Effect Of Famine Exposure Research Articles

Early Famine Exposure Results in Left Ventricular Remodeled, Diastolic Dysfunction and Systolic Function Preserved in Adults

Introduction: Malnutrition during a critical window of development in a fetus or infant can result in abnormal cardiac remodeling and function. It is uncertain whether the contribution of these effects continues to impact the cardiac remodeling and function of adults over the course of several decades of growth. Our study examined the impact of early Chinese famine exposure on cardiac remodeling, left ventricular (LV) diastolic function, and LV systolic function in adults. Methods: Participants at high risk of cardiovascular disease from the China Patient-Centered Evaluative Assessment of Cardiac Events Million Persons Project (PEACE MPP) were enrolled. The famine in China lasted from 1959 to 1962. A total of three groups were formed based on the participants’ birth dates: pre-famine group, famine exposure group, and post-famine group. Logistic regression and linear mixed models were used to explore the association between famine exposure and cardiac remodeling, LV diastolic function and LV systolic function in adults. Results: The study included 2,758 participants, the mean age was 57.05 years, 62.8% were female, 26.4% had LV hypertrophy (LVH), 59.6% had LV diastolic dysfunction (LVDD), and 10.5% had reduced global longitudinal strain (GLS). Compared to post-famine exposure, participants had independently increased risk of LVH in the famine exposure group (OR: 2.02, 95% CI: 1.60–2.56) and pre-famine exposure (OR: 1.36, 95% CI: 1.06–1.76). Compared to post-famine exposure, the risk of LVDD remarkably increased in the famine exposure group (OR: 3.04, 95% CI: 2.49–3.71) and pre-famine exposure group (OR: 1.87, 95% CI: 1.52–2.31). Famine exposure had no significant impact on GLS but was associated with a significant increase in LV ejection fraction (LVEF) and LV end-diastolic diameter (LVEDD). Significant interactions were observed between the effects of famine exposure and other clinical/sociodemographic variables (gender, systolic blood pressure [SBP] ≥140 mm Hg or not, high school or above or not, and annual income <50,000 RMB or not) on these outcomes. Conclusion: Exposure to famine, particularly during fetal and infant stages, increases the risk of LVH and LVDD in adults. However, the LV systolic function remains preserved. These impacts are more pronounced in females, individuals with SBP ≥140 mm Hg, those with low income, or those with high educational status.

Adolescence exposure to China\u2019s great famine period and the association of metabolic syndrome in adulthood: a retrospective study

BackgroundExposure to famine during early life is related to several adverse health outcomes in adulthood, but the effect of famine exposure during adolescence is unclear. This study aims to examine whether exposure to famine in adolescence is associated with metabolic syndrome (MetS) in adulthood.MethodsThis study included 4130 Chinese adults (2059 males and 2071 females) aged 59–71 from the 2011 China Health and Retirement Longitudinal Study (CHARLS). All the selected participants were exposed to the three-year time period (1959–1961) of China’s Great Famine. Participants were categorized into an adolescent-exposed group (born 01/01/1944–12/31/1948) and a non-adolescent-exposed group (born 01/01/1940–12/31/1941 and 01/01/1951–12/31/1952). Sex-stratified multiple logistic regression models were used to estimate the association between exposure to famine in adolescence and MetS.ResultsParticipants exposed to famine during adolescence were more likely to report MetS (aOR = 1.35; 95%CI 1.01–1.78) compared to the non-adolescent-exposed group. Further, males were 45% less likely to report MetS than females (aOR = 0.55; 95%CI 0.36–0.83). After stratification by sex, the effects of famine exposure during adolescence on MetS were detected among males only (aOR = 1.97; 95%CI 1.20–3.24). Additionally, males with a history of drinking were more likely to report MetS compared to those with no history of drinking (aOR = 2.63; 95%CI 1.41–4.90).ConclusionsOur findings reveal that exposure to famine during adolescence is associated with higher odds of MetS in adulthood overall, and this association is only pronounced among males. This study emphasizes that undernutrition in early life, including adolescence, may have a long-term effect and be associated with adverse health events in middle-to-late life. Targeting those elderly people who suffered famine during adolescence may help prevent the development of MetS in later life.

