Metabolic SyndromeNCT03279432
Vitamin D-related Genes and Metabolic Disorders
An observational study of Metabolic Syndrome and Obesity, run by National Institute on Aging (NIA).
Trial summary
The link between metabolic disturbances and vitamin D receptor (VDR) and MEGALIN (or LRP2) gene polymorphisms remains unclear, particularly among African-American adults. The associations of single nucleotide polymorphisms (SNPs) for VDR [rs1544410(BsmI:G/A), rs7975232(ApaI:A/C), rs731236(TaqI:G/A)] and MEGALIN… Read more about this study
- Who is it for?
- Ages 30 to 64 yearsHealthy volunteers can take part
- Conditions the study is for
- Metabolic Syndrome, Obesity, Central Obesity
- How many people
- 1,021 participants
- Where
- No sites listed yet
- Study dates
- 18 Aug 2004to 7 Jul 2013
- Phase
- Observational
- Are there results?
- None posted in the registry
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 30 to 64 years
- All sexes
- Healthy volunteers accepted
- Adult
Study population: Of the 3,720 baseline participants (mean±SD age(y) of 48.3±9.4, 45.3% men, and 59.1% African-American), genetic data were available on 1,024 African-American participants. Incomplete covariate data reduced the sample to n=769, while additional exclusions lead to a sample size ranging between 574 and 598 participants, with 539 having complete data on all baseline and follow-up outcome measures (cross-sectional part of the analysis). In the longitudinal analysis, metabolic disturbance-free at baseline participants were selected for each outcome. Sample sizes ranged from n=246 (central obesity-free) to n=466 (hyperglycemia-free). There were n=294 MetS-free individuals at baseline (Figure 1).
Who may be able to join
- 3,720 baseline participants (mean±SD age(y) of 48.3±9.4, 45.3% men, and 59.1% African-American),
- Genetic data were available on 1,024 African-American participants.
- Incomplete covariate data reduced the sample to n=769, while additional exclusions lead to a sample size ranging between 574 and 598 participants, with 539 having complete data on all baseline and follow-up outcome measures (cross-sectional part of the analysis).
- In the longitudinal analysis, metabolic disturbance-free at baseline participants were selected for each outcome. Sample sizes ranged from n=246 (central obesity-free) to n=466 (hyperglycemia-free).
- There were n=294 MetS-free individuals at baseline.
Who cannot join
- Whites in HANDLS, since they did not have any genetic data collected.
- All African-Americans in HANDLS without genetic data collected.
- All African-Americans in HANDLS with genetic data collected, who had incomplete data on key outcome variables and/or basic covariates of interest.
About this study
Official title: Vitamin D Receptor and Megalin Gene Polymorphisms and Their Association With Obesity, Central Obesity and the Metabolic Syndrome
The link between metabolic disturbances and vitamin D receptor (VDR) and MEGALIN (or LRP2) gene polymorphisms remains unclear, particularly among African-American adults. The associations of single nucleotide polymorphisms (SNPs) for VDR [rs1544410(BsmI:G/A), rs7975232(ApaI:A/C), rs731236(TaqI:G/A)] and MEGALIN [rs3755166:G/A,rs2075252:C/T, rs2228171:C/T] genes with incident and prevalent metabolic disturbances, including obesity, central obesity and metabolic syndrome (MetS) were evaluated.
From 1,024 African-Americans participating in the Healthy Aging in Neighborhoods of Diversity across the Life Span (HANDLS, Baltimore, MD, 2004-2013) study, 539 subjects were selected who had complete genetic data as well as covariates selected for metabolic outcomes at two consecutive examinations (visits 1 and 2) with a mean follow-up time of 4.64±0.93y. Haplotype (HAP) analyses generated polymorphism groups that were linked to incident and prevalent metabolic disturbances.
