Pub Date : 2026-01-20DOI: 10.17849/insm-53-1-1-4.2
Timothy Meagher
Multi-cancer early detection (MCED) tests are increasingly popular. Are these tests "genetic," and if so, can insurers use them in the risk assessment process? This article reviews definitions of genetic tests. It then reviews the motivation for limiting insurers' access to genetic tests and examines the wording in the legislation in 3 countries and 1 US state. It then attempts to establish whether MECD results are included in the legislation.
{"title":"When Is a Test Genetic? The Case of Multi-Cancer Early Detection Tests.","authors":"Timothy Meagher","doi":"10.17849/insm-53-1-1-4.2","DOIUrl":"https://doi.org/10.17849/insm-53-1-1-4.2","url":null,"abstract":"<p><p>Multi-cancer early detection (MCED) tests are increasingly popular. Are these tests \"genetic,\" and if so, can insurers use them in the risk assessment process? This article reviews definitions of genetic tests. It then reviews the motivation for limiting insurers' access to genetic tests and examines the wording in the legislation in 3 countries and 1 US state. It then attempts to establish whether MECD results are included in the legislation.</p>","PeriodicalId":39345,"journal":{"name":"Journal of insurance medicine (New York, N.Y.)","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146012841","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-20DOI: 10.17849/insm-53-1-1-3.2
Muhammed Adil Khan
Background.—: Cardiovascular risk estimation for life insurance underwriting relies on risk estimation from conventional metrics: age, sex, smoking status, body mass index, systolic and diastolic blood pressure, total and high-density lipoprotein cholesterol and stress electrocardiogram. Coronary artery calcium (CAC) scoring via CT is a validated predictor of cardiovascular risk but remains costly, invasive, and unsuitable for large-scale underwriting. A novel artificial intelligence (AI) model, RetiCAC, predicts CAC scores from retinal photographs, offering a non-invasive and scalable alternative.
Objective.—: To assess the potential role of RetiCAC in life insurance underwriting for improved cardiovascular risk stratification and pricing accuracy.
Methods.—: This review draws on evidence from The Lancet Digital Health study of RetiCAC and evaluates its accuracy to and prognostic value compared with traditional CAC scoring. Potential underwriting applications were considered, including risk stratification, replacement of costly diagnostics, predictive augmentation, improvement in customer experience and integration with dynamic underwriting models and wellness programs.
Results.—: RetiCAC demonstrated incremental predictive prognostic value, particularly in borderline and intermediate-risk groups, and showed comparable performance to CT-derived CAC scoring in external cohorts. For insurers, RetiCAC could enable scalable, non-invasive cardiovascular risk assessment, refine mortality predictions, and improve classification of substandard applicants. Its digital nature supports remote underwriting models and wellness integration.
Conclusion.—: RetiCAC has potential as a non-invasive adjunct to traditional underwriting, enhancing cardiovascular risk prediction while reducing reliance on invasive testing. Broader adoption will require further validation, regulatory approval, and ethical safeguards, but integration could provide insurers with competitive advantages and align risk assessment with preventive health strategies.
