scholarly journals Prenatal and early-life exposure to the Great Chinese Famine increased the risk of tuberculosis in adulthood across two generations

2020 ◽  
Vol 117 (44) ◽  
pp. 27549-27555
Author(s):  
Qu Cheng ◽  
Robert Trangucci ◽  
Kristin N. Nelson ◽  
Wenjiang Fu ◽  
Philip A. Collender ◽  
...  
Keyword(s):  
Incidence Rate ◽  
Early Life ◽  
Food System ◽  
Cohort Analysis ◽  
Host Susceptibility ◽  
Sexually Transmitted ◽  
Global Food Security ◽  
Household Transmission ◽  
Early Life Exposure ◽  
Increased Risk

Global food security is a major driver of population health, and food system collapse may have complex and long-lasting effects on health outcomes. We examined the effect of prenatal exposure to the Great Chinese Famine (1958–1962)—the largest famine in human history—on pulmonary tuberculosis (PTB) across consecutive generations in a major center of ongoing transmission in China. We analyzed >1 million PTB cases diagnosed between 2005 and 2018 in Sichuan Province using age–period–cohort analysis and mixed-effects metaregression to estimate the effect of the famine on PTB risk in the directly affected birth cohort (F1) and their likely offspring (F2). The analysis was repeated on certain sexually transmitted and blood-borne infections (STBBI) to explore potential mechanisms of the intergenerational effects. A substantial burden of active PTB in the exposed F1 cohort and their offspring was attributable to the Great Chinese Famine, with more than 12,000 famine-attributable active PTB cases (>1.23% of all cases reported between 2005 and 2018). An interquartile range increase in famine intensity resulted in a 6.53% (95% confidence interval [CI]: 1.19–12.14%) increase in the ratio of observed to expected incidence rate (incidence rate ratio, IRR) in the absence of famine in F1, and an 8.32% (95% CI: 0.59–16.6%) increase in F2 IRR. Increased risk of STBBI was also observed in F2. Prenatal and early-life exposure to malnutrition may increase the risk of active PTB in the exposed generation and their offspring, with the intergenerational effect potentially due to both within-household transmission and increases in host susceptibility.

scholarly journals Determinants of Influenza Mortality Trends: Age-Period-Cohort Analysis of Influenza Mortality in the United States, 1959–2016

Demography ◽  
2019 ◽  
Vol 56 (5) ◽  
pp. 1723-1746 ◽  
Author(s):  
Enrique Acosta ◽  
Stacey A. Hallman ◽  
Lisa Y. Dillon ◽  
Nadine Ouellette ◽  
Robert Bourbeau ◽  
...  
Keyword(s):  
United States ◽  
Influenza Virus ◽  
Early Life ◽  
Baby Boom ◽  
Cohort Analysis ◽  
The Elderly ◽  
The United States ◽  
Birth Cohorts ◽  
Mortality Trends ◽  
Early Life Exposure

Abstract This study examines the roles of age, period, and cohort in influenza mortality trends over the years 1959–2016 in the United States. First, we use Lexis surfaces based on Serfling models to highlight influenza mortality patterns as well as to identify lingering effects of early-life exposure to specific influenza virus subtypes (e.g., H1N1, H3N2). Second, we use age-period-cohort (APC) methods to explore APC linear trends and identify changes in the slope of these trends (contrasts). Our analyses reveal a series of breakpoints where the magnitude and direction of birth cohort trends significantly change, mostly corresponding to years in which important antigenic drifts or shifts took place (i.e., 1947, 1957, 1968, and 1978). Whereas child, youth, and adult influenza mortality appear to be influenced by a combination of cohort- and period-specific factors, reflecting the interaction between the antigenic experience of the population and the evolution of the influenza virus itself, mortality patterns of the elderly appear to be molded by broader cohort factors. The latter would reflect the processes of physiological capital improvement in successive birth cohorts through secular changes in early-life conditions. Antigenic imprinting, cohort morbidity phenotype, and other mechanisms that can generate the observed cohort effects, including the baby boom, are discussed.

scholarly journals Maternal Obesity, Birth Size, and Risk of Childhood Cancer Development

