| 1. |
- Crump, Casey, et al.
(författare)
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Aerobic fitness, muscular strength and obesity in relation to risk of heart failure
- 2017
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Ingår i: Heart. - : BMJ. - 1355-6037 .- 1468-201X. ; 103:22, s. 1780-1787
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Tidskriftsartikel (refereegranskat)abstract
- Objective Low physical fitness and obesity have been associated with higher risk of developing heart failure (HF), but their interactive effects are unknown. Elucidation of interactions among these common modifiable factors may help facilitate more effective primary prevention. Methods We conducted a national cohort study to examine the interactive effects of aerobic fitness, muscular strength and body mass index (BMI) among 1 330 610 military conscripts in Sweden during 1969-1997 (97%-98% of all 18-year-old men) on risk of HF identified from inpatient and outpatient diagnoses through 2012 (maximum age 62 years). Results There were 11 711 men diagnosed with HF in 37.8 million person-years of follow-up. Low aerobic fitness, low muscular strength and obesity were independently associated with higher risk of HF, after adjusting for each other, socioeconomic factors, other chronic diseases and family history of HF. The combination of low aerobic fitness and low muscular strength (lowest vs highest tertiles) was associated with a 1.7-fold risk of HF (95% CI 1.6 to 1.9; p<0.001; incidence rates per 100 000 person-years, 43.2 vs 10.8). These factors had positive additive and multiplicative interactions (p<0.001) and were associated with increased risk of HF even among men with normal BMI. Conclusions Low aerobic fitness, low muscular strength and obesity at the age of 18 years were independently associated with higher risk of HF in adulthood, with interactive effects between aerobic fitness and muscular strength. These findings suggest that early-life interventions may help reduce the long-term risk of HF and should include both aerobic fitness and muscular strength, even among persons with normal BMI.
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| 2. |
- Crump, Casey, et al.
(författare)
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Cardiorespiratory fitness and long-term risk of sleep apnea : A national cohort study
- 2019
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Ingår i: Journal of Sleep Research. - : Wiley. - 0962-1105 .- 1365-2869. ; 28:6
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Tidskriftsartikel (refereegranskat)abstract
- Sleep apnea is increasing in prevalence, and is an important cause of cardiometabolic diseases and mortality worldwide. Its only established modifiable risk factor is obesity; however, up to half of all sleep apnea cases may occur in non-obese persons, and hence there is a pressing need to identify other modifiable risk factors to facilitate more effective prevention. We sought to examine, for the first time, cardiorespiratory fitness in relation to the risk of sleep apnea, independent of obesity. A national cohort study was conducted to examine cardiorespiratory fitness in all 1,547,478 Swedish military conscripts during 1969–1997 (97%–98% of all 18-year-old men) in relation to risk of sleep apnea through 2012 (maximum age 62 years). Cardiorespiratory fitness was measured as maximal aerobic workload in Watts, and sleep apnea was identified from nationwide outpatient and inpatient diagnoses. A total of 44,612 (2.9%) men were diagnosed with sleep apnea in 43.7 million person-years of follow-up. Adjusting for age, height, weight, socioeconomic factors and family history of sleep apnea, low cardiorespiratory fitness at age 18 years was associated with a significantly increased risk of sleep apnea in adulthood (lowest versus highest cardiorespiratory fitness tertile: incidence rate ratio, 1.44; 95% confidence interval, 1.40–1.49; p < 0.001; continuous cardiorespiratory fitness per 100 Watts: incidence rate ratio, 0.71; 95% confidence interval, 0.70–0.73; p < 0.001). An increased risk was observed even among men with normal body mass index (lowest versus highest cardiorespiratory fitness tertile: incidence rate ratio, 1.30; 95% confidence interval, 1.26–1.35; p < 0.001). These findings identify low cardiorespiratory fitness early in life as a new modifiable risk factor for development of sleep apnea in adulthood.
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| 3. |
- Crump, Casey, et al.