Read the detailed description
Adiposity, especially central adiposity, is a key component of the metabolic syndrome (MetS), which is accompanied by hyperglycemia, elevated blood pressure, lower HDL cholesterol and hypertriglyceridemia.(Ford, et al., 2003,Grundy, 1999)_ENREF_4 MetS increases the risk of type 2 diabetes (T2D) and cardiovascular disease by 1.7- and 5-folds, respectively.(Alberti, et al., 2009,Ford, et al., 2003,Galassi, et al., 2006) MetS is heritable and polygenic.(Maes, et al., 1997) Genetic variability contributes to 16%-85% of changes in Body Mass Index (BMI)(Yang, et al., 2007) and 37%-81% in waist circumference (WC) (e.g.(Ochs-Balcom, et al., 2011)). MetS is a major public health concern, increasing all-cause mortality rates, disability and health care costs.(Appels and Vandenbroucke, 2006,Bender, et al., 2006,Colditz, 1999,Doig, 2004,Ferrucci and Alley, 2007,Hill, et al., 2004,Solomon and Manson, 1997,Stevens, 2000,Wolf and Colditz, 1998) Obesity is implicated in the etiology of vitamin D deficiency. Serum 25-hydroxyvitamin D [25(OH)D] concentration correlates inversely with adiposity.(Beydoun, et al., 2010,Dorjgochoo, et al., 2012) Conversely, vitamin D3 may play a role in obesity by modulating intracellular calcium homeostasis, because higher intracellular calcium triggers lipogenesis and suppresses lipolysis.(Zemel, 2003) Many organs express vitamin D receptor (VDR), a part of the nuclear hormone receptor super-family. The VDR-1,25(OH)2D3 complex modulates transcription of vitamin D responsive genes(Kato, 2000) and influences adipocyte differentiation both in vitro and in vivo.(Wood, 2008) Epidemiological studies have shown associations of VDR gene polymorphisms with adiposity and related metabolic disorders.(Filus, et al., 2008,Grundberg, et al., 2004,Gu, et al., 2009,Ochs-Balcom, et al., 2011,Oh and Barrett-Connor, 2002,Ortlepp, et al., 2001,Ortlepp, et al., 2003,Speer, et al., 2001,Ye, et al., 2001) However, studies specifically examining adiposity outcomes either had small sample sizes (<400), (e.g.(Filus, et al., 2008,Grundberg, et al., 2004,Speer, et al., 2001)) or were restricted to one sex, (e.g. (Grundberg, et al., 2004,Ochs-Balcom, et al., 2011)) but more importantly were all cross-sectional or case-control by design.(Filus, et al., 2008,Grundberg, et al., 2004,Gu, et al., 2009,Ochs-Balcom, et al., 2011,Oh and Barrett-Connor, 2002,Ortlepp, et al., 2001,Ortlepp, et al., 2003,Speer, et al., 2001,Ye, et al., 2001) MEGALIN (aka low-density lipoprotein receptor-related protein-2 [LRP-2]), is the endocytic vitamin D-binding protein receptor which allows vitamin D entry into cells and whose expression is directly regulated by both vitamin D (Gressner, et al., 2008)) and vitamin A.(Liu, et al., 1998) MEGALIN may influences obesity by mediating leptin transport through the blood-brain barrier and modulating leptin signaling,(Dietrich, et al., 2008) or by facilitating transcytosis of its precursor hormone thyroglobulin.(Lisi, et al., 2005) Collectively, leptin and thyroid hormones affect adiposity through energy metabolism regulation.(Beydoun, et al., 2011) MEGALIN acting also as the receptor for sex-hormone binding globulin (SHBG) may play a role in the interaction between estrogen, vitamin D and intracellular calcium in adipocytes, resulting in sex-specific effects of MEGALIN polymorphisms on obesity phenotypes.(Ding, et al., 2008) In this study, it is hypothesized that selected polymorphisms in VDR and MEGALIN genes have sex-specific associations with several key metabolic disturbances in a longitudinal study of African-American urban adults.
- Conditions
- Metabolic Syndrome, Obesity, Central Obesity
- Keywords
- VDR, MEGALIN, haplotypes, obesity, metabolic syndrome
- Medical subject headings
- Metabolic Syndrome, Obesity, Obesity, Abdominal
What is being measured
The primary outcome is the main question the study is designed to answer.
