Tick-borne infections are the most common vector-borne diseases in the USA. Ticks harbor and transmit several infections with Lyme disease being the most common tickborne infection in the US and Europe. Lack of awareness about tick populations, specific diagnostic tests, and overlapping signs and symptoms of tick-borne infections can often lead to misdiagnosis affecting treatment and the prevalence data reported especially for non-Lyme tick-borne infections. The diagnostic tests currently available for tick-borne diseases are severely limited in their ability to provide accurate results and cannot detect multiple pathogens in a single run. The multiplex protein microarray developed at Vibrant was designed to detect multiple serological antibodies thereby detecting exposure to multiple pathogens simultaneously. Our microarray in its present form can accommodate 400 antigens (molecules that can bind to specific antibodies) and can multiplex across antigen types, whole cell lysates, recombinant proteins, and peptides. A designed array containing multiple antigens of several microbes including Borrelia burgdorferi, the Lyme disease spirochete, was manufactured and evaluated. The immunoglobulin M (IgM) and G (IgG) responses against several tick-borne microbes and other infectious agents were analyzed for analytical and clinical performance. The microarray improved IgM and IgG sensitivities and specificities of individual microbes when compared with the respective gold standards. The testing was also performed in a single run in comparison to multiple runs needed for comparable testing standards. In summary, our study presents a flexible multiplex microarray platform that can provide quick results with high sensitivity and specificity for evaluating exposure to varied infectious agents especially tick-borne pathogens.

Introduction Cardiovascular diseases (CVDs) remain the leading cause of mortality globally. The role of micronutrients in maintaining cardiovascular health has gained increasing attention, as deficiencies or imbalances in vitamins, minerals, and amino acids may influence the risk and progression of CVDs. This study aimed to evaluate the relationship between serum micronutrient levels and critical lipid and lipoprotein markers indicative of cardiovascular health. Materials and methods A retrospective analysis was conducted on 358 individuals who underwent testing for the Cardio Health and Micronutrients Panel at Vibrant America Clinical Laboratory. The participants were divided into three groups based on their serum lipid and lipoprotein concentrations: 'Low', 'Normal', and 'High'. The levels of vitamins (A, D, E, and K), minerals (zinc, iron, calcium, and magnesium), and amino acids (leucine, isoleucine, and valine) were measured, and their correlation with cardiovascular markers such as cholesterol, LDL, HDL, and Apo B was analyzed using Pearson's correlation. Results The study found significant associations between micronutrient levels and cardiovascular markers. Vitamins D, E, and K and minerals like zinc, calcium, and magnesium showed positive correlations with lipid markers. Asparagine was negatively correlated with cholesterol and LDL, while amino acids such as isoleucine and valine negatively correlated with HDL but showed a positive association with LDL and Apo B. Fat-soluble vitamins demonstrated strong positive associations with total cholesterol and triglycerides. Conclusion These findings suggest that certain micronutrients play a critical role in regulating lipid profiles and overall cardiovascular health. Further studies are necessary to explore the therapeutic potential of micronutrient supplementation in preventing or managing CVDs.

Objective To evaluate the association between thyroid disease and diabetes markers.Design Retrospective cohort study.Setting The study was conducted in a diagnostic setting where the primary care providers recommended the patients to test for thyroid and diabetes panels.Participants The thyroid and diabetes markers were tested in 32 787 subjects with suspected thyroid and related conditions who visited Vibrant America Clinical Laboratory between January 2015 and June 2019.Results Our general prevalence results showed that homeostatic model assessment-insulin resistance (HOMA-IR) was elevated in overt hypothyroid subjects (43.7%) and overt hyperthyroid subjects (42.2%). Glycated hemoglobin (HbA1C) was elevated in subclinical hypothyroid subjects (19.2%), overt hypothyroid subjects (22.3%) and overt hyperthyroid subjects (21.2%). Glucose was significantly elevated in subclinical hypothyroid subjects (24.2%) and overt hyperthyroid subjects (31.0%). Insulin was significantly elevated in overt hypothyroid subjects (15.1%). Interestingly, we found that 70.3% of subjects who had their HOMA-IR score escalated from negative (HOMA-IR<2.7) to positive (HOMA-IR>2.7) during their multiple visits had anti-thyroid peroxidase (anti-TPO) 369 (±242) days prior to the onset of this change.Conclusion Our findings showed that anti-TPO levels are elevated before the onset of insulin resistance, indicating its potential use as a predictive marker.