(författare)
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Comorbidities and Mortality in Bipolar Disorder A Swedish National Cohort Study
- 2013
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Ingår i: JAMA Psychiatry. - : American Medical Association (AMA). - 2168-6238 .- 2168-622X. ; 70:9, s. 931-939
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Tidskriftsartikel (refereegranskat)abstract
- IMPORTANCE Bipolar disorder is associated with premature mortality, but the specific causes and underlying pathways are unclear. OBJECTIVE To examine the physical health effects of bipolar disorder using outpatient and inpatient data for a national population. DESIGN, SETTING, AND PARTICIPANTS National cohort study of 6 587 036 Swedish adults, including 6618 with bipolar disorder. MAIN OUTCOMES AND MEASURES Physical comorbidities diagnosed in any outpatient or inpatient setting nationwide and mortality (January 1, 2003, through December 31, 2009). RESULTS Women and men with bipolar disorder died 9.0 and 8.5 years earlier on average than the rest of the population, respectively. All-cause mortality was increased 2-fold among women (adjusted hazard ratio [aHR], 2.34; 95% CI, 2.16-2.53) and men (aHR, 2.03; 95% CI, 1.85-2.23) with bipolar disorder, compared with the rest of the population. Patients with bipolar disorder had increased mortality from cardiovascular disease, diabetes mellitus, chronic obstructive pulmonary disease (COPD), influenza or pneumonia, unintentional injuries, and suicide for both women and men and cancer for women only. Suicide risk was 10-fold among women (aHR, 10.37; 95% CI, 7.36-14.60) and 8-fold among men (aHR, 8.09; 95% CI, 5.98-10.95) with bipolar disorder, compared with the rest of the population. Substance use disorders contributed only modestly to these findings. The association between bipolar disorder and mortality from chronic diseases (ischemic heart disease, diabetes, COPD, or cancer) was weaker among persons with a prior diagnosis of these conditions (aHR, 1.40; 95% CI, 1.26-1.56) than among those without a prior diagnosis (aHR, 2.38; 95% CI, 1.95-2.90; P-interaction = .01). CONCLUSIONS AND RELEVANCE In this large national cohort study, patients with bipolar disorder died prematurely from multiple causes, including cardiovascular disease, diabetes, COPD, influenza or pneumonia, unintentional injuries, and suicide. However, chronic disease mortality among those with more timely medical diagnosis approached that of the general population, suggesting that better provision of primary medical care may effectively reduce premature mortality among persons with bipolar disorder.
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| 4. |
- Crump, Casey, et al.
(författare)
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Comorbidities and Mortality in Persons With Schizophrenia: A Swedish National Cohort Study
- 2013
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Ingår i: American Journal of Psychiatry. - : American Psychiatric Association Publishing. - 1535-7228 .- 0002-953X. ; 170:3, s. 324-333
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Tidskriftsartikel (refereegranskat)abstract
- Objective: Schizophrenia is associated with premature mortality, but the specific causes and pathways are unclear. The authors used outpatient and inpatient data for a national population to examine the association between schizophrenia and mortality and comorbidities. Method: This was a national cohort study of 6,097,834 Swedish adults, including 8,277 with schizophrenia, followed for 7 years (2003-2009) for mortality and comorbidities diagnosed in any outpatient or inpatient setting nationwide. Results: On average, men with schizophrenia died 15 years earlier, and women 12 years earlier, than the rest of the population, and this was not accounted for by unnatural deaths. The leading causes were ischemic heart disease and cancer. Despite having twice as many health care system contacts, schizophrenia patients had no increased risk of nonfatal ischemic heart disease or cancer diagnoses, but they had an elevated mortality from ischemic heart disease (adjusted hazard ratio for women, 3.33 [95% CI=2.73-4.05]; for men, 2.20 [95%, CI=1.83-2.65]) and cancer (adjusted hazard ratio for women, 1.71 [95% CI=1.38-2.10; for men, 1.44 [95% CI=1.15-1.80]). Among all people who died from ischemic heart disease or cancer, schizophrenia patients Were less likely than others to have been diagnosed previously with these conditions (for ischemic heart disease, 26.3% compared with 43.7%; for cancer, 73.9% compared with 82.3%). The association between schizophrenia and mortality was stronger among women and the employed. Lack of antipsychotic treatment was also associated with elevated mortality.. Conclusions: Schizophrenia patients had markedly premature mortality, and the leading causes were ischemic heart disease and cancer, which appeared to be under-diagnosed. Preventive interventions should prioritize primary health care tailored to this population, including more effective risk modification and screening for cardiovascular disease and cancer. (Am J Psychiatty 2013; 170:324-333)
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| 5. |
- Crump, Casey, et al.
