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PubMed2004

Evaluation of a multi-parameter biomarker set for oxidative damage in man: increased urinary excretion of lipid, protein and DNA oxidation products after one hour of exercise.

The objective of the present study was to evaluate a comprehensive set of urinary biomarkers for oxidative damage to lipids, proteins and DNA, in man. Eighteen moderately trained males (mean age 24.6+/-0.7) exercised 60min at 70% of maximal O2 uptake on a cycle ergometer. Urine fractions for 12 h were collected 1 day before, and for 3 consecutive days after exercise. As biomarkers of lipid peroxidation, 8 aldehydes (i.e. propanal, butanal, pentanal, hexanal, heptanal, octanal, nonanal and malondialdehyde-MDA)and acetone were analyzed in urines by gas chromatography with electron capture detection (GC-ECD). As a biomarker of protein oxidation, o,o'-dityrosine was analyzed in urine samples by a recently developed isotope dilution HPLC-atmospheric pressure chemical ionization (APCI)-tandem-mass spectrometry (HPLC-APCI-MS/MS) methodology. As a biomarker of oxidative DNA damage, urinary excretion of 8-hydroxy-2'-deoxyguanosine (8-OHdG) was measured by an ELISA method. On the day of exercise, significant increases were observed in urinary excretions of acetone (p < 0.025, n = 18) and butanal (p < 0.01, n = 18) in the 12h daytime fractions compared to the daytime fraction before exercise. The urinary acetone excretion was also significantly (p < 0.05) increased on the 1st day after exercise. Octanal and nonanal were increased in the daytime urine fraction on the 2nd day after exercise. However, these increases were of borderline significance (p = 0.09 and p = 0.07, respectively). Significantly elevated urinary o,o'-dityrosine amounts were observed in the daytime fraction on the day of exercise (p < 0.025) and on the 1st day after exercise (p = 0.07) compared to the before exercise daytime fraction. Excretion of urinary 8-OHdG was statistically significantly increased in the daytime fractions on the day of exercise (p = 0.07) and on the 1st day after exercise (p < 0.025) compared to before exercise daytime fraction. Increases in urinary excretions of acetone, propanal, pentanal, MDA and 8-OHdG significantly correlated with training status (hours of exercise/week) of the volunteers, while o,o'-dityrosine did not. To our knowledge, the present study is the first to evaluate a multi-parameter non-invasive biomarker set for damage to three main cellular targets of ROS. It shows that 1 h of exercise may already induce oxidative damage in moderately trained individuals and that the chosen urinary biomarkers are sensitive enough to monitor such damage.

8-Hydroxy-2'-Deoxyguanosine↗
PubMedDate not supplied

Biomarkers of apoptosis: release of cytochrome c, activation of caspase-3, induction of 8-hydroxy-2'-deoxyguanosine, increased 3-nitrotyrosine, and alteration of p53 gene.

Biomarkers rely on biochemical, histological, morphological, and physiological changes in whole organisms. Their use is becoming an important tool to examine changes at cellular and molecular levels, especially in nucleic acids and proteins. Biomarkers are used to measure exposure to a toxic agent, to detect severity of any toxic response, and to predict the possible outcome. Information on the mechanisms of action of toxicants can allow the development of potential biomarkers of effect and thus improvement of the risk assessment processes. Use of biomarkers as a tool to predict induction of apoptosis allows identification of biological signs that may indicate increased risk for disease. In cells undergoing apoptosis, the release of cytochrome c from the mitochondria to the cytoplasm and the activation of caspase-3, a key enzyme to execution stage of apoptotic pathway, have been studied as biomarkers of cell death (apoptosis). Products of DNA fragmentation that either accumulate in the cellular tissues or are excreted in the urine are useful markers of DNA damage. The induction level of urinary or cellular level of 8-hydroxy-2-deoxyguanosine and 3-nitrotyrosine has been used as a marker to measure extent of DNA oxidative damage. Furthermore, alteration or overexpression of the p53 gene was considered an indication of apoptosis. This article reviews some of the aspects of biomarkers of apoptosis, indicating relevance of their uses to predict apoptosis following exposure to environmental toxicants.

8-Hydroxy-2'-Deoxyguanosine↗
PubMedDate not supplied

Data-driven analysis approach for biomarker discovery using molecular-profiling technologies.

