Student Updates
BUSM Researchers Find Link Between Childhood Abuse and Age at Menarche
Researchers from Boston University School of Medicine (BUSM) have found an association between childhood physical and sexual abuse and age at menarche. The findings are published online in the Journal of Adolescent Health.
Researchers led by corresponding author, Renée Boynton-Jarrett, MD, assistant professor of pediatrics at BUSM, found a 49 percent increase in risk for early onset menarche (menstrual periods prior to age 11 years) among women who reported childhood sexual abuse compared to those who were not abused. In addition, there was a 50 percent increase in risk for late onset menarche (menstrual periods after age 15 years) among women who reported severe physical abuse in childhood. The participants in the study included 68,505 women enrolled in the Nurses’ Health Study II, a prospective cohort study.
"In our study child abuse was associated with both accelerated and delayed age at menarche and importantly, these associations vary by type of abuse, which suggest that child abuse does not have a homogenous effect on health outcomes,” said Boynton-Jarrett. “There is a need for future research to explore characteristics of child abuse that may influence health outcomes including type, timing and severity of abuse, as well as the social context in which the abuse occurs.”
Child abuse is associated with a significant health burden over the life course. Early menarche has been associated with risks such as cardiovascular disease, metabolic dysfunction, cancer and depression, while late menarche has been associated with lower bone mineral density and depression.
“We need to work toward better understanding how child abuse influences health and translate these research findings into clinical practice and public health strategies to improve the well-being of survivors of child abuse,” added Boynton-Jarrett.
This research was supported by the William T Grant Foundation, the Charles Hood Foundation, and the Building Interdisciplinary Research Careers in Women’s Health K12 HD043444 NIH Office of Women’s Health Research funded data analysis, manuscript preparation. The Nurses' Health Study II is supported by Public Health Service grant CA50385 from the National Cancer Institute, National Institutes of Health, and U.S. Department of Health and Human Services. The Nurses‟ Mothers‟ Cohort Study was funded by the Intramural Research Program of the National Cancer Institute, Research Contract N02-RC-17027 from the National Cancer Institute, and by P.O. 263 MQ 411027 from the National Cancer Institute. The 2001 supplemental violence assessment questionnaire was funded by R01 HL064108.
BUSM Study Identifies Adenosine Receptor’s Role in Regulating High Fat Diet-Induced Obesity and Type 2 Diabetes
A recent study led by Boston University School of Medicine (BUSM) demonstrates that the A2b-type adenosine receptor, A2bAR, plays a significant role in the regulation of high fat, high cholesterol diet-induced symptoms of type 2 diabetes. The findings, which are published online in PLoS ONE, also identify A2bAR as a potential target for the treatment of type 2 diabetes.
Katya Ravid, DSc/PhD, professor of medicine and biochemistry and director of the Evans Center for Interdisciplinary Biomedical Research at BUSM, led this study. Colleagues from Ravid’s lab who collaborated on this research include Hillary Johnston-Cox, BSc (MD/PhD, 2014) and Milka Koupenova-Zamor, PhD. Noyan Gokce, MD, associate professor of medicine at BUSM, and Melissa Farb, PhD, a postdoctoral fellow at BUSM, also collaborated on the study.
Diets that are high in fat and cholesterol induce changes in how the body regulates blood glucose levels. Exercise induces an increased production adenosine, a metabolite produced naturally by cells. A2bAR, a naturally occurring protein receptor found in the cell membrane, is activated by adenosine. This receptor is known to play an important role in regulating inflammation, which is associated with type 2 diabetes and obesity.
To examine the association of A2bAR activation with a diet high in fat and cholesterol, the researchers used an experimental model that lacked A2bAR and compared the results with a control group. When the experimental model group was given a diet high in fat and cholesterol, there was an increase in the development of obesity and signs of type 2 diabetes. The signs demonstrated in the study included elevated blood glucose levels and increased in insulin levels. When the control group was given the same diet, however, the levels of A2bAR increased, resulting in decreased insulin and glucose levels and obesity.
A novel link also was identified between the expression of A2bAR, insulin receptor substrate 2 (IRS-2) and insulin signaling. The results showed that the level of IRS-2, a protein that has previously been shown to mediate the effect of insulin, was impaired in tissues of the experimental model lacking A2bAR, causing higher concentrations of blood glucose. When A2bAR was activated in the control group using a pharmacologic agent with a diet high in fat and cholesterol, the level of IRS-2 was upregulated, lowering blood glucose.
