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PURPOSE: Disparities in oral cavity and pharyngeal cancer based on race/ethnicity and socioeconomic status have been reported, but the impact of living within areas that are persistently poor at the time of diagnosis and outcome is unknown. This study aimed to investigate whether the incidence, 5-year relative survival, stage at diagnosis, and mortality among patients with oral cavity and pharyngeal cancers varied by persistent poverty. METHODS: Data were drawn from the SEER database (2006-2017) and included individuals diagnosed with oral cavity and pharyngeal cancers. Persistent poverty (at census tract) is defined as areas where ≥ 20% of the population has lived below the poverty level for ~ 30 years. Age-adjusted incidence and 5-year survival rates were calculated. Multivariable logistic regression was used to estimate the association between persistent poverty and advanced stage cancer. Cumulative incidence and multivariable subdistribution hazard models were used to evaluate mortality risk. In addition, results were stratified by cancer primary site, sex, race/ethnicity, and rurality. RESULTS: Of the 90,631 patients included in the analysis (61.7% < 65 years old, 71.6% males), 8.8% lived in persistent poverty. Compared to non-persistent poverty, patients in persistent poverty had higher incidence and lower 5-year survival rates. Throughout 10 years, the cumulative incidence of cancer death was greater in patients from persistent poverty and were more likely to present with advanced-stage cancer and higher mortality risk. In the stratified analysis by primary site, patients in persistent poverty with oropharyngeal, oral cavity, and nasopharyngeal cancers had an increased risk of mortality compared to the patients in non-persistent poverty. CONCLUSION: This study found an association between oral cavity and pharyngeal cancer outcomes among patients in persistent poverty indicating a multidimensional strategy to improve survival.
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Neoplasias de la Boca , Neoplasias Faríngeas , Pobreza , Programa de VERF , Humanos , Masculino , Femenino , Neoplasias Faríngeas/epidemiología , Neoplasias Faríngeas/mortalidad , Incidencia , Neoplasias de la Boca/epidemiología , Neoplasias de la Boca/mortalidad , Pobreza/estadística & datos numéricos , Persona de Mediana Edad , Anciano , Tasa de Supervivencia , Estados Unidos/epidemiología , Adulto , Disparidades en el Estado de SaludRESUMEN
BACKGROUND: Secondhand smoke (SHS) poses a significant public health threat. Cancer survivors are at a greater risk of adverse health outcomes from SHS because of its association with poor prognosis and other downstream clinical events. METHODS: A nationally representative sample of US adults aged 20 years and older was analyzed from the National Health and Nutrition Examination Survey between 2013 and 2020. Data on indoor SHS exposure were reported by 16,778 adults who were not currently smoking (1775 cancer survivors; 15,003 individuals without a cancer history). The weighted prevalence of SHS exposure was estimated and compared across sociodemographic and health-related characteristics. Multivariable logistic regression models were fitted to identify correlates of SHS exposure. RESULTS: Of the 1775 nonsmoking cancer survivors (mean age, 64.9 years; 57.0% female; 84.4% non-Hispanic Whites), 15.8% reported SHS exposure. No significant change in trends of SHS exposure was observed during the study period. The prevalence of SHS exposure was higher in cancer survivors who were younger, racial minorities, and had a household income below 130% of the federal poverty level. After adjustment for multiple correlates, age below 40 years, low income, smoking history, and diagnosis within 2 years were associated with SHS exposure. Cancer survivors were most likely to report that SHS exposure occurred at home or in a car. CONCLUSIONS: The prevalence of SHS exposure among cancer survivors remained steady in the past decade. However, disparities exist in SHS exposure among cancer survivors across sociodemographic characteristics and smoking status. Smoking cessation programs should be promoted among caregivers and families of cancer survivors.