High-throughput molecular-profiling technologies provide rapid, efficient and systematic approaches to search for biomarkers. Supervised learning algorithms are naturally suited to analyse a large amount of data generated using these technologies in biomarker discovery efforts. The study demonstrates with two examples a data-driven analysis approach to analysis of large complicated datasets collected in high-throughput technologies in the context of biomarker discovery. The approach consists of two analytic steps: an initial unsupervised analysis to obtain accurate knowledge about sample clustering, followed by a second supervised analysis to identify a small set of putative biomarkers for further experimental characterization. By comparing the most widely applied clustering algorithms using a leukaemia DNA microarray dataset, it was established that principal component analysis-assisted projections of samples from a high-dimensional molecular feature space into a few low dimensional subspaces provides a more effective and accurate way to explore visually and identify data structures that confirm intended experimental effects based on expected group membership. A supervised analysis method, shrunken centroid algorithm, was chosen to take knowledge of sample clustering gained or confirmed by the first step of the analysis to identify a small set of molecules as candidate biomarkers for further experimentation. The approach was applied to two molecular-profiling studies. In the first study, PCA-assisted analysis of DNA microarray data revealed that discrete data structures exist in rat liver gene expression and correlated with blood clinical chemistry and liver pathological damage in response to a chemical toxicant diethylhexylphthalate, a peroxisome-proliferator-activator receptor agonist. Sixteen genes were then identified by shrunken centroid algorithm as the best candidate biomarkers for liver damage. Functional annotations of these genes revealed roles in acute phase response, lipid and fatty acid metabolism and they are functionally relevant to the observed toxicities. In the second study, 26 urine ions identified from a GC/MS spectrum, two of which were glucose fragment ions included as positive controls, showed robust changes with the development of diabetes in Zucker diabetic fatty rats. Further experiments are needed to define their chemical identities and establish functional relevancy to disease development.

Algorithms↗
PubMedDate not supplied

Biomarkers of exposure and potential harm in adult smokers of 3-7 mg tar yield (Federal Trade Commission) cigarettes and in adult non-smokers.

The paper reports levels of 24-h urine nicotine and five of its major metabolites (expressed as nicotine-equivalents) and blood carboxyhaemoglobin as biomarkers of exposure to particulate- and gas-phase cigarette smoke, respectively, from an exploratory pilot study of adult smokers of 3.0-6.9 mg tar delivery (Federal Trade Commission (FTC) method) cigarettes. On multiple occasions over 6 weeks, blood high-sensitivity C-reactive protein (hs-CRP), fibrinogen, HDL- and LDL-cholesterol, and 24-h urine 8-epi-prostaglandin F2alpha (8-epi-PGF2alpha) and 11-dehydro-thromboxane B2 (11-dehydro-TxB2) were also evaluated as biomarkers of potential harm. All the biomarkers examined, except for LDL-cholesterol, discriminated with high sensitivity and specificity between adult smokers and non-smokers overall. Except for HDL-cholesterol, all biomarker medians were greater in adult smokers than in non-smokers: urine nicotine-equivalents 64.514 versus < 0.034 nmol mg-1 creatinine (p<0.001), carboxyhaemoglobin 4.0 versus 0.4% saturation (p<0.001), hs-CRP 0.27 versus 0.12 mg dl-1 (p=0.05), fibrinogen 292 versus 248 mg dl-1 (p<0.001), HDL-cholesterol 46 versus 53 mg dl-1 (p=0.003), LDL-cholesterol 119 versus 109 mg dl-1 (p=0.18), urine 8-epi-PGF2alpha 1935 versus 1034 pg mg-1 creatinine (p<0.001) and urine 11-dehydro-TxB2 973 versus 710 pg mg-1 creatinine (p<0.001). All the biomarkers of exposure and most of the biomarkers of potential harm showed no time of sampling (by visit week) effect.

Biomarkers↗
PubMed2003

Biomarkers of tobacco exposure or harm: application to clinical and epidemiological studies. 25-26 October 2001, Minneapolis, Minnesota.

Adverse outcomes from tobacco use may take decades to develop. Biomarkers are measures that can be used in the early stages of tobacco use to assess exposure to tobacco toxins or to predict adverse health outcomes with which they are associated. Examples of biomarkers include specific chemical components of tobacco or their metabolites; early biochemical, histological, or physiological effects; and early health effects. Mechanistically relevant and quantitatively valid biomarkers are essential for assessing the ultimate impact of new products, treatments, preventive measures, and public health policies on tobacco-related disease. The tobacco industry's recent introduction of a variety of new tobacco products or devices with implied claims of reduced health risks highlights the need to develop methods for assessing their potential for benefit or harm. A wide variety of biomarkers for tobacco exposure or harm has been studied. Although many questions about their use remain unanswered, substantial data exist regarding their validity and utility. This conference reviewed both the general issues surrounding biomarker use and the current state of knowledge regarding the most widely studied and promising biomarkers.