“The pharmacologic activation of A2bAR demonstrated its newly identified role in signaling down to regulate the levels of IRS-2, which then improved the signs of high fat diet-induced type 2 diabetes,” said Ravid.
The prevalence of type 2 diabetes and obesity continues to increase in developed countries and both factors are known to contribute to the development of cardiovascular disease. According to the World Health Organization, 346 million people worldwide have diabetes and 90 percent of those people have type 2 diabetes.
To correlate these results in humans, the researchers then examined fat tissue samples from obese individuals. The results showed that A2bAR expression is high in fat from obese individuals, marked by inflammation, compared to lean ones, and is strongly correlated with IRS-2 expression.
“Our study suggests the important role of A2bAR in maintaining the level of IRS-2, a regulator of glucose and insulin homeostasis,” added Ravid.
This study was funded in part by the National Heart, Lung and Blood Institute under award numbers HL93149 (Katya Ravid) and HL084213 (Noyan Gokce). Click on the following link to view the study online: http://dx.plos.org/10.1371/journal.pone.0040584
BUSM Researchers Identify Genetic Markers for Testosterone, Estrogen Level Regulation
A research study led by Boston University School of Medicine (BUSM) and the University of Exeter in the United Kingdom, in collaboration with a global consortium, has identified genetic markers that influence a protein involved in regulating estrogen and testosterone levels in the bloodstream. The results, published online in PLoS Genetics, also reveal that some of the genetic markers for this protein are near genes related to liver function, metabolism and type 2 diabetes, demonstrating an important genetic connection between the metabolic and reproductive systems in men and women.
Andrea D. Coviello, MD, assistant professor of medicine at BUSM and an endocrinologist at Boston Medical Center, is one of the paper’s lead authors. This study was done in collaboration with the Framingham Heart Study and investigators from 15 international epidemiologic studies participating in the Cohorts for Heart and Aging Research in Genetic Epidemiology (CHARGE) consortium.
Sex hormone-binding globulin (SHBG) is the key protein that carries testosterone and estrogen in the bloodstream in both men and women. As the main carrier of these sex hormones, SHBG helps to regulate their effects in different tissues and organs in the body. In addition to effects on reproduction in men and women through regulation of sex hormones, SHBG has been linked to many chronic diseases including type 2 diabetes and hormone-sensitive cancers such as breast and prostate.
Previous family studies have demonstrated that approximately 50 percent of the variation in SHBG concentrations in the bloodstream is inherited from parents, suggesting that SHBG levels are under significant genetic control. However, little has been known about the specific genes that influence SHBG levels.
Investigators examined human genomes from 21,791 men and women to determine which genes influence SHBG levels and validated the results from this genome-wide association study (GWAS) in an additional 7,046 men and women. They identified 12 single-nucleotide polymorphisms (SNPs), or DNA sequence variations, associated with the concentration of SHBG circulating in the bloodstream. However, these SNPs combined explain only 16 percent of the variation of SHBG in men and eight percent in women, respectively, indicating that SHBG levels are affected by many other factors as well.
The results also showed that the SNPs that influence SHBG levels are near genes related to liver function, fat and carbohydrate metabolism and type 2 diabetes. In addition, there were genes that had stronger effects in one sex compared to the other.
“These findings underscore the connection between the reproductive system and metabolism in both men and women, and may help explain sex differences observed in some metabolic diseases, particularly type 2 diabetes,” said Coviello.
Funding for this study was provided by multiple sources. For complete information, go to http://www.plosgenetics.org/article/info%3Adoi%2F10.1371%2Fjournal.pgen.1002805.
Geriatric Re-Admission Rates Can be Minimized, Finds BUMC Study
Despite their greater frailty, patients cared for in an interdisciplinary geriatrics practice at Boston Medical Center (BMC) were no more likely to be re-hospitalized than adults receiving “usual care” according to researchers from Boston University School of Medicine (BUSM) and Boston University School of Public Health. The findings, which appeared in the American Journal of Medical Quality, demonstrate that it is possible to achieve re-hospitalization rates comparable to those of younger and healthier older adults using current care delivery models.
According to the authors, BU Geriatric Services uses specific practices to reduce re-hospitalizations including: case management and care coordination led by advanced practice nurses; discharge communication (documented in the electronic health records and sent to the primary care team) between the inpatient geriatric service attending physician and the primary care team on the day of discharge and attending physician review of medication reconciliation performed by house staff at discharge.
