scholarly journals Dietary Intake of Tomato and Lycopene and Risk of All-Cause and Cause-Specific Mortality: Results From a Prospective Study

2021 ◽  
Vol 8 ◽  
Author(s):  
Xin Xu ◽  
Shiqi Li ◽  
Yi Zhu

Evidence on the relationship between consumption of tomato or lycopene and mortality is limited. We investigated the associations of raw tomato, tomato catsup or lycopene intake with all-cause and cause-specific mortality using data from the Prostate, Lung, Colorectal, and Ovarian (PLCO) screening trial. A multivariate Cox proportional hazards model was used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs). During a total of 1,672,715 follow-up years, 24,141 all-cause deaths, 7,534 cardiovascular disease (CVD) deaths and 7,161 cancer deaths occurred. Total mortality was statistically significantly inversely associated with intake of raw tomato (Q5 vs. Q1; HR, 0.95 [95% CI, 0.91–0.99]), tomato catsup (Q5 vs. Q1; HR, 0.93 [95% CI, 0.89–0.97]), and moderate lycopene (Q4 vs. Q1; HR, 0.88 [95% CI, 0.85–0.93]). CVD mortality was significantly inversely related with intake of moderate raw tomato (Q4 vs. Q1; HR, 0.90 [95% CI, 0.83–0.97]), tomato catsup (Q5 vs. Q1; HR, 0.92 [95% CI, 0.85–0.99]), and moderate lycopene (Q4 vs. Q1; HR, 0.90 [95% CI, 0.83–0.98]). Dietary intake of raw tomato (Q5 vs. Q1; HR, 1.04 [95% CI, 0.96–1.14]) and tomato catsup (Q5 vs. Q1; HR, 1.00 [95% CI, 0.93–1.08]) were not related with cancer mortality. Moderate dietary intake of lycopene was significantly associated with a lower cancer mortality (Q4 vs. Q1; HR, 0.89 [95% CI, 0.82–0.96]). There was a non-linear J-shaped association between consumption of raw tomato, tomato catsup or lycopene and total mortality (P for non-linearity <0.001). In conclusion, in this large nationally representative sample of US adult population, tomato products, and lycopene intake were associated with lower risks of total and CVD mortality. Moderate consumption of lycopene was also related with a reduced cancer mortality. Further clinical studies and dietary intervention studies are warranted to confirm our premilitary findings.

Neurology ◽  
2017 ◽  
Vol 90 (2) ◽  
pp. e135-e141 ◽  
Author(s):  
Yinge Li ◽  
Yanping Li ◽  
John W. Winkelman ◽  
Arthur S. Walters ◽  
Jiali Han ◽  
...  

ObjectiveWe prospectively examined whether women with physician-diagnosed restless legs syndrome (RLS) had a higher risk of total and cardiovascular disease (CVD) mortality relative to those without RLS.MethodsThe current study included 57,417 women (mean age 67 years) from the Nurses' Health Study without cancer, renal failure, and CVD at baseline (2002). Main outcomes were total and CVD mortality. We used the Cox proportional hazards model to calculate hazard ratios (HRs) and 95% confidence intervals (CIs) for all-cause and CVD-specific mortality based on RLS status, adjusting for age, presence of major chronic diseases, and other potential confounders.ResultsWe documented 6,448 deaths during 10 years of follow-up. We did not observe a significant association between presence of physician-diagnosed RLS and high risk of total mortality (adjusted HR 1.15, 95% CI 0.98–1.34). When cause-specific mortality was studied, participants with RLS had a significantly higher risk of CVD mortality (adjusted HR 1.43, 95% CI 1.02–2.00) relative to those without RLS after adjustment for potential confounders. Longer duration of RLS diagnosis was significantly associated with a higher risk of CVD mortality (p for trend = 0.04). Excluding participants with common RLS comorbidities strengthened the association between RLS and total (adjusted HR 1.43, 95% CI 1.03–1.97) and CVD mortality (adjusted HR 2.27, 95% CI 1.21–4.28). However, we did not find a significant association between RLS and mortality due to cancer and other causes.ConclusionsWomen with RLS had a higher CVD mortality rate, which may not be fully explained by common co-occurring disorders of RLS.


BMC Nutrition ◽  
2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Akiko Nakanishi ◽  
Erika Homma ◽  
Tsukasa Osaki ◽  
Ri Sho ◽  
Masayoshi Souri ◽  
...  