Obesity
Obesity was defined as BMI≥30 kg/m2.
Measured: 2004-2013
Central Obesity
Central obesity was defined based on waist circumference (WC) ≥ 102 cm or 40 inches (men), ≥ 88 cm or 35 inches (women)
Measured: 2004-2013
Metabolic Syndrome
Participants who screened positive on at least 3 of 5 conditions ((1) central obesity (see above); (2) dyslipidemia: TAG≥1.695 mmol/L (150 mg/dl); (3) dyslipidemia: HDL-C<40 mg/dL (male), <50 mg/dL (female); (4) blood pressure≥130/85 mmHg; (5) fasting plasma glucose≥6.1 mmol/L (110 mg/dl).(39)) were classified as MetS-positive (2) Similarly, continuous annual rates of change (Δ) in metabolic outcomes were considered, specifically number of metabolic disturbances (MetD), BMI, WC, SBP, DBP, TAG, HDL-C, and Glucose. Binary incident outcomes included obesity, central obesity, MetS and other metabolic disturbance (i.e. hypertension, dyslipidemia-TAG, dyslipidemia-HDL and hyperglycemia).
Measured: 2004-2013
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted12 Sep 2017
- Study start18 Aug 2004
- Primary completion7 Jul 2013
- Study completion7 Jul 2013
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (35)Papers the sponsor has linked to this study.
- Other trials for Metabolic SyndromeStudies of the same condition, open and under way.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Observational
- Observational model
- Cohort
- Time perspective
- Prospective
- Enrolment
- 1,021 participants (actual)
Sponsor and investigators
- Lead sponsor
- National Institute on Aging (NIA)
- Sponsor type
- US National Institutes of Health
- Responsible party
- Principal investigator, May Ahmad Baydoun, National Institute on Aging (NIA)
- Investigators
- Alan B Zonderman, PhD, Principal investigator, National Institute on Aging (NIA)Michele K Evans, MD, Principal investigator, National Institute on Aging (NIA)
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT03279432
- Sponsor's protocol ID
- NIA
- Status last verified
- Sep 2017
- First submitted
- 8 Sep 2017
- Last updated
- 12 Sep 2017
- Results posted
- No
- Data monitoring committee
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
- Individual data sharing
- No
Publications
Ford ES, Mokdad AH, Giles WH, Brown DW. The metabolic syndrome and antioxidant concentrations: findings from the Third National Health and Nutrition Examination Survey. Diabetes. 2003 Sep;52(9):2346-52. doi: 10.2337/diabetes.52.9.2346.
PubMed 12941775Grundy SM. Hypertriglyceridemia, insulin resistance, and the metabolic syndrome. Am J Cardiol. 1999 May 13;83(9B):25F-29F. doi: 10.1016/s0002-9149(99)00211-8.
PubMed 10357572Galassi A, Reynolds K, He J. Metabolic syndrome and risk of cardiovascular disease: a meta-analysis. Am J Med. 2006 Oct;119(10):812-9. doi: 10.1016/j.amjmed.2006.02.031.
PubMed 17000207Alberti KG, Eckel RH, Grundy SM, Zimmet PZ, Cleeman JI, Donato KA, Fruchart JC, James WP, Loria CM, Smith SC Jr; International Diabetes Federation Task Force on Epidemiology and Prevention; Hational Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International Atherosclerosis Society; International Association for the Study of Obesity. Harmonizing the metabolic syndrome: a joint interim statement of the International Diabetes Federation Task Force on Epidemiology and Prevention; National Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International Atherosclerosis Society; and International Association for the Study of Obesity. Circulation. 2009 Oct 20;120(16):1640-5. doi: 10.1161/CIRCULATIONAHA.109.192644. Epub 2009 Oct 5.
PubMed 19805654Maes HH, Neale MC, Eaves LJ. Genetic and environmental factors in relative body weight and human adiposity. Behav Genet. 1997 Jul;27(4):325-51. doi: 10.1023/a:1025635913927.
