Changes in Fasting Lipids during Puberty

Eissa, Mona A.; Mihalopoulos, Nicole L.; Holubkov, Richard; Dai, Shifan; Labarthe, Darwin R.

doi:10.1016/j.jpeds.2015.11.018

Cited by 89 publications

(106 citation statements)

References 42 publications

(53 reference statements)

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“…This difference watch first appears at puberty and is likely hormonally mediated. 42 A similar pattern was noted for the plot of HDL-C against BMI ( Figure 4B).…”

Section: Resultssupporting

confidence: 79%

Upper body fat predicts metabolic syndrome similarly in men and women

Grundy

Williams

Vega

2018

Eur J Clin Investigation

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BackgroundThe metabolic syndrome is a constellation of risk factors including dyslipidemia, dysglycemia, hypertension, a pro‐inflammatory state, and a prothrombotic state. All of these factors are accentuated by obesity. However, obesity can be defined by body mass index (BMI), percent body fat, or by body fat distribution. The latter consists of upper body fat (subcutaneous and visceral fat) and lower body fat (gluteofemoral fat). Waist circumference is a common surrogate marker for upper body fat.MethodsData from the National Health and Nutrition Examination Survey (NHANES) for the years 1999‐2006 was examined for associations of metabolic risk factors with percent body fat, waist circumference, and BMI.ResultsAssociations between absolute measures of waist circumference and risk factors were similiar for men and women. The similarities of associations between waist circumference and risk factors suggests that greater visceral fat in men does not accentuate the influence of upper body fat on risk factors.ConclusionsDifferent waist concumference values should not be used to define abdominal obesity in men and women.

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“…This difference watch first appears at puberty and is likely hormonally mediated. 42 A similar pattern was noted for the plot of HDL-C against BMI ( Figure 4B).…”

Section: Resultssupporting

confidence: 79%

Upper body fat predicts metabolic syndrome similarly in men and women

Grundy

Williams

Vega

2018

Eur J Clin Investigation

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“…54,55 In studies tracking serum lipids and lipoproteins from childhood to adulthood, levels of HDL cholesterol dropped in boys, but were not changed in girls after puberty. 56, 57 These results suggest effects of endogenous testosterone during development to regulate HDL cholesterol. Moreover, the decline in testosterone levels with age 58 is associated with age-dependent increases in atherosclerosis in males, 59–61 although other age-related factors could be causal.…”

Section: Atherosclerosismentioning

confidence: 82%

Sex Hormones and Sex Chromosomes Cause Sex Differences in the Development of Cardiovascular Diseases

Arnold

Cassis

Eghbali

et al. 2017

ATVB

254

176

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This review summarizes recent evidence concerning hormonal and sex chromosome effects in obesity, atherosclerosis, aneurysms, ischemia/reperfusion injury, and hypertension. Cardiovascular diseases (CVD) occur and progress differently in the two sexes, because biological factors differing between the sexes have sex-specific protective and harmful effects. By comparing the two sexes directly, and breaking down sex into its component parts, one can discover sex-biasing protective mechanisms that might be targeted in the clinic. Gonadal hormones, especially estrogens and androgens, have long been found to account for some sex differences in CVD, and molecular mechanisms mediating these effects have recently been elucidated. More recently the inherent sexual inequalities in effects of sex chromosome genes have also been implicated as contributors in animal models of CVDs, especially a deleterious effect of the second X chromosome found in females but not in males. Hormonal and sex chromosome mechanisms interact in the sex-specific control of certain diseases, sometimes by opposing the action of the other.

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“…During puberty, circulating levels of many lipids decrease (45, 46). Therefore, the inverse relations of MCPP, MEP, and ΣDBP with total cholesterol and LDL-C in boys could be driven by pubertal status.…”

Section: Discussionmentioning

confidence: 99%

Exposure to phthalates is associated with lipid profile in peripubertal Mexican youth

Perng

Watkins

Cantoral³

et al. 2017

Environmental Research

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Animal models indicate that endocrine disrupting chemicals (EDCs) affect circulating lipid concentrations by interfering with hepatic fatty acid oxidation. Little is known of the relationship between EDC exposure and lipid profile in humans. We measured bisphenol A (BPA) and 9 phthalate metabolites in maternal urine collected at up to three time points during pregnancy as a measure of in utero exposure, and in the child’s urine at 8–14 years as a measure of concurrent, peripubertal exposure among 248 participants of a Mexico City pre-birth cohort. We used linear regression to examine relations of BPA and phthalate exposure with peripubertal serum lipids, while also adjusting for child age, sex, and specific gravity. While in utero EDC exposure was not associated with lipid profile, higher concurrent levels of mono-3-carboxypropyl phthalate (MCPP), monoethyl phthalate (MEP), and dibutyl phthalate metabolites (DBP) corresponded with lower total cholesterol and low-density lipoprotein (LDL-C) in boys; e.g., an interquartile range increment in MCPP corresponded with 7.4% (2.0%, 12.8%) lower total cholesterol and 12.7% (3.8%, 21.6%) lower LDL-C. In girls, higher urinary di-2-ethylhexyl phthalate metabolites (ΣDEHP) correlated with lower LDL-C (−7.9% [−15.4%, −0.4%]). Additional longitudinal research is needed to determine whether these associations persist beyond adolescence.

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Changes in Fasting Lipids during Puberty

Cited by 89 publications

References 42 publications

Upper body fat predicts metabolic syndrome similarly in men and women

Upper body fat predicts metabolic syndrome similarly in men and women

Sex Hormones and Sex Chromosomes Cause Sex Differences in the Development of Cardiovascular Diseases

Exposure to phthalates is associated with lipid profile in peripubertal Mexican youth

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