(författare)
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Exercise is medicine : Primary care counseling on aerobic fitness and muscle strengthening
- 2019
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Ingår i: Journal of the American Board of Family Medicine. - : American Board of Family Medicine (ABFM). - 1557-2625 .- 1558-7118. ; 32:1, s. 103-107
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Tidskriftsartikel (refereegranskat)abstract
- Patient counseling on physical fitness remains underutilized in primary care, despite its clinical and cost effectiveness. Most counseling interventions have focused on aerobic activity and neglected another vital component of physical fitness, muscle strengthening, which has recently been shown to be independently protective against cardiometabolic diseases and premature mortality. This article reviews the latest scientific evidence and makes recommendations toward a more comprehensive approach for promoting physical fitness in primary care. Given the high prevalence and wide-ranging health impacts of physical inactivity, counseling on physical fitness should be a standard part of wellness promotion and disease prevention and treatment for all patients. Interventions that include muscle strengthening will have a significantly greater impact on health outcomes than those focused on aerobic fitness alone. Counseling to promote both aerobic fitness and muscle strengthening is indicated for all patients, irrespective of body weight, and should begin early in life and continue across the life course.
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| 6. |
- Crump, Casey, et al.
(författare)
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Fetal growth and subsequent maternal risk of thyroid cancer.
- 2016
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Ingår i: International Journal of Cancer. - : Wiley. - 0020-7136. ; 138:5, s. 1085-1093
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Tidskriftsartikel (refereegranskat)abstract
- Thyroid cancer has peak incidence among women of reproductive age, and growth factors, which have procarcinogenic properties, may play an important etiologic role. However, the association between fetal growth rate during a woman's pregnancy and her subsequent risk of thyroid cancer has not been previously examined. We conducted a national cohort study of 1,837,634 mothers who had a total of 3,588,497 live-births in Sweden in 1973-2008, followed up for thyroid cancer incidence through 2009. There were 2,202 mothers subsequently diagnosed with thyroid cancer in 36.8 million person-years of follow-up. After adjusting for maternal age, height, weight, smoking, and sociodemographic factors, high fetal growth (birth weight standardized for gestational age and sex) was associated with a subsequent increased risk of thyroid cancer in the mother (incidence rate ratio [IRR] per additional 1 standard deviation, 1.05; 95% CI, 1.01-1.09; P=0.02). Each 1,000 g increase in the infant's birth weight was associated with a 13% increase in the mother's subsequent risk of thyroid cancer (IRR, 1.13; 95% CI, 1.05-1.22; P=0.001). These findings appeared to involve both papillary and follicular subtypes, and did not vary significantly by the mother's height, weight, or smoking status. In this large national cohort study, high fetal growth during a woman's pregnancy was independently associated with a subsequent increased risk of her developing thyroid cancer. If confirmed, these findings suggest an important role of maternal growth factors in the development of thyroid cancer, and potentially may help facilitate the identification of high-risk subgroups of women. This article is protected by copyright. All rights reserved. © 2014 Wiley Periodicals, Inc.
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| 7. |
- Crump, Casey, et al.