PubMed 9519560Yang W, Kelly T, He J. Genetic epidemiology of obesity. Epidemiol Rev. 2007;29:49-61. doi: 10.1093/epirev/mxm004. Epub 2007 Jun 12.
PubMed 17566051Ochs-Balcom HM, Chennamaneni R, Millen AE, Shields PG, Marian C, Trevisan M, Freudenheim JL. Vitamin D receptor gene polymorphisms are associated with adiposity phenotypes. Am J Clin Nutr. 2011 Jan;93(1):5-10. doi: 10.3945/ajcn.2010.29986. Epub 2010 Nov 3.
PubMed 21048058Appels CW, Vandenbroucke JP. Overweight, obesity, and mortality. N Engl J Med. 2006 Dec 21;355(25):2699; author reply 2700-1. doi: 10.1056/NEJMc062590. No abstract available.
PubMed 17182999Bender R, Zeeb H, Schwarz M, Jockel KH, Berger M. Causes of death in obesity: relevant increase in cardiovascular but not in all-cancer mortality. J Clin Epidemiol. 2006 Oct;59(10):1064-71. doi: 10.1016/j.jclinepi.2006.01.006. Epub 2006 May 30.
PubMed 16980146Doig GS. Obesity-related excess mortality: What should we do now? Crit Care Med. 2004 Apr;32(4):1084-5. doi: 10.1097/01.ccm.0000119934.01548.af. No abstract available.
PubMed 15071413Ferrucci L, Alley D. Obesity, disability, and mortality: a puzzling link. Arch Intern Med. 2007 Apr 23;167(8):750-1. doi: 10.1001/archinte.167.8.750. No abstract available.
PubMed 17452535Solomon CG, Manson JE. Obesity and mortality: a review of the epidemiologic data. Am J Clin Nutr. 1997 Oct;66(4 Suppl):1044S-1050S. doi: 10.1093/ajcn/66.4.1044S.
PubMed 9322585Stevens J. Obesity and mortality in African-Americans. Nutr Rev. 2000 Nov;58(11):346-53. doi: 10.1111/j.1753-4887.2000.tb01832.x.
PubMed 11140906Colditz GA. Economic costs of obesity and inactivity. Med Sci Sports Exerc. 1999 Nov;31(11 Suppl):S663-7. doi: 10.1097/00005768-199911001-00026.
PubMed 10593542Hill JO, Sallis JF, Peters JC. Economic analysis of eating and physical activity: a next step for research and policy change. Am J Prev Med. 2004 Oct;27(3 Suppl):111-6. doi: 10.1016/j.amepre.2004.06.010.
PubMed 15450621
Study at a glance
From the registry record, last updated by the sponsor on 12 Sep 2017. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Vitamin D Receptor and Megalin Gene Polymorphisms and Their Association With Obesity, Central Obesity and the Metabolic Syndrome
- ClinicalTrials.gov ID
- NCT03279432
- Acronym / sponsor ID
- NIA
- Conditions
- Metabolic Syndrome, Obesity, Central Obesity
- Keywords
- VDR, MEGALIN, haplotypes, obesity, metabolic syndrome
- Study type
- Observational
- Recruitment status
- Completed
- Enrolment
- 1,021 participants (actual)
- Lead sponsor
- National Institute on Aging (NIA)US National Institutes of Health
- Study start
- 18 Aug 2004 (actual)
- Primary completion
- 7 Jul 2013 (actual)
- Study completion
- 7 Jul 2013 (actual)
- First posted
- 12 Sep 2017 (actual)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
The link between metabolic disturbances and vitamin D receptor (VDR) and MEGALIN (or LRP2) gene polymorphisms remains unclear, particularly among African-American adults. The associations of single nucleotide polymorphisms (SNPs) for VDR [rs1544410(BsmI:G/A), rs7975232(ApaI:A/C), rs731236(TaqI:G/A)] and MEGALIN [rs3755166:G/A,rs2075252:C/T, rs2228171:C/T] genes with incident and prevalent metabolic disturbances, including obesity, central obesity and metabolic syndrome (MetS) were evaluated.