“The odds of re-hospitalization among older, sicker geriatric patients cared for at BMC which uses a multidisciplinary, team-based, integrated geriatric practice model, were no different when compared with older adults cared for in a general medical services who tended to be younger and healthier,” explained lead author Daniel Oates, MD, MSc, an assistant professor of medicine at BUSM and a geriatrician at BMC. “In fact, this was the case even though 71 percent of BU Geriatrics’ patients admitted to the inpatient geriatrics service came from home care or nursing home programs and were significantly more likely to have a diagnosis of dementia, depression or weight loss; a history of delirium; or a pressure ulcer,” he added. Additionally, BU Geriatrics’ patients were more likely to be discharged to a skilled nursing facility (43 percent for geriatric patients vs 17 percent for general medical patients) or home with services from a certified home health agency (26 percent for geriatric patients vs 16 percent for general medical patients), which are further indicators of the illness severity and complexity of the geriatric patients.
Oates added, “BU Geriatric Services is a “working model” of geriatric care, not a costly “add on” to what is already in place. This study demonstrates that it is possible to limit re-hospitalizations within current care delivery models.”
BUSM Researchers Identify Role of FOXO1 Gene in Parkinson’s Disease
A recent study led by researchers at Boston University School of Medicine (BUSM) revealed that the FOXO1 gene may play an important role in the pathological mechanisms of Parkinson’s disease. These findings are published online in PLoS Genetics, a peer-reviewed open-access journal published by the Public Library of Science.
The study was led by Alexandra Dumitriu, PhD, a postdoctoral associate in the department of neurology at BUSM. Richard Myers, PhD, professor of neurology at BUSM, is the study’s senior author.
According to the Parkinson’s Disease Foundation, 60,000 Americans are diagnosed with Parkinson’s disease each year and approximately one million Americans are currently living with the disease.
Parkinson’s disease is a complex neurodegenerative disorder characterized by a buildup of proteins in nerve cells that lead to their inability to communicate with one another, causing motor function issues, including tremors and slowness in movement, as well as dementia. The substantia nigra is an area of the midbrain that helps control movement, and previous research has shown that this area of the brain loses neurons as Parkinson’s disease progresses.
The researchers analyzed gene expression differences in brain tissue between 27 samples with known Parkinson’s disease and 26 samples from neurologically healthy controls. This data set represents the largest number of brain samples used in a whole-genome expression study of Parkinson’s disease to date. The novel aspect of this study is represented by the researchers’ emphasis on removing possible sources of variation by minimizing the differences among samples. They used only male brain tissue samples that showed no significant marks of Alzheimer’s disease pathology, one of the frequently co-occurring neurological diseases in Parkinson’s disease patients. The samples also had similar tissue quality and were from the brain’s prefrontal cortex, one of the less studied areas for the disease. The prefrontal cortex does not show neuronal death to the same extent as the substantia nigra, although it displays molecular and pathological modifications during the disease process, while also being responsible for the dementia present in a large proportion of Parkinson’s disease patients.
Results of the expression experiment showed that the gene FOXO1 had increased expression in the brain tissue samples with known Parkinson’s disease. FOXO1 is a transcriptional regulator that can modify the expression of other genes. Further examination of the FOXO1 gene showed that two single-nucleotide polymorphisms (SNPs), or DNA sequence variations, were significantly associated with age at onset of Parkinson’s disease.
“Our hypothesis is that FOXO1 acts in a protective manner by activating genes and pathways that fight the neurodegeneration processes,” said Dumitriu. “If this is correct, there could be potential to explore FOXO1 as a therapeutic drug target for Parkinson’s disease.”
Research reported in this publication was supported in part by the National Institute of Neurological Disorders and Stroke under award number 1R01NS076843-01, the Cogan Family Foundation, the Robert P. & Judith N. Goldberg Foundation and the William N. and Bernice E. Bumpus Foundation.
BUSM and VA Researchers Discover Dissociative Subtype of Posttraumatic Stress Disorder
A recent study by Erika J. Wolf, PhD, and Principal Investigator Mark W. Miller, PhD, both from the National Center for PTSD at the VA Boston Healthcare System and Department of Psychiatry at Boston University School of Medicine (BUSM), found an association between posttraumatic stress disorder (PTSD) and dissociation. The findings, published in the Archives of General Psychiatry, suggest that symptoms of dissociation, which reflect problems in consciousness and awareness, are a prominent feature of PTSD in a distinct subtype of individuals with the disorder.
