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

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.

Nutrients ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 4063
Author(s):  
Jing Liu ◽  
Guimin Wang ◽  
Yiling Wu ◽  
Ying Guan ◽  
Zhen Luo ◽  
...  

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.


Rheumatology ◽  
2019 ◽  
Vol 58 (Supplement_3) ◽  
Author(s):  
Trishna Rathod-Mistry ◽  
Edward Roddy ◽  
Kelvin Jordan ◽  
Christian D Mallen ◽  
Milisa Blagojevic-Bucknall

2021 ◽  
pp. 1-24
Author(s):  
Yuhan Shao ◽  
Li Liu ◽  
Xiaojing Li ◽  
Jianping Sun ◽  
Xiaomei Huang

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.


BMJ Open ◽  
2019 ◽  
Vol 9 (2) ◽  
pp. e024980 ◽  
Author(s):  
Tiia T M Reho ◽  
Salla A Atkins ◽  
Nina Talola ◽  
Markku P T Sumanen ◽  
Mervi Viljamaa ◽  
...  

ObjectivesFrequent attenders (FAs) create a substantial portion of primary care workload but little is known about FAs’ sickness absences. The aim of the study is to investigate how occasional and persistent frequent attendance is associated with sickness absences among the working population in occupational health (OH) primary care.Setting and participantsThis is a longitudinal study using medical record data (2014–2016) from an OH care provider in Finland. In total, 59 676 patients were included and categorised into occasional and persistent FAs or non-FAs. Sick-leave episodes and their lengths were collected along with associated diagnostic codes. Logistic regression was used to analyse associations between FA status and sick leaves of different lengths (1–3, 4–14 and ≥15 days).ResultsBoth occasional and persistent FA had more and longer duration of sick leave than non-FA through the study years. Persistent FAs had consistently high absence rates. Occasional FAs had elevated absence rates even 2 years after their frequent attendance period. Persistent FAs (OR=11 95% CI 7.54 to 16.06 in 2016) and occasional FAs (OR=2.95 95% CI 2.50 to 3.49 in 2016) were associated with long (≥15 days) sickness absence when compared with non-FAs. Both groups of FAs had an increased risk of long-term sick leaves indicating a risk of disability pension.ConclusionBoth occasional and persistent FAs should be identified in primary care units caring for working-age patients. As frequent attendance is associated with long sickness absences and possibly disability pensions, rehabilitation should be directed at this group to prevent work disability.


2020 ◽  
Vol 0 (0) ◽  
Author(s):  
Thorsten Braun ◽  
Vivien Filleböck ◽  
Boris Metze ◽  
Christoph Bührer ◽  
Andreas Plagemann ◽  
...  

AbstractObjectivesTo compare the long-term effects of antenatal betamethasone (ANS, ≤16 mg, =24 mg and >24 mg) in twins on infant and childhood growth.MethodsA retrospective cohort follow up study among 198 twins after ANS including three time points: U1 first neonatal examination after birth and in the neonatal period; U7 examination from the 21st to the 24th month of life and U9 examination from the 60th to the 64th month of life using data from copies of the children’s examination booklets. Inclusion criteria are twin pregnancies with preterm labor, cervical shortening, preterm premature rupture of membranes, or vaginal bleeding, and exposure to ANS between 23+5 and 33+6 weeks. Outcome measures are dosage-dependent and sex-specific effects of ANS on growth (body weight, body length, head circumference, body mass index and ponderal index) up to 5.3 years.ResultsOverall, 99 live-born twin pairs were included. Negative effects of ANS on fetal growth persisted beyond birth, altered infant and childhood growth, independent of possible confounding factors. Overall weight percentile significantly decreased between infancy and early childhood by 18.8%. Birth weight percentiles significantly changed in a dose dependent and sex specific manner, most obviously in female-female and mixed pairs. The ponderal index significantly decreased up to 42.9%, BMI index increased by up to 33.8%.ConclusionsANS results in long-term alterations in infant and childhood growth. Changes between infancy and early childhood in ponderal mass index and BMI, independent of dose or twin pair structure, might indicate an ANS associated increased risk for later life disease.SynopsisFirst-time report on long-term ANS administration growth effects in twin pregnancies, showing persisting alterations beyond birth in infant and childhood growth up to 5.3 years as potential indicator of later life disease risk.