{"title":"Retinal Coronary Artery Calcium Scoring - A Scalable Tool for Life Insurers.","authors":"Muhammed Adil Khan","doi":"10.17849/insm-53-1-1-3.2","DOIUrl":"https://doi.org/10.17849/insm-53-1-1-3.2","url":null,"abstract":"<p><strong>Background.—: </strong>Cardiovascular risk estimation for life insurance underwriting relies on risk estimation from conventional metrics: age, sex, smoking status, body mass index, systolic and diastolic blood pressure, total and high-density lipoprotein cholesterol and stress electrocardiogram. Coronary artery calcium (CAC) scoring via CT is a validated predictor of cardiovascular risk but remains costly, invasive, and unsuitable for large-scale underwriting. A novel artificial intelligence (AI) model, RetiCAC, predicts CAC scores from retinal photographs, offering a non-invasive and scalable alternative.</p><p><strong>Objective.—: </strong>To assess the potential role of RetiCAC in life insurance underwriting for improved cardiovascular risk stratification and pricing accuracy.</p><p><strong>Methods.—: </strong>This review draws on evidence from The Lancet Digital Health study of RetiCAC and evaluates its accuracy to and prognostic value compared with traditional CAC scoring. Potential underwriting applications were considered, including risk stratification, replacement of costly diagnostics, predictive augmentation, improvement in customer experience and integration with dynamic underwriting models and wellness programs.</p><p><strong>Results.—: </strong>RetiCAC demonstrated incremental predictive prognostic value, particularly in borderline and intermediate-risk groups, and showed comparable performance to CT-derived CAC scoring in external cohorts. For insurers, RetiCAC could enable scalable, non-invasive cardiovascular risk assessment, refine mortality predictions, and improve classification of substandard applicants. Its digital nature supports remote underwriting models and wellness integration.</p><p><strong>Conclusion.—: </strong>RetiCAC has potential as a non-invasive adjunct to traditional underwriting, enhancing cardiovascular risk prediction while reducing reliance on invasive testing. Broader adoption will require further validation, regulatory approval, and ethical safeguards, but integration could provide insurers with competitive advantages and align risk assessment with preventive health strategies.</p>","PeriodicalId":39345,"journal":{"name":"Journal of insurance medicine (New York, N.Y.)","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146012838","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-20DOI: 10.17849/insm-53-1-1-8.2
Rodney C Richie
There was a steady decrease in cardiovascular disease (CVD ischemic heart disease and stroke) mortality from 1960 to 2020, but since then, this decline has reversed. There have been over 228,000 excess CVD deaths through 2022,1 undoubtedly partially due to the COVID-19 pandemic, but the mortality rate continues to rise (arguably due to the rising epidemic of obesity and diabetes). CVD remains the leading cause of death in developed countries, accounting for over 30% of deaths, and risk estimation is a cornerstone approach to guiding CVD prevention in clinical medicine. Data from the CDC reveal that 36% of US adults have no CVD risk factors, 35% have 1, and 29% have 2 or more risk factors. The age-adjusted percentage of adults with 2 or more CVD risk factors has increased between 2013-2014 to August 2021-August 2023, especially in older age groups.2 Assessing the risk for CVD mortality is essential for the disability and life insurance industry required to assess that risk at a single point in time (at the issuance of an insurance policy). Evaluating this risk requires careful attention to modifiable and non-modifiable factors, including hypertension and other co-morbidities, abnormal lipid profiles, and lifestyle inequalities. The goal of this treatise is to evaluate the various CVD calculators, but also to review other risk factors that may not be routinely sought in estimating CVD risk. The importance of apolipoproteinB (apoB) and lipoprotein A (LpA) as better risk predictors than just elevated LDL levels will be emphasized, and evidence of systemic inflammation and insulin resistance will be proposed as essential early indicators of future cardiovascular disease.
{"title":"Evaluating Cardiovascular Disease Risk.","authors":"Rodney C Richie","doi":"10.17849/insm-53-1-1-8.2","DOIUrl":"https://doi.org/10.17849/insm-53-1-1-8.2","url":null,"abstract":"<p><p>There was a steady decrease in cardiovascular disease (CVD ischemic heart disease and stroke) mortality from 1960 to 2020, but since then, this decline has reversed. There have been over 228,000 excess CVD deaths through 2022,1 undoubtedly partially due to the COVID-19 pandemic, but the mortality rate continues to rise (arguably due to the rising epidemic of obesity and diabetes). CVD remains the leading cause of death in developed countries, accounting for over 30% of deaths, and risk estimation is a cornerstone approach to guiding CVD prevention in clinical medicine. Data from the CDC reveal that 36% of US adults have no CVD risk factors, 35% have 1, and 29% have 2 or more risk factors. The age-adjusted percentage of adults with 2 or more CVD risk factors has increased between 2013-2014 to August 2021-August 2023, especially in older age groups.2 Assessing the risk for CVD mortality is essential for the disability and life insurance industry required to assess that risk at a single point in time (at the issuance of an insurance policy). Evaluating this risk requires careful attention to modifiable and non-modifiable factors, including hypertension and other co-morbidities, abnormal lipid profiles, and lifestyle inequalities. The goal of this treatise is to evaluate the various CVD calculators, but also to review other risk factors that may not be routinely sought in estimating CVD risk. The importance of apolipoproteinB (apoB) and lipoprotein A (LpA) as better risk predictors than just elevated LDL levels will be emphasized, and evidence of systemic inflammation and insulin resistance will be proposed as essential early indicators of future cardiovascular disease.</p>","PeriodicalId":39345,"journal":{"name":"Journal of insurance medicine (New York, N.Y.)","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146012854","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-10-09DOI: 10.17849/insm-52-3-1-10.2
Antoine Moll, Eric Raymond, Théo Schneider, Anthony Vuillaume, Mark Li, Denis Charles, Valentine Sarrazin, Manuel Plisson
Introduction.—: Prostate cancer is one of the most common cancers, with an approximate global annual incidence of 1.5 million men and nearly 400,000 deaths. Treatment options include surgical resection, radiotherapy, and high-intensity focused ultrasounds, often combined with hormone deprivation therapy. Insurability of prostate cancer patients is evaluated based on tumor severity using the AJCC and TNM classifications, along with PSA levels and Gleason Scores. To control the risk, life insurers use medical selection, albeit many individuals may be excluded from coverage. Regulations, such as France's "Right to Be Forgotten," allow standard rate acceptance for certain prostate cancer survivors under specific conditions.