From 1,024 African-Americans participating in the Healthy Aging in Neighborhoods of Diversity across the Life Span (HANDLS, Baltimore, MD, 2004-2013) study, 539 subjects were selected who had complete genetic data as well as covariates selected for metabolic outcomes at two consecutive examinations (visits 1 and 2) with a mean follow-up time of 4.64±0.93y. Haplotype (HAP) analyses generated polymorphism groups that were linked to incident and prevalent metabolic disturbances.
Detailed description
Adiposity, especially central adiposity, is a key component of the metabolic syndrome (MetS), which is accompanied by hyperglycemia, elevated blood pressure, lower HDL cholesterol and hypertriglyceridemia.(Ford, et al., 2003,Grundy, 1999)_ENREF_4 MetS increases the risk of type 2 diabetes (T2D) and cardiovascular disease by 1.7- and 5-folds, respectively.(Alberti, et al., 2009,Ford, et al., 2003,Galassi, et al., 2006) MetS is heritable and polygenic.(Maes, et al., 1997) Genetic variability contributes to 16%-85% of changes in Body Mass Index (BMI)(Yang, et al., 2007) and 37%-81% in waist circumference (WC) (e.g.(Ochs-Balcom, et al., 2011)). MetS is a major public health concern, increasing all-cause mortality rates, disability and health care costs.(Appels and Vandenbroucke, 2006,Bender, et al., 2006,Colditz, 1999,Doig, 2004,Ferrucci and Alley, 2007,Hill, et al., 2004,Solomon and Manson, 1997,Stevens, 2000,Wolf and Colditz, 1998) Obesity is implicated in the etiology of vitamin D deficiency. Serum 25-hydroxyvitamin D [25(OH)D] concentration correlates inversely with adiposity.(Beydoun, et al., 2010,Dorjgochoo, et al., 2012) Conversely, vitamin D3 may play a role in obesity by modulating intracellular calcium homeostasis, because higher intracellular calcium triggers lipogenesis and suppresses lipolysis.(Zemel, 2003) Many organs express vitamin D receptor (VDR), a part of the nuclear hormone receptor super-family. The VDR-1,25(OH)2D3 complex modulates transcription of vitamin D responsive genes(Kato, 2000) and influences adipocyte differentiation both in vitro and in vivo.(Wood, 2008) Epidemiological studies have shown associations of VDR gene polymorphisms with adiposity and related metabolic disorders.(Filus, et al., 2008,Grundberg, et al., 2004,Gu, et al., 2009,Ochs-Balcom, et al., 2011,Oh and Barrett-Connor, 2002,Ortlepp, et al., 2001,Ortlepp, et al., 2003,Speer, et al., 2001,Ye, et al., 2001) However, studies specifically examining adiposity outcomes either had small sample sizes (<400), (e.g.(Filus, et al., 2008,Grundberg, et al., 2004,Speer, et al., 2001)) or were restricted to one sex, (e.g. (Grundberg, et al., 2004,Ochs-Balcom, et al., 2011)) but more importantly were all cross-sectional or case-control by design.(Filus, et al., 2008,Grundberg, et al., 2004,Gu, et al., 2009,Ochs-Balcom, et al., 2011,Oh and Barrett-Connor, 2002,Ortlepp, et al., 2001,Ortlepp, et al., 2003,Speer, et al., 2001,Ye, et al., 2001) MEGALIN (aka low-density lipoprotein receptor-related protein-2 [LRP-2]), is the endocytic vitamin D-binding protein receptor which allows vitamin D entry into cells and whose expression is directly regulated by both vitamin D (Gressner, et al., 2008)) and vitamin A.(Liu, et al., 1998) MEGALIN may influences obesity by mediating leptin transport through the blood-brain barrier and modulating leptin signaling,(Dietrich, et al., 2008) or by facilitating transcytosis of its precursor hormone thyroglobulin.(Lisi, et al., 2005) Collectively, leptin and thyroid hormones affect adiposity through energy metabolism regulation.(Beydoun, et al., 2011) MEGALIN acting also as the receptor for sex-hormone binding globulin (SHBG) may play a role in the interaction between estrogen, vitamin D and intracellular calcium in adipocytes, resulting in sex-specific effects of MEGALIN polymorphisms on obesity phenotypes.(Ding, et al., 2008) In this study, it is hypothesized that selected polymorphisms in VDR and MEGALIN genes have sex-specific associations with several key metabolic disturbances in a longitudinal study of African-American urban adults.