Alkaloids↗
PubMedDate not supplied

Assessing biomarker use in risk assessment--a survey of practitioners.

Advances in molecular epidemiology and mechanistic toxicology have provided increased opportunities for incorporating biomarkers in the human health risk assessment process. For years, the published literature has lauded the concept of incorporating biomarkers into risk assessments as a means to reduce uncertainty in estimating health risk. For all the potential benefits, one would think that markers of effective dose, markers of early biological effects, and markers of human susceptibility are frequently selected as the basis for quantitative human health risk assessments. For this article, we sought to determine the degree to which this evolution in risk assessment has come to pass. The extent to which biomarkers are being used in current human health risk assessment was determined through an informal survey of leading risk assessment practitioners. Case studies highlighting the evolution of risk assessment methods to include biomarkers are also described. The goal of this review was to enhance the implementation of biomarker technology in risk assessment by (1) highlighting successes in biomarker implementation, (2) identifying key barriers to overcome, and (3) describing evolutions in risk assessment methods.

Biomarkers↗
PubMedDate not supplied

Biomarkers of exposure in community settings.

Biomonitoring is a valuable tool for assessing human exposures to chemical contaminants in the environment. Biomonitoring tests can be divided into biomarkers of exposure, effect, and susceptibility. In studies of community exposure to an environmental contaminant, biomarkers of exposure are most often used. The ideal biomarker should be sensitive, specific, biologically relevant, practical, inexpensive, and available. Seldom does a biomarker meet all of these criteria--most biomarkers represent a compromise of these criteria. In designing a community exposure study, consideration should also be given to the selection of the test population, the practicality of collecting biological samples, temporal or seasonal variations in exposure, the availability of background comparison ranges, and interpretation of the test results. Biomonitoring tests provide unequivocal evidence of exposure, but they do not typically identify the source of exposure. Furthermore, rarely do the test results predict a health outcome. For many chemicals, testing must be conducted soon after exposure has occurred. In spite of these limitations, the use of biomonitoring is finding wider application in many scientific disciplines. Recent advances in analytical techniques are expanding the utility of biomarker testing in public health investigations.

Biomarkers↗
PubMed2006

Interpretation of serum ferritin concentrations as indicators of total-body iron stores in survey populations: the role of biomarkers for the acute phase response.

BACKGROUND: Nutritional surveys use acute phase protein (APP) biomarkers such as C-reactive protein (CRP) and alpha1-acid glycoprotein (AGP) to identify the influence of inflammation on the distribution of iron status biomarkers. Few, however, have examined which biomarker better identifies persons with spurious elevations in iron status markers. OBJECTIVE: We explored the relations of APP biomarkers to iron-status biomarkers in infants and school-age children. DESIGN: In screening surveys, we identified a sample of African American infants (n = 351) and Guatemalan school-age children (n = 375). We used a common set of APP and iron-status biomarkers to examine the association between the 2 sets of markers (laboratory variables). RESULTS: The overall prevalence of either inflammation or iron deficiency was <10% in both samples. The log AGP and CRP values were significantly correlated (r = 0.70), but the unexplained variance still was >50%. Serum ferritin-but not transferrin receptor, transferrin receptor index, or serum iron-was related to APP concentrations, but poor positive predictive value (<72%) and low kappa scores were found. Ferritin concentrations >1 geometric SD above the geometric mean were poorly predicted by either elevated AGP or CRP. Qualitative CRP analysis was not effective in identifying persons who had other indications of mild inflammation. CONCLUSIONS: These analyses show that a low prevalence of inflammation has little influence on the distribution of ferritin, and 2 common indicators of inflammation do not perform equally well in identifying persons who may have elevations in ferritin due to inflammation.

Acute-Phase Proteins↗
PubMed2006

Dependence network modeling for biomarker identification.

