Bio


Dr. Kevin L’Esperance is a cancer epidemiologist who focuses on the interplay between adiposity, lifestyle, and social drivers of health in kidney and ovarian cancer risk, prevention, and survivorship. His work involves patients, clinicians, and population-level perspectives to improve health literacy, integrate lived experiences, and enhance cancer care and management. In parallel, Dr. L’Esperance is actively engaged in science communication, working to raise awareness about cancer and shift the narrative from fatalism to empowerment and actionable change.

Stanford Advisors


All Publications


  • Trajectories of body fatness in adulthood and the risk of ovarian cancer. Cancer epidemiology L'Espérance, K., Madathil, S., Ritonja, J. A., Abrahamowicz, M., Ho, V., Nicolau, B., O'Loughlin, J., Koushik, A. 2025; 96: 102814

    Abstract

    While excess body fatness in older adulthood has been linked to ovarian cancer, the influence of changes in body fatness over time is unclear. This study examined the association between adulthood trajectories of body mass index (BMI), a proxy for body fatness, and ovarian cancer.In a population-based case-control study (440 cases, 820 controls), we used a group-based trajectory approach to identify BMI trajectories from age 20-70. Using unconditional logistic regression, we estimated adjusted odds ratios (aOR) and 95 % confidence intervals (95 % CI) for the associations between the estimated trajectories and ovarian cancer.We identified three distinct BMI trajectories: a normal-stable trajectory, a normal-to-overweight trajectory and an overweight-to-obese trajectory, which included 63.2 %, 31.0 % and 6.8 % of the population, respectively. Multivariable aORs suggested that participants with normal weight at the onset of adulthood who became overweight over their adulthood time did not differ in their risk of ovarian cancer compared to those who maintained a normal weight throughout adulthood (aOR (95 %CI): 0.89 (0.69-1.16)). Among those in the overweight-to-obese trajectory, the aOR (95 %CI) was 1.45 (0.87-2.43), and thus in the direction of an increased ovarian cancer risk compared to those who maintained a normal weight.Our findings underscore the need for further research to clarify the role of body fatness across the lifetime in the etiology of ovarian cancer.

    View details for DOI 10.1016/j.canep.2025.102814

    View details for PubMedID 40245771

  • Body fatness across the adult life course and ovarian cancer risk. European journal of epidemiology Ritonja, J. A., Madathil, S., Nicolau, B., L'Espérance, K., Ho, V., Abrahamowicz, M., Koushik, A. 2024; 39 (10): 1139-1149

    Abstract

    Excess body fatness in late adulthood has been observed to increase ovarian cancer risk, but the association is relatively weak. Body fatness can change over time, and timing may differently influence risk. We used a life course epidemiology approach to identify whether the relation between body fatness and ovarian cancer risk is best described by a critical period, accumulation or sensitive period hypothesis. In a population-based case-control study of ovarian cancer in Montreal, Canada (2011-16), data on body mass index (BMI) at each decade starting at age 20 was available. Among 363 cases and 707 controls aged ≥ 50 years, we used a Bayesian relevant life course exposure model to estimate the relative importance of BMI for three pre-specified periods across the adult life course, i.e., early childbearing years, late childbearing years, and peri/postmenopause, on ovarian cancer risk. The accumulation hypothesis best described BMI in relation to ovarian cancer overall, with an odds ratio (OR) for the lifetime effect of BMI (per 5 kg/m2 increase) of 1.10 (95% credible interval [CrI]: 0.90-1.35). For invasive ovarian cancer, the OR (95% CrI) for the lifetime effect was 1.16 (0.92-1.48), with BMI during early childbearing years showing the highest relative importance, suggesting this may be a sensitive period. For borderline cancer, the lifetime effect OR was not strongly supportive of an association (OR: 0.90, 95% CrI: 0.53-1.32). The results suggest that a sensitive period of early childbearing years is a candidate hypothesis for further investigation.