Secular trends of age at menarche and the effect of famine exposure on age at menarche in rural Chinese women

Background Over the past few decades, more studies have suggested that the age at menarche (AAM) has continued to decline. However, the AAM for women in resource-constrained areas is not clear. Moreover, the association between the Chinese famine and AAM is still unclear in rural regions. Aim The study aimed to investigate the secular trends of AAM for women born between 1935 and 2000 and to further explore the effect of famine on AAM in rural China. Subjects and methods The study included 23,444 women participants from the baseline study of the Henan Rural Cohort study. Changing AAM over time was analysed using linear regressions. Multinomial logistic regression was conducted to analyse the association between famine exposure and AAM subgroups. Results The age-standardised mean AAM was 14.74 years. The average AAM declined from 16.98 years for those born in 1935 to 13.87 years for those born in 2000, a decline of 0.077 years per 1 year and 0.729 years per decade. Compared to the reference group, women exposed to famine during foetal, early childhood, middle childhood, and late childhood were 1.376 (95% CI = 1.071–1.769), 1.848 (95% CI = 1.512–2.259), 2.084 (95% CI = 1.725–2.518), and 2.146 (95% CI = 1.788–2.576) times more likely to be ≥18 years AAM than women unexposed to famine, respectively. Conclusion AAM showed a decreasing trend in rural China. Furthermore, both foetal and childhood famine exposure, especially in late childhood, were positively associated with increased AAM compared to unexposed famine.

The relationship between famine exposure during early life and ascending aorta dilatation in adults.

The relationship between exposure to famine in early life and the risk of ascending aorta dilatation (AAD) in adulthood is still unclear; therefore, we aimed to examine the association in the Chinese population. We investigated the data of 2598 adults who were born between 1952 and 1964 in Guangdong, China. All enrolled subjects were categorised into five groups: not exposed to famine, exposed during fetal period, and exposed during early, mid or late childhood. AAD was assessed by cardiac ultrasound. Multivariate logistic regression and interaction tests were performed to estimate the OR and CI on the association between famine exposure and AAD. There were 2598 (943 male, mean age 58·3 ± 3·68 years) participants were enrolled, and 270 (10·4 %) subjects with AAD. We found that famine exposure (OR = 2·266, 95 % CI 1·477, 3·477,P = 0·013) was associated with elevated AAD after adjusting for multiple confounders. In addition, compared with the non-exposed group, the adjusted OR for famine exposure during fetal period, early, mid or late childhood were 1·374 (95 % CI 0·794, 2·364, P = 0·251), 1·976 (95 % CI 1·243, 3·181, P = 0·004), 1·929 (95 % CI 1·237, 3·058, P = 0·004) and 2·227 (95 % CI 1·433, 3·524, P < 0·001), respectively. Subgroup analysis showed that the effect of famine exposure on the association with AAD was more pronounced in female, current smokers, people with BMI ≥ 24 kg/m2 and hypertensive patients. We observed that exposure to famine during early life was linked to AAD in adulthood.

Exposure to the Chinese Great Famine in Early Life and Thyroid Function and Disorders in Adulthood: A Cross-Sectional Study.

Background: Malnutrition in early life may permanently change the structure and function of the body, which lead to a number of diseases in adulthood. The effect of famine exposure during the early life on thyroid function and disorders remains unclear. This study investigated the association between exposure to the Great Chinese Famine (1959-1961) in early life and thyroid function and disorders in adulthood. Methods: Nine thousand eight hundred eighty-one subjects with appropriate birth dates derived from the Thyroid disorders, Iodine status, and Diabetes Epidemiological survey were included. Thyroid function and disorders were defined by the test results of blood sample and ultrasonography of all participants. Associations between famine exposure in early life and thyroid function and disorders in adulthood were assessed with binary logistic regression and linear regression. Results: Participants exposed to the Great Chinese Famine during the fetal stage was associated with a higher thyrotropin (TSH) level in adulthood (β = 0.024; p = 0.038), compared with the nonexposed participants. The association was significant among rural participants (β = 0.039; p = 0.02) but not in urban participants (β = 0.005; p = 0.77). Fetal-exposed group did not show a higher risk of thyroid disorders than the age-matched balanced control group, including overt hyperthyroidism, subclinical hyperthyroidism, overt hypothyroidism, subclinical hypothyroidism, autoimmune thyroiditis, and thyroid nodules (p > 0.05). Conclusions: Famine exposure during the fetal stage was associated with a higher TSH level in adulthood. The fetal stage could be the critical period for programming the pituitary-thyroid axis.