2019 ◽  
Vol 188 (8) ◽  
pp. 1503-1511 ◽  
Author(s):  
Shaina L Stacy ◽  
Jeanine M Buchanich ◽  
Zhen-qiang Ma ◽  
Christina Mair ◽  
Linda Robertson ◽  
...  
Keyword(s):  
Childhood Cancer ◽  
Early Life ◽  
Maternal Obesity ◽  
Birth Certificate ◽  
Cancer Development ◽  
Related Factors ◽  
Early Life Exposure ◽  
Increased Risk ◽  
Development Accounting ◽  
Newborn Size

Abstract Infants and children are particularly vulnerable to in utero and early-life exposures. Thus, a mother’s exposures before and during pregnancy could have important consequences for her child’s health, including cancer development. We examined whether birth certificate–derived maternal anthropometric characteristics were associated with increased risk of subsequent childhood cancer development, accounting for established maternal and infant risk factors. Pennsylvania birth and cancer registry files were linked by the state Department of Health, yielding a virtual cohort of births and childhood cancers from 2003 through 2016. The analysis included 1,827,875 infants (13,785,309 person-years at risk), with 2,352 children diagnosed with any cancer and 747 with leukemia before age 14 years. Children born to mothers with a body mass index (weight (kg)/height (m)2) of ≥40 had a 57% (95% confidence interval: 12, 120) higher leukemia risk. Newborn size of ≥30% higher than expected was associated with 2.2-fold and 1.8-fold hazard ratios for total childhood cancer and leukemia, respectively, relative to those with expected size. Being <30% below expected size also increased the overall cancer risk (P for curvilinearity < 0.0001). Newborn size did not mediate the association between maternal obesity and childhood cancer. The results suggest a significant role of early-life exposure to maternal obesity- and fetal growth–related factors in childhood cancer development.

scholarly journals Early-Life Exposure to Famine and Risk of MetabolicAssociated Fatty Liver Disease in Chinese Adults

Nutrients ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 4063
Author(s):  
Jing Liu ◽  
Guimin Wang ◽  
Yiling Wu ◽  
Ying Guan ◽  
Zhen Luo ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Liver Disease ◽  
Fatty Liver ◽  
Early Life ◽  
Fatty Liver Disease ◽  
Chinese Adults ◽  
Early Life Exposure ◽  
Increased Risk ◽  
Famine Exposure

Background: Early-life exposure to the Chinese famine has been related to the risk of obesity, type 2 diabetes, and nonalcoholic fatty liver disease later in life. Nevertheless, the long-term impact of famine exposure on metabolic associated fatty liver disease (MAFLD), a recently proposed term to describe liver disease associated with known metabolic dysfunction, remains unknown. The aim of our study was to explore the relationship between early famine exposure and MAFLD in adulthood. Methods: A total of 26,821 participants (10,994 men, 15,827 women) were recruited from a cohort study of Chinese adults in Shanghai. We categorized participants into four famine exposure subgroups based on the birth year as nonexposed (1963–1967), fetal-exposed (1959–1962), childhood-exposed (1949–1958), and adolescence-exposed (1941–1948). MAFLD was defined as liver steatosis detected by ultrasound plus one of the following three criteria: overweight/obesity, type 2 diabetes, or evidence of metabolic dysregulation. Multivariable logistic regression models were performed to examine the association between famine exposure and MAFLD. Results: The mean ± standard deviation age of the participants was 60.8 ± 6.8 years. The age-adjusted prevalence of MAFLD was 38.3, 40.8, 40.1, and 36.5% for the nonexposed, fetal-exposed, childhood-exposed, and adolescence-exposed subgroups, respectively. Compared with nonexposed participants, fetal-exposed participants showed an increased risk of adulthood MAFLD (OR = 1.10, 95% CI 1.00–1.21). The significant association between fetal famine exposure and MAFLD was observed in women (OR = 1.22, 95% CI 1.08–1.37), but not in men (OR = 0.88, 95% CI 0.75–1.03). In age-balanced analyses combining pre-famine and post-famine births as the reference, women exposed to famine in the fetal stage still had an increased risk of MAFLD (OR = 1.15, 95% CI 1.05–1.26). Conclusions: Prenatal exposure to famine showed a sex-specific association with the risk of MAFLD in adulthood.

scholarly journals Early Life Exposure in Mexico to ENvironmental Toxicants (ELEMENT) Project

