News from the latest research


Infants delivered by Caesarean section (CS) may be at risk for obesity as adults, a study recently published in PLOS One suggests.

Researchers, led by Karthik Darmasseelane, of Imperial College of London, note that in the last 20 years, there have been worldwide increases in obesity prevalence in children and adults, while at the same time, there has been a significant upward trend in CS births.

The scientists carried out a systematic review of 15 studies with a combined population of 142,702 subjects, “from ten countries, spanning four continents,” using a predefined search strategy, Pubmed, Google Scholar, and Web of Science. the studies reported adult anthropometry (BMI, height, weight, incidence of overweight/ obesity) by mode of delivery. The review was conducted using an a prioriprotocol (registered on PROSPERO) following PRISMA guidelines for reporting systematic reviews and meta-analyses. “Results [were] illustrated using forest plots and funnel plots, and presented as mean differences or odds ratios (OR) and 95% confidence intervals,” the study says.

They then compared all CS to vaginal delivery (VD) in “pooled-gender unadjusted analyses” and found that “mean BMI difference was 0.44 kg•m-2 (0.17, 0.72; p = 0.002), OR for incidence of overweight was 1.26 (1.16, 1.38; p<0.00001) and OR for incidence of obesity was 1.22 (1.05, 1.42; p = 0.01).” “We found an average increase in BMI of almost 0.5 kg•m−2 in subjects delivered by CS compared to VD,” the authors wrote, “and an increased odds of overweight and obesity >20%; these findings are consistent across sexes.” The researchers concluded that there is a strong association between CS and increased offspring BMI, being overweight and obese as adults. However, they pointed out that these findings were based on observational studies and “there is a need to determine whether this is causal, or reflective of confounding influences.”


Vitamin D deficiency may be linked to compromised immune function in older individuals, according to a paper recently published in the Journal of Clinical Endocrinology & Metabolism.

Sean Strain, director of the Northern Ireland Centre for Food and Health at the University of Ulster, and the team investigated 957 Irish adults from the TUDA (Trinity Ulster Department of Agriculture) aging cohort study, aged 60 and older. the researchers measured serum 25-hydroxyvitamin D (25(OH)D), as well as the following biomarkers of inflammation; serum cytokines IL-6, TNF-a, IL-10, and C-reactive protein (CRP).

They found that participants who were vitamin D deficient were more likely to have high levels of these biomarkers, writing, “Concentrations of IL-6, CRP, and the ratios of IL-6 to IL-10 and CRP to IL-10 were significantly higher in individuals with deficient (<25 nmol/L) serum 25(OH)D compared with those with sufficient (>75 nmol/L) status after adjustment for age, sex, and body mass index (P <.05). Vitamin D status was a significant predictor of the IL-6 to IL-10 cytokine ratio, and those participants defined as deficient were significantly more likely to have an IL-6 to IL-10 ratio >2:1 compared with those defined as sufficient.”

the authors noted that the inflammatory markers in question have been linked to cardiovascular disease, multiple sclerosis, Crohn’s disease, and rheumatoid arthritis, and wrote that the findings of this study could lead to potential health benefits for those conditions.

“The results indicate immune function may be compromised in older individuals with vitamin D deficiency,” according to lead author Eamon Laird, PhD, of Trinity College in Dublin. “Ensuring older individuals have optimal vitamin D levels may benefit immune function in this population, but this needs to be confi rmed in randomized controlled trials.”


Overweight eight- to 10-year-old children who had increased exposure to perfluorinated and polyfluorinated compounds (PFCs) — chemicals commonly found in stain and water repellants in carpet and furniture — show early signs of developing metabolic syndromes such as heart disease and diabetes, according to research recently published in the Journal of Clinical Endocrinology & Metabolism.

Clara Amalie G. Timmerman, MSC, of the University of Southern Denmark, and her team assessed PFC exposure and body mass index (BMI), skinfold thickness, waist circumference, leptin, adiponectin, insulin, glucose, and triglyceride concentrations in 499 eight- to 10-year-old children in 1997, using a subset of the European Youth Heart Study.