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Supervivientes de Cáncer , Neoplasias , Cese del Hábito de Fumar , Contaminación por Humo de Tabaco , Adulto , Humanos , Femenino , Persona de Mediana Edad , Anciano , Masculino , Contaminación por Humo de Tabaco/efectos adversos , Encuestas Nutricionales , Pobreza , Exposición a Riesgos Ambientales/efectos adversos , Prevalencia , Neoplasias/epidemiología , Neoplasias/inducido químicamenteRESUMEN
Helicobacter pylori infection has been suggested to be associated with lung cancer risk. However, information is lacking on whether the association differs by H. pylori antigen. We conducted a nested case-control study within the Southern Community Cohort Study, including 295 incident lung cancer cases and 295 controls. Helicobacter pylori multiplex serology assay was performed to detect antibodies to 15 H. pylori proteins. Conditional logistic regression was used to estimate odds ratios (ORs) and confidence intervals (95% CIs) after adjustment for covariates. Overall H. pylori+ was associated with a non-statistically significant increased risk of lung cancer (OR: 1.29; 95% CI: 0.85-1.95). Significant associations, however, were observed for H. pylori+ VacA+ (OR: 1.64; 95% CI: 1.02-2.62) and H. pylori+ Catalase+ (OR: 1.75; 95% CI: 1.11-2.77). The positive association of H. pylori+ Catalase+ with lung cancer risk was predominantly seen among African Americans (OR: 2.09; 95% CI: 1.11-3.95) but not European Americans (OR: 1.20; 95% CI: 0.56-2.54). Among participants who smoked ≥ 30 pack-years, overall H. pylori+ (OR: 1.85; 95% CI: 1.02-3.35), H. pylori+ CagA+ (OR: 2.77; 95% CI: 1.35-5.70), H. pylori+ VacA+ (OR: 2.53; 95% CI: 1.25-5.13) and H. pylori+ HP1564+ (OR: 2.01; 95% CI: 1.07-3.77) were associated with increased risk of lung cancer. Our study provides novel evidence that associations of H. pylori infection with lung cancer risk differ by H. pylori biomarker, may be more evident among African Americans and may be modified by smoking habits. Furthermore, studies are warranted to confirm our findings.
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Infecciones por Helicobacter , Neoplasias Pulmonares , Antígenos Bacterianos , Proteínas Bacterianas , Biomarcadores , Estudios de Casos y Controles , Catalasa , Estudios de Cohortes , Infecciones por Helicobacter/complicaciones , Humanos , Neoplasias Pulmonares/epidemiología , Neoplasias Pulmonares/etiología , Factores de RiesgoRESUMEN
BACKGROUND AND AIMS: Studies have linked several metabolites to the risk of coronary heart disease (CHD) among Western populations, but prospective studies among Asian populations on the metabolite-CHD association remain limited. METHODS AND RESULTS: We evaluated the association of urinary metabolites with CHD risk among Chinese adults in a nested case-control study of 275 incident cases and 275 matched controls (127 pairs of men and 148 pairs of women). Fifty metabolites were measured by a predefined metabolomics panel and adjusted using urinary creatinine. Conditional logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (95% CIs). After adjusting for traditional CHD risk factors, urinary tryptophan showed a positive association with incident CHD: OR (95% CI) for the highest vs. lowest quartiles was 2.02 (1.15-3.56) among all study participants (p-trend = 0.02). The tryptophan-CHD association was more evident among individuals with dyslipidemia than among those without the condition (OR [95% CI] for the highest vs. lowest quartiles = 3.90 [1.86-8.19] and 0.74 [0.26-2.06], respectively; p-interaction<0.01). Other metabolites did not show significant associations with CHD risk among all study participants. However, a positive association of methionine with CHD risk was observed only among women (OR [95% CI] for the highest vs. lowest quartiles = 2.77 [1.17-6.58]; p-interaction = 0.03), and an inverse association of inosine with CHD risk was observed only among men (OR [95% CI] for the highest vs. lowest quartiles = 0.29 [0.11-0.81]; p-interaction = 0.04). CONCLUSION: Elevated urinary tryptophan may be related to CHD risk among Chinese adults, especially for those with dyslipidemia.
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Enfermedad Coronaria/orina , Triptófano/orina , Salud Urbana , Adulto , Anciano , Biomarcadores/orina , Estudios de Casos y Controles , China/epidemiología , Enfermedad Coronaria/diagnóstico , Enfermedad Coronaria/epidemiología , Femenino , Humanos , Incidencia , Masculino , Metabolómica , Persona de Mediana Edad , Proyectos Piloto , Prevalencia , Estudios Prospectivos , Medición de Riesgo , Factores de Riesgo , Regulación hacia ArribaRESUMEN
BACKGROUND: The incidence and mortality of gastric cancer have declined rapidly over the past few decades, but reverse trends in the young generation's differential between sexes in some races have been reported in recent years. To investigate whether this divergent trend can be observed in Korea, a country with the highest incidence in the world, age- and sex-specific incidence and mortality trends were evaluated. METHODS: Gastric cancer incidence data for the years 1999-2010 and mortality data for the years 1983-2012 were obtained from the Korea Central Cancer Registry and National Statistical Office. Annual percentage changes were calculated by age group (20-39, 40-54, 55-69, 70-79) using Joinpoint regression analysis. Furthermore, age-period-cohort analysis was evaluated. RESULTS: Overall age-standardized gastric cancer incidence in adults aged between 20 and 79 was declining at a nonsignificant average annual percentage change (AAPC) of -0.2 % in males and -0.4 % in females in Korea during 1999-2010. Mortality was steeper at a significant rate of -4.3 and -5.9 % in males and females, respectively. However, age-specific analysis revealed a flat (males 0.2 %, 95 % CI -0.5-0.6) or increasing incidence trend (females 1.7 %, 95 % CI 0.9-2.5) in the 40-54 age group. APC analysis confirmed the decreasing incidence and mortality trend mainly by the cohort effect. CONCLUSIONS: The differential pattern between males and females in different age groups suggests a possible effect of detection by screening practice or a signal of the change in epidemiological factors in the incidence and mortality of gastric cancer that warrants further studies.
