Diabetes and cancer: two diseases with obesity as a common risk factor

There is a growing body of evidence to support a connection between diabetes (predominantly type 2), obesity and cancer. Multiple meta‐analyses of epidemiological data show that people with diabetes are at increased risk of developing many different types of cancers, along with an increased risk of cancer mortality. Several pathophysiological mechanisms for this relationship have been postulated, including insulin resistance and hyperinsulinaemia, enhanced inflammatory processes, dysregulation of sex hormone production and hyperglycaemia. In addition to these potential mechanisms, a number of common risk factors, including obesity, may be behind the association between diabetes and cancer. Indeed, obesity is associated with an increased risk of cancer and diabetes. Abdominal adiposity has been shown to play a role in creating a systemic pro‐inflammatory environment, which could result in the development of both diabetes and cancer. Here, we examine the relationship between diabetes, obesity and cancer, and investigate the potential underlying causes of increased cancer risk in individuals with diabetes. Current treatment recommendations for reducing the overall disease burden are also explored and possible areas for future research are considered.     

Obesity,intentional weight loss and physical disability in older adults

We examine obesity, intentional weight loss and physical disability in older adults. Based on prospective epidemiological studies, body mass index exhibits a curvilinear relationship with physical disability; there appears to be some protective effect associated with older adults being overweight. Whereas the greatest risk for physical disability occurs in older adults who are ≥class II obesity, the effects of obesity on physical disability appears to be moderated by both sex and race. Obesity at age 30 years constitutes a greater risk for disability later in life than when obesity develops at age 50 years or later; however, physical activity may buffer the adverse effects obesity has on late life physical disability. Data from a limited number of randomized clinical trials reinforce the important role that physical activity plays in weight loss programmes for older adults. Furthermore, short‐term studies have found that resistance training may be particularly beneficial in these programmes as this mode of exercise attenuates the loss of fat‐free mass during caloric restriction. Multi‐year randomized clinical trials are needed to examine whether weight loss can alter the course of physical disablement in aging and to determine the long‐term feasibility and effects of combining resistance exercise with weight loss in older adults.     

Insulin resistance/hyperinsulinemia and cancer mortality: the Cremona study at the 15th year of follow-up

Type 2 diabetes is associated with risk of cancer. Hyperinsulinemia and insulin resistance may be the link with cancer, but whether this is independent of the diabetes status, obesity/visceral obesity and metabolic syndrome is uncertain and the present study wanted to address this issue. Fifteen-year all-cause, CVD and cancer mortality data were obtained through the Regional Health Registry in 2,011 out of 2,074 Caucasian middle-aged individuals of the Cremona Study, a population study on the prevalence of diabetes mellitus in Italy in which anthropometric and metabolic characteristics were collected. During the 15-year observation period, 495 deaths were registered: 221 CVD related and 180 cancer related. Age and sex were independently associated with all-cause, cancer and CVD mortality rates. Age- and sex-adjusted analysis showed that HOMA-IR, cigarette smoking and diabetes were independently associated with all-cause mortality; HOMA-IR, systolic blood pressure and fibrinogen were independently associated with CVD mortality; HOMA-IR and smoking habit were independently associated with cancer mortality. Individuals in the highest quintile of serum insulin had a 62% higher risk of cancer mortality (HR?=?1.62 95% CI: 1.19?C2.20; P?<?0.0022) and 161% higher risk of gastrointestinal cancer mortality (HR?=?2.61 95% CI: 1.73?C3.94; P?<?0.0001). Age- and sex-adjusted analysis showed that hyperinsulinemia/insulin resistance is associated with cancer mortality independently of diabetes, obesity/visceral obesity and the metabolic syndrome.     

The GH/IGF-1 Axis in Obesity: Physiological and Pathological Aspects

The cluster of cardiovascular risk factors-abdominal obesity, dyslipidaemia, insulin resistance and hypertension-has been recognized as the core of the metabolic syndrome. Adults with severe growth hormone (GH) deficiency have, to a large extent, features of the metabolic syndrome, and there is a strong inverse association between visceral fat accumulation and blunted GH secretion in adults. Hyposomatotropism in abdominal obesity has therefore been suggested to be of importance for its metabolic consequences. However, the underlying pathophysiological mechanisms are poorly understood. Prevalence of the metabolic syndrome is steadily increasing worldwide. Overnutrition and sedentary habits are the stigmata of modern society that predispose genetically susceptible individuals to develop central obesity and other features of the metabolic syndrome including glucose intolerance, hypertension and dyslipidemia. Although there are still no unified definitions of the syndrome, it is clear that this condition is associated with an increased risk for development of cardiovascular disease (CVD) and diabetes mellitus (DM). In this review, we discuss current evidence regarding alterations in the GH-IGF- 1 axis in abdominal obesity and its possible impact on other features of the metabolic syndrome.     