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
S Selvaraj ◽  
B.L Claggett ◽  
D.V Veldhuisen ◽  
I.S Anand ◽  
B Pieske ◽  
...  

Abstract Background Serum uric acid (SUA) is a biomarker of several pathobiologies relevant to the pathogenesis of heart failure with preserved ejection fraction (HFpEF), though by itself may also worsen outcomes. In HF with reduced EF, SUA is independently associated with adverse outcomes and sacubitril/valsartan reduces SUA compared to enalapril. These effects in HFpEF have not been delineated. Purpose To determine the prognostic value of SUA, relationship of change in SUA to quality of life and outcomes, and influence of sacubitril/valsartan on SUA in HFpEF. Methods We analyzed 4,795 participants from the Prospective Comparison of ARNI with ARB Global Outcomes in HF with Preserved Ejection Fraction (PARAGON-HF) trial. We related baseline hyperuricemia to the primary outcome (CV death and total HF hospitalization), its components, myocardial infarction or stroke, and a renal composite outcome. At the 4-month visit, the relationship between SUA change and Kansas City Cardiomyopathy Questionnaire overall summary score (KCCQ-OSS) and several biomarkers including N-terminal pro-B-type natriuretic peptide (NT-proBNP) were also assessed. We simultaneously adjusted for baseline and time-updated SUA to determine whether lowering SUA was associated with clinical benefit. Results Average age was 73±8 years and 52% were women. After multivariable adjustment, hyperuricemia was associated with increased risk for most outcomes (primary outcome HR 1.61, 95% CI 1.37, 1.90, Fig 1A). The treatment effect of sacubitril/valsartan for the primary outcome was not modified by baseline SUA (interaction p=0.11). Sacubitril/valsartan reduced SUA −0.38 mg/dL (95% CI: −0.45, −0.31) compared with valsartan (Fig 1B), with greater effect in those with baseline hyperuricemia (−0.50 mg/dL) (interaction p=0.013). Change in SUA was independently and inversely associated with change in KCCQ-OSS (p=0.019) and eGFR (p&lt;0.001), but not NT-proBNP (p=0.52). Time-updated SUA was a stronger predictor of adverse outcomes over baseline SUA. Conclusions SUA independently predicts adverse outcomes in HFpEF. Sacubitril/valsartan significantly reduces SUA compared to valsartan, an effect that was stronger in those with higher baseline SUA, and reducing SUA was associated with improved outcomes. Funding Acknowledgement Type of funding source: Private company. Main funding source(s): Novartis


Author(s):  
Menglin Jiang ◽  
Dandan Gong ◽  
Yu Fan

AbstractElevated serum uric acid (SUA) levels may increase the risk of prehypertension. However, the findings from these studies remain conflicting. The objective of this study was to determine the relationship between SUA levels and risk of prehypertension by conducting a meta-analysis. We conducted a comprehensive literature search of PubMed, Embase, China National Knowledge Infrastructure, VIP, and the Wangfang database without language restrictions through May 2015. Observational studies assessing the relationship between SUA levels and prevalence of prehypertension were included. Pooled adjust odds ratio (OR) and corresponding 95% confidence intervals (CI) of prehypertension were calculated for the highest vs. lowest SUA levels. Prehypertension was defined as systolic blood pressure (BP) ranging from 120 to 139 mmHg or diastolic BP ranging from 80 to 89 mmHg. Eight cross-sectional studies with a total of 21,832 prehypertensive individuals were included. Meta-analysis showed that elevated SUA levels were associated with increased risk of prehypertension (OR: 1.84; 95% CI: 1.42–2.38) comparing the highest vs. lowest level of SUA levels. Subgroup analyses showed that elevated SUA levels significantly increased the risk of prehypertension among men (OR: 1.60; 95% CI: 1.12–2.21) and women (OR: 1.59; 95% CI: 1.17–2.16). Elevated SUA levels are positively associated with the risk of prehypertension in the general population. However, more well-designed longitudinal studies are needed before a definitive conclusion can be drawn due to the cross-sectional studies included are susceptible to bias.