Background  The study aims to assess the association of apolipoprotein E (APOE) gene polymorphisms with serological lipid and inflammatory markers to determine their potential role in predicting the risk of cardiovascular diseases (CVDs) and Alzheimer's disease (AD).  Methodology  A total of 915 individuals underwent testing for lipid and inflammatory biomarkers at Vibrant America Clinical Laboratory. Clinical data, blood lipid and inflammatory profiles, and APOE genotyping were analyzed using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP).  Results Compared to the E3/E3 genotype, individuals with E2/E3 genotypes showed higher levels of high-density lipoprotein (HDL), triglycerides, apolipoprotein A (APOA), high-sensitivity C-reactive protein (hs-CRP), and myeloperoxidase (MPO). E2/E4 genotype carriers had higher levels of HDL, triglycerides, Lp(a), and N-terminal pro b-type natriuretic peptide (BNPNT). E3/E4 genotypes were associated with elevated levels of total cholesterol, LDL, Lp(a), hs-CRP, small-density low-density lipoprotein (SDLDL), oxidized LDL (OXLDL), MPO, LDL-CAL, PLAC, and APOB. The E4/E4 group displayed higher concentrations of total cholesterol, LDL, APOB, Lp(a), hs-CRP, SDLDL, OXLDL, MPO, LDLCAL, and PLAC compared to E3/E3 carriers. These findings highlight the potential atherogenic effect of the ε4 allele and the protective effect of the ε2 allele based on lipid and inflammatory marker profiles.  Conclusions This study provides strong evidence linking APOE gene polymorphism to abnormal serum lipid and inflammatory profiles. Individuals carrying the ε4 alleles exhibited dysregulated lipid metabolism and abnormal inflammatory markers, increasing their risk of CVD and AD. Early detection and prompt diagnosis are crucial for implementing therapeutic, dietary, and lifestyle interventions to mitigate risks and prevent or delay lipid and inflammation-related disorders.

Purpose of review: This review investigates the oral microbiome’s composition, functions, influencing factors, connections to oral and systemic diseases, and personalized oral care strategies. Recent findings: The oral microbiome is a complex ecosystem consisting of bacteria, fungi, archaea, and viruses that contribute to oral health. Various factors, such as diet, smoking, alcohol consumption, lifestyle choices, and medical conditions, can affect the balance of the oral microbiome and lead to dysbiosis, which can result in oral health issues like dental caries, gingivitis, periodontitis, oral candidiasis, and halitosis. Importantly, our review explores novel associations between the oral microbiome and systemic diseases including gastrointestinal, cardiovascular, endocrinal, and neurological conditions, autoimmune diseases, and cancer. We comprehensively review the efficacy of interventions like dental probiotics, xylitol, oral rinses, fluoride, essential oils, oil pulling, and peptides in promoting oral health by modulating the oral microbiome. Summary: This review emphasizes the critical functions of the oral microbiota in dental and overall health, providing insights into the effects of microbial imbalances on various diseases. It underlines the significant connection between the oral microbiota and general health. Furthermore, it explores the advantages of probiotics and other dental care ingredients in promoting oral health and addressing common oral issues, offering a comprehensive strategy for personalized oral care.