Methods.—: By matching patient data from the SEER database with mortality tables, we established a Cox survival prostate cancer model for patients sharing similar long-term survival risk and compared it with that of the general population.
Results.—: By investigating risks in populations of various age ranges, we defined groups with variable survival risk. To distinguish insurable from uninsurable, we have defined a so-called "acceptance corridor," which delimits the boundary within the expected normal range of survival for a group of age and the highest acceptable premium. This corridor is delimited with an upper boundary depicted where the risk is equal to the standard population and a lower boundary where the risk of death is higher than that of the normal population or where the risk overpasses the maximum acceptable premium of 250%.
Conclusion.—: In this paper, we have revisited the risk of individuals with a history of prostate cancer and have provided estimates of risk belonging within an acceptance corridor of insurability, broadening options for standard rate. This method may be further used to evaluate the impacts of regulatory guidelines, rules, and regulations, such as the right to be forgotten, to cancer patient populations.
{"title":"Prostate Cancer Insurability: Population Identification Within the Insurability Corridor and the Right to be Forgotten.","authors":"Antoine Moll, Eric Raymond, Théo Schneider, Anthony Vuillaume, Mark Li, Denis Charles, Valentine Sarrazin, Manuel Plisson","doi":"10.17849/insm-52-3-1-10.2","DOIUrl":"10.17849/insm-52-3-1-10.2","url":null,"abstract":"<p><strong>Introduction.—: </strong>Prostate cancer is one of the most common cancers, with an approximate global annual incidence of 1.5 million men and nearly 400,000 deaths. Treatment options include surgical resection, radiotherapy, and high-intensity focused ultrasounds, often combined with hormone deprivation therapy. Insurability of prostate cancer patients is evaluated based on tumor severity using the AJCC and TNM classifications, along with PSA levels and Gleason Scores. To control the risk, life insurers use medical selection, albeit many individuals may be excluded from coverage. Regulations, such as France's \"Right to Be Forgotten,\" allow standard rate acceptance for certain prostate cancer survivors under specific conditions.</p><p><strong>Methods.—: </strong>By matching patient data from the SEER database with mortality tables, we established a Cox survival prostate cancer model for patients sharing similar long-term survival risk and compared it with that of the general population.</p><p><strong>Results.—: </strong>By investigating risks in populations of various age ranges, we defined groups with variable survival risk. To distinguish insurable from uninsurable, we have defined a so-called \"acceptance corridor,\" which delimits the boundary within the expected normal range of survival for a group of age and the highest acceptable premium. This corridor is delimited with an upper boundary depicted where the risk is equal to the standard population and a lower boundary where the risk of death is higher than that of the normal population or where the risk overpasses the maximum acceptable premium of 250%.</p><p><strong>Conclusion.—: </strong>In this paper, we have revisited the risk of individuals with a history of prostate cancer and have provided estimates of risk belonging within an acceptance corridor of insurability, broadening options for standard rate. This method may be further used to evaluate the impacts of regulatory guidelines, rules, and regulations, such as the right to be forgotten, to cancer patient populations.</p>","PeriodicalId":39345,"journal":{"name":"Journal of insurance medicine (New York, N.Y.)","volume":" ","pages":"116-125"},"PeriodicalIF":0.0,"publicationDate":"2025-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145087742","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-10-09DOI: 10.17849/insm-52-3-1-2.2
John R Iacovino
Some underwriting departments believe hiring a board-certified specialist from a clinical background will improve their life underwriting, expectancy estimations, and profitability. This is not a panacea for solving adverse underwriting expectations. The need is a potential red flag indicating internal underwriting deficiencies. The specialist comes with their own limitations, the most prominent being the lack of any experience in insurance medicine and risk selection. You will be depending on the least experienced medical director to correct your problems. Likely, one or more internal underwriting practices could be the root cause of the unfavorable results.