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Neoplasias Gástricas/epidemiología , Adulto , Factores de Edad , Anciano , Estudios de Cohortes , Femenino , Humanos , Masculino , Persona de Mediana Edad , Análisis de Regresión , República de Corea/epidemiología , Factores Sexuales , Neoplasias Gástricas/mortalidad , Adulto JovenRESUMEN
BACKGROUND: To investigate whether preeclampsia is independently associated with risk of future metabolic syndrome and whether any such primary associations are modified by different ages at first pregnancy. METHODS: Based on the Health Examinees Study, a cross-sectional analysis was conducted. Data of women (n = 49 780) who had experienced at least 1 pregnancy during their lifetime and had never been diagnosed with any metabolic disorder before their pregnancy were analyzed using multiple logistic regression models. Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated after adjusting for age, lifestyle characteristics, and reproductive factors. A stratified analysis was also conducted to estimate the extent of the primary association between preeclampsia and future metabolic syndrome by age at first pregnancy. RESULTS: Women with a history of preeclampsia had significantly increased odds of developing metabolic syndrome (adjusted OR 1.23; 95% CI, 1.12-1.35), central obesity (adjusted OR 1.36; 95% CI, 1.25-1.47), elevated blood pressure (adjusted OR 1.53; 95% CI, 1.41-1.67), or elevated fasting glucose (adjusted OR 1.13; 95% CI, 1.03-1.25) in later life. In the stratified analysis, women who first became pregnant at ages >35 years and had preeclampsia were found to be at significantly increased likelihood of metabolic syndrome later in life (adjusted OR 4.38; 95% CI, 1.62-11.9). CONCLUSIONS: Our findings suggest that preeclampsia increases the risk of metabolic syndrome in later life, and late age at first pregnancy can further exacerbate this risk.
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Síndrome Metabólico/epidemiología , Preeclampsia/epidemiología , Adulto , Anciano , Estudios de Cohortes , Estudios Transversales , Femenino , Humanos , Edad Materna , Persona de Mediana Edad , Embarazo , República de Corea/epidemiología , RiesgoRESUMEN
OBJECTIVE: This study is a pilot study to assess the clinical outcomes of percutaneous disc decompression using the L'DISQ in patients with lumbar discogenic pain. STUDY DESIGN: An institutional, prospective clinical data analysis. METHODS: We ablated the torn annulus using L'DISQ on 20 patients with axial low back pain for at least 3 months (average 29 months) unresponsive to conservative management. Before the therapeutic procedure, all the patients had been diagnosed with lumbar discogenic pain through provocation discography, which had confirmed the level of painful discs. The torn annulus was identified through lumbosacral magnetic resonance image and computed tomographic discogram. Baseline data were prospectively gathered before the procedure and at 1, 4, 12, 24, and 48 weeks post-procedure. Data included pain intensity (visual analog scale [VAS]), measure of disability (Oswestry Disability Index [ODI] and Rolando-Morris Disability Questionnaire [RM]), and health-related quality of life (Bodily Pain Scale of Short Form-36 version 2 [SF-36 BP]). RESULTS: At 48 weeks, the VAS fell from 7.55 ± 1.28 to 3.60 ± 2.28 scores, the ODI and RM had decreased significantly, and the SF-36 BP showed significant improvement (P < 0.05). The success rates of procedure were 55.0% at 48 weeks. There were no complications with the exception of a minor venous bleeding at the site of needle puncture. CONCLUSIONS: The L'DISQ device is specifically designed to ablate adjacent disc tissue using a wand that can be navigated into a torn annulus. Following ablation, we measured clinically significant pain improvement and decreased disability for patients with axial low back pain.