The relationship of dissociation and PTSD is controversial but important for accurately classifying PTSD and better understanding its course. The researchers studied PTSD and dissociative symptoms in 492 veterans and their intimate partners, all of whom had histories of trauma. Participants reported exposure to a variety of traumatic events including combat, childhood physical and sexual abuse, partner abuse, motor vehicle accidents and natural disasters with most participants reporting exposure to multiple types of traumatic events.
In the study, participants were interviewed by clinicians using the Clinician Administered PTSD Scale (CAPS), a diagnostic instrument that measures the frequency and severity of PTSD and dissociation symptoms. Analysis revealed a small but distinct subset of participants characterized by high symptoms of dissociation and PTSD along with high rates of sexual assault history. This study contributes to a growing body of research, providing a basis for adding the new dissociative subtype distinction to the PTSD diagnosis in the American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders (DSM-5).
"This study helps to identify a small group of individuals who show a unique pattern of post-traumatic symptoms marked by derealization, or feeling that one's surroundings are unreal or unfamiliar, and depersonalization, or feeling that one’s body is unfamiliar or strange," said Wolf. "The results clarify that these symptoms are not a core part of PTSD for most people with the disorder. However, identification of this group of individuals is important for maximizing PTSD treatment effectiveness."
Funding for this study was provided by National Institute on Mental Health award RO1 MH079806 and a VA Merit Review Grant awarded to Mark Miller and by a VA Career Development Award to Erika Wolf.
BUSM In Vitro Study Identifies Potential Combination Therapy for Breast Cancer
A study conducted at Boston University School of Medicine (BUSM) demonstrates an effective combination therapy for breast cancer cells in vitro. The findings, published in the July 2012 issue of Anticancer Research, raise the possibility of using this type of combination therapy for different forms of breast cancer, including those that develop resistance to chemotherapy and other treatments.
The study was led by researchers at the Boston University Cancer Center. Sibaji Sarkar, PhD, adjunct instructor of medicine at BUSM, is the study’s corresponding author.
According to the Centers for Disease Control and Prevention, breast cancer is the most common cancer among women in the United States aside from non-melanoma skin cancer. Breast cancer also is one of the leading causes of cancer death among women of all races and Hispanic origin populations.
Triple negative breast cancer, which accounts for approximately 14 to 20 percent of all breast cancer cases, is a type of the disease that occurs when the cancer cells lack hormone receptors, including the receptor called HER-2, and typically will not respond to hormone and herceptin-based therapies. Triple negative breast cancer occurs more often in African-American women and is considered to be a more aggressive form of the disease with higher rates of recurrence and mortality than other forms of breast cancer.
“Cancer is like a car without brakes. Cell growth speeds up and it doesn’t stop,” said Sarkar. “When expressed, tumor suppressor genes, which work in a protective way to limit tumor growth, function as the brakes. They are not expressed in most cancers, causing the cancer to grow and potentially metastasize.”
A major focus in the area of anti-cancer drug development is to find a way to re-express tumor suppressor genes so that they can help inhibit cancer cell growth. Some tumor suppressor genes are imprinted, meaning that from the two genes inherited from the mother and father, only one of the genes is functional. In cancer, both imprinted tumor suppressor genes may become non-functional and unable to stop tumor growth.
The researchers tested, in vitro, a combination therapy of an epigenetic drug with a protease inhibitor on breast cancer cell lines that are hormone responsive and breast cancer lines, like triple negative, that are not hormone responsive. They utilized histone deacetylases inhibitors (HDACi) and calpeptin, which inhibits calpain, a protein involved in the regulation of signaling proteins. Calpain inhibition is being studied as a potential treatment model for blood clots and other neurological diseases.
In this study, they found that the combination therapy both inhibited cell growth and increased cell death in both cancer cell lines by inducing cell cycle arrest and cell death. However, the mechanism of how the combination therapy stops the cells from growing was different. Cells in the hormone responsive line stopped the cell cycle in an earlier phase compared to the non-hormone responsive cells. In the triple negative breast cancer cell line, the inhibitors allowed an imprinted tumor suppressing gene, ARHI, to re-express, which helped stop the growth of the cancer cells and led to cancer cell death.
“The study data demonstrates that HDACi’s bring back the brakes of the car, halting cell growth and promoting cell death,” added Sarkar, who also is a faculty member at the Genome Science Institute at Boston University. “These results provide a model to investigate the re-expression of tumor suppressor genes, including imprinted genes, in many forms of breast cancer.”
