Babies who are exposed to high levels of air pollution while in the womb have worse lung function as children and teenagers, study claims

Same old, same old crap.  Pollution and poverty confounded as a cause of poor health.

Pollution encountered was meaured by whether the person lived in a polluted area.  But pollution is not uniform in an area.  And poor people tend to live in more polluted areas.  And poor people tend to have poorer health. So was it pollution or poverty that caused the poorer health?  Unknowable.

The article is only a conference paper so details of the research are not publically available and hence are not open for critical examination.  But by relying on previous studies of that ilk we can be pretty certain that income was not controlled for and that the effects found were minute

Tedious.  Let's hope it does not get past peer review


Babies who are exposed to high air pollution develop worse lung function as children and teenagers, research suggests.

A study of 915 children found that the higher the levels of air pollution they were exposed to in infancy, the worse their lung function became as they grew into adolescence.

Researchers in Germany measured the infants' air pollution exposure and then repeatedly assessed their breathing, carrying out tests at the ages of six, ten and 15.

The team, who presented their findings at the European Respiratory Society International Congress, found an even bigger impact on lung function in children who developed asthma.

But they also found that babies who were breastfed for at least the first 12 weeks of their life were given some degree of protection.

SOURCE

The old BPA nonsense again

Using extreme tertiles for the analysis suggests that there was no overall connection between BPA and anything else.  And even after throwing away a third of their data, the correlations were trivial,  too low to be a basis for public policy

Association Between Bisphenol A Exposure and Risk of All-Cause and Cause-Specific Mortality in US Adults

Wei Bao et al.

Abstract

Importance:  Bisphenol A (BPA) is a major public health concern because of its high-volume industrial production, ubiquitous exposure to humans, and potential toxic effects on multiple organs and systems in humans. However, prospective studies regarding the association of BPA exposure with long-term health outcomes are sparse.

Objective:  To examine the association of BPA exposure with all-cause mortality and cause-specific mortality among adults in the United States.

Design, Setting, and Participants:  This nationally representative cohort study included 3883 adults aged 20 years or older who participated in the US National Health and Nutrition Examination Survey 2003-2008 and provided urine samples for BPA level measurements. Participants were linked to mortality data from survey date through December 31, 2015. Data analyses were conducted in July 2019.

Exposures:  Urinary BPA levels were quantified using online solid-phase extraction coupled to high-performance liquid chromatography–isotope dilution tandem mass spectrometry.

Main Outcomes and Measures:  Mortality from all causes, cardiovascular disease, and cancer.

Results:  This cohort study included 3883 adults aged 20 years or older (weighted mean [SE] age, 43.6 [0.3] years; 2032 women [weighted, 51.4%]). During 36 514 person-years of follow-up (median, 9.6 years; maximum, 13.1 years), 344 deaths occurred, including 71 deaths from cardiovascular disease and 75 deaths from cancer. Participants with higher urinary BPA levels were at higher risk for death. After adjustment for age, sex, race/ethnicity, socioeconomic status, dietary and lifestyle factors, body mass index, and urinary creatinine levels, the hazard ratio comparing the highest vs lowest tertile of urinary BPA levels was 1.49 (95% CI, 1.01-2.19) for all-cause mortality, 1.46 (95% CI, 0.67-3.15) for cardiovascular disease mortality, and 0.98 (95% CI, 0.40-2.39) for cancer mortality.

Conclusions and Relevance:  In this nationally representative cohort of US adults, higher BPA exposure was significantly associated with an increased risk of all-cause mortality. Further studies are needed to replicate these findings in other populations and determine the underlying mechanisms.

SOURCE

Does losing weight increase your lifespan?

Most studies show little effect of fat on life expectancy but the one below seems to.  So what is going on?  Easy.  There WAS  in fact a benefit from weight loss but it was very small. Which is what previous studies have shown

Association of Weight Loss Between Early Adulthood and Midlife With All-Cause Mortality Risk in the US

Wubin Xie et al.

Abstract

Importance:  Describing potential mortality risk reduction associated with weight loss between early adulthood and midlife is important for informing primary and secondary prevention efforts for obesity.

Objective:  To examine the risk of all-cause mortality among adults who lost weight between early adulthood and midlife compared with adults who were persistently obese over the same period.