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Descompresión Quirúrgica/instrumentación , Desplazamiento del Disco Intervertebral/cirugía , Adulto , Femenino , Humanos , Vértebras Lumbares , Masculino , Persona de Mediana Edad , Dimensión del Dolor , Proyectos Piloto , Adulto JovenRESUMEN
BACKGROUND: Physician-patient discussions regarding lung cancer screening (LCS) are uncommon and its racial and ethnic disparities are under-investigated. We examined the racial and ethnic disparities in the trends and frequency of LCS discussion among the LCS-eligible United States (US) population. METHODS: We analyzed data from the Health Information National Trends Survey from 2014 to 2020. LCS-eligible individuals were defined as adults aged 55 to 80 years old who have a current or former smoking history. We estimated the trends and frequency of LCS discussions and adjusted the probability of having an LCS discussion by racial and ethnic groups. RESULTS: Among 2136 LCS-eligible participants (representing 22.7 million US adults), 12.9% (95% CI, 10.9%-15%) reported discussing LCS with their providers in the past year. The frequency of LCS discussion was lowest among non-Hispanic White participants (12.3%, 95% CI, 9.9%-14.7%) compared to other racial and ethnic groups (14.1% in Hispanic to 15.3% in non-Hispanic Black). A significant increase over time was only observed among non-Hispanic Black participants (10.1% in 2014 to 22.1% in 2020; P = .05) and non-Hispanic Whites (8.5% in 2014 to 14% in 2020; P = .02). In adjusted analyses, non-Hispanic Black participants (14.6%, 95% CI, 12.3%-16.7%) had a significantly higher probability of LCS discussion than non-Hispanic Whites (12.1%, 95% CI, 11.4%-12.7%). CONCLUSION: Patient-provider LCS discussion was uncommon in the LCS-eligible US population. Non-Hispanic Black individuals were more likely to have LCS discussions than other racial and ethnic groups. There is a need for more research to clarify the discordance between LCS discussions and the actual screening uptake in this population.
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Etnicidad , Neoplasias Pulmonares , Anciano , Anciano de 80 o más Años , Humanos , Persona de Mediana Edad , Detección Precoz del Cáncer , Hispánicos o Latinos , Neoplasias Pulmonares/diagnóstico , Neoplasias Pulmonares/epidemiología , Estados Unidos/epidemiología , Negro o AfroamericanoRESUMEN
Iron is an essential nutrient required for various physiological processes in the body. However, iron imbalance can potentially contribute to initiating and promoting cancer development. Epidemiological studies have investigated the relationship between dietary iron intake and the risk of different types of cancer, yet, not all studies have consistently shown a significant association between dietary iron and cancer risk. Also, studies have shown different effects of dietary heme and non-heme iron intake on cancer risk. While some epidemiological studies suggest a possible link between high dietary iron (mainly heme-iron) intake and increased cancer risk, the evidence remains inconsistent. Moreover, multiple iron biomarkers, which can mirror physiological iron status, have demonstrated varied correlations with the risk of cancer, contingent upon the specific biomarker analyzed and the type of cancer being investigated. Here, we have investigated the current evidence on the potential relationship between dietary iron intake on one hand, and iron biomarkers on the other hand, with the risk of developing different types of cancer, including breast, prostate, lung, pancreatic, colon, colorectal, and liver cancers. Further research is warranted to better understand the complex relationship between dietary iron, physiological iron and cancer development. Future research should account for factors that affect and interact with dietary iron and physiological iron levels, such as genetic susceptibility, overall diet quality, and lifestyle habits.
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Iron plays a crucial role in many physiological processes, including oxygen transport, bioenergetics, and immune function. Iron is assimilated from food and also recycled from senescent red blood cells. Iron exists in two dietary forms: heme (animal based) and non-heme (mostly plant based). The body uses iron for metabolic purposes, and stores the excess mainly in splenic and hepatic macrophages. Physiologically, iron excretion in humans is inefficient and not highly regulated, so regulation of intestinal absorption maintains iron homeostasis. Iron losses occur at a steady rate via turnover of the intestinal epithelium, blood loss, and exfoliation of dead skin cells, but overall iron homeostasis is tightly controlled at cellular and systemic levels. Aging can have a profound impact on iron homeostasis and induce a dyshomeostasis where iron deficiency or overload (sometimes both simultaneously) can occur, potentially leading to several disorders and pathologies. To maintain physiologically balanced iron levels, reduce risk of disease, and promote healthy aging, it is advisable for older adults to follow recommended daily intake guidelines and periodically assess iron levels. Clinicians can evaluate body iron status using different techniques but selecting an assessment method primarily depends on the condition being examined. This review provides a comprehensive overview of the forms, sources, and metabolism of dietary iron, associated disorders of iron dyshomeostasis, assessment of iron levels in older adults, and nutritional guidelines and strategies to maintain iron balance in older adults.