This study needs further investigation but raises the possibility of using this type of combination therapy for diverse types of breast cancers including those that are hormone refractory and develop drug resistance to conventional chemotherapy.
This study was funded by the American Cancer Society.
Researchers Find Abuse During Childhood and Adolescence may Contribute to Obesity in Adulthood
Investigators from Boston University School of Medicine (BUSM) and Boston University’s Slone Epidemiology Center report research findings that may shed light on influences on obesity during adulthood. Appearing in the journal Pediatrics, the study found an association of severity of sexual and physical abuse during childhood and adolescence with obesity during adulthood.
The findings were based on the ongoing Black Women’s Health Study, which has followed a large cohort of African-American women since 1995. Information provided in 2005 by more than 33,000 participants on early life experiences of abuse was assessed in relation to two measures of obesity: body mass index of 30 kg/m2 or more as a measure of overall obesity and waist circumference greater than 35 inches as a measure of central obesity.
The risk of obesity in 2005 by either measure was estimated to be approximately 30 percent greater among women in the highest category of physical and sexual abuse than in women who reported no abuse. The association was dampened but not fully explained by allowance for reproductive history, diet, physical activity and depressive symptoms, which might have been intermediates between abuse and weight gain.
According to the researchers, the findings add to growing evidence that experiences during childhood may have long-term health consequences. “Abuse during childhood may adversely shape health behaviors and coping strategies, which could lead to greater weight gain in later life,” explained Renee Boynton-Jarrett, MD, the lead investigator of the study and a pediatric primary care physician at Boston Medical Center. She also noted that metabolic and hormonal disruptions resulting from abuse could have that effect and that childhood abuse could be a marker for other adversities. “Ultimately, greater understanding of pathways between early life abuse and adult weight status may inform obesity prevention and treatment approaches.” Boynton-Jarrett cautioned that further studies are needed to clarify just which factors are responsible for the association of abuse with obesity and noted there is a consensus that pediatric providers should screen for abuse.
Other BUSPH researchers include: Lynn Rosenberg, professor of epidemiology and PI of the Black Women’s Health Study; Julie R. Palmer, professor of epidemiology and Co-PI of the study; Lauren A. Wise, associate professor of epidemiology; and Deborah Boggs, post-doctoral fellow at BU's Slone Epidemiology Center."
Funding for the Black Women’s Health Study is provided by a grant from the National Cancer Institute (CA 058420). Dr. Boynton-Jarrett is supported by the William T Grant Foundation, Boston University Building Interdisciplinary Research Careers in Women’s Health K12 HD043444 NIH Office of Women’s Health Research, and the Academic Pediatric Association.
BUSM Study Finds Genes Associated with Hippocampal Atrophy
In a genome-wide association (GWA) study, researchers from Boston University Schools of Medicine (BUSM) and Public Health (BUSPH) have identified several genes which influence degeneration of the hippocampus, the part of the brain most associated with Alzheimer disease (AD). The study, which currently appears online as a Rapid Communication in the Annals of Neurology, demonstrates the efficacy of endophenotypes for broadening the understanding of the genetic basis of and pathways leading to AD.
AD is a progressive neurodegenerative disorder for which there are no prevention methods. Available drugs only marginally affect disease severity and progression, making AD effectively untreatable.
GWA studies using very large samples have increased the number of robust associations to 10 genes, including APOE. However, these genes account for no more than 35 percent of the inherited risk of AD and most of the genetic underpinning of the disorder remains unexplained. According to the researchers, magnetic resonance imaging (MRI) of the brain provides in vivo quantitative measures of neurodegenerative and cerebrovascular brain injury that may represent AD-related changes long before clinical symptoms appear. These measures are more powerful than comparisons of individuals with AD with cognitively healthy persons because they avoid misclassification of normal persons who will develop disease in the future.
BUSM researchers conducted a two-stage GWA study for quantitative measures of hippocampal volume (HV), total cerebral volume (TCV) and white matter hyperintensities (WMH). Brain MRI measures of HV, TCV and WMH were obtained from 981 Caucasian and 419 African-American AD cases and their cognitively normal siblings in the MIRAGE (Multi Institutional Research in Alzheimer’s Genetic Epidemiology) Study. In addition, similar MRI measures were obtained from 168 AD cases, 336 individuals with mild cognitive impairment and 188 controls (all Caucasian) in the AD Neuroimaging Initiative (ADNI) Study. The MIRAGE Caucasian families and ADNI subjects were included in the first stage and the MIRAGE African American families were added in stage two. Results from the two Caucasians data sets were combined by meta-analysis.