(författare)
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Gestational age at birth and mortality from infancy into mid-adulthood : a national cohort study
- 2019
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Ingår i: The Lancet Child and Adolescent Health. - 2352-4642. ; 3:6, s. 408-417
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Tidskriftsartikel (refereegranskat)abstract
- Background: Breakthroughs in the treatment of preterm birth approximately 40 years ago have enabled a generation of preterm survivors to now reach mid-adulthood. Understanding their health sequelae is essential for guiding their long-term care. We did a study to examine preterm birth in relation to mortality into mid-adulthood. Methods: A national cohort study was done of all 4 296 814 singleton livebirths in Sweden between 1973 and 2015, who were followed up for mortality through Dec 31, 2017 (maximum age 45 years). Cox regression was used to examine gestational age at birth in relation to all-cause and cause-specific mortality, and cosibling analyses assessed for potential confounding by shared familial (genetic or environmental)factors. Findings: In 103·5 million person-years of follow-up, 43 916 (1·0%)deaths were reported. Gestational age at birth was inversely associated with mortality from infancy to mid-adulthood. Relative to full-term birth (39–41 weeks), the adjusted hazard ratios for mortality associated with gestational age at birth were: 66·14 (95% CI 63·09–69·34)for extremely preterm (22–27 weeks), 8·67 (8·32–9·03)for very preterm (28–33 weeks), 2·61 (2·52–2·71)for late preterm (34–36 weeks), and 1·34 (1·30–1·37)for early term (37–38 weeks), from birth to age 45 years; and 2·04 (0·92–4·55)for extremely preterm, 1·48 (1·17–1·87)for very preterm, 1·22 (1·07–1·39)for late preterm, and 1·16 (1·08–1·25)for early term, at ages 30–45 years. Preterm birth accounted for more deaths among males than females (additive interaction p<0·001). Multiple underlying causes were identified, including congenital anomalies; respiratory, endocrine, cardiovascular, and neurological diseases; cancer; and external causes. Cosibling analyses suggested that the observed associations were not due to shared genetic or environmental factors in families. Interpretation: Preterm and early term birth should be recognised as chronic conditions that require long-term follow-up for adverse health sequelae in adulthood. Funding: National Heart, Lung, and Blood Institute at the National Institutes of Health.
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| 8. |
- Crump, Casey, et al.
(författare)
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Gestational Age at Birth and Mortality in Young Adulthood
- 2011
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Ingår i: JAMA: The Journal of the American Medical Association. - : American Medical Association (AMA). - 1538-3598. ; 306:11, s. 1233-1240
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Tidskriftsartikel (refereegranskat)abstract
- Context Preterm birth is the leading cause of infant mortality in developed countries, but the association between gestational age at birth and mortality in adulthood remains unknown. Objective To examine the association between gestational age at birth and mortality in young adulthood. Design, Setting, and Participants National cohort study of 674 820 individuals born as singletons in Sweden in 1973 through 1979 who survived to age 1 year, including 27 979 born preterm (gestational age <37 weeks), followed up to 2008 (ages 29-36 years). Main Outcome Measures All-cause and cause-specific mortality. Results A total of 7095 deaths occurred in 20.8 million person-years of follow-up. Among individuals still alive at the beginning of each age range, a strong inverse association was found between gestational age at birth and mortality in early childhood (ages 1-5 years: adjusted hazard ratio [aHR] for each additional week of gestation, 0.92; 95% CI, 0.89-0.94; P<.001), which disappeared in late childhood (ages 6-12 years: aHR, 0.99; 95% CI, 0.95-1.03; P=.61) and adolescence (ages 13-17 years: aHR, 0.99; 95% CI, 0.95-1.03; P=.64) and then reappeared in young adulthood (ages 18-36 years: aHR, 0.96; 95% CI, 0.94-0.97; P<.001). In young adulthood, mortality rates (per 1000 person-years) by gestational age at birth were 0.94 for 22 to 27 weeks, 0.86 for 28 to 33 weeks, 0.65 for 34 to 36 weeks, 0.46 for 37 to 42 weeks (full-term), and 0.54 for 43 or more weeks. Preterm birth was associated with increased mortality in young adulthood even among individuals born late preterm (34-36 weeks, aHR, 1.31; 95% CI, 1.13-1.50; P<.001), relative to those born full-term. In young adulthood, gestational age at birth had the strongest inverse association with mortality from congenital anomalies and respiratory, endocrine, and cardiovascular disorders and was not associated with mortality from neurological disorders, cancer, or injury. Conclusion After excluding earlier deaths, low gestational age at birth was independently associated with increased mortality in early childhood and young adulthood. JAMA. 2011;306(11):1233-1240 www.jama.com
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| 9. |
- Crump, Casey, et al.