Background Colorectal cancer (CRC) is a growing global health challenge with a multifactorial etiology encompassing genetic susceptibility, nutrition, and inflammation in the bowel. Objective To examine micronutrient status in CRC patients undergoing CRC resection. Design We performed a case-control study including 13 consecutive CRC patients and 10 healthy controls (CTRL) comparing the serum levels of 29 micronutrients, namely Copper, Zinc, Selenium, Chromium, Manganese, Carnitine, Choline, Inositol, Methylmalonic acid (MMA), Vitamin (Vit) B1, Vit B2, Vit B3, Vit B5, Vit B6, Vit C, Vit A, Vit D3, Vit E, Vit K1, Vit K2 and the amino acids Serine, Valine, Leucine, Isoleucine, Asparagine, Glutamine, Arginine, Citrulline and Cysteine. Results After considering the effect of age and sex, copper, arginine, and cysteine were increased, while zinc, selenium, chromium, Vit B1, Vit K1, and Vit A were decreased in CRC patients in comparison with CTRL. Zinc levels perfectly predicted the diagnosis of CRC, and were associated with lymph nodes (pN), of the pTNM staging. Copper levels in serum were strongly associated with the pathological pTNM staging of CRC. Conclusion Though this is a preliminary study that needs confirmation with a larger longitudinal cohort, our results show that serum micronutrients are linked to tumor growth, likely caused by increased demand from tumor tissue associated with an aberrant cell proliferation and changes in the antioxidant function.

Oxidative species, generated endogenously via metabolism or from exogenous sources, play crucial roles in the body. At low levels, these species support immune functions by participating in phagocytosis. They also aid in cellular signaling and contribute to vasomodulation. However, when the levels of oxidative species exceed the body’s antioxidant capacity to neutralize them, oxidative stress occurs. This stress can damage cellular macromolecules such as lipids, DNA, RNA, and proteins, driving the pathogenesis of diseases and aging through the progressive deterioration of physiological functions and cellular structures. Therefore, the body’s ability to manage oxidative stress and maintain it at optimal levels is essential for overall health. Understanding the fundamentals of oxidative stress, along with its reliable quantification, can enable consistency and comparability in clinical practice across various diseases. While direct quantification of oxidant species in the body would be ideal for assessing oxidative stress, it is not feasible due to their high reactivity, short half-life, and the challenges of quantification using conventional techniques. Alternatively, quantifying lipid peroxidation, damage products of nucleic acids and proteins, as well as endogenous and exogenous antioxidants, serves as appropriate markers for indicating the degree of oxidative stress in the body. Along with the conventional oxidative stress markers, this review also discusses the role of novel markers, focusing on their biological samples and detection techniques. Effective quantification of oxidative stress may enhance the understanding of this phenomenon, aiding in the maintenance of cellular integrity, prevention of age-associated diseases, and promotion of longevity.

Oxidative stress refers to the imbalance between the production of oxidant species and the body’s ability to quench them using antioxidants, favoring the rise in oxidant levels. This leads to the damage of cellular macromolecules such as lipids, DNA, RNA, and proteins. The body’s ability to manage oxidative stress and maintain it at an optimum level is crucial for overall health. Oxidative damage, if left unmitigated, contributes to the aging process characterized by the progressive deterioration of physiological functions and cellular structures. Understanding the mechanisms of oxidative stress along with its reliable quantification can enable consistency and comparability in clinical practice across diseases. While direct quantification of oxidant species in the body would be ideal for assessing oxidative stress, it is not feasible owing to their high reactivity, short half-life, and quantification challenges using conventional techniques. Quantifying oxidative damage products and antioxidants pose as appropriate markers, indicating the degree of oxidative stress in the body. This review comprehensively discusses the mechanism of generation of key oxidant species, their sources, the beneficial roles played by them at low levels and the detrimental effects exerted by their elevated levels. The review also provides insights into the effective quantification techniques for damage products of lipids nucleic acids, and proteins along with the endogenous and exogenous antioxidant markers. Effective quantification of oxidative stress may improve our understanding on the phenomenon which may aid in maintaining cellular integrity, preventing age-associated diseases, and thereby promoting optimal well-being and longevity.