    View details for DOI 10.1007/s10654-024-01161-1

    View details for PubMedID 39404972

    View details for PubMedCentralID 5421437

  • Predicted 25-hydroxyvitamin D over the adult lifetime and the risk of ovarian cancer. American journal of epidemiology Ritonja, J. A., Danieli, C., Pana, M. P., Palmer, M. J., L'Espérance, K., Ho, V., Abrahamowicz, M., Koushik, A. 2024; 193 (9): 1233

    Abstract

    The evidence from previous studies of serum 25-hydroxyvitamin D (25(OH)D) and ovarian cancer risk is not conclusive. However, the 25(OH)D levels were generally only measured in late adulthood, which may not capture the etiologically relevant exposure periods. We investigated predicted 25(OH)D over the adult lifetime in relation to ovarian cancer risk in a population-based case-control study conducted from 2011 to 2016 in Montreal, Canada (n = 490 cases and 896 controls). Predicted 25(OH)D was computed using previously validated regression models. Unconditional multivariable logistic regression models were used to estimate adjusted odds ratios (aORs) and 95% CIs for average predicted 25(OH)D over the adult lifetime and ovarian cancer risk. In addition, the relative importance of different periods of past 25(OH)D exposure was explored using a weighted cumulative exposure (WCE) model. For each 20-nmol/L increase in average predicted 25(OH)D over the adult lifetime, the aOR (95% CI) was 0.73 (0.55-0.96). In WCE analyses, the inverse association was strongest for exposures 5 to 20 years and 35 to 55 years prior to diagnosis, with aORs (95% CIs) of 0.82 (0.69-0.94) and 0.79 (0.66-1.02), respectively, for each 20-nmol/L increase in predicted 25(OH)D. These results support an inverse association between 25(OH)D levels in adulthood and ovarian cancer risk. This article is part of a Special Collection on Gynecological Cancers.

    View details for DOI 10.1093/aje/kwae070

    View details for PubMedID 38754871

    View details for PubMedCentralID PMC11369219

  • An empirical evaluation of approximate and exact regression-based causal mediation approaches for a binary outcome and a continuous or a binary mediator for case-control study designs. BMC medical research methodology Caubet, M., L'Espérance, K., Koushik, A., Lefebvre, G. 2024; 24 (1): 72

    Abstract

    In the causal mediation analysis framework, several parametric regression-based approaches have been introduced in past years for decomposing the total effect of an exposure on a binary outcome into a direct effect and an indirect effect through a target mediator. In this context, a well-known strategy involves specifying a logistic model for the outcome and invoking the rare outcome assumption (ROA) to simplify estimation. Recently, exact estimators for natural direct and indirect effects have been introduced to circumvent the challenges prompted by the ROA. As for the approximate approaches relying on the ROA, these exact approaches cannot be used as is on case-control data where the sampling mechanism depends on the outcome.Considering a continuous or a binary mediator, we empirically compare the approximate and exact approaches using simulated data under various case-control scenarios. An illustration of these approaches on case-control data is provided, where the natural mediation effects of long-term use of oral contraceptives on ovarian cancer, with lifetime number of ovulatory cycles as the mediator, are estimated.In the simulations, we found few differences between the performances of the approximate and exact approaches when the outcome was rare, both marginally and conditionally on variables. However, the performance of the approximate approaches degraded as the prevalence of the outcome increased in at least one stratum of variables. Differences in behavior were also observed among the approximate approaches. In the data analysis, all studied approaches were in agreement with respect to the natural direct and indirect effects estimates.In the case where a violation of the ROA applies or is expected, approximate mediation approaches should be avoided or used with caution, and exact estimators favored.

    View details for DOI 10.1186/s12874-024-02156-y

    View details for PubMedID 38509513

    View details for PubMedCentralID PMC10953265

  • Childhood body fatness and the risk of epithelial ovarian cancer: A population-based case-control study in Montreal, Canada. Preventive medicine L'Espérance, K., Abrahamowicz, M., O'Loughlin, J., Koushik, A. 2024; 178: 107794