BMJ Open ◽  
2019 ◽  
Vol 9 (8) ◽  
pp. e030427 ◽  
Author(s):  
Wei Perng ◽  
Marcela Tamayo-Ortiz ◽  
Lu Tang ◽  
Brisa N Sánchez ◽  
Alejandra Cantoral ◽  
...  
Keyword(s):  
Lead Exposure ◽  
Early Life ◽  
Calcium Supplementation ◽  
Dietary Factors ◽  
Environmental Toxicants ◽  
Neurocognitive Deficits ◽  
Early Life Exposure ◽  
Increased Risk ◽  
Maternity Hospitals ◽  
Pregnancy And Lactation

PurposeThe Early Life Exposure in Mexico to ENvironmental Toxicants (ELEMENT) Project is a mother–child pregnancy and birth cohort originally initiated in the mid-1990s to explore: (1) whether enhanced mobilisation of lead from maternal bone stores during pregnancy poses a risk to fetal and subsequent offspring neurodevelopment; and (2) whether maternal calcium supplementation during pregnancy and lactation can suppress bone lead mobilisation and mitigate the adverse effects of lead exposure on offspring health and development. Through utilisation of carefully archived biospecimens to measure other prenatal exposures, banking of DNA and rigorous measurement of a diverse array of outcomes, ELEMENT has since evolved into a major resource for research on early life exposures and developmental outcomes.Participantsn=1643 mother–child pairs sequentially recruited (between 1994 and 2003) during pregnancy or at delivery from maternity hospitals in Mexico City, Mexico.Findings to dateMaternal bone (eg, patella, tibia) is an endogenous source for fetal lead exposure due to mobilisation of stored lead into circulation during pregnancy and lactation, leading to increased risk of miscarriage, low birth weight and smaller head circumference, and transfer of lead into breastmilk. Daily supplementation with 1200 mg of elemental calcium during pregnancy and lactation reduces lead resorption from maternal bone and thereby, levels of circulating lead. Beyond perinatal outcomes, early life exposure to lead is associated with neurocognitive deficits, behavioural disorders, higher blood pressure and lower weight in offspring during childhood. Some of these relationships were modified by dietary factors; genetic polymorphisms specific for iron, folate and lipid metabolism; and timing of exposure. Research has also expanded to include findings published on other toxicants such as those associated with personal care products and plastics (eg, phthalates, bisphenol A), other metals (eg, mercury, manganese, cadmium), pesticides (organophosphates) and fluoride; other biomarkers (eg, toxicant levels in plasma, hair and teeth); other outcomes (eg, sexual maturation, metabolic syndrome, dental caries); and identification of novel mechanisms via epigenetic and metabolomics profiling.Future plansAs the ELEMENT mothers and children age, we plan to (1) continue studying the long-term consequences of toxicant exposure during the perinatal period on adolescent and young adult outcomes as well as outcomes related to the original ELEMENT mothers, such as their metabolic and bone health during perimenopause; and (2) follow the third generation of participants (children of the children) to study intergenerational effects of in utero exposures.Trial registration numberNCT00558623.

scholarly journals Early-life exposure to the Chinese famine of 1959–61 and risk of Hyperuricemia: results from the China health and retirement longitudinal study

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Wenqiang Zhang ◽  
Rongsheng Luan
Keyword(s):  
Early Childhood ◽  
Uric Acid ◽  
Longitudinal Study ◽  
Serum Uric Acid ◽  
Early Life ◽  
Early Life Exposure ◽  
Long Term Effect ◽  
Increased Risk ◽  
Famine Exposure

Abstract Background Short-term starvation has been related to hyperuricemia. However, little is known about the long-term effect of early-life exposure to famine on hyperuricemia risk in adulthood. Methods The analysis included 2383 participants from the China Health and Retirement Longitudinal Study in 2015. Hyperuricemia was diagnosed as serum uric acid ≥7 mg/dL in men and serum uric acid ≥6 mg/dL in women. Famine exposure subgroups were defined as unexposed (born between October 1, 1962, and September 30, 1964), fetal-exposed (born between October 1, 1959, and September 30, 1961), and early-childhood exposed (born between October 1, 1956, and September 1, 1958). The association between early-life famine exposure and hyperuricemia risk was assessed using multivariate logistic regression. Results The prevalence of hyperuricemia in the unexposed, fetal-exposed, and early-childhood exposed participants was 10.7, 14.1, 11.1%, respectively. Compared with unexposed and early-childhood exposed participants combined as an age-balanced control, fetal-exposed participants showed an increased risk of hyperuricemia in adulthood (OR = 1.41; 95% CI: 1.06–1.88), after adjusting for gender, marital status, famine severity, residence, smoking, drinking, BMI, hypertension, and diabetes. The famine effect on hyperuricemia was accentuated by overweight or obesity (P for interaction = 0.042). Compared with unexposed and BMI < 24 kg/m2 participants, the OR (95%CI) of hyperuricemia was 3.66 (2.13–6.30) for fetal-exposed and overweight/obesity participants. However, combined unexposed and early-childhood exposed participants as an age-balanced control, the interaction of famine exposure and BMI was not statistically significant (P for interaction = 0.054). Conclusion Famine exposure in the fetal stage was associated with an increased risk of hyperuricemia in adulthood.