{"title":"Will Hiring a Board-Certified Specialist Improve Your Company's Unfavorable Underwriting Results?","authors":"John R Iacovino","doi":"10.17849/insm-52-3-1-2.2","DOIUrl":"10.17849/insm-52-3-1-2.2","url":null,"abstract":"<p><p>Some underwriting departments believe hiring a board-certified specialist from a clinical background will improve their life underwriting, expectancy estimations, and profitability. This is not a panacea for solving adverse underwriting expectations. The need is a potential red flag indicating internal underwriting deficiencies. The specialist comes with their own limitations, the most prominent being the lack of any experience in insurance medicine and risk selection. You will be depending on the least experienced medical director to correct your problems. Likely, one or more internal underwriting practices could be the root cause of the unfavorable results.</p>","PeriodicalId":39345,"journal":{"name":"Journal of insurance medicine (New York, N.Y.)","volume":" ","pages":"126-127"},"PeriodicalIF":0.0,"publicationDate":"2025-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145075985","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-10-09DOI: 10.17849/insm-52-3-1-32.1
Anthony F Milano
Leukemia is a broad term for a heterogenous group of hematologic malignancies that arise from the abnormal proliferation of leukocytes. It occurs most often in adults older than 55, but also is the most common cancer in children younger than 15, and accounts for more than 25% of cancer deaths in this age group. In this United States long term retrospective population-based analysis of 143,713 microscopically confirmed leukemia cases, mortality and survival study, 1975-2022, data is derived from the NCI Surveillance, Epidemiology and End-Results Programs, SEER*Stat software versions 8.4.5 and SEER*Stat 9.0.40.0, and, SEER Registry - Incidence - SEER Research Data, 8 Registries, Nov 2024 Sub (1975-2022). This comparative cohort entry time-period analysis is intended to provide age-adjusted epidemiologic, demographic, short and long-term survival and mortality data for convenient reference by all physicians, scientists, insurance underwriters, and others interested in cancer mortality follow-up.
{"title":"Leukemia - 20-Year Comparative Survival and Mortality Analysis by Age, Sex, Race, Cohort Entry Time-Period, Disease Duration, Major Subtypes and Other Histologic Categories: A Systematic Review of 142,713 Cases for Diagnosis Years 1975-2022.","authors":"Anthony F Milano","doi":"10.17849/insm-52-3-1-32.1","DOIUrl":"10.17849/insm-52-3-1-32.1","url":null,"abstract":"<p><p>Leukemia is a broad term for a heterogenous group of hematologic malignancies that arise from the abnormal proliferation of leukocytes. It occurs most often in adults older than 55, but also is the most common cancer in children younger than 15, and accounts for more than 25% of cancer deaths in this age group. In this United States long term retrospective population-based analysis of 143,713 microscopically confirmed leukemia cases, mortality and survival study, 1975-2022, data is derived from the NCI Surveillance, Epidemiology and End-Results Programs, SEER*Stat software versions 8.4.5 and SEER*Stat 9.0.40.0, and, SEER Registry - Incidence - SEER Research Data, 8 Registries, Nov 2024 Sub (1975-2022). This comparative cohort entry time-period analysis is intended to provide age-adjusted epidemiologic, demographic, short and long-term survival and mortality data for convenient reference by all physicians, scientists, insurance underwriters, and others interested in cancer mortality follow-up.</p>","PeriodicalId":39345,"journal":{"name":"Journal of insurance medicine (New York, N.Y.)","volume":"52 3","pages":"148-179"},"PeriodicalIF":0.0,"publicationDate":"2025-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145276246","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-10-09DOI: 10.17849/insm-52-3-1-9.2
Rodney C Richie
Liver steatosis is now the politically correct term for excessive fat in the liver (fatty liver). Its incidence and prevalence, in lockstep with diabetes and obesity, continue to climb to over 2 billion persons worldwide. It is the most common cause of chronic liver disease and the leading cause of liver-related morbidity and mortality. This treatise, resulting from a selection of PubMed literature of relevant steatosis studies since the nomenclature change in 2023, will include the change in the names for the steatotic liver entities, documenting the contribution of metabolic dysfunctions (obesity, diabetes, hypertension, and dyslipidemias) to the pathology of insulin resistance and alcohol in the evolution of these liver diseases. The various modalities for measuring the degree of fat, fibrosis, and cirrhotic scarring of the liver will be discussed, followed by a review of the mortality implications of the subcategories of liver steatosis, including intrahepatic cirrhosis and malignancy, extrahepatic malignancies, and cardiovascular disease. Finally, a review of treatments to address these entities will be briefly reviewed.