Abstract Background Dairy products are known as health-promoting foods. This study prospectively examined the association between milk and yogurt intake and mortality in a community-based population. Methods The study population comprised of 14,264 subjects aged 40–74 years who participated in an annual health checkup. The frequency of yogurt and milk intake was categorized as none (< 1/month), low (< 1/week), moderate (1–6/week), and high (> 1/day) intake. The association between yogurt and milk intake and total, cardiovascular, and cancer-related mortalities was determined using the Cox proportional hazards model. Results During the follow-up period, there were 265 total deaths, 40 cardiovascular deaths and 90 cancer-related deaths. Kaplan–Meier analysis showed that the total mortality in high/moderate/low yogurt intake and moderate/low milk intake groups was lower than that in none group (log-rank, P < 0.01). In the multivariate Cox proportional hazard analysis adjusted for possible confounders, the hazard ratio (HR) for total mortality significantly decreased in high/moderate yogurt intake group (HR: 0.62, 95% confidence interval [CI]: 0.42–0.91 for high intake, HR: 0.70, 95%CI: 0.49–0.99 for moderate intake) and moderate milk intake group (HR: 0.67, 95% CI: 0.46–0.97) compared with the none yogurt and milk intake groups. A similar association was observed for cancer-related mortality, but not for cardiovascular mortality. Conclusions Our study showed that yogurt and milk intake was independently associated with a decrease in total and cancer-related mortalities in the Japanese population.


Circulation ◽  
2018 ◽  
Vol 137 (suppl_1) ◽  
Author(s):  
Paulette D Chandler ◽  
Deirdre Tobias ◽  
Jule E Buring ◽  
I-Min Lee ◽  
Daniel Chasman ◽  
...  

Background: Given the increased prevalence of cancer survivors in the United States, it is imperative to define risk factors for potential reductions in total and cause-specific mortality. Physical activity (PA) represents a promising target for intervention. Design: We prospectively evaluated PA from questionnaires before and after cancer diagnosis with total and cause-specific mortality among 13,297 subjects diagnosed with invasive cancer combined from the Physicians’ Health Study (PHS) (n=6328), Physicians’ Health Study II (PHS II) (n=912), and Women's Health Study (WHS) (n=6057). WHS and PHS participants were free of baseline cancer; PHS II participants reported no active cancer at baseline. We ascertained PA before and after an incident cancer diagnosis based on reports on repeated follow-up questionnaires. Death was ascertained by medical records and death certificates. Cox regression estimated combined hazard ratios (HRs) of mortality by PA adjusted for age, randomized treatments, BMI, and other lifestyle/demographic factors. We evaluated the interaction between PA before and after cancer diagnosis by comparing PA ≤1 versus ≥2 times/wk. Results: The mean follow-up after cancer diagnosis was 8.0, 7.5, and 5.2 y for WHS, PHS, and PHS II, respectively, during which there were 5623 deaths (WHS, 2164; PHS, 3269; PHS II; 190). Higher PA before cancer diagnosis was associated with significantly lower mortality. Compared with PA ≤ once/wk, the HRs (95% CIs) associated with PA 2-4 and >4 times/wk were 0.87 (0.82-0.93) and 0.88 (0.82-0.94) for total mortality; 0.77 (0.63-0.95) and 0.79 (0.62-0.997) for CVD mortality, and 0.90 (0.83-0.98) and 0.90 (0.83-0.98) for cancer mortality. Higher PA after cancer diagnosis was associated with significantly lower total and cancer mortality and non-significantly lower CVD mortality, with HRs (95% CIs) of 0.65 (0.58-0.72) and 0.66 (0.59-0.73) for total mortality; 0.78 (0.59-1.03) and 0.82 (0.61-1.10) for CVD mortality, and 0.66 (0.57-0.77) and 0.64 (0.55-0.74) for cancer mortality. There was a significant interaction of PA before and after cancer diagnosis for total (p int =0.02) and cancer (p int =0.007) mortality, but not CVD mortality (p int =0.38). Conclusions: Greater PA both before and after cancer diagnosis were significantly associated with lower total and cancer mortality. Higher PA before cancer diagnosis was also associated with lower CVD mortality. PA may be an important target for lower mortality after cancer diagnosis.