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Alzheimer's disease (AD) is the most common type of dementia and neurodegenerative disease characterized by neurofibrillary tangles (NFTs) and amyloid plaque. Familial AD is caused by mutations in the APP, PSEN1, and PSEN2 genes and these mutations result in the early onset of the disease. Sporadic AD usually affects older adults over the age of 65 years and is, therefore classified as late-onset AD (LOAD). Several risk factors associated with LOAD including the APOE gene have been identified. Moreover, GWAS studies have identified a wide array of genes and polymorphisms that are associated with LOAD risk. Currently, the diagnosis of AD involves the evaluation of memory and personality changes, cognitive impairment, and medical and family history to rule out other diseases. Laboratory tests to assess the biomarkers in the body fluids as well as MRI, CT, and PET scans to analyze the presence of plaques and NFTs are also included in the diagnosis of AD. It is important to diagnose AD before the onset of clinical symptoms, i.e. during the preclinical stage, to delay the progression and for better management of the disease. Research has been conducted to identify biomarkers of AD in the CSF, serum, saliva, and urine during the preclinical stage. Current research has identified several biomarkers and potential biomarkers in the body fluids that enhance diagnostic accuracy. Aside from genetics, other factors such as diet, physical activity, and lifestyle factors may influence the risk of developing AD. Clinical trials are underway to find potential biomarkers, diagnostic measures, and treatments for AD mainly in the preclinical stage. This review provides an overview of the genes and biomarkers of AD.

Background and aims: Elevated high-sensitivity C-reactive protein (hs-CRP) levels are associated with an increased risk of cardiovascular disease, indicating systemic inflammation. Abnormal lipid levels and deficiencies in certain vitamins and minerals could also contribute to elevated hs-CRP levels. By broadly looking at the cross-correlations between inflammatory, lipid, and micronutrient markers, we aim to highlight the key associations at the serological levels. Methods: A retrospective analysis was conducted on 1,014 free-living individuals who tested for cardiovascular and micronutrient panels along with hs-CRP at Vibrant America Clinical Laboratory. Results and conclusion: Based on parametric t-tests, significant variations between the sexes (Ma1) were observed for cholesterol, high-density lipoprotein (HDL), triglycerides, vitamin A, vitamin D3, serum copper, and valine. Pearson's correlation showed a high-significant positive correlation between hs-CRP and triglycerides, folate, serum copper, and manganese.

Genetics is a key factor that governs the susceptibility to oxidative stress. In the body, oxidative burden is regulated by the balance between the prooxidant genes that orchestrate processes that produce oxidant species, while the antioxidant genes aid those involved in scavenging these species. Together, the two components aid in maintaining the oxidative balance in the body. Genetic variations can influence the expression and activity of the encoded proteins which can then affect their efficiency in regulating redox processes, thereby increasing the risk of oxidative stress. This review studies single nucleotide polymorphisms (SNPs) that bear relevance to oxidative stress by exploring the variations in the prooxidant genes, such as XDH, CYBA, CYP1A1, PTGS2, NOS, and MAO and antioxidant genes including SOD, CAT, GPX, GSS, GLUL, GSR, GSTM1, GSTM5, GSTP1, TXN and HMOX1. Early identification of individuals at the increased risk of oxidative stress is possible from the assessment of sequence of these genes. Integrating genetic insights into oxidative stress management measures can pave the way for personalized medicine that tailors’ healthcare approaches to individual genetic profiles. Effective genetic assessment along with routine quantification of biological markers can improve and monitor treatment strategies, enhancing mitigation approaches that maintain cellular health and promote longevity.

Food sensitivity, a common but overlooked condition, has been associated with a variety of gastrointestinal symptoms. Typically, patients suffering from food sensitivity are placed on elimination diets, although the success of this approach has not been sufficiently validated. We aimed to assess whether effective serological assessment for food sensitivity and the implementation of a subsequent elimination diet improved patients’ symptoms and overall well-being. In this study, 52 participants were tested for serum IgG and IgA levels against 262 food antigens. Based on the results, participants followed personalized elimination diets excluding foods they were reactive to, for a period of 4 weeks. Symptoms were assessed weekly using the ‘Food Sensitivity-Symptom Severity Scale’ (FS-SSS), which was seen to decrease in 88.46% of participants from baseline to week 4 (p < 0.05). The physician’s evaluation of participants' responses was analyzed using the ‘Food Sensitivity-Global Improvement Scale’ (FS-GIS), where 84.61% of participants saw notable improvements. Antibody titers post-intervention showed improved IgG levels in 96.15% of the participants while IgA levels showed improvement in 84.61% of the participants. Serological assessment followed by a personalized elimination diet effectively addressed food sensitivity, evidenced by reduced symptoms, improved antibody titers, and favorable physician assessments of patient response.