2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Shingo Nakayama ◽  
Michihiro Satoh ◽  
Takahisa Murakami ◽  
Yukako Tatsumi ◽  
Tomoko Muroya ◽  
...  

Abstract Background and Aims While previous studies have reported the association between serum uric acid (SUA) and chronic kidney disease (CKD) incidence, the sex differences in this association remain controversial. Therefore, we examined the association between SUA levels and CKD incidence in middle-aged adults stratified by sex using data from a large-scale health check-up. Method We analyzed information from the JMDC database, which included the annual health check-up data of Japanese employees and their dependents aged &lt;75 years. Among those individuals, we analyzed data from 138,511 individuals without CKD, kidney disease, or a history of cardiovascular disease at baseline. CKD was defined as an estimated glomerular filtration rate (eGFR) &lt;60 mL/min/1.73 m2 and/or proteinuria. We divided the participants into 9 and 7 groups according to SUA levels for men and women, respectively. A Cox model was applied to assess the adjusted hazard ratios (HRs) for CKD incidence in each SUA level group using an SUA concentration of 4.0–4.9 mg/dL as the reference after adjusting for age, body mass index, current or ex-smoker, current or ex-drinker, diabetes mellitus, dyslipidemia, systolic blood pressure, use of anti-hyperuricemic drugs, and baseline eGFR. Results The mean participant age was 44.1 years, and 29.6% were women. The mean SUA levels were 5.9 mg/dL and 4.1 mg/dL in men and women, respectively. During the mean follow-up period of 4.68 years, 12,589 participants developed CKD. The age-standardized incidence rates for CKD were 17.88/17.80 per 1000 person-years in men/women with SUA concentrations of 4.0–4.9 mg/dL, 209.76 per 1000 person-years in men with SUA ≥11.0 mg/dL, and 73.38 per 1000 person-years in women with SUA ≥ 9.0 mg/dL. The fully adjusted HRs (95% confidence interval [CI], P value) for CKD incidence in the groups with SUA concentrations of &lt;4.0, 10.0–10.9, and ≥11.0 mg/dL compared with those with SUA of 4.0–4.9 mg/dL among men were 1.13 (1.01–1.26, P=0.030), 1.98 (1.32–2.97, P=0.0010), and 3.74 (1.68–8.35, P=0.0013), respectively. In women, the fully adjusted HRs for CKD incidence in the groups with SUA concentrations of &lt;4.0, 8.0–8.9, and ≥9.0 mg/dL were 1.08 (1.01–1.16, P=0.032), 2.39 (1.07–5.35, P=0.034), and 3.20 (0.80–12.8, P=0.10), respectively. Similar results were observed when we performed the sensitivity analysis excluding 8,411 individuals with hypertensive treatment from the main analysis. The HRs for the outcomes caused by the onset of eGFR &lt;60 mL/min/1.73 m2 or proteinuria separately were similar to those for the main results. Conclusion The results of the present study demonstrated an increased risk of CKD in men with SUA concentrations of &lt;4.0 and ≥10.0 mg/dL and &lt;4.0 and ≥8.0 mg/dL in women compared to those with SUA concentrations of 4.0–4.9 mg/dL after adjusting for various covariates. Both high and low SUA levels were risk factors for CKD in middle-aged men and women. Hyperuricemia was demonstrated to cause renal injury due to the intraluminal deposition of uric acid crystals in the renal collecting duct. Hyperuricemia may also induce endothelial dysfunction, activation of the renin-angiotensin system, and induction of inflammation and stimulation of vascular smooth muscle cell proliferation by the induction of cyclooxygenase-2. However, as uric acid is one of the most important antioxidants in human plasma, low SUA levels may increase the risk of CKD incidence through decreased antioxidant activity. These mechanisms are implicated in the pathogenesis of CKD caused by high and low SUA levels. In addition, the SUA levels and ranges associated with increased risks of CKD incidence differed by sex.


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