A small amount of emerging research has observed variations between individual sensitivity, preference and intake of salt in the presence of single nucleotide polymorphisms (SNP) on the genes encoding salt taste receptors. Sodium intake is a significant risk factor for common diseases in elderly populations such as hypertension and cardiovascular disease; however, this does not fully explain the risk. Research into the influence of salt taste genetics on diet quality is yet to be undertaken and current research on indicators of health is limited and mixed in the direction of associations. Therefore, a secondary analysis of data from a well-characterised elderly cohort (the cross-sectional Retirement Health and Lifestyle Study, n = 536) was conducted to explore relationships between the salt taste-related SNP TRPV1-rs8065080 (assessed by Taqman genotyping assay), dietary habits and biomarkers of health. Data were analysed with standard least squares regression modelling and Tukey’s HSD post hoc tests. No association was found between the TRPV1-rs8065080 genotype, sodium intake or multiple diet quality indices (assessed by food frequency questionnaire). Sodium-related markers of health including blood pressure and markers of kidney function (urinary creatinine and albumin/creatinine ratio) and general health markers, such as Body Mass Index (BMI), were also not related to TRPV1-rs8065080 genotype. To date, this study is the most comprehensive investigation conducted to determine if the TRPV1-rs8065080 genotype relates to sodium intake and health markers influenced by sodium intake. Although no significant relationships were found, these findings are an important contribution to the limited body of knowledge surround this SNP. In addition to further research across other ages and cultures, the TRPV1-rs8065080 genotype may interact with other ion channels, and so further studies are required to determine if polymorphic variations influence sodium intake, diet and health.
(1) Background: The aetiology of oral disease is multifactorial, involving genetic and environmental factors, including dietary ones. Bitter taste genetics may be related to oral health through dietary modulation or non-gustatory roles, including modulation of inflammation. Investigations of bitter taste and oral health associations to date have been restricted to specific polymorphisms, limited outcomes (caries), and age-groups (children), and links to inflammation remain to be elucidated. (2) Methods: A cross-sectional study (n = 65) investigated the correlations between bitter taste genotypes, oral health outcomes, and oral inflammation markers. Oral examinations were conducted, including saliva testing with evaluation of flow rate, pH, and buffering and antioxidant capacity (FRAP) and IL-1β, TNF-α, IL-6 levels. DNA was collected via buccal swabs and used to evaluate the presence of multiple bitter-taste receptor gene polymorphisms. (3) Results: The major allele for TAS2R4-rs2233998, TAS2R5-rs2227264, TAS2R50-rs1376251, and TAS2R9-rs3741845 was associated with a higher mean of unstimulated salivary flow rate, FRAP, TNF-α, IL-1β, and likelihood of filled teeth. Presence of the major allele for TAS2R4-rs2234001 and TAS2R9-rs3741845 was associated with lower means FRAP, TNF-α, IL-1β, DMFT index, and likelihood of missing teeth. (4) Conclusions: These findings suggest relationships between bitter-taste genotypes, oral health outcomes, and inflammatory markers. These findings justify the need for further studies that could help identify risk groups and develop novel agents for maintaining oral health.
Introduction: Wilson's disease (WD) is a disorder of copper metabolism leading to the accumulation of this metal in different organs. Hepatic manifestations tend to occur in the first decade and neurological symptoms in the third decade. Neurological manifestations are said to worsen with chelation therapy. Case report: In our patient however the initial manifestation was head tremor at the age of 43 years which improved with treatment. The patient for some reason stopped the therapy for 8 years after which he decided to resume it only to precipitate the liver cirrhosis clinically-something that has not been reported earlier. The diagnosis was missed initially. However treatment produced good results. Conclusion: The case also serves as a reminder not to dismiss this disease as a rare theoretical possibility but to suspect it in a case of liver cirrhosis of unknown etiology or when the patient presents with an obscure isolated neurological sign such as tremor. Delayed recognition of the disease or stopping therapy can lead to a progression of the disease. The patient had many unusual features which are being reported for future reference by researchers and practioners.
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