Alzheimer’s disease (AD) is the most common type of dementia and neurodegenerative disease characterized by neurofibrillary tangles (NFTs) and amyloid plaque. Familial AD is caused by mutations in the APP, PSEN1, and PSEN2 genes and these mutations result in the early onset of the disease. Sporadic AD usually affects older adults over the age of 65 years and is, therefore classified as late-onset AD (LOAD). Several risk factors associated with LOAD including the APOE gene have been identified. Moreover, GWAS studies have identified a wide array of genes and polymorphisms that are associated with LOAD risk. Currently, the diagnosis of AD involves the evaluation of memory and personality changes, cognitive impairment, and medical and family history to rule out other diseases. Laboratory tests to assess the biomarkers in the body fluids as well as MRI, CT, and PET scans to analyze the presence of plaques and NFTs are also included in the diagnosis of AD. It is important to diagnose AD before the onset of clinical symptoms, i.e. during the preclinical stage, to delay the progression and for better management of the disease. Research has been conducted to identify biomarkers of AD in the CSF, serum, saliva, and urine during the preclinical stage. Current research has identified several biomarkers and potential biomarkers in the body fluids that enhance diagnostic accuracy. Aside from genetics, other factors such as diet, physical activity, and lifestyle factors may influence the risk of developing AD. Clinical trials are underway to find potential biomarkers, diagnostic measures, and treatments for AD mainly in the preclinical stage. This review provides an overview of the genes and biomarkers of AD.

Renal involvement is a common occurrence in subjects with systemic autoimmune diseases. The renal manifestation and its severity depend on the underlying condition and may reversely complicate the clinical course of autoimmune diseases. Renal function markers have been widely used in the assessment of normal functioning of kidneys including glomerular filtration rate and concentrating and diluting capacity of the kidney. An increase or decrease in the values of these markers may indicate kidney dysfunction. In this study, a number of critical renal markers were examined in seropositive autoimmune diseases including systemic lupus erythematosus (SLE), connective tissue disorder (CTD), and rheumatoid arthritis (RA). The data from three cohorts of subjects enrolled in renal markers and autoimmune antibody testing between January 2015 to August 2019 were retrospectively studied. The prevalence of renal markers that were out of the reference range and their average levels in female and male subgroups across SLE, CTD, and RA cohorts were compared and analyzed. The levels of renal markers are significantly affected by the presence of autoantibodies, in particular eGFR, cystatin C, and albumin. Autoantibodies were also more frequent in subjects with severe renal function damage. Close follow-up of both renal markers and autoantibodies may potentially assist in the early diagnosis of kidney diseases and improve the survival and life expectancy of autoimmune patients.

ABSTRACTThe association of thyroid disease and diabetes has been classically described. However, the comorbidity of thyroid disparities and insulin resistance is not frequently assessed, especially the sequence of the occurrence of these markers. We performed a retrospective analysis to evaluate the association between thyroid disease and diabetes markers. We further investigated the sequence of occurrence of thyroid and diabetes markers to identify any predictive capabilities of these markers. We evaluated 32787 subjects who were classified based on their serum thyroid hormones and autoantibody levels. Our general prevalence results showed that HOMA-IR was elevated in overt hypothyroid subjects (43.7%) and overt hyperthyroid subjects (42.2%). HbA1C was elevated in subclinical hypothyroid subjects (19.2%), overt hypothyroid subjects (22.3%) and overt hyperthyroid subjects (21.2%). Glucose was significantly elevated in subclinical hypothyroid subjects (24.2%) and overt hyperthyroid subjects (31.0%). Insulin was only significantly elevated in overt hypothyroid subjects (15.1%). Interestingly, we found that 70.3% of subjects who had their HOMA-IR score escalated from negative (HOMA-IR<2.7) to positive (HOMA-IR>2.7) during their multiple visits had anti-TPO 369 (±242) days prior to the onset of this change. Our comprehensive study provided evidence that the presence of anti-TPO may suggest a predictive role in developing insulin resistance later in life.Strengths and limitations of the studyThe strength of our study is the large population size including a larger set of markers from both thyroid disease and diabetes.The limitation in our study is the distorted male and female ratio.