Early-life exposure to the Chinese famine and risk of carotid intima-media thickness increased in adulthood

Background and aimsLittle was known about the effect of famine exposure on carotid intima-media thickness (cIMT). The present study aimed to explore the relationship in a Chinese population. Methods and resultsParticipants were divided into five groups: not exposed to famine, exposed to famine in fetal, early, mid or late childhood. Elevated cIMT was defined as a thickness of >0.9 mm measured by carotid ultrasound. Multivariate logistic regression was performed to calculate odds ratio (OR) and confidence interval (CI) between famine exposure and cIMT. A total of 2637 (970 male, mean age 59.1 ± 3.65 years) participants were recruited, and 491 (18.62%) of them had elevated cIMT. When compared with the non-exposure group, the fully adjusted ORs for increased cIMT for exposure in fetal, early, mid to late childhood were 1.321 (95%CI: 0.872, 1.994, P = 0.186), 1.713 (95% CI: 1.188, 2.483, P = 0.004), 2.359 (95% CI: 1.674, 3.357, P < 0.001) and 2.485 (95% CI: 1.773, 3.518, P < 0.001), respectively. Subgroup analyses showed that the exposure to famine did not interact with body mass index, gender, smoking status, hypertension and diabetes history on its effect on cIMT. ConclusionOur findings indicated that early-life exposure to the Chinese famine might be associated with an increased risk of increased cIMT in adulthood.

The relationship between famine exposure in early life and left atrial enlargement in adulthood.

Increased left atrium diameter (LAD) is associated with an elevated risk of cardiovascular diseases. The relationship between nutrition status and left atrial enlargement (LAE) is still unclear. The present study aimed to investigate the association of famine exposure in early life with LAE in adulthood. Participants were divided into non-exposed, fetal, early, middle and late childhood exposed groups according to birth data. LAE was defined when LAD was ≥3.9cm in women and ≥4.1cm in men, or ≥2.3cmm-2 by a sex-independent cut-off normalised for body surface area. Multivariate logistic regression was performed to calculate the odds ratio (OR) and confidence interval (CI) between famine exposure and LAE. In total, 2522 [905 male, mean (SD) age 59.1(3.65)years] subjects were enrolled, including 392 (15.5%) LAE subjects. The prevalence of LAE in non-exposed, fetal, early, middle and late childhood exposed groups was 55 (10.8%), 38 (11.2%), 88 (18.1%), 102 (16.7%) and 109 (19.0%), respectively. Compared to the non-exposed group, the ORs for LAE were in fetal (OR=0.956, 95% CI=0.605-1.500, P=0.847), late (OR=1.748, 95% CI=1.208-2.555, P=0.003), middle (OR=1.647, 95% CI=1.140-2.403, P=0.008) and early (OR=1.630, 95% CI=1.116-2.399, P=0.012) childhood exposed groups after adjusting potential cofounders. When stratified by gender, smoking, body mass index, hypertension and diabetes, we found that the effect of famine exposure on LAE was only modified by diabetes (Pinteraction =0.007). Famine exposure during childhood stage might increase the risk of LAE in adults, and this effect interacts with diabetes.

The relationship between famine exposure during early life and body mass index in adulthood: A systematic review and meta-analysis.

BackgroundPrevious epidemiologic studies have reported famine exposure during early life association with overweight or obesity in adulthood, but a consistent perspective has not been established to date.PurposeTo determine, by conducting a systematic review and meta-analysis, whether exposure to famine could increase body mass index (BMI) in adult or not, and assess the association between famine exposure and the risk of overweight or obesity.MethodsPublished articles were systematically searched (until August, 2017) from PubMed, ScienceDirect, Cochrane, and China National Knowledge Infrastructure. Initially, comparing differences in BMI between exposed and non-exposed groups that weight mean difference (WMD) were used. Subsequently, the effect of famine exposure on overweight or obesity risk, which pooled relative risks (RRs), odds ratios (ORs) or hazard ratios (HRs) with 95% confidence intervals (CIs) were calculated using a random-effects model.ResultTwenty studies were included in this systematic review and meta-analysis. Compared with non-exposed group, famine exposure group significantly increased the risk of overweight (OR = 1.10, 95% CI: 1.04–1.16) and obesity (OR = 1.15, 95% CI: 1.05–1.24). Sensitivity analyses revealed no significant change in the famine exposure and BMI, the risk of overweight and obesity study when any one study was excluded. Subgroup analyses showed that age, gender, exposure type, study type, continent, famine cause and paper publication date were associated with BMI, the risk of overweight and obesity. Meta-regression analyses suggested that continent, famine cause could partially explain heterogeneity for famine exposure and BMI studies.ConclusionThe systematic review and meta-analysis indicates that famine exposure during early life may increase BMI, the risk of overweight and obesity, especially for female, fetal famine exposure or subject age less than 50. Furthermore, famine exposure group the risk of overweight and obesity in cross-sectional studies, Asian studies, famine cause by natural disaster or paper published from 2015 to the present studies are higher than that of non-exposed group.