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Homeostasis , Hierro de la Dieta , Hierro , Necesidades Nutricionales , Humanos , Homeostasis/fisiología , Anciano , Hierro de la Dieta/administración & dosificación , Hierro/metabolismo , Envejecimiento/fisiología , Estado Nutricional , Anemia Ferropénica/prevención & control , Deficiencias de Hierro , Sobrecarga de HierroRESUMEN
IMPORTANCE: Epidemiologic evidence regarding the outcomes of dietary sodium intake on mortality remains limited for low-income individuals, particularly Black people. OBJECTIVE: To investigate the associations of excessive dietary sodium with all-cause and cause-specific mortality among predominantly low-income Black and White Americans. DESIGN, SETTING, AND PARTICIPANTS: This cohort study included participants aged 40 to 79 years from the Southern Community Cohort Study who were recruited at Community Health Centers in 12 southeastern states from 2002 to 2009. Analyses were conducted between March 2022 and June 2023. EXPOSURES: Dietary sodium intake was assessed using a validated food frequency questionnaire at baseline. MAIN OUTCOMES AND MEASURES: Multivariable-adjusted Cox regression was used to estimate hazard ratios (HRs) and 95% CIs for mortality outcomes (all-cause, cardiovascular disease [CVD], coronary heart disease [CHD], stroke, heart failure, cancer, and other) associated with sodium intake. Nonlinear associations and population-attributable risk (PAR) of the mortality burden associated with excess sodium were further assessed. RESULTS: Among the 64â¯329 participants, 46â¯185 (71.8%) were Black, 18â¯144 (28.2%) were White, and 39â¯155 (60.9%) were female. The mean (SD) age at study enrollment was 51.3 (8.6) years for Black participants and 53.3 (9.3) years for White counterparts. Mean (SD) dietary sodium intake was 4512 (2632) mg/d in Black individuals and 4041 (2227) mg/d in White individuals; 37â¯482 Black individuals (81.2%) and 14â¯431 White individuals (79.5%) exceeded the current dietary recommendations of 2300 mg/d. During a median (IQR) follow-up of 13.8 (11.3-15.8) years, 17â¯811 deaths were documented, including 5701 from CVD. After adjustment for potential confounders, in Black individuals, HRs per 1000-mg increase in daily sodium intake were 1.07 (95% CI, 1.03-1.10) and 1.08 (95% CI, 1.02-1.14) for deaths from total CVD and CHD, respectively; while in White individuals, the corresponding HRs were 1.08 (95% CI, 1.02-1.14) and 1.13 (95% CI, 1.03-1.23). No significant associations were found for cancer mortality. PAR estimates suggest that sodium intake above the recommended threshold may account for 10% of total CVD, 13% of CHD, and 30% of heart failure deaths in this low-income southern population. CONCLUSIONS AND RELEVANCE: In this cohort study of 64â¯329 low-income Americans, nearly 80% of study participants consumed sodium exceeding the current recommended daily amount, which was associated with 10% to 30% of CVD mortality. Public health programs targeted to reduce sodium intake among this underserved population may be beneficial.
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Enfermedades Cardiovasculares , Insuficiencia Cardíaca , Neoplasias , Sodio en la Dieta , Femenino , Humanos , Masculino , Población Negra , Causas de Muerte , Estudios de Cohortes , Sodio , Sodio en la Dieta/efectos adversos , Blanco , Estados Unidos , Negro o Afroamericano , Adulto , Persona de Mediana Edad , AncianoRESUMEN
BACKGROUND: Despite the various anticancer activities of tocopherols, little is known about tocopherols associated with lung cancer risk among low-income African Americans (AA) and European Americans (EA) who are disproportionately affected by the disease. METHODS: We conducted a nested case-control study that included 209 incident lung cancer cases and 406 matched controls within the Southern Community Cohort Study. Using biospecimens collected at cohort enrollment, plasma levels of α-, ß/γ-, δ-, and total-tocopherols were measured by high-performance liquid chromatography with photodiode array detection. Conditional logistic regression was used to estimate ORs and 95% confidence intervals (CI) for lung cancer risk after adjusting for potential confounders. Stratified analyses were also conducted. RESULTS: Plasma levels of total-tocopherols were inversely associated with lung cancer risk overall [OR (95% CI) for the highest vs. lowest tertile = 0.51 (0.30-0.90)]. The inverse association remained significant among EAs [0.20 (0.06-0.65)], men [0.43 (0.21-0.90)], current smokers [0.49 (0.26-0.93)], and cases diagnosed within 2 years of blood draw [0.36 (0.15-0.86)], though we did not find a significant risk reduction among AAs [0.75 (0.39-1.45)]. Notably, we found significant interactions between α-tocopherol and race after controlling the FDR to correct for multiple comparisons (Pinteraction = 0.02). CONCLUSIONS: Our results indicate that plasma total-tocopherols are inversely associated with lung cancer risk, but the association may differ across specific isomeric forms of tocopherols, race, or other individuals' characteristics. Further large-scale studies are warranted to confirm our findings. IMPACT: Recommendations on tocopherols for lung cancer prevention should take isomers, race, and smoking behaviors into consideration.