MOTIVATION: Our purpose is to develop a statistical modeling approach for cancer biomarker discovery and provide new insights into early cancer detection. We propose the concept of dependence network, apply it for identifying cancer biomarkers, and study the difference between the protein or gene samples from cancer and non-cancer subjects based on mass-spectrometry (MS) and microarray data. RESULTS: Three MS and two gene microarray datasets are studied. Clear differences are observed in the dependence networks for cancer and non-cancer samples. Protein/gene features are examined three at one time through an exhaustive search. Dependence networks are constructed by binding triples identified by the eigenvalue pattern of the dependence model, and are further compared to identify cancer biomarkers. Such dependence-network-based biomarkers show much greater consistency under 10-fold cross-validation than the classification-performance-based biomarkers. Furthermore, the biological relevance of the dependence-network-based biomarkers using microarray data is discussed. The proposed scheme is shown promising for cancer diagnosis and prediction. AVAILABILITY: See supplements: http://dsplab.eng.umd.edu/~genomics/dependencenetwork/

Algorithms↗
PubMed1995

Levels of aflatoxin-albumin biomarkers in rat plasma are modulated by both long-term and transient interventions with oltipraz.

The validation process for biomarkers to be used for monitoring the efficacy of preventive interventions in humans includes assessments of whether levels of the biomarker can be modulated in experimental models. From this perspective, the influence of two intervention protocols with the chemopreventive agent oltipraz on rates of formation and disappearance of aflatoxin-albumin adducts has been evaluated in rats chronically exposed to aflatoxin B1. Male F344 rats were treated daily with 20 micrograms aflatoxin B1, p.o. for 35 days. The first strategy employed a standard, long-term intervention in which basal AIN-76A diet was supplemented with 0.05% oltipraz beginning one week before AFB1 treatment and continuing throughout the period of carcinogen exposure. In this setting, treatment with oltipraz reduced the rate of formation of aflatoxin-albumin adducts such that steady-state levels were lowered by > 50% from control values of 400 pmol aflatoxin adducts/mg albumin. The time-course for reaching respective steady-state levels was unchanged, with or without oltipraz intervention. The second intervention strategy utilized a delayed, transient protocol in which oltipraz was fed for 2 weeks beginning 1 week after AFB1 dosing began and ending 2 weeks before AFB1 dosing was completed. This second strategy, which models clinical interventions in chronically exposed individuals, produced a steady decline in aflatoxin-albumin adduct levels that approached a 50% reduction by the end of the AFB1 exposure period. Development of smooth curve functions allowed for the estimation of the ratio of effects between the non-intervention and intervention groups as well as the simultaneous 90% confidence intervals for the aflatoxin-albumin adduct levels. These analyses indicated that long-term intervention with oltipraz produced a statistically significant reduction in levels of the aflatoxin-albumin biomarker at all times throughout aflatoxin exposure. By contrast, a statistically significant decrease in biomarker levels was not seen in the delayed, transient intervention protocol until the ninth day of the intervention. However, once achieved, significant differences from the control group were maintained for the remainder of the aflatoxin exposure period. These changes in aflatoxin biomarker levels are consistent with the cancer chemopreventive outcomes of these intervention protocols in rats. Collectively, these results support the utility of measuring this biomarker as a means for assessing the efficacy or chemopreventive interventions in individuals at high risk for aflatoxin exposure and development of hepatocellular carcinoma.

Aflatoxin B1↗
PubMed2003

Laboratory issues: use of nutritional biomarkers.

Biomarkers of nutritional status provide alternative measures of dietary intake. Like the error and variation associated with dietary intake measures, the magnitude and impact of both biological (preanalytical) and laboratory (analytical) variability need to be considered when one is using biomarkers. When choosing a biomarker, it is important to understand how it relates to nutritional intake and the specific time frame of exposure it reflects as well as how it is affected by sampling and laboratory procedures. Biological sources of variation that arise from genetic and disease states of an individual affect biomarkers, but they are also affected by nonbiological sources of variation arising from specimen collection and storage, seasonality, time of day, contamination, stability and laboratory quality assurance. When choosing a laboratory for biomarker assessment, researchers should try to make sure random and systematic error is minimized by inclusion of certain techniques such as blinding of laboratory staff to disease status and including external pooled standards to which laboratory staff are blinded. In addition analytic quality control should be ensured by use of internal standards or certified materials over the entire range of possible values to control method accuracy. One must consider the effect of random laboratory error on measurement precision and also understand the method's limit of detection and the laboratory cutpoints. Choosing appropriate cutpoints and reducing error is extremely important in nutritional epidemiology where weak associations are frequent. As part of this review, serum lipids are included as an example of a biomarker whereby collaborative efforts have been put forth to both understand biological sources of variation and standardize laboratory results.

Behavior↗
PubMed2003

Biomarkers of trace mineral intake and status.

