Immaculata DeVivo

Brigham and Women's Hospital, Boston, Massachusetts, United States

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Publications (10)55.33 Total impact

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    ABSTRACT: Abuse victimization in childhood is associated with a variety of age-related cardiometabolic diseases, but the mechanisms remain unknown. Telomeres, which form the protective caps at the ends of chromosomes, have been proposed as measures of biological age, and a growing body of research suggests that telomere attrition may help to explain relationships between stress and cardiometabolic degradation. We examined the association between childhood abuse victimization and leukocyte telomere length among 1,135 participants in the Nurses' Health Study II (NHSII). The NHSII ascertained physical and sexual child abuse histories in 2001. Telomere length was measured in genomic DNA extracted from peripheral blood leukocytes collected between 1996 and 1999. The ratio of telomere repeat copy number to a single gene copy number (T/S) was determined by a modified version of the quantitative real-time PCR telomere assay. Telomere length was log-transformed and corrected for assay variation across batch. We regressed telomere length on childhood abuse exposure variables and covariates using linear regression. We observed a reduction in telomere length associated with moderate physical abuse versus no physical abuse, but there was no evidence of a dose-response relationship for increased severity of physical abuse. No associations were noted for sexual abuse. We found no evidence of an association between severity of childhood physical or sexual abuse and leukocyte telomere length in the NHSII.
    PLoS ONE 06/2015; 10(6):e0124493. DOI:10.1371/journal.pone.0124493 · 3.23 Impact Factor
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    ABSTRACT: Shortened telomeres have been linked to poorer health outcomes. Exposure to psychological stress is associated with accelerated telomere shortening, and a well-established body of evidence indicates that families with a child with autism spectrum disorder (ASD) experience heightened levels of psychological stress. Also, alterations in a number of biological processes implicated in telomere length dynamics (i.e., oxidative stress, DNA methylation) have been linked to ASD susceptibility. We examined whether families of children with ASD who have an infant show shortened telomeres. Saliva samples were collected from infants, their older sibling (proband), and parents in families with or without a child with ASD. Infants and their families were designated as high-risk for ASD (HRA; n = 86) or low-risk for ASD (LRA; n = 118) according to the older siblings' diagnostic status. We used the real-time polymerase chain reaction (PCR) telomere assay to determine relative average telomere length for each participant. HRA families demonstrated significantly shorter telomere length relative to LRA families. This effect was observed at the individual family member level, with infants, probands, and mothers in HRA families showing reduced relative telomere length compared to individuals in LRA families; although not significant, fathers of high-risk infants showed a similar pattern of decreased telomere length. Families of children with ASD who have an infant show shortened telomeres relative to families with no history of ASD. These results suggest that such "high-risk" families should be monitored for the physical and mental health consequences that are often associated with accelerated telomere shortening. Copyright © 2015 American Academy of Child and Adolescent Psychiatry. Published by Elsevier Inc. All rights reserved.
    Journal of the American Academy of Child & Adolescent Psychiatry 04/2015; 54(7). DOI:10.1016/j.jaac.2015.04.006 · 7.26 Impact Factor
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    ABSTRACT: Leukocyte telomere length (LTL) is a marker of cellular turnover and oxidative stress. Studies suggest major depressive disorder (MDD) is associated with oxidative stress, but examinations of MDD and LTL have yielded mixed results, likely because of differences in measurement methods and unmeasured confounding. This study examined LTL and telomerase activity in 166 individuals with MDD compared to 166 age- and gender-matched matched controls free of any psychiatric disorder, using well-validated assays and clinical assessment methods, and controlling for a range of potential confounders. Subjects aged 18 to 70 were evaluated by trained raters and provided blood for LTL and telomerase activity measurement. LTL was assayed using Southern blot and replicated with qPCR, and telomerase activity was assayed with a repeat amplification protocol using a commercial kit. There was no significant difference in telomere length for individuals with MDD [mean (SD)=9.1 (3.0)kbp] compared to controls [mean(SD)=8.9(2.5)kbp] measured by Southern blot (p=0.65) or by confirmatory qPCR (p=0.91) assays. Controlling for potential confounders did not alter the results. Telomerase activity did not differ by MDD diagnosis overall (p=0.40), but the effect of MDD was significantly modified by gender (t(299)=2.67, p=0.0079) even after controlling for potential confounders, with telomerase activity significantly greater only in males with MDD versus controls. Our well-characterized, well-powered examination of concurrently assessed telomere length and telomerase activity in individuals with clinically significant, chronic MDD and matched controls failed to provide strong evidence of an association of MDD with shorter LTL, while telomerase activity was lower in men with MDD. Copyright © 2015 Elsevier Ltd. All rights reserved.