In stage two, one genetic marker (i.e. single nucleotide polymorphism or SNP) from each of the gene regions that were most significantly associated with AD in the Caucasian data sets was evaluated in the African-American data set.
Novel genome-wide significant associations were observed for HV with SNPs in the APOE, F5/SELP, LHFP, and GCFC2 gene regions. All of these associations were supported by evidence in each data set.
“Our two-stage GWAS identified highly significant associations between a measure of degeneration in the brain region most strongly correlated with AD and several genes in both Caucasian and African American samples containing AD, cognitively impaired and cognitively healthy subjects. One of these associations was with the ε4 variant of APOE which is the most well-established genetic risk factor for AD. Other associations were demonstrated with markers in F5/SELP, LHFP, and GCFC2, genes not previously implicated in this disease” explained senior author Lindsay Farrer, PhD, chief of biomedical genetics at BUSM. He also noted, “previous studies showed that blood level of P-selectin (the protein encoded by SELP) has been correlated with rate of cognitive decline in AD patients.”
Farrer believes it is very likely that the number and specificity of these associations will increase in future studies using larger samples and focused on additional precise structural and functional MRI measures. “These findings will inform experiments designed to increase our understanding of disease-causing mechanism and may lead to new therapeutics targets,” added Farrer.
Researchers from Massachusetts General Hospital, Indiana University School of Medicine and University of California at Davis also collaborated on this study.
This study was supported by the National Institute on Aging (NIA), the Dana Foundation and the National Institutes of Health Clinical and Translational Science Institute. ADNI is funded by the NIA and the National Institute of Biomedical Imaging and Bioengineering, and through generous contributions from the following: Abbott, AstraZeneca AB, Bayer Schering Pharma AG, Bristol-Myers Squibb, Eisai Global Clinical Development, Elan Corporation, Genentech, GE Healthcare, GlaxoSmithKline, Innogenetics, Johnson and Johnson, Eli Lilly and Co., Medpace, Merck and Co., Novartis AG, Pfizer, F. Hoffman-La Roche, Schering-Plough, Synarc, and Wyeth, as well as nonprofit partners the Alzheimer’s Association and Alzheimer’s Drug Discovery Foundation, with participation from the US Food and Drug Administration. Private sector contributions to ADNI are facilitated by the Foundation for the National Institutes of Health (www.fnih.org).
BUSM Study Finds Gout and Hyperuricemia on the Rise in the U.S.
Boston University School of Medicine (BUSM) researchers have found that the incidence of gout and hyperuricemia (high uric acid levels) in the U.S. has risen significantly over the last 20 years and is associated with major medical disorders like hypertension and chronic kidney disease. The study, which is published in the American Journal of Medicine, was led by Hyon Choi, MD, DrPH, professor of medicine in the section of rheumatology and the clinical epidemiology unit at BUSM and rheumatologist at Boston Medical Center (BMC).
Gout is a common inflammatory arthritis triggered by crystallization of uric acid within the joints, causing severe pain and swelling.
Using data from the latest U.S. National Health and Nutrition Examination Survey (NHANES) conducted in 2007 and 2008, which included data from 5,707 participants, the researchers found that gout now affects 8.3 million Americans, or four percent of the population. They also found that hyperuricemia affects 43.3 million U.S. adults, or 21 percent of the population.
The study results demonstrated that participants with gout have remarkably high rates of hypertension (74 percent) and chronic kidney disease (71 percent). More than half of this patient population was obese (53 percent) and a significant number had diabetes (26 percent) and kidney stones (24 percent). These participants also showed high rates of heart attack (14 percent), heart failure (11 percent) and stroke (10 percent).
Additionally, study results showed that among individuals with the highest uric acid levels, rates of kidney disease (86 percent), hypertension (66 percent) and obesity (65 percent) were high. Approximately one third of the survey participants had heart failure and diabetes, and the prevalence of heart attack (23 percent) and stroke (12 percent) also were high.
“These findings highlight the remarkable prevalences and population estimates of medical disorders associated with gout and hyperuricemia in the U.S.,” said Choi, the study’s senior author. “Appropriate preventive and management measures of these associated conditions should be implemented in gout management, and when considering treatment strategies in gout, the lifestyle and pharmacologic measures that can concurrently improve serum uric acid and reduce associated disorders should be preferred.”
The research was supported by Takeda Pharmaceuticals International, Inc.