyroid disease, which is associated with a number of autoimmune ‘susceptibility’ loci, but not obviously with size at birth.…”

Section: Discussionmentioning

confidence: 72%

TSH Levels in Relation to Gestation, Birth Weight and Sex

et al. 2009

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Aims: Low birth weight is associated with hypothyroidism and an adverse metabolic profile in later life. Our aim was to examine the relationship between neonatal TSH and birth weight, gestational age and sex. Methods: We compared blood spot filter paper TSH levels with birth weight, gestational age and sex in a 10% sample of infants screened for congenital hypothyroidism at a single centre in Northern England. All gestational ages were included with infants suspected of having congenital hypothyroidism excluded. Results: Data on 1,728 male and 1,662 female infants were analysed. The distribution of TSH was significantly different between males and females, with males having a higher median TSH (0.7 vs. 0.6). Correlations were shown between TSH and birth weight (ρ = –0.07, p = 0.0001) and gestational age (ρ = –0.05, p = 0.008), with the birth weight association remaining independent of gestational age. The functional form of the model suggested that higher TSH in the lowest birth weight categories was responsible for the association between TSH and birth weight. Conclusions: Low birth weight is related to neonatal TSH levels. Further research is required to assess whether this association explains the relationship between higher TSH and an adverse metabolic profile in later life.

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Section: Discussionmentioning

confidence: 72%

TSH Levels in Relation to Gestation, Birth Weight and Sex

et al. 2009

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“…Twenty-five years ago, Barker and colleagues (2,3) proposed that poor placental growth was prognostic for adult onset ischemic heart disease. Barker and colleagues also showed that small body size at birth predicts both increases in thyroglobulin and thyroid peroxidase autoantibodies in adult women (34) and spontaneous hypothyroidism among women (25). Ovine studies show that either high or low T 3 concentrations are powerful regulators of myocardial maturation (6) and alter the number of cardiomyocytes in the heart at birth (Chattergoon and Thornburg; unpublished data).…”

Section: Discussionmentioning

confidence: 98%

Unexpected maturation of PI3K and MAPK-ERK signaling in fetal ovine cardiomyocytes

Chattergoon

Louey

Stork

et al. 2014

American Journal of Physiology-Heart and Circulatory Physiology

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In the first two-thirds of gestation, ovine fetal cardiomyocytes undergo mitosis to increase cardiac mass and accommodate fetal growth. Thereafter, some myocytes continue to proliferate while others mature and terminally differentiate into binucleated cells. At term (145 days gestational age; dGA) about 60% of cardiomyocytes become binucleated and exit the cell cycle under hormonal control. Rising thyroid hormone (T3) levels near term (135 dGA) inhibit proliferation and stimulate maturation. However, the degree to which intracellular signaling patterns change with age in response to T3 is unknown. We hypothesized that in vitro activation of ERK, Akt, and p70(S6K) by two regulators of cardiomyocyte cell cycle activity, T3 and insulin like growth factor-1 (IGF-1), would be similar in cardiomyocytes at gestational ages 100 and 135 dGA. IGF-1 and T3 each independently stimulated phosphorylation of ERK, Akt, and p70(S6K) in cells at both ages. In the younger mononucleated myocytes, the phosphorylation of ERK and Akt was reduced in the presence of IGF-1 and T3. However, the same hormone combination led to a dramatic twofold increase in the phosphorylation of these signaling proteins in the 135 dGA cardiomyocytes-even in cells that were not proliferating. In the older cells, both mono- and binucleated cells were affected. In conclusion, fetal ovine cardiomyocytes undergo profound maturation-related changes in signaling in response to T3 and IGF-1, but not to either factor alone. Differences in age-related response are likely to be related to milestones in fetal cardiac development as the myocardium prepares for ex utero life.

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“…In patients with the metabolic syndrome, obesity, and insulin resistance have been found to stimulate thyroid cell proliferation and increase thyroid volume and stimulate the production of THs (Sari et al 2003, Pergola et al 2008, Rezzonico et al 2008, Ayturk et al 2009). In a birth cohort study, Kajantie et al (2006) found that a small body size at birth and during childhood increases the risk of spontaneous hypothyroidism in adult women, whereas Brix et al (2000) found, in a populationbased twin case-control study, that low birth weight is not associated with thyroid autoimmunity or nonautoimmune thyroid disease. Thyroid gland metabolism has been shown to be downregulated in both nutrientrestricted suckling rats , Lisboa et al 2010 and in fetal growth-restricted lambs (Rae et al 2002); in the rat study by Lisboa et al (2010), thyroid gland metabolism remained downregulated into adulthood.…”

Section: Introductionmentioning

confidence: 99%

Prenatal undernutrition and postnatal overnutrition alter thyroid hormone axis function in sheep

Johnsen

Kongsted

Nielsen

2013

Journal of Endocrinology

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Mounting evidence led us to hypothesize that i) function of the thyroid hormone (TH) axis can be programed by late gestation undernutrition (LG-UN) and ii) early-postnatal-life overnutrition (EL-ON) exacerbates the fetal impacts on TH axis function. In a 2!2 factorial experiment, 21 twin-bearing sheep were fed one of two diets during late gestation: NORM (fulfilling energy and protein requirements) or LOW (50% of NORM). From day 3 to 6 months after birth (around puberty), the twin lambs were assigned to each their diet: conventional (CONV) or high-carbohydrate, high-fat, where after half the lambs were killed. Remaining sheep (exclusively females) were fed the same moderate diet until 2 years of age (young adults). At 6 months and 2 years of age, fasting challenges were conducted and target tissues were collected at autopsy. LG-UN caused adult hyperthyroidism associated with increased thyroid expression of genes regulating TH synthesis and deiodination. In one or more of the target tissues, liver, cardiac muscle, and longissimus dorsi muscle, gene expressions were increased by LG-UN for TH receptors (THRA and THRB) and deiodinases but were decreased in visceral and subcutaneous adipose tissues. EL-ON increased TH levels in adolescent lambs, but this was reversed after diet correction and not evident in adulthood. We conclude that LG-UN programed TH axis function at the secretory level and differentially in target tissues, which was increasingly manifested with age. Differential TH signaling in adipose vs other tissues may be part of a mechanism whereby fetal malnutrition can predispose for obesity and other metabolic disorders.

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Spontaneous Hypothyroidism in Adult Women Is Predicted by Small Body Size at Birth and during Childhood

Abstract: Small body size at birth and during childhood increases the risk of spontaneous hypothyroidism in adult women.

Cited by 44 publications

References 16 publications

TSH Levels in Relation to Gestation, Birth Weight and Sex

TSH Levels in Relation to Gestation, Birth Weight and Sex

Unexpected maturation of PI3K and MAPK-ERK signaling in fetal ovine cardiomyocytes

Prenatal undernutrition and postnatal overnutrition alter thyroid hormone axis function in sheep

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