{"title":"Steatotic Liver Diseases (SLDs): A Review.","authors":"Rodney C Richie","doi":"10.17849/insm-52-3-1-9.2","DOIUrl":"10.17849/insm-52-3-1-9.2","url":null,"abstract":"<p><p>Liver steatosis is now the politically correct term for excessive fat in the liver (fatty liver). Its incidence and prevalence, in lockstep with diabetes and obesity, continue to climb to over 2 billion persons worldwide. It is the most common cause of chronic liver disease and the leading cause of liver-related morbidity and mortality. This treatise, resulting from a selection of PubMed literature of relevant steatosis studies since the nomenclature change in 2023, will include the change in the names for the steatotic liver entities, documenting the contribution of metabolic dysfunctions (obesity, diabetes, hypertension, and dyslipidemias) to the pathology of insulin resistance and alcohol in the evolution of these liver diseases. The various modalities for measuring the degree of fat, fibrosis, and cirrhotic scarring of the liver will be discussed, followed by a review of the mortality implications of the subcategories of liver steatosis, including intrahepatic cirrhosis and malignancy, extrahepatic malignancies, and cardiovascular disease. Finally, a review of treatments to address these entities will be briefly reviewed.</p>","PeriodicalId":39345,"journal":{"name":"Journal of insurance medicine (New York, N.Y.)","volume":" ","pages":"128-136"},"PeriodicalIF":0.0,"publicationDate":"2025-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145126065","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-10-09DOI: 10.17849/insm-52-3-1-11.1
Steven J Rigatti, Stephanie Tanasia Saputra, Jean-Marc Fix
Objectives.—: This study seeks to quantify the mortality effect of high levels of body mass index (BMI) on life insurance applicants and participants in the National Health and Nutrition Examination Survey (NHANES) in univariate models and in successive models controlling for BMI-related diseases and conditions.
Background.—: It is well established that a high BMI is associated with increased all-cause and cardiovascular mortality; however, the quantitative effect of controlling for related diseases and conditions is not well understood.
Methods.—: Data were collected from over 7 million life insurance applicants submitting samples to Clinical Reference Laboratories (CRL) and 23,486 NHANES participants with available BMI and mortality status. Cox models were utilized, treating BMI as both a continuous predictor and as a categorical variable within various age and sex groups. Six Cox models were constructed in each age-sex-data group: a univariate model controlled only for age, then 5 more successively controlling for disease status (hypertension, diabetes, and heart disease), liver function tests, blood pressure/renal function, and finally hemoglobin A1c.
Results.—: Overall, the effect of high BMI on mortality hazard was highest in the univariate model, and lower with successively controlled models. In the life insurance data, the residual effect of BMI in the final models was still significant above a BMI of about 35. In the NHANES data, the effect remained significant only above a BMI of about 40. In the continuous models, the hazard of BMI was persistently significant for both sexes in the CRL models, only for men in the final NHANES model.
Conclusion.—: Based on this study, the effect of high BMI on mortality is significantly blunted when accounting for diseases and conditions that are associated with high BMI.