2018 ◽  
Vol 122 (5) ◽  
pp. 552-563 ◽  
Author(s):  
Cecilie Kyrø ◽  
Kirsten Frederiksen ◽  
Marianne Holm ◽  
Natalja P. Nørskov ◽  
Knud E. B. Knudsen ◽  
...  

AbstractThe association between lifestyle and survival after colorectal cancer has received limited attention. The female sex hormone, oestrogen, has been associated with lower colorectal cancer risk and mortality after colorectal cancer. Phyto-oestrogens are plant compounds with structure similar to oestrogen, and the main sources in Western populations are plant lignans. We investigated the association between the main lignan metabolite, enterolactone and survival after colorectal cancer among participants in the Danish Diet, Cancer and Health cohort. Prediagnosis plasma samples and lifestyle data, and clinical data from time of diagnosis from 416 women and 537 men diagnosed with colorectal cancer were used. Enterolactone was measured in plasma using a liquid chromatography–tandem mass spectrometry (LC–MS/MS) method. Participants were followed from date of diagnosis until death or end of follow-up. During this time, 210 women and 325 men died (170 women and 215 men died due to colorectal cancer). The Cox proportional hazards model was used to estimate hazard ratios (HR) and 95 % CI. Enterolactone concentrations were associated with lower colorectal cancer-specific mortality among women (HRper doubling: 0·88, 95 % CI 0·80, 0·97, P=0·0123). For men, on the contrary, enterolactone concentrations were associated with higher colorectal cancer-specific mortality (HRper doubling: 1·10, 95 % CI 1·01, 1·21, P=0·0379). The use of antibiotics affects enterolactone production, and the associations between higher enterolactone and lower colorectal cancer-specific mortality were more pronounced among women who did not use antibiotics (analysis on a subset). Our results suggest that enterolactone is associated with lower risk of mortality among women, but the opposite association was found among men.


Circulation ◽  
2019 ◽  
Vol 140 (12) ◽  
pp. 979-991 ◽  
Author(s):  
Megu Y. Baden ◽  
Gang Liu ◽  
Ambika Satija ◽  
Yanping Li ◽  
Qi Sun ◽  
...  

Background: Plant-based diets have been associated with lower risk of type 2 diabetes mellitus and cardiovascular disease (CVD) and are recommended for both health and environmental benefits. However, the association between changes in plant-based diet quality and mortality remains unclear. Methods: We investigated the associations between 12-year changes (from 1986 to 1998) in plant-based diet quality assessed by 3 plant-based diet indices (score range, 18–90)—an overall plant-based diet index (PDI), a healthful PDI, and an unhealthful PDI—and subsequent total and cause-specific mortality (1998–2014). Participants were 49 407 women in the Nurses’ Health Study (NHS) and 25 907 men in the Health Professionals Follow-Up Study (HPFS) who were free from CVD and cancer in 1998. Multivariable-adjusted Cox proportional-hazards models were used to estimate hazard ratios (HRs) and 95% CIs. Results: We documented 10 686 deaths including 2046 CVD deaths and 3091 cancer deaths in the NHS over 725 316 person-years of follow-up and 6490 deaths including 1872 CVD deaths and 1772 cancer deaths in the HPFS over 371 322 person-years of follow-up. Compared with participants whose indices remained stable, among those with the greatest increases in diet scores (highest quintile), the pooled multivariable-adjusted HRs for total mortality were 0.95 (95% CI, 0.90–1.00) for PDI, 0.90 (95% CI, 0.85–0.95) for healthful PDI, and 1.12 (95% CI, 1.07–1.18) for unhealthful PDI. Among participants with the greatest decrease (lowest quintile), the multivariable-adjusted HRs were 1.09 (95% CI, 1.04–1.15) for PDI, 1.10 (95% CI, 1.05–1.15) for healthful PDI, and 0.93 (95% CI, 0.88–0.98) for unhealthful PDI. For CVD mortality, the risk associated with a 10-point increase in each PDI was 7% lower (95% CI, 1–12%) for PDI, 9% lower (95% CI, 4–14%) for healthful PDI, and 8% higher (95% CI, 2–14%) for unhealthful PDI. There were no consistent associations between changes in plant-based diet indices and cancer mortality. Conclusions: Improving plant-based diet quality over a 12-year period was associated with a lower risk of total and CVD mortality, whereas increased consumption of an unhealthful plant-based diet was associated with a higher risk of total and CVD mortality.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Hang Li ◽  
Xiulong Wu ◽  
Yansen Bai ◽  
Wei Wei ◽  
Guyanan Li ◽  
...  