Early-Life Exposure to the Chinese Famine and Risk of Hyperuricemia in Adult Females in Qingdao

2021 ◽  
pp. 1-24
Author(s):  
Yuhan Shao ◽  
Li Liu ◽  
Xiaojing Li ◽  
Jianping Sun ◽  
Xiaomei Huang
Keyword(s):  
Early Life ◽  
Population Based ◽  
Exposed Group ◽  
Childhood And Adolescence ◽  
Cross Sectional ◽  
Logistic Regression Models ◽  
Adult Females ◽  
Early Life Exposure ◽  
Increased Risk ◽  
Famine Exposure

Abstract Purpose: We aimed to explore whether exposure to the Chinese famine in early life was associated with hyperuricemia in adulthood. Methods and Results: Two population-based cross-sectional surveys involving randomly selected Chinese adults aged 35–74 years were conducted in Qingdao, China in 2006 and 2009. 9055 subjects from the two surveys were grouped into four birth groups of fetal/infant exposed(born between 1959/1/1 and 1962/12/31), childhood exposed(born between 1950/1/1 and 1958/12/31), adolescence exposed(born between 1942/1/1 and 1949/12/31) and the unexposed(born before 1941 and after 1963). Multivariate logistic regression models were used to calculate the odd ratios (ORs) and 95% confidence intervals (CIs) of hyperuricemia in different exposed groups. Overall, famine exposure in the fetal/infant period, childhood and adolescence was not associated with adulthood hyperuricemia (all P>0.05). In females, childhood exposed group(OR=1.59, 95%CI:1.25-2.02) and adolescence exposed group(OR=1.74, 95%CI:1.30-2.33) both had higher risks to have hyperuricemia in adult. However, this difference was not found in fetal/infant exposed group. In males, no significant relation was observed in any famine exposed group (all P>0.05). Conclusions: Exposure to famine in childhood and adolescence is associated with an increased risk of hyperuricemia for adulthood of females, but not in males. Adequate nutrition during early life appears to be beneficial to prevent hyperuricemia of adult females.

Fibromyalgia and the Risk of a Subsequent Motor Vehicle Crash

2015 ◽  
Vol 42 (8) ◽  
pp. 1502-1510 ◽  
Author(s):  
Donald A. Redelmeier ◽  
Jeremy D. Zung ◽  
Deva Thiruchelvam ◽  
Robert J. Tibshirani
Keyword(s):  
Incidence Rate ◽  
Traffic Safety ◽  
Rate Ratio ◽  
Incidence Rate Ratio ◽  
Motor Vehicle ◽  
Cohort Analysis ◽  
Motor Vehicle Crash ◽  
Vehicle Crash ◽  
Increased Risk ◽  
Population Norm

Objective.Motor vehicle crashes are a widespread contributor to mortality and morbidity, sometimes related to medically unfit motorists. We tested whether patients diagnosed with fibromyalgia (FM) have an increased risk of a subsequent serious motor vehicle crash.Methods.We conducted a population-based self-matched longitudinal cohort analysis to estimate the incidence rate ratio of crashes among patients diagnosed with FM relative to the population norm in Ontario, Canada. We included adults diagnosed from April 1, 2006, to March 31, 2012, excluding individuals younger than 18 years, living outside Ontario, lacking valid identifiers, or having only a single visit for the diagnosis. The primary outcome was an emergency department visit as a driver involved in a motor vehicle crash.Results.The patients (n = 137,631) accounted for 738 crashes during the first year of followup after diagnosis, equal to an incidence rate ratio of 2.44 compared with the population norm (95% CI 2.27–2.63, p < 0.001). The crash rate was more than twice the population norm for those with a new or a persistent diagnosis. The increased risk included patients with diverse characteristics, approached the rate observed among other patients diagnosed with alcoholism, and was mitigated among those who received dedicated FM care or a physician warning for driving safety.Conclusion.A diagnosis of FM is associated with an increased risk of a subsequent motor vehicle crash that might justify medical interventions for traffic safety.