Cardiovascular diseases (CVD) are among the most preventable chronic disorders accounting for about one-third of general mortality around the globe. Micronutrients have been shown to have a significant impact on cardiovascular health. Micronutrients have been looked at as the most adoptable lifestyle choice which could reduce the burden of disease around the world. In this context, it is important to study the levels of micronutrients and see their correlation to cardiac disease biomarkers. The present study, has attempted to investigate the relationship between the diverse class of micronutrients and serum levels of the key lipids and lipoproteins. A retrospective analysis was carried out between the serum levels of micronutrients and vital cardiovascular markers. The study was carried out in a group of 358 individuals tested for the Cardio Health and Micronutrients Panel at Vibrant America Clinical Laboratory. The study population was categorized based on the serum concentration of lipids and lipoproteins into 3 groups ‘Low’ ‘Normal’ and ‘High’ and the levels of micronutrients were compared among these groups. The results revealed a significant association of several cardiovascular markers with vitamins including Vit D, Vit E, Vit K, and minerals including zinc, iron, calcium, magnesium, and amino acids including leucine, isoleucine, and valine. Quantitative analysis by Pearson’s correlation exhibited a negative correlation of asparagine with serum levels of cholesterol and LDL. Amino acids such as cysteine, isoleucine, and valine were found to have a significant negative correlation with HDL. A positive correlation was observed between valine and serum levels of LDL and Apo B. Vitamins such as Vit A, Vit D3, Vit E, and Vit K1 were found to have a strong positive correlation with levels of total cholesterol and triglycerides. The study summarizes micronutrients and modulation of several lipid markers which are critical for the management of cardiovascular diseases. Micronutrients such as vitamins B1, B3, asparagine, and glutamine have a strong positive association, and fat-soluble vitamins, and BCAA has a strong negative association with cardiovascular health.

Background: Homocysteine (tHcy) has emerged as a new risk factor for cardiovascular diseases (CVD) The Methylenetetrahydrofolate reductase (MTHFR) polymorphisms are seen to give rise to high levels of tHcy which can be a causative factor in the progression of CVD due to its thrombogenic effect. Serum cardiac biomarkers help in the diagnosis, prognosis, or surveillance of CVD. The present study evaluated the association of the two MTHFR mutations, rs1801133 and rs1801131 with 16 well-established serum cardiac markers. Additionally, the influence of age and gender on the association of the two MTHFR polymorphisms with serum cardiac marker levels was also investigated. Methods: The study was carried out on 1295 individuals who visited Vibrant America Clinical Lab for regular or suspected CVD check-ups. The serological markers and genomic variant analysis were carried out as per the standard laboratory protocol under CLIA. The association between serological markers and the rs1801133 and rs1801131 genetic variants with respect to age and gender was evaluated using a one-way ANNOVA test. Results: No significant association was observed in tHcy levels with respect to gender, however, plasma total tHcy levels were higher in males than females. tHcy levels increased with increasing age in the wild and heterozygous genotypes for the mutations, rs1801133 and rs1801131. Additionally, the serum cardiac markers, High Density Lipoprotein (HDL), Low Density Lipoprotein (LDL), Cholesterol (CHOL), Apolipoprotein A (APOA), Apolipoprotein B (APOB), N-terminal (NT)-pro hormone BNP (BNPNT), LDL calculated (LDLCAL), Small Density Low Density Lipoprotein (SDLDL), APOBAR, Oxidised Low Density Lipoprotein (OXLDL), Lipoprotein (A) (LPA), Triglycerides (TRIG), and Lipoprotein-Associated Phospholipase (Lp-PLA2) Test (PLAC) showed significant associations with respect to gender and age for rs1801133 and rs1801131 (P < 0.05) However, these markers were seen to have different trends in correlation with gender and age. Conclusions: The present study reports the association of tHcy, HDL, LDL, CHOL, APOA, APOB, BNPNT, LDLCAL, SDLDL, APOBAR, OXLDL, LPA, TRIG, and PLAC with respect to age and gender for the mutations, rs1801133 and rs1801131. We observed that tHcy levels were high in males and the levels increased with increasing age in males for both polymorphisms. rs1801131 mutant males have high levels of triglyceride whereas rs1801133 mutant postmenopausal females showed high levels of cholesterol. Further analysis will be required to understand the pattern of association of the rest of the serum cardiac markers with age and gender for rs1801133 and rs1801131 mutations.