Association between the visceral adiposity index and risks of all-cause and cause-specific mortalities in a large cohort: Findings from the UK biobank

Background and aimsThe visceral adiposity index (VAI) has been recently established as a measure of visceral fat distribution and is shown to be associated with a wide range of adverse health events. However, the precise associations between the VAI score and all-cause and cause-specific mortalities in the general population remain undetermined.Methods and resultsIn this large-scale prospective epidemiological study, 357,457 participants (aged 38–73 years) were selected from the UK Biobank. We used Cox competing risk regression models to estimate the association between the VAI score and all-cause, cardiovascular disease (CVD), cancer, and other mortalities. The VAI score was significantly correlated with an increased risk of all-cause mortality (hazard ratio [HR], 1.200; 95% confidence interval [CI], 1.148–1.255; P < 0.0001), cancer mortality (HR, 1.224; 95% CI, 1.150–1.303; P < 0.0001), CVD mortality (HR, 1.459; 95% CI, 1.148–1.255; P < 0.0001), and other mortalities (HR, 1.200; 95% CI, 1.148–1.255; P < 0.0001) after adjusting for a series of confounders. In addition, the subgroup analyses showed that HRs were significantly higher in participants who were male, aged below 65 years, and body mass index less than 25.ConclusionIn summary, VAI was positively associated with an increased risk of all-cause and cause-specific mortalities in a nationwide, well-characterised population identified in a UK Biobank. The VAI score might be a complementary traditional predictive indicator for evaluating the risk of adverse health events in the population of Western adults aged 38 years and older.     

Obesity and cardiovascular disease risk: research update

The obesity epidemic has reached unprecedented proportions in Western society. Evidence continues to accumulate that obesity is associated with significant morbidity and mortality and in particular that it is an independent risk factor for cardiovascular disease (CVD). The association of obesity with CVD and its risk factors, including hypertension, dyslipidemia, glucose intolerance, and impaired hemostasis is becoming more clearly understood. An increasing body of data indicates that risk factors tend to cluster in obese individuals and may act synergistically to increase these people's risk for CVD. Individuals with disproportionate visceral adiposity are at significantly greater risk for CVD. Adult weight gain also underlies the development of many risk factors and augments the risk of CVD. Physicians can play a vital and active role in the prevention and treatment of obesity and overweight and thereby reduce patients' CVD risk.     

Hearing sensitivity in older adults: associations with cardiovascular risk factors in the health, aging and body composition study

OBJECTIVES: To examine the association between cardiovascular disease (CVD) and its risk factors and age‐associated hearing loss in a cohort of older black and white adults. DESIGN: Cross‐sectional cohort study. SETTING: The Health, Aging, and Body Composition (Health ABC) Study, a community‐based cohort study of older adults from Pittsburgh, Pennsylvania, and Memphis, Tennessee. PARTICIPANTS: Two thousand forty‐nine well‐functioning adults (mean age 77.5; 37% black). MEASUREMENTS: Pure‐tone audiometry measurement and history of clinical CVD were obtained at the fourth annual follow‐up visit. Pure‐tone averages in decibels reflecting low (250, 500, and 1,000 Hz), middle (500, 1,000, and 2,000 Hz), and high (2,000, 4,000, and 8,000 Hz) frequencies were calculated for each ear. CVD risk factors, aortic pulse‐wave velocity (PWV), and ankle–arm index (AAI) were obtained at study baseline. RESULTS: In sex‐stratified models, after adjustment for age, race, study site, and occupational noise exposure, risk factors associated with poorer hearing sensitivity in men included high triglyceride levels, high resting heart rate, and history of smoking. In women, poor hearing sensitivity was associated with high body mass index, high resting heart rate, fast PWV, and low AAI. CONCLUSION: Modifiable risk factors for CVD may play a role in the development of age‐related hearing loss.     