Design, Setting, and Participants:  Combined repeated cross-sectional analysis was conducted using data from the National Health and Nutrition Examination Survey III (1988-1994) and continuous waves collected in 2-year cycles between 1999 and 2014. The data analysis was conducted from February 10, 2019, to April 20, 2020. Individuals aged 40 to 74 years at the time of survey (baseline) were included in the analyses (n = 24 205).

Exposures:  Weight history was assessed by self-reported weight at age 25 years, at 10 years before baseline (midlife: mean age, 44 years; interquartile range, 37-55), and measured weight at baseline. Body mass index (BMI) (calculated as weight in kilograms divided by height in meters squared) at each time was categorized as normal (18.5-24.9), overweight (25.0-29.9), and obese (≥30.0). Weight change patterns were assessed from age 25 years (early adulthood) to 10 years before baseline (midlife).

Main Outcomes and Measures:  Incident all-cause mortality using linked data from the National Death Index.

Results:  Of the 24 205 participants, 11 617 were women (49.0%) and 11 567 were non-Hispanic White (76.9%). The mean (SD) BMI was 29.0 (6.1) at baseline. During a mean (SD) follow-up of 10.7 (7.2) years, 5846 deaths occurred. Weight loss from obese to overweight was associated with a 54% (hazard ratio, 0.46; 95% CI, 0.27-0.77) reduction in mortality risk compared with individuals with stable obesity between early adulthood and midlife. An estimated 3.2% (95% CI, 1.6%-4.9%) of early deaths could have been avoided if those who maintained an obese BMI instead lost weight to an overweight BMI by midlife. Overall, an estimated 12.4% (95% CI, 8.1%-16.5%) of early deaths may be attributable to having weight in excess of the normal BMI range at any point between early and mid-adulthood.

Conclusions and Relevance:  In this study, weight loss from obesity to overweight between early adulthood through midlife appeared to be associated with a mortality risk reduction compared with persistent obesity.

SOURCE 

Vitamin D no good for depression

Effect of Long-term Vitamin D3 Supplementation vs Placebo on Risk of Depression or Clinically Relevant Depressive Symptoms and on Change in Mood Scores

Olivia I. Okereke et al.

Abstract

Importance:  Low levels of 25-hydroxyvitamin D have been associated with higher risk for depression later in life, but there have been few long-term, high-dose large-scale trials.

Objective:  To test the effects of vitamin D3 supplementation on late-life depression risk and mood scores.

Design, Setting, and Participants:  There were 18 353 men and women aged 50 years or older in the VITAL-DEP (Vitamin D and Omega-3 Trial-Depression Endpoint Prevention) ancillary study to VITAL, a randomized clinical trial of cardiovascular disease and cancer prevention among 25 871 adults in the US. There were 16 657 at risk for incident depression (ie, no depression history) and 1696 at risk for recurrent depression (ie, depression history but no treatment for depression within the past 2 years). Randomization occurred from November 2011 through March 2014; randomized treatment ended on December 31, 2017, and this was the final date of follow-up.

Intervention:  Randomized assignment in a 2 × 2 factorial design to vitamin D3 (2000 IU/d of cholecalciferol) and fish oil or placebo; 9181 were randomized to vitamin D3 and 9172 were randomized to matching placebo.

Main Outcomes and Measures:  The primary outcomes were the risk of depression or clinically relevant depressive symptoms (total of incident and recurrent cases) and the mean difference in mood scores (8-item Patient Health Questionnaire depression scale [PHQ-8]; score range, 0 points [least symptoms] to 24 points [most symptoms]; the minimal clinically important difference for change in scores was 0.5 points).

Results:  Among the 18 353 randomized participants (mean age, 67.5 [SD, 7.1] years; 49.2% women), the median treatment duration was 5.3 years and 90.5% completed the trial (93.5% among those alive at the end of the trial). Risk of depression or clinically relevant depressive symptoms was not significantly different between the vitamin D3 group (609 depression or clinically relevant depressive symptom events; 12.9/1000 person-years) and the placebo group (625 depression or clinically relevant depressive symptom events; 13.3/1000 person-years) (hazard ratio, 0.97 [95% CI, 0.87 to 1.09]; P = .62); there were no significant differences between groups in depression incidence or recurrence. No significant differences were observed between treatment groups for change in mood scores over time; mean change in PHQ-8 score was not significantly different from zero (mean difference for change in mood scores, 0.01 points [95% CI, −0.04 to 0.05 points]).