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Neoplasias Pulmonares , Tocoferoles , Masculino , Humanos , Estudios de Cohortes , Neoplasias Pulmonares/epidemiología , Neoplasias Pulmonares/etiología , Estudios de Casos y Controles , Modelos Logísticos , Factores de RiesgoRESUMEN
OBJECTIVES: The association between long sleep duration and mortality is frequently attributed to the confounding influence of comorbidities. Nevertheless, past efforts to account for comorbidities have yielded inconsistent outcomes. The objective of this study was to evaluate this relationship using a large prospective cohort in Korea. METHODS: The study included 114 205 participants from the Health Examinees Study, who were followed for a median of 9.1 years. A composite comorbidity score was developed to summarize the effects of 21 diseases. Using Cox proportional hazards regression, hazard ratios (HRs) and 95% confidence intervals (CIs) for all-cause, cancer, and cardiovascular mortality associated with sleep duration were estimated. These estimates were adjusted for socio-demographic factors, lifestyle factors, body mass index, and comorbidity score. Additionally, a stratified analysis by subgroups with and without comorbidities was conducted. RESULTS: Throughout the follow-up period, 2675 deaths were recorded. After all adjustments, an association was observed between a sleep duration of 8 hours or more and all-cause mortality (HR, 1.10; 95% CI, 1.01 to 1.20). However, no such association was detected in the stratified analysis for the subgroups based on comorbidity status. CONCLUSIONS: Long sleep duration was found to be associated with all-cause mortality among Koreans, even after adjusting for comorbidities. Additional studies are required to explore the mechanism underlying the association between sleep duration and major causes of mortality.
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Duración del Sueño , Sueño , Humanos , Estudios Prospectivos , Comorbilidad , Modelos de Riesgos Proporcionales , República de Corea/epidemiología , Factores de RiesgoRESUMEN
Background: Allostatic load has been linked to an increased risk of death in various populations. However, to date, there is no research specifically investigating the effect of allostatic load on mortality in older cancer survivors. Aims: To investigate the association between allostatic load (AL) and mortality in older cancer survivors. Method: A total of 1,291 adults aged 60 years or older who survived for ≥1 year since cancer diagnoses were identified from the 1999-2010 National Health and Nutrition Examination Survey. AL was the exposure of interest incorporating 9 clinical measures/biomarkers; one point was added to AL if any of the measures/biomarkers exceeded the normal level. The sum of points was categorized as an ordinal variable to reflect low, moderate, and high AL. Our outcomes of interest were all-cause, cancer-specific, and cardiovascular disease (CVD)-specific mortality. Death was identified by linkage to the National Death Index. Multivariable Cox proportional hazards models were used to estimate adjusted hazard ratio (aHR) and 95% confidence intervals (CI) of mortality by AL category. Results: Overall, 53.6% of participants were male and 78.4% were white. The mean age of study participants at interview was 72.8 years (SD=7.1). A total of 546 participants died during the follow-up (median follow-up time: 8.0 years). Among them, 158 died of cancer and 106 died of cardiovascular events. Results from multivariable Cox proportional hazards models showed that higher ALS was positively associated with higher all-cause mortality (ALS=4-9 vs. ALS =0-1: aHR=1.52, 95% CI =1.17-1.98, p-trend<0.01) and higher cancer-specific mortality (ALS=4-9 vs. ALS =0-1: aHR=1.80, 95% CI =1.12-2.90, p-trend=0.01). The association between ALS and cardiovascular mortality was positive but non-significant (ALS=4-9 vs. ALS =0-1: aHR=1.59, 95% CI =0.86-2.94, p-trend=0.11). Conclusions: Our study suggests that older cancer survivors can have a higher risk of death if they have a high burden of AL.