(författare)
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Gestational Age at Birth and Mortality in Young Adulthood EDITORIAL COMMENT
- 2012
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Ingår i: Obstetrical and Gynecological Survey. - 0029-7828. ; 67:1, s. 12-13
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- Preterm birth is associated with increased rates of neonatal and infant mortality. It has been hypothesized that gestational age at birth may also be associated with increased mortality rates in adulthood, but to date, no studies have demonstrated this relationship. This national cohort study investigated the association between gestational age at birth and mortality in young adulthood. Data obtained from the Swedish Birth Registry identified 678,528 individuals who were born as singletons between 1973 and 1979 and survived to age 1 year. Among this cohort, 674,820 were included in the final analysis. Of these, 27,979 (4.1%) born preterm (<37 weeks) were followed to age 29 to 36 years (up to 2008). The primary study outcome measures were all-cause and cause-specific mortality. Cox proportional hazards regression was used to estimate the association between gestational age at birth and mortality for 4 age categories: early childhood (age, 1-5 years), late childhood (age, 6-12 years), adolescence (age, 13-17 years), and young adulthood (age, 18-36 years). There were 7095 deaths reported in 20.8 million person-years of follow-up. A strong inverse association was found between gestational age at birth for 2 of the age categories and mortality among individuals still alive at the beginning of each age range. The adjusted hazard ratio [aHR] for each additional week of gestation in early childhood was 0.92 (95% confidence interval [CI], 0.89-0.94; P < 0.001). This inverse association disappeared in late childhood (aHR, 0.99; 95% CI, 0.95-1.03; P = 0.61) and adolescence (aHR, 0.99; 95% CI, 0.95-1.03; P = 0.64), and reappeared in young adulthood (aHR, 0.96; 95% CI, 0.94-0.97; P < 0.001). In young adulthood, the gestational age at birth was associated with mortality rates (per 1000 person-years) as follows: the aHR was 0.94 for 22 to 27 weeks, 0.86 for 28 to 33 weeks, 0.65 for 34 to 36 weeks, 0.46 for 37 to 42 weeks (full-term), and 0.54 for 43 or more weeks (P < 0.001 for all). Relative to individuals born full-term, preterm birth was associated with increased mortality in young adulthood even among individuals born late preterm (34-36 weeks); the aHR was 1.31, with a 95% CI of 1.13-1.50; P < 0.001). Moreover, gestational age at birth in young adulthood had the strongest inverse association with mortality from congenital anomalies, as well as respiratory, endocrine, and cardiovascular disorders, and it had no association with mortality from neurological disorders, cancer, or injury.
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| 10. |
- Crump, Casey, et al.
(författare)
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Gestational age at birth and risk of allergic rhinitis in young adulthood
- 2011
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Ingår i: Journal of Allergy and Clinical Immunology. - : Elsevier BV. - 1097-6825 .- 0091-6749. ; 127:5, s. 1173-1179
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Tidskriftsartikel (refereegranskat)abstract
- Background: Previous studies of the association between gestational age or birth weight and allergic rhinitis in later life have had various limitations, including the inability to estimate risk among subjects born extremely preterm or to examine specific contributions of gestational age and fetal growth. Objective: We sought to determine whether gestational age at birth independent of fetal growth is associated with allergic rhinitis medication prescription in a national cohort of young adults. Methods: We conducted a national cohort study of 630,090 infants born in Sweden from 1973 through 1979 including 27,953 born preterm (<37 weeks) and followed for prescription of nasal corticosteroids and oral antihistamines in 2005-2009 (age, 25.5-37.0 years). Medication data were obtained from all outpatient and inpatient pharmacies throughout Sweden. Results: The overall prevalence of nasal corticosteroid and oral antihistamine prescription was 16.3% and 16.8%, respectively, which is similar to the reported prevalence of allergic rhinitis in this population. Low gestational age at birth was associated with a decreased risk of nasal corticosteroid and oral antihistamine prescription in young adulthood after adjusting for fetal growth and other potential confounders. For subjects born extremely preterm (23-28 weeks), adjusted odds ratios were 0.70 (95% CI, 0.51-0.96) for nasal corticosteroid prescription and 0.45 (95% CI, 0.27-0.76) for both nasal corticosteroid and oral antihistamine prescription relative to those born at full term. Conclusion: These findings suggest that low gestational age at birth independent of fetal growth is associated with a decreased risk of allergic rhinitis in young adulthood, possibly because of a protective effect of earlier exposure to pathogens. (J Allergy Clin Immunol 2011;127:1173-9.)
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