Mechanisms of disease: adipokines and breast cancer - endocrine and paracrine mechanisms that connect adiposity and breast cancer

A vast number of epidemiological studies suggest an important, but still controversial, role for obesity and adipose tissue mass in breast cancer risk and an association with tumor phenotype. The main conclusions from these studies raise the possibility that the adipose tissue can act as an effector organ that influences both cancer risk and tumor behavior. Here we also review heterotypic mechanisms in breast-cancer tumorigenesis; these mechanisms involve soluble secreted factors from peritumoral cells, extracellular-matrix components and interactions between stromal cells and tumor cells that create a specific and local peritumoral microenvironment. As a special focus, we discuss the increasing evidence for a role of peritumoral adipose tissue and secreted adipokines (such as adiponectin and leptin) in breast cancer; furthermore, the cellular and molecular basis of the peritumoral 'desmoplastic' tissue reaction observed in breast cancer is reviewed in detail.     

An evidence-based assessment of federal guidelines for overweight and obesity as they apply to elderly persons

BACKGROUND: The US Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults set the body mass index (BMI; weight in kilograms divided by the square of height in meters) of 25 as the upper limit of ideal weight for all adults regardless of age. However, the prognostic importance of overweight and obesity in elderly persons (>/=65 years) is controversial. We sought to analyze the guidelines in the context of currently available evidence that is relevant to older adults. METHODS: We searched MEDLINE for all English-language studies of the association between BMI and all-cause or cardiovascular mortality or coronary heart disease events from January 1966 through October 1999. Additional pertinent articles were identified through bibliographies of the MEDLINE articles. We selected studies for detailed review if they reported on the association between BMI and mortality for nonhospitalized subjects who were 65 years or older and had been followed up for at least 3 years. We controlled for age, smoking, and baseline health status. Of the 444 screened articles, 13 were selected to assess the guidelines. We extracted information regarding publication year, study design, population, recruitment period, follow-up duration, number of subjects, sex, age range, inclusion and exclusion criteria, and statistical models, including variables and end points. RESULTS: These data do not support the BMI range of 25 to 27 as a risk factor for all-cause and cardiovascular mortality among elderly persons. The results were not substantially different for men and women. Most studies showed a negative or no association between BMI and all-cause mortality. Three studies indicated overweight (BMI >/=27) as a significant prognostic factor for all-cause and cardiovascular mortality among 65- to 74-year-olds, and one study showed a significant positive association between overweight (BMI >/=28) and all-cause mortality among those 75 years or older. Higher BMI values were consistent with a smaller relative mortality risk in elderly persons compared with young and middle-aged populations. CONCLUSIONS: Federal guideline standards for ideal weight (BMI 18.7 to <25) may be overly restrictive as they apply to the elderly. Studies do not support overweight, as opposed to obesity, as conferring an excess mortality risk. Future guidelines should consider the evidence for specific age groups when establishing standards for healthy weight.     

Metabolic syndrome as a predictor of type 2 diabetes,and its clinical interpretations and usefulness

Metabolic syndrome is defined as a cluster of glucose intolerance, hypertension, dyslipidemia and central obesity with insulin resistance as the source of pathogenesis. Although several different combinations of criteria have been used to define metabolic syndrome, a recently published consensus recommends the use of ethnic‐specific criteria, including waist circumference as an indicator of central obesity, triglyceride and high‐density lipoprotein (HDL) cholesterol as indicators of dyslipidemia, and blood pressure greater than 130/85 mmHg. The definition of dysglycemia, and whether central obesity and insulin resistance are essential components remain controversial. Regardless of the definition, the prevalence of metabolic syndrome is increasing in Western and Asian countries, particularly in developing areas undergoing rapid socioenvironmental changes. Numerous clinical trials have shown that metabolic syndrome is an important risk factor for cardiovascular disease (CVD), type 2 diabetes mellitus and all‐cause mortality. Therefore, metabolic syndrome might be useful as a practical tool to predict these two major metabolic disorders. Comprehensive management of risk factors is very important to the improvement of personal and public health. However, recent studies have focused on the role metabolic syndrome plays as a risk factor for CVD; its importance in the prediction of incident diabetes is frequently overlooked. In the present review, we summarize the known evidence supporting metabolic syndrome as a predictor for type 2 diabetes mellitus and CVD. Additionally, we suggest how metabolic syndrome might be useful in clinical practice, especially for the prediction of diabetes.     