    Psychoneuroendocrinology 04/2015; 58:9-22. DOI:10.1016/j.psyneuen.2015.04.004 · 4.94 Impact Factor
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    Y Je · I DeVivo · E Giovannucci
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    ABSTRACT: Background: Previous epidemiologic studies have shown inconsistent results for the association between alcohol intake and endometrial cancer risk. Most of the studies, however, assessed alcohol intake after cancer diagnosis, or measured alcohol intake at baseline only. Methods: We prospectively examined the association between alcohol intake and endometrial cancer risk in the Nurses' Health Study with 68 067 female participants aged 34–59 years in 1980. Alcohol intake was measured several times with validated dietary questionnaires. We calculated cumulative average alcohol intake to represent long-term intakes of individual subjects. Using Cox proportional hazards models, we estimated incidence rate ratios (RRs) and 95% confidence intervals (CIs) for endometrial cancer risk after controlling for several risk factors simultaneously. Results: We identified a total of 794 invasive endometrial adenocarcinoma from 1980 to 2010. We found an inverse association among alcohol drinkers (multivariable RR=0.81; 95% CI: 0.68–0.96) compared with nondrinkers. Women with light alcohol intake of <5 g per day (∼half drink per day) had a 22% lower risk of endometrial cancer (multivariable RR=0.78; 95% CI: 0.66–0.94). Higher intake of alcohol, however, did not provide additional benefits against endometrial cancer: multivariable RRs for 5–14.9 g (∼1 drink), 15–29.9 g (∼2 drinks), or ⩾30 g (⩾2 drinks) versus 0 g per day were 0.88, 0.83, and 0.78 (95% CI: 0.49–1.25), respectively. The lower risk among drinkers (∼half drink per day) appeared to be stronger for obese women, but no significant interaction by body mass index was found. Conclusions: This study provides prospective evidence for an inverse association between light alcohol intake (∼half drink per day) in the long term and endometrial cancer risk, but above that level no significant association was found.
    British Journal of Cancer 05/2014; 111(1). DOI:10.1038/bjc.2014.257 · 4.84 Impact Factor
  • Cancer Research 08/2013; 73(8 Supplement):2542-2542. DOI:10.1158/1538-7445.AM2013-2542 · 9.33 Impact Factor
  • Cancer Research 08/2013; 73(8 Supplement):153-153. DOI:10.1158/1538-7445.AM2013-153 · 9.33 Impact Factor
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    ABSTRACT: Relatively short telomere length may serve as a marker of accelerated aging, and shorter telomeres have been linked to chronic stress. Specific lifestyle behaviors that can mitigate the effects of stress might be associated with longer telomere lengths. Previous research suggests a link between behaviors that focus on the well-being of others, such as volunteering and caregiving, and overall health and longevity. We examined relative telomere length in a group of individuals experienced in Loving-Kindness Meditation (LKM), a practice derived from the Buddhist tradition which utilizes a focus on unselfish kindness and warmth towards all people, and control participants who had done no meditation. Blood was collected by venipuncture, and Genomic DNA was extracted from peripheral blood leukocytes. Quantitative real time PCR was used to measure relative telomere length (RTL) (Cawthon, 2002) in fifteen LKM practitioners and 22 control participants. There were no significant differences in age, gender, race, education, or exposure to trauma, but the control group had a higher mean body mass index (BMI) and lower rates of past depression. The LKM practitioners had longer RTL than controls at the trend level (p=.083); among women, the LKM practitioners had significantly longer RTL than controls, (p=.007), which remained significant even after controlling for BMI and past depression. Although limited by small sample size, these results offer the intriguing possibility that LKM practice, especially in women, might alter RTL, a biomarker associated with longevity.
    Brain Behavior and Immunity 04/2013; 32. DOI:10.1016/j.bbi.2013.04.005 · 5.89 Impact Factor