AbstractSystemic immune-inflammation index (SII) emerged as a biomarker of chronic inflammation and an independent prognostic factor for many cancers. We aimed to investigate the associations of SII level with total and cause-specific mortality risks in the general populations, and the potential modification effects of lifestyle-related factors on the above associations. In this study, we included 30,521 subjects from the Dongfeng-Tongji (DFTJ) cohort and 25,761 subjects from the National Health and Nutrition Examination Survey (NHANES) 1999–2014. Cox proportional hazards regression models were used to estimate the associations of SII with mortality from all-cause, cardiovascular diseases (CVD), cancer and other causes. In the DFTJ cohort, compared to subjects in the low SII subgroup, those within the middle and high SII subgroups had increased risks of total mortality [hazard ratio, HR (95% confidence interval, CI) = 1.12 (1.03–1.22) and 1.26 (1.16–1.36), respectively) and CVD mortality [HR (95%CI) = 1.36 (1.19–1.55) and 1.50 (1.32–1.71), respectively]; those within the high SII subgroup had a higher risk of other causes mortality [HR (95%CI) = 1.28 (1.09–1.49)]. In the NHANES 1999–2014, subjects in the high SII subgroup had higher risks of total, CVD, cancer and other causes mortality [HR (95%CI) = 1.38 (1.27–1.49), 1.33 (1.11–1.59), 1.22 (1.04–1.45) and 1.47 (1.32–1.63), respectively]. For subjects with a high level of SII, physical activity could attenuate a separate 30% and 32% risk of total and CVD mortality in the DFTJ cohort, and a separate 41% and 59% risk of total and CVD mortality in the NHANES 1999–2014. Our study suggested high SII level may increase total and CVD mortality in the general populations and physical activity exerted a beneficial effect on the above associations.


Author(s):  
Natalia S Gavrilova ◽  
Leonid A Gavrilov

Abstract It is known that biological relatives of long-lived individuals demonstrate lower mortality and longer lifespan compared to relatives of shorter-lived individuals, and at least part of this advantage is likely to be genetic. Less information, however, is available about effects of familial longevity on age-specific mortality trajectories. We compared mortality patterns after age 50 years for 10,045 siblings of U.S. centenarians and 12,308 siblings of shorter-lived individuals (died at age 65 years). Similar comparisons were made for sons and daughters of longer-lived parents (both parents lived 80 years and more) and shorter-lived parents (both parents lived less than 80 years) within each group of siblings. Although relatives of longer-lived individuals have lower mortality at younger ages compared to relatives of shorter lived individuals, this mortality advantage practically disappears by age 100 years. To validate this observation further, we analyzed survival of 3,408 U.S. centenarians born in 1890-97 with known information on maternal and paternal lifespan. We found using the Cox proportional hazards model that both maternal and paternal longevity (lifespan 80+ years) is not significantly associated with survival after age 100 years. The results are compatible with the predictions of reliability theory of aging suggesting higher initial levels of system redundancy (reserves) in individuals with protective familial/genetic background and hence lower initial mortality. Heterogeneity hypothesis is another possible explanation for the observed phenomena.


2021 ◽  
Author(s):  
Eilon Krashin ◽  
Barbara Silverman ◽  
David M Steinberg ◽  
Daniel Yekutieli ◽  
Shmuel Giveon ◽  
...  

Research on the association between thyroid hormone levels and cancer mortality remains limited and inconclusive. We determined the relation of thyroid stimulating hormone (TSH), free T4 (FT4) and free T3 (FT3) levels with mortality in overall cancer and specific tumor types. Thyroid hormone levels one to five years prior to cancer diagnosis, as well as multiple clinical and demographic parameters, were retrospectively collected for 10,325 Israeli cancer patients, diagnosed between 2000 and 2016. Patients treated with thyroid altering medications were excluded. Cancer diagnosis was determined via the Israel National Cancer Registry (INCR). Multivariate adjusted Cox proportional hazards model was used to assess the hazard ratios (HR) based on thyroid hormone function for cancer mortality. 5,265 patients died during the follow-up period (median of 4.4 years). TSH, FT4 and FT3 levels in the hypothyroid range were associated with increase in overall mortality (adjusted HR 1.20; 1.74; 1.87, respectively). We further analyzed the association between TSH and mortality in fourteen cancer subgroups. Specifically, TSH in both the hyperthyroid and hypothyroid range was associated with melanoma mortality (adjusted HR 2.20 ; 4.47, respectively). In conclusion, pre-diagnosis thyroid dysfunction is associated with increased cancer mortality, a relation likely driven by specific cancer types. These findings suggest that thyroid hormones may potentially serve as prognostic markers in cancer.