The emerging public health importance of zinc and selenium and the continuing public health challenges of iron and iodine draw attention to the unmet need for improved biomarkers of trace element status. Currently available biomarkers of these four trace elements are critiqued including the outstanding lack of satisfactory biomarkers for the assessment of zinc intake and status. Other trace elements are reviewed briefly including copper, for which human dietary deficiencies and excesses have been documented, and chromium, which is of possible but unconfirmed public health significance. Evolving strategies of considerable potential include molecular techniques such as the measurement of metallothionein mRNA in lymphocytes as a biomarker of zinc status, an assay that can now be performed with a dried blood spot. The judicious application of tracer techniques also has a role in advancing the quality of zinc biomarkers. Also of special current interest is full definition of the potential of plasma-soluble transferrin receptor concentrations as the biomarker of choice for the detection of early functional iron deficiency.

Anemia, Iron-Deficiency↗
PubMed2001

Validated biomarker responses influence medical surveillance of individuals exposed to genotoxic agents.

There is currently a vast armamentarium of biomarkers for evaluating human exposures to environmental carcinogens, the effects of such exposures and/or susceptibility to disease outcome. Before application, however, these biomarkers require validation in terms of truly reflecting what is claimed. Transitional epidemiological studies bridge the gap between laboratory and field. In a transitional study, a biomarker response is the dependent variable being evaluated, while the intended measure, i.e. exposure effect or susceptibility, is the independent variable. Once validated, biomarker responses provide valuable data for use in making human health risk assessments and as guides for individual medical surveillance programmes. An analysis of medical decision-making illustrates how biomarker responses that increase the relative risk of subsequent disease occurrence change the 'pre-test likelihood' of having the disease, thereby influencing interpretation of medical diagnostic tests and even the choice of tests to be performed. This argues that an individual's response using salidated biomarkers should be made part of the medical record.

Biomarkers↗
PubMed2006

Biomarkers in cardiovascular disease: integrating pathophysiology into clinical practice.

Biomarkers play an important role in the diagnosis, prognostic assessment, and management of patients with suspected acute coronary syndromes (ACS). Specific biomarkers identify different components of the pathophysiology of ACS: troponins are prototype markers of myocyte necrosis, natriuretic peptides reflect neurohormonal activation and hemodynamic stress, soluble CD40 ligand is an indicator of platelet activation, and C-reactive protein, myeloperoxidase, and monocyte chemoattractant protein-1 reflect various inflammatory processes. When combined, multiple biomarkers reflecting different pathophysiologic processes appear to enhance risk stratification, as compared with using individual markers alone. Advances in proteomic technology promise to identify additional novel biomarkers that facilitate diagnosis, risk stratification, and selection of therapies in ACS. In the future, it is hoped that multiple biomarker panels will form the basis of an individualized approach to the treatment of ACS, in which therapy is tailored to individual biomarker profiles.

Biomarkers↗
PubMed2001

Ki-67, cyclin E, and p16INK4 are complimentary surrogate biomarkers for human papilloma virus-related cervical neoplasia.

Prior studies of Ki-67, cyclin E, and p16 expression have suggested that these biomarkers may be preferentially expressed in cervical neoplasia. This study examined and compared the distribution of staining for these three antigens in 1) normal and reactive epithelial changes, 2) diagnostically challenging cases (atypical metaplasia and atypical atrophy), 3) squamous intraepithelial lesions (SIL), and 4) high-and low-risk human papilloma virus (HPV) type-specific SIL. One hundred four epithelial foci from 99 biopsies were studied, including low-grade squamous intraepithelial lesions (LSIL; 24), high-grade squamous intraepithelial lesions (HSIL; 36), mature or immature (metaplastic) squamous epithelium (29), and atrophic or metaplastic epithelium with atypia (15). Cases were scored positive for Ki-67 expression if expression extended above the basal one third of the epithelium, for cyclin E if moderate to strong staining was present, and for p16 if moderate to strong diffuse or focal staining was present. HPV status was scored by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) analysis of extracted DNA. Immunohistochemical findings were correlated with histologic and viral data. Overall, a histologic diagnosis of SIL correlated strongly with all of the biomarkers used (p <0.001). Positive scores for Ki-67, cyclin E, and p16 were seen in 68.4%, 96.7%, and 100% of LSILs and 94.7%, 91.6%, and 100% of HSILs, respectively. Positive predictive values of these three biomarkers for HPV were 82.4%, 89.5%, and 91.4%, respectively. The positive predictive value for HPV of either cyclin E or p16 was 88.7%. Strong diffuse staining for p16 was significantly associated with high-risk HPV-associated lesions. Normal or reactive epithelial changes scored positive for the three biomarkers in 7.7%, 8.0%, and 12%, respectively. Limitations in specificity included minimal or no suprabasal staining for Ki-67 in immature condylomas and occasional suprabasal staining of reactive epithelial changes (10%), diffuse weak nuclear cyclin E staining in some normal or metaplastic epithelia, and diffuse weak basal p16 staining and occasional stronger focal positivity in normal epithelia. Ki-67, cyclin E, and p16 are complementary surrogate biomarkers for HPV-related preinvasive squamous cervical disease. (Because cyclin E and p16 are most sensitive for LSIL and HSIL [including high-risk HPV], respectively, use of these biomarkers in combination for resolving diagnostic problems, with an appreciation of potential background staining, is recommended.)