Body mass index and all‐cause mortality in older adults: A scoping review of observational studies

In older age, body composition changes as fat mass increases and redistributes. Therefore, the current body mass index (BMI) classification may not accurately reflect risk in older adults (65+). This study aimed to review the evidence on the association between BMI and all‐cause mortality in older adults and specifically, the findings regarding overweight and obese BMI. A systematic search of the OVID MEDLINE and Embase databases was conducted between 2013 and September 2018. Observational studies examining the association between BMI and all‐cause mortality within a community‐dwelling population aged 65+ were included. Seventy‐one articles were included. Studies operationalized BMI categorically (n = 60), continuously (n = 8) or as a numerical change/group transition (n = 7). Reduced risk of mortality was observed for the overweight BMI class compared with the normal BMI class (hazard ratios [HR] ranged 0.41‐0.96) and for class 1 or 2 obesity in some studies. Among studies examining BMI change, increases in BMI demonstrated lower mortality risks compared with decreases in BMI (HR: 0.83‐0.95). Overweight BMI classification or a higher BMI value may be protective with regard to all‐cause mortality, relative to normal BMI, in older adults. These findings demonstrate the potential need for age‐specific BMI cut‐points in older adults.     

Body mass index,waist circumference and waist–hip ratio: which is the better discriminator of cardiovascular disease mortality risk? Evidence from an individual‐participant meta‐analysis of 82 864 participants from nine cohort studies

Few studies have examined both the relative magnitude of association and the discriminative capability of multiple indicators of obesity with cardiovascular disease (CVD) mortality risk. We conducted an individual‐participant meta‐analysis of nine cohort studies of men and women drawn from the British general population resulting in sample of 82 864 individuals. Body mass index (BMI), waist circumference (WC) and waist‐to‐hip ratio (WHR) were measured directly. There were 6641 deaths (1998 CVD) during a mean of 8.1 years of follow‐up. After adjustment, a one SD higher in WHR and WC was related to a higher risk of CVD mortality (hazard ratio [95% CI]): 1.15 (1.05–1.25) and 1.15 (1.04–1.27), respectively. The risk of CVD mortality also increased linearly across quintiles of both these abdominal obesity markers with a 66% increased risk in the highest quintile of WHR. In age‐ and sex‐adjusted models only, BMI was related to CVD mortality but not in any other analyses. No major differences were revealed in the discrimination capabilities of models with BMI, WC or WHR for cardiovascular or total mortality outcomes. In conclusion, measures of abdominal adiposity, but not BMI, were related to an increased risk of CVD mortality. No difference was observed in discrimination capacities between adiposity markers.     

Resistance training,visceral obesity and inflammatory response: a review of the evidence

Intra‐abdominal obesity is an important risk factor for low‐grade inflammation, which is associated with increased risk for diabetes mellitus and cardiovascular disease. For the most part, recommendations to treat or prevent overweight and obesity via physical activity have focused on aerobic endurance training as it is clear that aerobic training is associated with much greater energy expenditure during the exercise session than resistance training. However, due to the metabolic consequences of reduced muscle mass, it is understood that normal ageing and/or decreased physical activity may lead to a higher prevalence of metabolic disorders. Whether resistance training alters visceral fat and the levels of several pro‐inflammatory cytokines produced in adipose tissue has not been addressed in earlier reviews. Because evidence suggests that resistance training may promote a negative energy balance and may change body fat distribution, it is possible that an increase in muscle mass after resistance training may be a key mediator leading to a better metabolic control. Considering the benefits of resistance training on visceral fat and inflammatory response, an important question is: how much resistance training is needed to confer such benefits? Therefore, the purpose of this review was to address the importance of resistance training on abdominal obesity, visceral fat and inflammatory response.     