{"title":"Mortality Risk of High BMI in Life Insurance Applicants and the US Population.","authors":"Steven J Rigatti, Stephanie Tanasia Saputra, Jean-Marc Fix","doi":"10.17849/insm-52-3-1-11.1","DOIUrl":"https://doi.org/10.17849/insm-52-3-1-11.1","url":null,"abstract":"<p><strong>Objectives.—: </strong>This study seeks to quantify the mortality effect of high levels of body mass index (BMI) on life insurance applicants and participants in the National Health and Nutrition Examination Survey (NHANES) in univariate models and in successive models controlling for BMI-related diseases and conditions.</p><p><strong>Background.—: </strong>It is well established that a high BMI is associated with increased all-cause and cardiovascular mortality; however, the quantitative effect of controlling for related diseases and conditions is not well understood.</p><p><strong>Methods.—: </strong>Data were collected from over 7 million life insurance applicants submitting samples to Clinical Reference Laboratories (CRL) and 23,486 NHANES participants with available BMI and mortality status. Cox models were utilized, treating BMI as both a continuous predictor and as a categorical variable within various age and sex groups. Six Cox models were constructed in each age-sex-data group: a univariate model controlled only for age, then 5 more successively controlling for disease status (hypertension, diabetes, and heart disease), liver function tests, blood pressure/renal function, and finally hemoglobin A1c.</p><p><strong>Results.—: </strong>Overall, the effect of high BMI on mortality hazard was highest in the univariate model, and lower with successively controlled models. In the life insurance data, the residual effect of BMI in the final models was still significant above a BMI of about 35. In the NHANES data, the effect remained significant only above a BMI of about 40. In the continuous models, the hazard of BMI was persistently significant for both sexes in the CRL models, only for men in the final NHANES model.</p><p><strong>Conclusion.—: </strong>Based on this study, the effect of high BMI on mortality is significantly blunted when accounting for diseases and conditions that are associated with high BMI.</p>","PeriodicalId":39345,"journal":{"name":"Journal of insurance medicine (New York, N.Y.)","volume":"52 3","pages":"180-190"},"PeriodicalIF":0.0,"publicationDate":"2025-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145276284","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-10-09DOI: 10.17849/insm-52-3-1-7.2
Clifton P Titcomb
Chronic myeloid leukemia (CML) is a myeloproliferative disorder in which there is a neoplastic proliferation of mature granulocytes. The cancer results from a reciprocal translocation of the breakpoint cluster region (BCR) on chromosome 22 and the ABL1 gene region on chromosome 9 - t (9;22). The result is an abnormal fusion gene on chromosome 22 known as the Philadelphia chromosome. It represents 15% to 20% of all leukemias in the United States with an estimated incidence rate of 1 to 2 cases per 100,000. About 50% of affected individuals are asymptomatic. Diagnosis depends on demonstrating the presence of the Philadelphia chromosome. CML occurs in 3 phases. The most common is the chronic phase characterized by an indolent course and <15% blast cells in the myeloid space. The remaining advanced phases are the accelerated (15%-30% blasts) and the blast phase (>30% blasts). Without treatment, progression is slow but relentless to the advanced stages and occurs over 3 to 5 years. Survival is markedly reduced once these latter stages are reached. The recognition that the BCR-ABL1 fusion gene was a key driver of the disease process led to the development of tyrosine kinase inhibitor (TKI) drugs that targeted the genetic basis for the cancer. The first of these was imatinib, which was released in 2001. Since then both second and third generations of the drug class have been approved. These medications have been demonstrated to reduce the ratio of abnormal to normal BCR:ABL1 transcripts. They are most effective if used in the chronic phase. The degree of this molecular response has been demonstrated to correlate with limitation of progression of disease and improvement, often marked, of survival. Most individuals who respond well require lifelong use of the medication. However, a subset of the responders may achieve treatment-free remission (TFR) without ongoing therapy. For those individuals who are in the advanced state of the disease, do not respond to the TKI drugs or cannot tolerate them, allogeneic hematopoietic stem cell transplantation (SCT) is an alternative therapy that can achieve long-term survival in some cases.