Conclusions and Relevance:  Among adults aged 50 years or older without clinically relevant depressive symptoms at baseline, treatment with vitamin D3 compared with placebo did not result in a statistically significant difference in the incidence and recurrence of depression or clinically relevant depressive symptoms or for change in mood scores over a median follow-up of 5.3 years. These findings do not support the use of vitamin D3 in adults to prevent depression.

SOURCE

Ya gotta be joking

Leftists are determined to believe anything that suits their Leftist idology.  The research below is about Mrs Obama's school lunch program.  The academic article seriously tells us that the kids indeed got improved food from it -- improved according to the conventional wisdom at the time.

What it fails to consider is what the kids actually ate.  That the kids turned up their noses at a lot of it and threw it in the bin is not mentioned.  They assume that the kids ate what they said they ate.

What idiocy.  What a kid should eat is often a contested matter between parent and child so the kids would all be pretty aware of what they needed to say in order to get approval.  So the amount they threw in the bin would not be mentioned to a nosy stranger. They would say they ate it


Association of the Healthy, Hunger-Free Kids Act With Dietary Quality Among Children in the US National School Lunch Program

Kelsey Kinderknecht et al.

Abstract

Importance:  The Healthy, Hunger-Free Kids Act of 2010, implemented nationwide in 2012, was intended to improve the nutritional quality of meals served in the National School Lunch Program (NSLP).

Objective:  To assess whether there was an association between the Healthy, Hunger-Free Kids Act of 2010 and dietary quality of lunch for students participating in the NSLP, stratified by income.

Design, Setting, Participants:  Serial cross-sectional study design, using National Health and Nutrition Examination Survey (NHANES) data from 2007-2008, 2009-2010, 2013-2014, and 2015-2016, of students who were surveyed in the NHANES and were attending schools participating in the NSLP. Individuals who were aged 5 to 18 years, in kindergarten through 12th grade, enrolled in a school that served school lunch, and had a reliable weekday dietary recall were included.

Exposures:  The Healthy, Hunger-Free Kids Act of 2010 (prepolicy period: 2007-2010; postpolicy period: 2013-2016), with participation in the NSLP estimated based on an algorithm.

Main Outcomes and Measures:  The primary outcome was dietary quality of intake for lunch, measured by the Healthy Eating Index-2010 (HEI-2010) score (range, 0-100; 0 indicates a diet with no adherence to the 2010 Dietary Guidelines for Americans and 100 indicates a diet with complete adherence to the guidelines).

Results:  Among 6389 students included in the surveys (mean age, 11.7 [95% CI, 11.6-11.9] years; 3145 [50%] female students; 1880 [56%] were non-Hispanic white), 32% were low-income, 12% were low-middle–income, and 56% were middle-high–income students. A total of 2472 (39%) were participants in the NSLP. Among low-income students, the adjusted mean prepolicy HEI-2010 score was 42.7 and the postpolicy score was 54.6 among NSLP participants and the adjusted mean prepolicy score was 34.8 and postpolicy score was 34.1 among NSLP nonparticipants (difference in differences, 12.6 [95% CI, 8.9-16.3]). Among low-middle–income students, the adjusted mean prepolicy HEI-2010 score was 40.4 and postpolicy score was 54.8 among NSLP participants and the adjusted mean prepolicy score was 34.2 and postpolicy score was 36.1 among NSLP nonparticipants (difference in differences, 12.4 [95% CI, 4.9-19.9]). Among middle-high–income students, the adjusted mean HEI-2010 prepolicy score was 42.7 and postpolicy score 55.5 for NSLP participants and the adjusted mean prepolicy score was 38.9 and prepolicy score was 43.6 for NSLP nonparticipants (difference in differences, 8.1 [95% CI, 4.2-12.0]).

Conclusions and Relevance:  In a serial cross-sectional study of students, the Healthy, Hunger-Free Kids Act of 2010 was associated with better changes in dietary quality for lunch among presumed low-income, low-middle–income, and middle-high–income participants in the NSLP compared with nonparticipants.

SOURCE