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    ABSTRACT: Coffee has been reported to lower levels of estrogen and insulin, two hormones implicated in endometrial carcinogenesis, but prospective data on the relation between coffee consumption and risk of endometrial cancer are limited. We prospectively assessed coffee consumption in relation to endometrial cancer risk in the Nurses' Health Study (NHS) with 67,470 female participants aged 34 to 59 in 1980. Cumulative average coffee intake was calculated with all available questionnaires to assess long-term effects. Cox regression models were used to calculate incidence rate ratios (RR), controlling for other risk factors. Fewer than 4 cups of coffee per day were not associated with endometrial cancer risk. However, women who consumed 4 or more cups of coffee had 25% lower risk of endometrial cancer than those who consumed less than 1 cup per day (multivariable RR = 0.75; 95% CI = 0.57-0.97; P(trend) = 0.02). We found the similar association with caffeinated coffee consumption (RR for ≥4 vs. <1 cup/d = 0.70; 95% CI = 0.51-0.95). For decaffeinated coffee consumption, a suggestive inverse association was found among women who consumed 2 or more cups per day versus <1 cup/mo. Tea consumption was not associated with endometrial cancer risk. These prospective data suggest that four or more cups of coffee per day are associated with a lower risk of endometrial cancer. Drinking of coffee, given its widespread consumption, might be an additional strategy to reduce endometrial cancer risk. However, addition of substantial sugar and cream to coffee could offset any potential benefits.
    Cancer Epidemiology Biomarkers & Prevention 11/2011; 20(12):2487-95. DOI:10.1158/1055-9965.EPI-11-0766 · 4.13 Impact Factor
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    ABSTRACT: Inflammation and non-steroidal anti-inflammatory agents (NSAIDs) may play important role in ovarian cancer. However, epidemiologic data are inconsistent, possibly reflecting inter-individual genetic differences affecting the metabolism of NSAIDs. We examined whether common polymorphisms affecting the metabolism of NSAIDs modify the association between NSAIDs and ovarian cancer risk. We genotyped 1,353 DNA samples from women who developed ovarian cancer and 1,823 samples from matched controls participating in the New England Case-Control study and the Nurses' Health Studies. Conditional logistic regression estimated odds ratios (ORs) and 95% confidence intervals (CIs) associated with regular use of NSAIDs and with relevant polymorphisms on ovarian cancer risk. Multivariable unconditional logistic regression estimated the association of NSAID use across stratum of each genotype. Regular use of NSAIDs was not associated with ovarian cancer risk. Multivariable OR (95% CI) associated with use NSAIDs was 0.85 (95% CI: 0.71-1.02). Associations between NSAID use and ovarian cancer risk did not differ significantly across strata of genotypes. None of the studied polymorphisms was associated with ovarian cancer risk. The multivariable ORs (95% CI) associated with CYP2C9 and UGT1A6 variant genotypes were 0.99 (0.90-1.08) and 0.93 (0.82-1.05), respectively. The multivariable ORs (95% CI) associated with PPAR-γ, COX-2 -765G>C, and COX-2 Ex10+837T>C polymorphisms were 1.02 (0.87-1.20), 0.87 (0.75-1.00), and 0.97 (0.87-1.09), respectively. In this relatively large study, we found no convincing evidence supporting an association between NSAIDs use and ovarian cancer risk. Furthermore, data did not suggest interaction between selected polymorphisms and use of NSAIDs in relation to ovarian cancer risk.
    International Journal of Molecular Epidemiology and Genetics 01/2010; 1(4):320-31. · 1.30 Impact Factor
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    ABSTRACT: A functional promoter polymorphism in the progesterone receptor (PR) gene previously has been associated with an increased risk of postmenopausal breast cancer. Whether the relationship between genetic variation in PR and risk of breast cancer is modified by postmenopausal hormone (PMH) use is unknown. Thus, we conducted a case-control study nested within the prospective Nurses' Health Study to evaluate if the risk of breast cancer associated with having the +331 A risk allele was modified by PMH use. Genotyping of this SNP was available for 1,664 postmenopausal breast cancer cases and 2,391 controls. Logistic regression was used to estimate the odds ratios (ORs) and 95% confidence intervals (CIs) for breast cancer. Women who were carriers of 1 or both variant A alleles had a 31% increased risk of developing breast cancer (95% CI 1.04-1.65). PMH use significantly modified the association between the +331G/A polymorphism and risk (p-interaction <0.05). Among never users of PMH, women who were variant carriers had a significantly increased risk of breast cancer compared to those with the wild-type genotype (OR = 2.57; 95% CI 1.64-4.02). The +331G/A polymorphism was not associated with breast cancer risk among past (OR = 1.23; 95% CI 0.77-1.97) or current (OR = 1.14; 95% CI 0.84-1.56) PMH users. The data from this large prospective study provide evidence for a 2-fold increased risk of developing postmenopausal breast cancer among never users of PMH with the +331G/A SNP. This finding adds to the evidence that the PR has an important etiologic role in breast cancer and should be evaluated in future studies.
    International Journal of Cancer 10/2009; 125(7):1685-91. DOI:10.1002/ijc.24477 · 5.09 Impact Factor

Publication Stats

46 Citations
55.33 Total Impact Points


  • 2015
    • Brigham and Women's Hospital
      • Channing Division of Network Medicine
      Boston, Massachusetts, United States
  • 2009–2014
    • Harvard Medical School
      • Department of Medicine
      Boston, Massachusetts, United States
  • 2013
    • Massachusetts General Hospital
      • Department of Psychiatry
      Boston, Massachusetts, United States
  • 2011–2013
    • Harvard University
      Cambridge, Massachusetts, United States