Study design
- Observational model
- Cohort
- Time perspective
- Prospective
Who may qualify
- Ages
- 30 to 64 years
- Sex
- All
- Healthy volunteers
- Accepted
- Age groups
- Adult
- Study population
- Of the 3,720 baseline participants (mean±SD age(y) of 48.3±9.4, 45.3% men, and 59.1% African-American), genetic data were available on 1,024 African-American participants. Incomplete covariate data reduced the sample to n=769, while additional exclusions lead to a sample size ranging between 574 and 598 participants, with 539 having complete data on all baseline and follow-up outcome measures (cross-sectional part of the analysis). In the longitudinal analysis, metabolic disturbance-free at baseline participants were selected for each outcome. Sample sizes ranged from n=246 (central obesity-free) to n=466 (hyperglycemia-free). There were n=294 MetS-free individuals at baseline (Figure 1).
Key inclusion criteria (5 listed)
- 3,720 baseline participants (mean±SD age(y) of 48.3±9.4, 45.3% men, and 59.1% African-American),
- Genetic data were available on 1,024 African-American participants.
- Incomplete covariate data reduced the sample to n=769, while additional exclusions lead to a sample size ranging between 574 and 598 participants, with 539 having complete data on all baseline and follow-up outcome measures (cross-sectional part of the analysis).
- In the longitudinal analysis, metabolic disturbance-free at baseline participants were selected for each outcome. Sample sizes ranged from n=246 (central obesity-free) to n=466 (hyperglycemia-free).
- There were n=294 MetS-free individuals at baseline.
Key exclusion criteria (3 listed)
- Whites in HANDLS, since they did not have any genetic data collected.
- All African-Americans in HANDLS without genetic data collected.
- All African-Americans in HANDLS with genetic data collected, who had incomplete data on key outcome variables and/or basic covariates of interest.
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Primary outcome
Obesity
Time frame: 2004-2013
Obesity was defined as BMI≥30 kg/m2.
Central Obesity
Time frame: 2004-2013
Central obesity was defined based on waist circumference (WC) ≥ 102 cm or 40 inches (men), ≥ 88 cm or 35 inches (women)
Metabolic Syndrome
Time frame: 2004-2013
Participants who screened positive on at least 3 of 5 conditions ((1) central obesity (see above); (2) dyslipidemia: TAG≥1.695 mmol/L (150 mg/dl); (3) dyslipidemia: HDL-C<40 mg/dL (male), <50 mg/dL (female); (4) blood pressure≥130/85 mmHg; (5) fasting plasma glucose≥6.1 mmol/L (110 mg/dl).(39)) were classified as MetS-positive (2) Similarly, continuous annual rates of change (Δ) in metabolic outcomes were considered, specifically number of metabolic disturbances (MetD), BMI, WC, SBP, DBP, TAG, HDL-C, and Glucose. Binary incident outcomes included obesity, central obesity, MetS and other metabolic disturbance (i.e. hypertension, dyslipidemia-TAG, dyslipidemia-HDL and hyperglycemia).
Results and safety
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 12 Sep 2017.
- Background: PubMed 12941775Ford ES, Mokdad AH, Giles WH, Brown DW. The metabolic syndrome and antioxidant concentrations: findings from the Third National Health and Nutrition Examination Survey. Diabetes. 2003 Sep;52(9):2346-52. doi: 10.2337/diabetes.52.9.2346.
- Background: PubMed 10357572Grundy SM. Hypertriglyceridemia, insulin resistance, and the metabolic syndrome. Am J Cardiol. 1999 May 13;83(9B):25F-29F. doi: 10.1016/s0002-9149(99)00211-8.