Thyroid metabolism is orchestrated by the action of various minerals and trace elements including iron, iodine, selenium, and zinc.Iron deficiency, specifically deficiency in serum ferritin levels, is one of the common causes of thyroid dysfunction.Our objective was to evaluate the relationship between serum ferritin levels and circulating thyroid hormones.For this, a retrospective analysis was performed on 16,512 individuals who tested for serum levels of ferritin and thyroid profile at Vibrant America Clinical Laboratories.Subjects were stratified based on the serum levels of ferritin.Age (p < 0.0001) was found to be a significant factor in altering serum ferritin levels and also serum ferritin levels were significantly associated with varying levels of thyroid hormones in both males and females, with the levels of T4 (p < 0.0001) and RT3 (p < 0.0001) being the most significant.The levels of FT4 (p < 0.0001) and TSH (p = 0.0120) were significantly associated but did not exhibit any change in expression levels.Serum ferritin was found to be positively correlated with free thyroxine (r = 0.04325, p < 0.0001) and inversely correlated with serum triiodothyronine (r = -0.03232,p < 0.0001).Analysis of Linear association by Pearson's correlation exhibited a considerable correlation between varying serum ferritin levels with all tested thyroid hormones.The study concludes that serum ferritin levels were associated with thyroid hormone synthesis and metabolism in individuals with optimal levels of circulating ferritin.

Cardiovascular diseases (CVDs) are a leading cause of death worldwide which is why early risk prediction is crucial. Discrete Polygenic risk score (PRS) measurement using saliva or dried blood spot samples collected at home poses a convenient means for early CVD risk assessment. The present study assessed the effects of 28 disease-associated single nucleotide polymorphisms (SNPs) on 16 serological cardiac markers and also aggregated the risk alleles into a PRS to evaluate its applicability in CVD-risk prediction. The study assessed genetic and serological markers in 184 individuals. The association between serological markers and individual genetic variants was evaluated using a two-tailed t test while the associations of serum markers with the PRS was analyzed using the Pearson correlation. The comparative analysis of genotypes revealed statistically significant associations between serum markers and CVD-associated SNPs with Apo B: Apo A-1, LDL Direct, Apo B, sdLDL, hsCRP, Lp(a), NT-proBNP, and PLAC levels being significantly associated with the risk alleles of the SNPs, rs12526453, rs5186, rs10911021, rs1801131, rs670, rs10757274, and rs10757278. Increased PLAC levels were associated with rs10757274 and rs10757278 (P < .05). The SNPs, rs1801133, rs1549758, rs1799983, rs5082, and rs5186 were significantly associated with an increase in the cardioprotective markers, HDL and ApoA1 (P < .05). Furthermore, the PRS was associated with increasing levels of several serum cardiac markers (r2 > 0.6). Significant correlations were observed between high PRSs and NT-proBNP and ox-LDL levels with the r2 values being 0.82 (95% CI = 0.13-0.99; P = .03) and 0.94 (95% CI = 0.63-0.99; P = .005), respectively. The present study reports that SNPs have differential effects on serum markers with rs12526453, rs5186, rs10911021, rs1801131, rs670, rs10757274, and rs10757278 showing significant associations with elevated marker levels, which are indicators of deteriorating cardiac health. A unified PRS using several SNPs was also associated with an increase in serum markers levels, especially, NT-proBNP and ox-LDL. Genetic assessment via a convenient at-home collection to calculate the PRS can serve as an effective predictive tool for early CVD-risk assessment. This may help identify the risk groups that may require increased serological monitoring.