2006 ◽  
Vol 24 (18_suppl) ◽  
pp. 4571-4571 ◽  
Author(s):  
D. V. Makarov ◽  
B. J. Trock ◽  
E. B. Humphreys ◽  
L. A. Mangold ◽  
M. A. Carducci ◽  
...  

4571 Background: For men developing PSA failure after radical prostatectomy (RP), administration of immediate androgen deprivation therapy (ADT) has not been shown to improve survival compared to delaying ADT until evidence of metastatic disease. We evaluated factors influencing prostate cancer (PCa) specific mortality (PCSM) in a cohort of PSA era patients developing metastases after RP treated with delayed ADT. Methods: 3,658 men had RP by a single surgeon at Johns Hopkins Hospital from 4/82 until 6/05. 553 had PSA failure. 216 developed radiographically evident distant metastasis. Of these, 91 men formed the study cohort: initially treated during the PSA era (1987–2005), received ADT only after documented metastasis, and having complete data. 41 of these men died. Median failure times were estimated with the Kaplan-Meier method. Prognostic impact was estimated as the hazard ratio (HR) derived from the Cox proportional hazards model. Results: Median followup from RP was 10 yrs (range 2–18). Actuarial median failure times are: 1 yr from RP to PSA failure (range 1–11), 32 mos from PSA failure to metastasis (range 0–129), 79 mos from metastasis to death (range 7–181), and 13 yrs from RP to death (range 2–18). The following variables were significant prognostic factors for PCSM in univariate analyses: Pain at diagnosis of metastases (p < 0.01), time from RP to metastasis (p = 0.02), hematocrit at metastasis (p < 0.01) and PSADT <3 mos during the 2 years prior to metastasis (p < 0.01). A multivariable Cox proportional hazards model demonstrated the following independent predictors of PCSM: pain (HR = 10.5 p < 0.01), PSA at metastasis ≥100 ng/mL (HR = 5.3 p < 0.01) and PSADT < 3 months (HR = 7.1 p < 0.01). PSADT determined in the two years immediately after PSA failure (HR = 1.0 p = 0.37) and time from RP to bone metastasis (HR = 1.0 p = 0.80) were not independent predictors of PCSM. Conclusion: Men receiving delayed ADT for development of metastasis after RP may have a prolonged survival time (13 yrs post RP - range 2–18). Optimizing the time for ADT in these patients requires well-designed, prospective randomized studies. Our data may facilitate the selection of patients and thresholds for implementation of ADT. No significant financial relationships to disclose.


2011 ◽  
Vol 2011 ◽  
pp. 1-10 ◽  
Author(s):  
Erin K. Howie ◽  
Xuemei Sui ◽  
Duck-chul Lee ◽  
Steven P. Hooker ◽  
James R. Hébert ◽  
...  

This study examined the association between consumption of alcoholic beverages and all-cause and cardiovascular disease (CVD) mortality in a cohort of men (n=31,367). In the Cox proportional hazards model adjusted for age, year of examination, body mass index (BMI), smoking, family history of CVD, and aerobic fitness, there were no significant differences in risk of all-cause mortality across alcohol intake groups. Risk of CVD mortality was reduced 29% in quartile 1 (HR = 0.71, 95% confidence interval (CI): 0.53, 0.95) and 25% in quartile 2 (HR = 0.75, 95% CI: 0.58, 0.98). The amount of alcohol consumed to achieve this risk reduction was <6 drinks/week; less than the amount currently recommended. The addition of other potential confounders and effect modifiers including blood pressure, insulin sensitivity, lipid levels, and psychological variables did not affect the magnitude of association. Future research is needed to validate the current public health recommendations for alcohol consumption.


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