- Background: PubMed 17000207Galassi A, Reynolds K, He J. Metabolic syndrome and risk of cardiovascular disease: a meta-analysis. Am J Med. 2006 Oct;119(10):812-9. doi: 10.1016/j.amjmed.2006.02.031.
- Background: PubMed 19805654Alberti KG, Eckel RH, Grundy SM, Zimmet PZ, Cleeman JI, Donato KA, Fruchart JC, James WP, Loria CM, Smith SC Jr; International Diabetes Federation Task Force on Epidemiology and Prevention; Hational Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International Atherosclerosis Society; International Association for the Study of Obesity. Harmonizing the metabolic syndrome: a joint interim statement of the International Diabetes Federation Task Force on Epidemiology and Prevention; National Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International Atherosclerosis Society; and International Association for the Study of Obesity. Circulation. 2009 Oct 20;120(16):1640-5. doi: 10.1161/CIRCULATIONAHA.109.192644. Epub 2009 Oct 5.
- Background: PubMed 9519560Maes HH, Neale MC, Eaves LJ. Genetic and environmental factors in relative body weight and human adiposity. Behav Genet. 1997 Jul;27(4):325-51. doi: 10.1023/a:1025635913927.
- Background: PubMed 17566051Yang W, Kelly T, He J. Genetic epidemiology of obesity. Epidemiol Rev. 2007;29:49-61. doi: 10.1093/epirev/mxm004. Epub 2007 Jun 12.
- Background: PubMed 21048058Ochs-Balcom HM, Chennamaneni R, Millen AE, Shields PG, Marian C, Trevisan M, Freudenheim JL. Vitamin D receptor gene polymorphisms are associated with adiposity phenotypes. Am J Clin Nutr. 2011 Jan;93(1):5-10. doi: 10.3945/ajcn.2010.29986. Epub 2010 Nov 3.
- Background: PubMed 17182999Appels CW, Vandenbroucke JP. Overweight, obesity, and mortality. N Engl J Med. 2006 Dec 21;355(25):2699; author reply 2700-1. doi: 10.1056/NEJMc062590. No abstract available.
- Background: PubMed 16980146Bender R, Zeeb H, Schwarz M, Jockel KH, Berger M. Causes of death in obesity: relevant increase in cardiovascular but not in all-cancer mortality. J Clin Epidemiol. 2006 Oct;59(10):1064-71. doi: 10.1016/j.jclinepi.2006.01.006. Epub 2006 May 30.
- Background: PubMed 15071413Doig GS. Obesity-related excess mortality: What should we do now? Crit Care Med. 2004 Apr;32(4):1084-5. doi: 10.1097/01.ccm.0000119934.01548.af. No abstract available.
- Background: PubMed 17452535Ferrucci L, Alley D. Obesity, disability, and mortality: a puzzling link. Arch Intern Med. 2007 Apr 23;167(8):750-1. doi: 10.1001/archinte.167.8.750. No abstract available.
- Background: PubMed 9322585Solomon CG, Manson JE. Obesity and mortality: a review of the epidemiologic data. Am J Clin Nutr. 1997 Oct;66(4 Suppl):1044S-1050S. doi: 10.1093/ajcn/66.4.1044S.
- Related InfoLink provided by the sponsor.
- Individual participant dataSharing planned: No
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
Alan B Zonderman, PhD principal investigator
National Institute on Aging (NIA)
Michele K Evans, MD principal investigator
National Institute on Aging (NIA)
Questions about this trial
What is this clinical trial studying?
An observational study of Metabolic Syndrome and Obesity, run by National Institute on Aging (NIA).
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 5 inclusion and 3 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: finished, as of the sponsor's last update on 12 Sep 2017. Status can change between updates, so confirm with the study contact before making plans.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
Are results available for this study?
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Obesity (time frame: 2004-2013). The study lists 3 primary outcomes in all. It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT03279432, which also lists 35 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 12 Sep 2017.