{"title":"Chronic Myeloid Leukemia - A Review of Current Status.","authors":"Clifton P Titcomb","doi":"10.17849/insm-52-3-1-7.2","DOIUrl":"10.17849/insm-52-3-1-7.2","url":null,"abstract":"<p><p>Chronic myeloid leukemia (CML) is a myeloproliferative disorder in which there is a neoplastic proliferation of mature granulocytes. The cancer results from a reciprocal translocation of the breakpoint cluster region (BCR) on chromosome 22 and the ABL1 gene region on chromosome 9 - t (9;22). The result is an abnormal fusion gene on chromosome 22 known as the Philadelphia chromosome. It represents 15% to 20% of all leukemias in the United States with an estimated incidence rate of 1 to 2 cases per 100,000. About 50% of affected individuals are asymptomatic. Diagnosis depends on demonstrating the presence of the Philadelphia chromosome. CML occurs in 3 phases. The most common is the chronic phase characterized by an indolent course and <15% blast cells in the myeloid space. The remaining advanced phases are the accelerated (15%-30% blasts) and the blast phase (>30% blasts). Without treatment, progression is slow but relentless to the advanced stages and occurs over 3 to 5 years. Survival is markedly reduced once these latter stages are reached. The recognition that the BCR-ABL1 fusion gene was a key driver of the disease process led to the development of tyrosine kinase inhibitor (TKI) drugs that targeted the genetic basis for the cancer. The first of these was imatinib, which was released in 2001. Since then both second and third generations of the drug class have been approved. These medications have been demonstrated to reduce the ratio of abnormal to normal BCR:ABL1 transcripts. They are most effective if used in the chronic phase. The degree of this molecular response has been demonstrated to correlate with limitation of progression of disease and improvement, often marked, of survival. Most individuals who respond well require lifelong use of the medication. However, a subset of the responders may achieve treatment-free remission (TFR) without ongoing therapy. For those individuals who are in the advanced state of the disease, do not respond to the TKI drugs or cannot tolerate them, allogeneic hematopoietic stem cell transplantation (SCT) is an alternative therapy that can achieve long-term survival in some cases.</p>","PeriodicalId":39345,"journal":{"name":"Journal of insurance medicine (New York, N.Y.)","volume":" ","pages":"137-143"},"PeriodicalIF":0.0,"publicationDate":"2025-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145075991","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-10-09DOI: 10.17849/insm-52-3-1-9.2A
James A Mills, Jeffrey D Long, Robert A Philibert
Background.—: Previously we have shown that, in theory, a prediction algorithm that incorporates methylation sensitive digital PCR (MSdPCR) assessments of smoking and drinking could predict mortality. But the potential impact of these findings was speculative because limitations of the generalizability and available data from the study cohort.
Objective.—: To directly demonstrate the potential financial impact of using an epigenetic mortality index to assess potential applicants based off actual MSdPCR and survival data from a nationally representative cohort.
Methods.—: Using actual MSdPCR and survival data from our recent study of the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial, we modeled the survival and financial impact of a 55-year-old male smoker at the 25th, 50th and 75th percentile of Alcohol T Score (ATS) values.
Results.—: The likelihood of survival to maturation of 20 years was 86.2%, 80.8% and 74.4%. Using a simplified financial modeling of a 20-year term policy with $500K face value, insuring a client at the 25th percentile, would result in an average of $38,749 and $85,833 more in average net revenue than insuring the individuals at the 50th and 75th percentile.
Conclusions.—: Epigenetic survival indices can make financially impactful predictions. Real life pilots of this technology in the underwriting space are in order.
{"title":"An Illustration of the Protective Value of Epigenetics: Using the Alcohol T Score (ATS) in A Population of Known Smokers.","authors":"James A Mills, Jeffrey D Long, Robert A Philibert","doi":"10.17849/insm-52-3-1-9.2A","DOIUrl":"10.17849/insm-52-3-1-9.2A","url":null,"abstract":"<p><strong>Background.—: </strong>Previously we have shown that, in theory, a prediction algorithm that incorporates methylation sensitive digital PCR (MSdPCR) assessments of smoking and drinking could predict mortality. But the potential impact of these findings was speculative because limitations of the generalizability and available data from the study cohort.</p><p><strong>Objective.—: </strong>To directly demonstrate the potential financial impact of using an epigenetic mortality index to assess potential applicants based off actual MSdPCR and survival data from a nationally representative cohort.</p><p><strong>Methods.—: </strong>Using actual MSdPCR and survival data from our recent study of the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial, we modeled the survival and financial impact of a 55-year-old male smoker at the 25th, 50th and 75th percentile of Alcohol T Score (ATS) values.</p><p><strong>Results.—: </strong>The likelihood of survival to maturation of 20 years was 86.2%, 80.8% and 74.4%. Using a simplified financial modeling of a 20-year term policy with $500K face value, insuring a client at the 25th percentile, would result in an average of $38,749 and $85,833 more in average net revenue than insuring the individuals at the 50th and 75th percentile.</p><p><strong>Conclusions.—: </strong>Epigenetic survival indices can make financially impactful predictions. Real life pilots of this technology in the underwriting space are in order.</p>","PeriodicalId":39345,"journal":{"name":"Journal of insurance medicine (New York, N.Y.)","volume":" ","pages":"107-115"},"PeriodicalIF":0.0,"publicationDate":"2025-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145226100","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}