Increased plasma levels of retinol‐binding protein 4 with visceral obesity is associated with cardiovascular risk factors

Aims/Introduction: Visceral obesity has been suggested to be an independent risk factor for cardiovascular disease (CVD); the role of adipokines in the risk for CVD is less clear. Aim of this study was to investigate the relationship between parameters of visceral obesity and index of CVD risk factors. Materials and Methods: A cross‐sectional analysis of healthy males (n = 116) and females (n = 175) for evaluation of clinical, laboratory and anthropometric parameters were undertaken. Abdominal subcutaneous (SAT) and visceral adipose tissues (VAT) were measured by computed tomography. Adipokines, including retinol‐binding protein 4 (RBP4) and adiponectin, were determined. The risk for CVD was estimated using the 10‐year Framingham Coronary Heart Disease Risk Point scale (Framingham score). Results: The Framingham score was increased in subjects with metabolic syndrome, and significantly increased with various indices of obesity, traditional risk factors of CVD, C‐reactive protein (CRP) and RBP4, but decreased with adiponectin. With multiple linear regression analysis, the Framingham score independently associated with age, smoking status, body mass index, triglyceride and RBP4. The magnitude of the Framingham score showed a linear trend of increase with CRP, VAT and RBP4 (all P < 0.001), but of decrease with SAT and adiponectin (all P < 0.05) at stratified levels of obesity. Conclusions: RBP4 is increased with visceral fat accumulation and associated with CVD risk factors independent of obesity or traditional risk factors. (J Diabetes Invest, doi: 10.1111/j.2040‐1124.2012.00213.x , 2012)     

Menopausal obesity and metabolic syndrome - PolSenior study

Obesity is a common problem and its health consequences depend on the phenotype of obesity. Clinical aspects of three phenotypes of obesity: upper body (visceral), lower body (healthy) and metabolic obesity with normal weight are discussed. The PolSenior study and other data show that the incidence of obesity increases during hormonal climacteric transformation with special emphasis on visceral (72%) and metabolic obesity with normal weight (16%). The etiology of menopausal obesity and fat redistribution with an increase incidence of menopausal metabolic syndrome is presented. The role of sex hormones and SHBG of fat mass and fat distribution in postmenopausal women is discussed on the basis of PolSenior study. The diagnostic-therapeutic algorithm for climacteric women is recommended according to cardiovascular diseases risk (CVD), elevated waist circumference, serum triglicerides, decreased HDL cholesterol, elevated fasting glucose, HOMA over 1.69 and BP over 130/80 mmHg. In women with CVD risk factors the metformin therapy is a golden standard.     

The risk of overweight and obesity in children with autism spectrum disorders: A systematic review and meta‐analysis

Multiple studies have suggested that autism spectrum disorders seem to increase the risk of overweight and obesity. We examined the pooled prevalence and relative risk of developing overweight or obesity among children with autism spectrum disorders in a systematic review and meta‐analysis. We searched PubMed, Scopus, ProQuest, and Web of Science databases and subsequently screened the records to identify studies that reported prevalence of overweight and/or obesity in children with ASD and matched groups of neurotypical children. DerSimonian‐Laird random‐effects meta‐analyses were performed to examine pooled prevalence and relative risk of obesity in children with autism spectrum disorders using the “meta” package in R software. Among children with autism spectrum disorders, the prevalence of obesity was 22.2%. Children with ASD had a 41.1% greater risk (P = .018) of development of obesity. Non‐Caucasian race, increasing age, female sex, and living in the United States emerged as positive moderators of the association between autism spectrum disorders and prevalence of overweight or obesity. Autism spectrum disorders seem to increase the risk of childhood obesity. Increased awareness of this association may allow the implementation of early interventions to reduce obesity and prevent potential deterioration of quality‐of‐life in this population.     

Leptin and gastro‐intestinal malignancies

Obesity is a well‐established risk factor for the development and mortality from several cancers, including adenocarcinoma of the oesophagus, oesophago‐gastric junction and colorectum. Despite a large body of epidemiological evidence describing this relationship, the mechanisms relating obesity and cancer are only starting to be uncovered. The altered secretion of metabolically active, pro‐inflammatory adipocytokines from adipose tissue is believed to play a key role, and leptin is believed to be a key player in obesity‐related carcinogenesis, as well as being the most extensively studied of the adipokines. In this literature review, we aim to examine the association between leptin and cancers of the gastro‐intestinal tract. For each individual cancer, we examine and present the published data examining the role of leptin in both cell and animal models, the association between circulating leptin levels and cancer risk, and finally the expression of the leptin system in human gastro‐intestinal tract tumours, in relation to tumour biology, stage and patient outcome.     