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BACKGROUND: Head and neck cancer (HNC) mortality differs by race, ethnicity, and socioeconomic status (SES). However, it is unclear whether the relationship between race/ethnicity and HNC-specific mortality varies according to the residence-level SES. METHODS: Data from the Surveillance Epidemiology and End Results database included participants with primary HNC between 2006 and 2017 (followed through 2018) to assess the joint association of race/ethnicity and census-tract level SES Yost-index groups (quintiles) with all-cause and HNC-specific mortalities. Relative survival rates at 1, 5, and 10 years were calculated. Multivariable Cox proportional hazard regression models estimated hazard-ratios and 95% confidence intervals for all-cause mortality, and Fine-Gray subdistribution hazard models for HNC-specific mortality. Cumulative incidence curves for HNC-specific deaths were estimated. RESULTS: 76,095 patients were included in the analysis: 63.2% were <65 years, 73.4% male, and 11.3% non-Hispanic (NH) Black. Most patients (58.3%) were diagnosed at regional or distant stages and 20.6% died of HNC. The five-year relative survival rate increased with SES group, with 51.6% in the lowest SES group, and 74.1% in the highest SES group. NH-Black patients had higher risk of all-cause and HNC-specific mortality than NH-White patients, regardless of the SES group. NH-Asian/Pacific Islander and Hispanic patients had higher risk of HNC-specific mortality in some SES groups. CONCLUSIONS: NH-Black patients of all SES strata had significantly worse outcomes. Other factors, such as healthcare quality, may be associated with persistent disparities. IMPACT: The study highlights the persistence of significant racial disparities in HNC survival across socioeconomic categories. There is need to consider additional factors underlying these disparities.
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Etnicidad , Neoplasias de Cabeza y Cuello , Disparidades en el Estado de Salud , Factores Socioeconómicos , Femenino , Humanos , Masculino , Neoplasias de Cabeza y Cuello/etnología , Marco Interseccional , Programa de VERF , Clase Social , Grupos Raciales , Negro o AfroamericanoRESUMEN
Purpose: Small cell lung cancer (SCLC) is a highly fatal disease, but its treatment has remained relatively unchanged for decades. Randomized clinical trials evaluating radiation therapy (RT) dosing and fractionation have yielded mixed results on overall survival (OS). Methods and Materials: We identified 2261 patients with limited-stage (LS) SCLC undergoing definitive RT at 1.5, 1.8, and 2.0 Gy dose per fraction, concurrently with chemotherapy, between 2004 and 2015 within the National Cancer Database. Overall survival (OS) was evaluated using the Kaplan-Meier method, and Cox proportional hazards regression was used to investigate whether there was any survival difference among patients who received hyperfractionated, twice-daily RT at 1.5 Gy per fraction (HF1.5) and once-daily, standard fractionation RT at 1.8 Gy (SF1.8) or 2.0 Gy (SF2.0) per fraction. Subgroup analyses by age, sex, race, time to RT, facility type, and Charlson comorbidity index were also performed. Results: All stage median OS rates for HF1.5, SF1.8, and SF2.0 Gy groups were 21.6, 18.9, and 19.4 months, respectively (log-rank P = .0079). Multivariate analyses adjusting for demographic factors, socioeconomic status, tumor characteristics, and year of diagnosis showed SF1.8 (hazard ratio [HR] = 1.30, 1.03-1.63) and SF2.0 (HR = 1.20, 1.00-1.45) was associated with worse 1-year survival compared with HF1.5. This association was more evident in stage IIb-stage III than stage I to stage IIa patients. Propensity score-weighted analysis showed similar results. Stratified analyses showed the significant associations were confined to male or black patients, those aged >65 years, with 1 comorbidity, who had waited >60 days to start RT or were treated at an academic medical center. Conclusions: Analyses of real-world treatment outcome data showed that receiving hyperfractionated, twice-daily RT was associated with improved survival among patients with LS-SCLC compared with standard, once-daily fractionation regimens at 1 year after diagnosis, particularly for subsets of patients. Some associations retained statistical significance 3 years postdiagnosis.
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INTRODUCTION: Mutations of the TP53 gene lead to the production of autoantibodies against p53, a major tumor suppressor protein. Although studies have indicated the association of p53 autoantibodies with human cancers, epidemiologic evidence on lung cancer is still lacking. METHODS: In this nested case-control study conducted within the Southern Community Cohort Study, we investigated the association of circulating p53 autoantibodies with the subsequent risk of developing lung cancer. Using blood samples collected prior to any cancer diagnosis from 295 cases and their individually matched controls, seroreactivity to p53 was assessed by fluorescent bead-based multiplex serology. Conditional logistic regression models were used to estimate odds ratios (OR) and 95 % confidence intervals (CI) for lung cancer risk associated with p53 autoantibodies. RESULTS: After adjustment for potential confounders, p53 seropositivity was significantly associated with an increased risk of lung cancer (OR=2.98, 95 % CI: 1.10-8.06) among African Americans, but not among European Americans (OR=1.21, 95 % CI: 0.24-6.15). The positive associations were restricted to men (OR=4.59, 95 % CI: 1.30-16.16) and participants with a short interval (≤ 4 years) from blood collection to diagnosis (OR=4.30, 95 % CI: 1.33-13.89). CONCLUSION: Our findings add to the evidence supporting p53 autoantibodies as a biomarker of lung cancer.