The researchers found no association between PFC exposures and adiposity or markers of glycemic control in normal-weight children. Among overweight children, however, they found “an increase of 10 ng perfluorooctane sulfonic acid/mL plasma was associated with 16.2% (95% confidence interval [CI], 5.2%–28.3%) higher insulin concentration, 12.0% (95% CI, 2.4%–22.4%) higher β-cell activity, 17.6% (95% CI, 5.8%–30.8%) higher insulin resistance, and 8.6% (95% CI, 1.2%–16.5%) higher triglyceride concentrations, and an increase of 10 ng perfluorooctanoic acid/mL plasma was associated with 71.6% (95% CI, 2.4%–187.5%) higher insulin concentration, 67.5% (95% CI, 5.5%–166.0%) higher β-cell function, 73.9% (95% CI, 0.2%–202.0%) higher insulin resistance, and 76.2% (95% CI, 22.8%–153.0%) higher triglyceride concentrations.”

“Our results suggest that these chemicals, which linger in the environment for years, could represent an important public health hazard that merits further study,” says Timmerman. “Overweight children who were exposed to higher levels of PFCs tended to have higher concentrations of insulin and triglycerides in their blood, and these metabolic changes could signal the beginnings of the metabolic syndrome.” However, the authors noted that while this is the first study to associate PFC exposure to metabolic syndromes in “a large cohort of prepubertal children,” there were some limitations to this study. They wrote, “Chance findings may explain some of our results, and due to the cross-sectional design, reverse causation cannot be excluded. The findings therefore need to be confirmed in longitudinal studies.”


It seems that people are exposed to bisphenol A (BPA) almost everywhere they go, and there’s no shortage of research linking the endocrine disruptor to myriad conditions. Now, research in the journal Endocrinology has shown that exposure to BPA is associated with prostate cancer.

According to the article, prostate cancer is the second leading cause of cancer-related mortality in U.S. men. And while BPA itself is not a known carcinogen, the scientists note that in a study of 2,500 U.S. adults, 93% had detectable urine BPA, “indicating that humans are chronically exposed to this compound during routine daily activity.”

The study, led by Gail S. Prins, PhD, of the University of Illinois, utilized primary human prostate epithelial stem-like cells (PrEC) from the prostates of four disease-free donors aged 19-21. The PrECs were then combined with rat mesenchyme and grown as renal grafts in nude mice in order to assess in vivo carcinogenicity. The mice formed normal human prostate epithelium at one month.

Of their methods, the authors wrote, “Developmental BPA exposure was achieved through oral administration of 100 µg or 250 µg BPA/kg BW to hosts for two weeks post-grafting, producing free-BPA levels of 0.39 and 1.35 ng/ml serum, respectively. Carcinogenesis was driven by testosterone plus E2 treatment for two to four months to model rising E2 levels in aging men.” They found that the incidence of malignancies (intraepithelial neoplasia and adenocarcinoma) increased from 13% in oil-fed controls to 33%-36% in grafts exposed in vivo to BPA. “Continuous developmental BPA exposure through in vitro (200 nM) plus in vivo (250 µg/kg BW) treatments increased HG-PIN/cancer incidence to 45% (P< 0.01),” they wrote. The researchers also did in vitro work directly on the human prostate stem and progenitor cells, and found that BPA directly activates rapid signaling pathways in the stem and early progenitor cells, paralleling the actions of estradiol and resulting in increased self-renewal of the stem cell population, i.e., increasing their numbers. Thus, direct actions where shown, in addition to increased rates of estrogen-induced carcinogenesis in vivo. Prins and her team concluded that their findings demonstrate that “human prostate stem-progenitor cells are direct BPA targets and that developmental exposure to BPA at low doses increases hormone dependent cancer risk in the human prostate epithelium.” They go on to suggest that humans may be susceptible to prostate diseases after exposure to doses of BPA that are routinely found in humans.

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