Obesity and post‐operative complications in patients undergoing non‐bariatric surgery

As the prevalence of obesity continues to rise in society, an increasing number of patients undergoing non‐bariatric surgery will be obese. Obesity is known to increase morbidity and mortality in the general population and thus is perceived as a risk factor for adverse post‐surgical outcomes. This association is not clear‐cut, however, and there is a lack of consensus in the literature on the risk between obesity and specific complications, in particular relating to infection, wound healing, respiratory and venous thromboembolism. The paucity of studies, as well as a lack of consistency of definition of obesity, with an over‐reliance on body mass index rather than body composition analysis, may underlie this confusion. Emerging concepts position central/visceral adipose tissue as potentially key to the pathogenesis of the comorbidities associated with obesity, thus this article reviews emerging research investigating the association between visceral obesity, the metabolic syndrome and resulting post‐operative complications. It is hypothesized that the state of chronic inflammation and dysmetabolism observed in visceral obese patients negatively influences post‐operative outcomes and represents a potential target for pharmaconutrition. The need for further research investigating the influence of visceral adiposity on immune function post surgery and its impact on post‐operative morbidity and mortality is highlighted.     

Gut microbiota‐derived metabolite trimethylamine N‐oxide (TMAO) potentially increases the risk of obesity in adults: An exploratory systematic review and dose‐response meta‐ analysis

It has been suggested that trimethylamine N‐oxide (TMAO) is associated with increased risk of diabetes and cardiovascular disease (CVD) morbidity and mortality. However, it is not known whether increased TMAO concentrations is associated with obesity. In the current study, we summarized the evidence related to the association of circulating TMAO with the risk of obesity measurements, including body mass index (BMI), waist circumference (WC), and waist‐to‐hip ratio (WHR) in a two‐class and dose‐response meta‐analysis of observational studies. A systematic search carried out in PubMed, SCOPUS, Cochrane, and ProQuest through September 30, 2019 resulted in 12 eligible studies which were included in the current meta‐synthesis. In these studies, BMI was reported but there were no reports of WC or WHR. Meta‐analysis of two‐class variables and dose‐response meta‐analysis of continuous variables were performed. Subgroup analysis and meta‐regression were also performed to identify the source of heterogeneity. There was a dose‐response association between circulating TMAO concentration and increased BMI in studies involving healthy individuals (P nonlinearity = .007), while no evidence of departure from linearity was observed according to study design or among patients with CVD. Results showed the highest category of TMAO was associated with 0.56 kg/m² increase in BMI (weighted mean difference [WMD], 0.563; CI, 0.026‐1.100; P = .04). The results of the current meta‐analysis revealed a positive association between circulating TMAO and obesity as presented by increased BMI. Moreover, a dose‐dependent association between circulating TMAO and obesity was also identified in apparently healthy individuals. This is the first meta‐analysis to reveal positive dose‐dependent associations between circulating TMAO concentration and obesity.     

HIV/HCV coinfection and the risk of cardiovascular disease: A meta‐analysis

The emergence of improved antiretroviral therapy has increased the life expectancy of human immunodeficiency virus (HIV)‐infected individuals, although there is an increased susceptibility to developing cardiovascular diseases (CVD). The risk for CVD is purported to be even higher among people with HIV and hepatitis C virus (HCV) coinfection because of the increased inflammatory response, which may synergistically impact CVD risk. However, studies comparing CVD outcomes between HIV alone and HIV/HCV individuals have been discordant. Accordingly, we conducted a meta‐analysis to clarify and quantify the association between HIV/HCV coinfection and the risk for CVD. We searched EMBASE, CINAHL, Google Scholar, PubMed, and Web of Science from inception to December 2016 to identify studies that provided information on HIV/HCV coinfection and CVD, defined as coronary artery disease, congestive heart failure and stroke. We used a random‐effects model to abstract and pool data on the hazard ratios (HRs) for CVD. HRs were adjusted for traditional CVD risk factors including age, sex, smoking, hypertension, diabetes and LDL cholesterol. Among the 283 articles reviewed, four cohort studies met inclusion criteria with a total of 33 723 participants. The pooled adjusted HRs for the association between HIV/HCV coinfection and CVD were 1.24 (95% CI: 1.07‐1.40) compared to HIV monoinfection. The test for heterogeneity was not statistically significant (I²=0.0%, P=.397). In conclusion, individuals with HIV/HCV coinfection had an increased CVD risk compared to those with HIV monoinfection. More research is needed to further examine the nature of this association, and response to traditional risk‐reduction therapies.