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Background: Previous studies conducted among European and Asian decedents reported inverse associations of serum total bilirubin and albumin with lung cancer risk. Yet, no study has been conducted among African Americans or low-income European Americans. Methods: This study included 522 incident lung cancer cases and 979 matched controls nested in the Southern Community Cohort Study, a cohort of predominantly low-income African and European Americans. Serum levels of total bilirubin and albumin, collected up to 11 years prior to case diagnoses, were measured by a clinical chemistry analyzer. Conditional logistic regression models were applied to evaluate the associations of total bilirubin and albumin with lung cancer risk. Results: Overall, serum levels of total bilirubin (ORT3 vs. T1 = 0.96, 95% CI: 0.66-1.39) were not significantly associated with lung cancer risk. However, higher levels of serum total bilirubin were significantly associated with decreased risk of lung cancer among participants who were diagnosed within two years following sample collection (ORT3 vs. T1 = 0.36, 95% CI: 0.15-0.87) and among former/never smokers (ORT3 vs. T1 = 0.54, 95% CI: 0.32-0.93). Serum levels of albumin were significantly associated with decreased risk of lung cancer overall (ORT3 vs. T1 = 0.70, 95% CI: 0.50-0.98) and among African Americans (ORT3 vs. T1 = 0.62, 95% CI: 0.41-0.96), but not among European Americans. Conclusion: Our results indicate that in a low-income African American and European American population, serum levels of total bilirubin may be related to lung cancer progression and differ by smoking status. Meanwhile, the association of serum albumin levels with lung cancer risk may differ by race. Further studies are warranted to confirm these results.
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Observational studies found inverse associations of dietary carotenoids and vitamin A intakes with lung cancer risk. However, interventional trials among high-risk individuals showed that ß-carotene supplements increased lung cancer risk. Most of the previous studies were conducted among European descendants or Asians. We prospectively examined the associations of lung cancer risk with dietary intakes of carotenoids and vitamin A in the Southern Community Cohort Study, including 65,550 participants with 1204 incident lung cancer cases. Multivariate Cox regression was used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs). Lung cancer cases had lower energy-adjusted dietary intakes of all carotenoids and vitamin A than non-cases. However, dietary intakes of carotenoids and vitamin A were not associated with overall lung cancer risk. A significant positive association of dietary vitamin A intake with lung cancer risk was observed among current smokers (HRQ4 vs. Q1 = 1.23; 95% CI: 1.02-1.49; Ptrend = 0.01). In addition, vitamin A intake was associated with an increased risk of adenocarcinoma among African Americans (HRQ4 vs. Q1 = 1.55; 95%CI: 1.08-2.21; Ptrend = 0.03). Dietary lycopene intake was associated with an increased risk of lung cancer among former smokers (HRQ4 vs. Q1 = 1.50; 95% CI: 1.04-2.17; Ptrend = 0.03). There are positive associations of dietary ß-cryptoxanthin intake with squamous carcinoma risk (HRQ4 vs. Q1 = 1.49; 95% CI: 1.03-2.15; Ptrend = 0.03). Further studies are warranted to confirm our findings.
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Epidemiological evidence on tooth loss and lung cancer risk remains limited, especially for smoking-specific associations. To investigate the association between tooth loss and lung cancer risk by smoking status, we first analyzed data from the Shanghai Men's Health Study (n = 49,868) and the Shanghai Women's Health Study (n = 44,309). Cox regression models were applied to estimate the hazard ratios (HRs) and 95% confidence intervals (CIs) for lung cancer risk in relation to tooth loss. We also conducted a meta-analysis to summarize epidemiologic findings to date, incorporating results from the current study and six previously published studies. For 7.3 median follow-up years, 973 incident lung cancer cases (613 men and 360 women) were ascertained. After adjustment for major covariates, tooth loss was associated with an increased risk of lung cancer among men (HR [95% CI] for >10 teeth vs. none = 1.59 [1.21−2.11]) but not among women (0.86 [0.50−1.46]). The positive association was stronger among male current smokers (1.75 [1.26−2.45], p-interaction by smoking status = 0.04). In a meta-analysis incorporating 4052 lung cancer cases and 248,126 non-cases, tooth loss was associated with a 1.64-fold increased risk of developing lung cancer (relative risk [RR, 95% CI] for the uppermost with the lowest category = 1.64 [1.44−1.86]). The positive association was more evident among current smokers (1.86 [1.41−2.46]), but no significant associations were found among never or former smokers. Our findings suggest that tooth loss may be associated with an increased risk of lung cancer, and the association could be modified by smoking status.