Biomarkers↗
PubMed1995

Molecular biomarkers for aflatoxins and their application to human liver cancer.

The rationale for developing molecular biomarkers to monitor and assess risk from human exposure to aflatoxins have been justified by the association of these carcinogens with human liver cancer, a disease that causes at least 250000 deaths world-wide each year. The goal of our research has been the development of aflatoxin biomarkers based upon the knowledge of the biochemistry and toxicology of aflatoxins gleaned from both experimental and human studies. These biomarkers have been subsequently utilized in experimental chemoprotection models to provide data on the modulation of these markers under different situations of disease risk. Several of the aflatoxin specific biomarkers have been validated in epidemiologic studies and are now available to use as intermediate biomarkers in chemoprotection trials. This systematic approach provides encouragement for preventive interventions and should serve as a template for the development, validation and application of other chemical-specific biomarkers to cancer or other chronic diseases.

Aflatoxins↗
PubMed2005

Biomarkers in osteoarthritis.

PURPOSE OF REVIEW: Biomarker discovery and validation for osteoarthritis have accelerated over the past several years, coincident with an evolving understanding of joint tissue molecules and their complex interactions, and the compelling need for improved osteoarthritis outcome measures in clinical trials. This review highlights advances in osteoarthritis-related biomarker research within the past year. RECENT FINDINGS: The studies in the past year involving biochemical markers in humans can be assigned to one of four categories: new approaches and new biomarkers, exploratory studies in specialized disease subsets, large cross-sectional validation studies, and longitudinal studies, with and without an intervention. SUMMARY: Most these studies have examined the association of a biomarker with some aspect of the natural history of osteoarthritis. As illustrated by the six studies reviewed here that included therapeutic interventions, however, several biomarkers are emerging that display credible association with disease modification. The expanding pool of informative osteoarthritis-related biomarkers is expected to positively impact the development of therapeutics for this disease and, it is hoped, ultimately clinical care.

Biomarkers↗
PubMed2006

Combining serum biomarkers: the association of C-reactive protein, insulin sensitivity, and homocysteine with cardiovascular disease history in the general US population.

BACKGROUND: Elevated levels of serum biomarkers such as C-reactive protein (CRP) and homocysteine have been independently associated with cardiovascular risk. However, the prevalence of concurrent elevations of these biomarkers in the general population is unknown, as is their association with cardiovascular disease (CVD). METHODS: Data from adults (n = 4900) in the National Health and Nutrition Examination Survey were used to investigate the relationship between combinations of serum biomarkers of inflammation (CRP), atherosclerosis (homocysteine), and insulin sensitivity [homeostatic model assessment (HOMA) fasting insulin] and CVD. Using SUDAAN, logistic regression models were constructed to examine the relationships between elevated serum biomarkers (CRP, homocysteine, HOMA, or insulin), singly or in combination, and having a history of heart failure, myocardial infarction (MI), stroke, or any CVD, while controlling for age, race, sex, obesity, smoking, cholesterol level, diabetes history, hypertension history, exercise level, and dietary fiber intake. RESULTS: After adjustment for covariates, there was a significant relationship between concomitant elevations of CRP plus homocysteine and a history of MI [odds ratio (OR) 2.21], heart failure (OR 2.14), and any CVD (OR 1.87) that was stronger than the relationship between individual biomarkers alone and a history of CVD. In addition, combinations of elevated CRP plus HOMA and CRP plus insulin, remained significantly related to having a history of any CVD. CONCLUSION: Recent scientific evidence and the present findings demonstrate the possibility for improving cardiovascular risk stratification through the concurrent evaluation of multiple biomarkers. In particular, these findings demonstrate the need to evaluate the combination of CRP and homocysteine prospectively as predictors of CVD.

Adolescent↗