scholarly journals Early-life microbial intervention reduces colitis risk promoted by antibiotic-induced gut dysbiosis

2020 ◽  
Author(s):  
Jun Miyoshi ◽  
Sawako Miyoshi ◽  
Tom O. Delmont ◽  
Candace Cham ◽  
Sonny T.M. Lee ◽  
...  
Keyword(s):  
Immune Tolerance ◽  
Gut Microbiome ◽  
Early Life ◽  
Experimental Colitis ◽  
List Type ◽  
Immune Disorder ◽  
Gut Dysbiosis ◽  
Early Life Exposure ◽  
Increased Risk ◽  
Bowel Diseases

SummaryPerturbations in the early life gut microbiome are associated with increased risk to complex immune disorder like inflammatory bowel diseases. We previously showed maternal antibiotic-induced gut dysbiosis vertically passed to offspring increases experimental colitis risk in IL-10 gene deficient (IL-10−/−) mice. While this could arise from emergence of pathobionts or loss/lack of essential microbes needed for appropriate immunological education, our findings suggest the latter. A dominant Bacteroides strain absent following antibiotic-induced perturbation was cultivated from murine fecal samples. Addition of this strain into mice with antibiotic-induced dysbiosis significantly promoted immune tolerance and reduced incidence of colitis in IL-10−/− mice, but only if engrafted early in life, and not during adulthood. Thus, key members of the gut microbiome are essential for development of immune tolerance to commensal microbes in early life and their addition in presence of gut dysbiosis during this period can reduce colitis risk in genetically prone hosts.HighlightsSpecific gut microbes promote early life immune tolerance to key commensal microbesLoss of early life keystone microbes increases colitis risk in genetically prone hostsEmergence of absent commensal microbes late in life worsened colitis outcomeEarly life exposure to a missing keystone Bacteroides strain reduced colitis risk

Chemically Contaminated Eel Fed to Pregnant and Lactating Mouse Dams Causes Hyperactivity in Their Offspring

2016 ◽  
Vol 86 (1-2) ◽  
pp. 36-47 ◽  
Author(s):  
Imen Dridi ◽  
Nidhal Soualeh ◽  
Torsten Bohn ◽  
Rachid Soulimani ◽  
Jaouad Bouayed
Keyword(s):  
Open Field ◽  
Early Life ◽  
Home Cage ◽  
Anguilla Anguilla ◽  
Acetylcholinesterase Activity ◽  
Female Offspring ◽  
Significant Inhibition ◽  
Standard Diet ◽  
Early Life Exposure ◽  
Cage Test

Abstract.This study examined whether perinatal exposure to polluted eels (Anguilla anguilla L.) induces changes in the locomotor activity of offspring mice across lifespan (post-natal days (PNDs) 47 – 329), using the open field and the home cage activity tests. Dams were exposed during gestation and lactation, through diets enriched in eels naturally contaminated with pollutants including PCBs. Analysis of the eel muscle focused on the six non-dioxin-like (NDL) indicator PCBs (Σ6 NDL-PCBs: 28, 52, 101, 138, 153 and 180). Four groups of dams (n = 10 per group) received either a standard diet without eels or eels (0.8 mg/kg/day) containing 85, 216, or 400 ng/kg/day of ϵ6 NDL-PCBs. The open field test showed that early-life exposure to polluted eels increased locomotion in female offspring of exposed dams but not in males, compared to controls. This hyperlocomotion appeared later in life, at PNDs 195 and 329 (up to 32 % increase, p < 0.05). In addition, overactivity was observed in the home cage test at PND 305: exposed offspring females showed a faster overall locomotion speed (3.6 – 4.2 cm/s) than controls (2.9 cm/s, p <0.05); again, males remained unaffected. Covered distances in the home cage test were only elevated significantly in offspring females exposed to highest PCB concentrations (3411 ± 590 cm vs. 1377 ± 114 cm, p < 0.001). These results suggest that early-life exposure to polluted eels containing dietary contaminants including PCBs caused late, persistent and gender-dependent neurobehavioral hyperactive effects in offspring mice. Furthermore, female hyperactivity was associated with a significant inhibition of acetylcholinesterase activity in the hippocampus and the prefrontal cortex.

Sign in / Sign up

Export Citation Format

Share Document