    Abstract

    To assess the association between childhood body fatness and epithelial ovarian cancer (EOC), and whether this association differs by type of EOC.Using data from a population-based case-control study (497 cases and 902 controls) in Montreal, Canada conducted 2011-2016, we examined the association between childhood body fatness and EOC, overall and separately for invasive vs. borderline EOCs. A figure rating scale was used to measure body fatness at ages 5 and 10. Multivariable logistic regression was used to estimate adjusted odds ratios (aORs) and 95% confidence intervals (95% CI). Quantitative bias analyses were conducted to assess the impact of exposure misclassification and non-participation.The aOR (95% CI) of overall EOC for high vs. low body fatness was 1.07 (0.85-1.34) at age 5 and 1.28 (0.98-1.68) at age 10. The associations were stronger for invasive EOC, specifically the endometrioid histological type. For borderline cancers, the aORs were below the null value with wide confidence intervals. Bias analyses did not reveal a strong influence of non-participation. Non-differential exposure misclassification may have biased aORs towards the null for invasive cancers but did not appear to have an appreciable influence on the aORs for borderline cancers.Childhood body fatness may be a risk factor for invasive EOC in later adult life. Our study highlights the potential importance of examining early life factors for a comprehensive understanding of EOC development.

    View details for DOI 10.1016/j.ypmed.2023.107794

    View details for PubMedID 38072312

  • Alcohol intake and the risk of epithelial ovarian cancer. Cancer causes & control : CCC L'Espérance, K., Grundy, A., Abrahamowicz, M., Arseneau, J., Gilbert, L., Gotlieb, W. H., Provencher, D., Koushik, A. 2023; 34 (6): 533-541

    Abstract

    To investigate the association between alcohol intake over the lifetime and the risk of overall, borderline, and invasive ovarian cancer.In a population-based case-control study of 495 cases and 902 controls, conducted in Montreal, Canada, average alcohol intake over the lifetime and during specific age periods were computed from a detailed assessment of the intake of beer, red wine, white wine and spirits. Multivariable logistic regression was used to estimate odds ratios (ORs) with 95% confidence intervals (CIs) for the association between alcohol intake and ovarian cancer risk.For each one drink/week increment in average alcohol intake over the lifetime, the adjusted OR (95% CI) was 1.06 (1.01-1.10) for ovarian cancer overall, 1.13 (1.06-1.20) for borderline ovarian cancers and 1.02 (0.97-1.08) for invasive ovarian cancers. This pattern of association was similarly observed for alcohol intake in early (15- < 25 years), mid (25- < 40 years) and late adulthood (≥ 40 years), as well as for the intake of specific alcohol beverages over the lifetime.Our results support the hypothesis that a higher alcohol intake modestly increases the risk of overall ovarian cancer, and more specifically, borderline tumours.

    View details for DOI 10.1007/s10552-023-01681-3

    View details for PubMedID 36933150

    View details for PubMedCentralID 8192829

  • Vitamin D Exposure and Ovarian Cancer Risk and Prognosis. International journal of environmental research and public health L'Espérance, K., Datta, G. D., Qureshi, S., Koushik, A. 2020; 17 (4)

    Abstract

    Given the poor prognosis of ovarian cancer and limited population-level strategies for early detection and long-term treatment success, knowledge of modifiable risk factors for prevention and improved prognosis is important. Vitamin D has received wide scientific interest in cancer research as having the potential to be one such factor. We carried out a systematic narrative review of the literature on vitamin D and ovarian cancer risk and survival. We included 17 case-control and cohort studies on ovarian cancer incidence. Five analyses were of sun exposure, among which three reported an inverse association. Of 11 analyses of dietary vitamin D, two reported an inverse association. Among five studies of 25(OH)D levels, an inverse association was reported in two. Across all studies the findings were inconsistent, but some recent studies have suggested that vitamin D exposure at earlier ages may be important. Only three studies examining vitamin D exposure in relation to survival among ovarian cancer survivors were identified and the findings were inconsistent. The evidence to date supports a null influence of vitamin D on both ovarian cancer risk and survival. Future research should ensure that exposure assessment captures vitamin D exposure from all sources and for the etiologically or prognostically pertinent period.

    View details for DOI 10.3390/ijerph17041168

    View details for PubMedID 32059597

    View details for PubMedCentralID PMC7068491