Abstract P178: Famine Exposure in the Young and the Risk of Type 2 Diabetes in Adulthood

Background The developmental origins hypothesis proposes that undernutrition during early development is associated with an increased risk of type 2 diabetes mellitus (T2DM) in adulthood. We investigated the association between moderate and severe undernutrition during childhood and young adulthood and the risk of T2DM in later life. Methods We studied 7,837 women from the Prospect-EPIC cohort who were exposed at various degrees to the short but severe 1944-1945 Dutch Famine when they were between 0 and 21 years. We used Cox proportional hazard regression models to explore the effect of famine exposure on the risk of subsequent T2DM in adult life. We adjusted for potential confounders, including age at famine exposure, smoking, and level of education as a proxy for socio-economic status. Findings Famine exposure during childhood and young adulthood was associated with an increased T2DM risk in a dose-dependent manner (p for trend &lt;0·001). In those who were moderately famine exposed the T2DM hazard ratio (HR) was 1·36 (95% CI 1·09 to 1·69); in those severely famine exposed the HR was 1·64 (95% CI 1·26 to 2·13) relative to unexposed women. These effects did not materially change after adjustment for confounders (HR for moderate: 1·33, 95% CI 1·06 to 1·67; HR for severe: 1·51, 95% CI 1·16 to 1·98). Interpretation This study provides the first direct evidence, using individual famine exposure data, that a short period of moderate or severe undernutrition during postnatal development increases the risk of T2DM in adult life.

Timing in prenatal nutrition: a reprise of the Dutch Famine Study.

The array of results discussed in this paper is assembled by stage of gestation in the following table (Table 1). We must allow some uncertainty for some outcomes as to the precise stages of gestation in which they originate. For instance, with obesity, the effects of famine exposure may extend beyond the first trimester into the second. Yet, the table is perhaps sufficient in itself to support the point with which the paper opened, namely, that stage of development is crucial to the appreciation of the effects of prenatal nutrition.

Breast Cancer and the Brain: a Neurodevelopmental Hypothesis to Explain the Opposing Effects of Caloric Deprivation during the Dutch Famine of 1944–1945 on Breast Cancer and Its Risk Factors

Most studies on calorie deprivation and cancer risk in rodents show reductions in tumor occurrence. However, the few human studies on calorie restriction are conflicting. An overview is given of results in the DOM (diagnostic onderzoek mammacarcinoom) cohorts among women exposed to the Dutch Famine of 1944-1945. Opposing effects were found on risk factors (shortening of leg length, later menarche, and earlier menopause), whereas urinary estrogens and plasma insulin-like growth factor (IGF)-1 and IGF binding protein-3 were increased, as was breast cancer itself. Exposure between 2 and 10 y old was an unexpected window of susceptibility to the effects of calorie deprivation. The effects of famine exposure were most clearly seen in women who never gave birth. These opposing observations can be explained by a neurodevelopmental hypothesis on set-point shifts at the level of the diencephalons/hypothalamus, either directly or from rebound effects. Such a mechanism reflects old evolutionary adaptation systems in lower and higher organisms to cope with periods of stress and famine by adjusting, for example, reproductive functions. These effects in exposed women may later also affect their unexposed offspring. This hypothesis provides several testable, hormone-mediated corollaries on the relationships between the role of calories in a Westernized lifestyle and human cancer risk. The underlying developmental perspective, as opposed to a risk factor approach, can explain why certain ages, even before breast development, are especially sensitive to effects of large fluctuations in calories. The observations presented may have implications for preventive strategies such as promoting moderation of calorie intake to curb cancer risks.

Microalbuminuria in Adults after Prenatal Exposure to the Dutch Famine

Maternal undernutrition during gestation is associated with an increase in cardiovascular risk factors in the offspring in adult life. The effect of famine exposure during different stages of gestation on adult microalbuminuria (MA) was studied. MA was measured in 724 people, aged 48 to 53, who were born as term singletons in a university hospital in Amsterdam, the Netherlands, around the time of the Dutch famine 1944 to 1945. Twelve percent of people who were exposed to famine in mid gestation had MA (defined as albumin/creatinine ratio >/=2.5) compared with 7% of those who were not prenatally exposed to famine (odds ratio 2.1; 95% confidence interval 1.0 to 4.3). Correcting for BP, diabetes, and other influences that affect MA did not attenuate this association (adjusted odds ratio 3.2; 95% confidence interval 1.4 to 7.7). The effect of famine was independent of size at birth. Midgestation is a period of rapid increase in nephron number, which is critical in determining nephron endowment at birth. Fetal undernutrition may lead to lower nephron endowment with consequent MA in adult life.