Carbon Chemist

Tag: Tea

  • Blessed thistle compound Cnicin speeds nerve growth, study finds

    Blessed thistle compound Cnicin speeds nerve growth, study finds

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    Blessed thistle (Cnicus benedictus) is a plant in the family Asteraceae and also grows in our climate. For centuries, it has been used as a medicinal herb as an extract or tea, e.g. to aid the digestive system. Researchers at the Center for Pharmacology of University Hospital Cologne and at the Faculty of Medicine of the University of Cologne have now found a completely novel use for Cnicin under the direction of Dr Philipp Gobrecht and Professor Dr. Dietmar Fischer. Animal models as well as human cells have shown that Cnicin significantly accelerates axon (nerve fibres) growth. The study ‘Cnicin promotes functional nerve regeneration’ was published in Phytomedicine.

    Rapid help for nerves

    Regeneration pathways of injured nerves in humans and animals with long axons are accordingly long. This often makes the healing process lengthy and even frequently irreversible because the axons cannot reach their destination on time. An accelerated regeneration growth rate can, therefore, make a big difference here, ensuring that the fibers reach their original destination on time before irreparable functional deficits can occur. The researchers demonstrated axon regeneration in animal models and human cells taken from retinae donated by patients. Administering a daily dose of Cnicin to mice or rats helped improve paralysis and neuropathy much more quickly.

    Compared to other compounds, Cnicin has one crucial advantage: it can be introduced into the bloodstream orally (by mouth). It does not have to be given by injection.

    The correct dose is very important here, as Cnicin only works within a specific therapeutic window. Doses that are too low or too high are ineffective. This is why further clinical studies on humans are crucial.”


    Professor Dr. Dietmar Fischer

    The University of Cologne researchers are currently planning relevant studies. The Center for Pharmacology is researching and developing drugs to repair the damaged nervous system.

    The current study received funding of around 1,200,000 euros from the Federal Ministry of Education and Research within the framework of the project PARREGERON.

    Source:

    Journal reference:

    Gobrecht, P., et al. (2024). Cnicin promotes functional nerve regeneration. Phytomedicine. doi.org/10.1016/j.phymed.2024.155641.

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  • The association between diet and colorectal cancer risk

    The association between diet and colorectal cancer risk

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    In a nested case-control study published in JAMA Network Open, researchers from South Korea investigated the genetic variants that modify the association between diet and colorectal cancer (CRC) risk.

    They found that single-nucleotide polymorphisms (SNPs) in the EPDR1 gene can modify the impact of fish intake on the risk of CRC.

    Further, they highlighted the potential pathways underlying the link between the consumption of tea, milk, cheese, and alcohol and the development of CRC.

    Study: Genome-Wide Interaction Study of Dietary Intake and Colorectal Cancer Risk in the UK Biobank. Image Credit: BlurryMe/Shutterstock.comStudy: Genome-Wide Interaction Study of Dietary Intake and Colorectal Cancer Risk in the UK Biobank. Image Credit: BlurryMe/Shutterstock.com

    Background

    CRC is the second most prevalent cancer in Europe (12.9%) and stands among the top three most-diagnosed cancers in both men and women in the United Kingdom (UK). Evidence suggests that the consumption of meat and alcohol is associated with an increased risk of CRC.

    On the other hand, the intake of fish, milk, fruits, and vegetables shows an inverse association with CRC-risk. Genetic factors, accounting for 3.5% to 10.5% of variations, may influence dietary habits and CRC-risk.

    For example, specific genes impact the metabolism of carcinogens in cooked meat and modify associations. Similarly, cruciferous vegetables are found to be inversely linked to CRC in individuals with certain enzyme deficiencies.

    Advances in technology have enabled genome-wide association studies that reveal genetic susceptibility loci and facilitate the assessment of gene-diet interactions across the genome.

    Dietary factors may influence CRC pathogenesis by modulating gene expression through metabolites or activating complex metabolic pathways.

    Previous studies explored the role of nutrition in various carcinogenesis pathways, including deoxyribonucleic acid (DNA) synthesis, epigenetic control via one-carbon metabolism, DNA damage, phase 1 and 2 enzymes, tumor promotion, and polynucleotide repair.

    Although potential mechanisms suggesting the association between dietary intake and CRC have been proposed, the specific genes and pathways involved in this association have not been extensively documented.

    Therefore, researchers in the present study conducted a gene-diet interaction analysis using genetic data and CRC cases to identify genetic variants that influence the association between diet and CRC-risk.

    About the study

    Data was obtained from the UK Biobank of participants enrolled between 2006 and 2010. Individuals with sex mismatches, putative sex chromosome aneuploidy, non-White racial background, and prevalent cancer at recruitment were excluded.

    A total of 4,686 participants (mean age 60.7 years) and 14,058 matched controls (mean age 60.4 years) were included in the study. In both the cohorts, 57.8% of participants were male.

    Dietary intake information, including milk, cheese, poultry, red meat, processed meat, fish, coffee, tea, alcohol, and total fruit and vegetables, was collected through a touchscreen food frequency questionnaire.

    Although the median follow-up was 12.4 years, only 10.2% of participants had data from more than one follow-up visit. Imputed genotyping data underwent quality control, resulting in 4,122,345 variants for the genome-wide interaction (GWI) analysis.

    CRC cases were identified based on the International Statistical Classification of Diseases and Related Health Problems (revision 10).

    Gene-based and gene-enrichment analyses were conducted. Statistical analysis involved the Cochran-Mantel-Haenszel χ2 test, conditional logistic model, principal component analysis, and p-values for gene or gene-set levels interactions.

    Results and discussion

    As compared to controls, the cases had a higher proportion of smokers, higher frequency of alcohol consumption, and higher prevalence of obesity.

    Individuals consuming red meat ≥3 times per week and processed meat ≥2 times per week showed a higher CRC-risk (odds ratio 1.16) after adjusting for confounding factors.

    Additionally, those who consumed alcohol more than thrice a week showed an increased CRC-risk compared to those with alcohol intake less than once a week. Notably, a protective association against CRC was found for participants consuming ≥4 servings of fruit daily compared to those with ≤ 2 servings daily.

    324 SNPs were suggested to interact with dietary intake without statistical significance. Genes EPDR1 and ZNRF2 were identified in the gene-based analysis, with EPDR1 showing significance with fish consumption through multiple SNPs.

    Further, gene-set enrichment analysis revealed overrepresented pathways (OR, ART, KRT, PRM, and TNP) for genes interacting with cheese, milk, tea, and alcohol consumption, respectively.

    The study’s findings could contribute to personalized preventive strategies and interventions for CRC.

    However, the study is limited by the analysis of CRC-risk based on dietary information from a single time point, limited availability of dietary data at multiple follow-up visits, potential instability in certain nutritional factors, inability to confirm specific SNPs modifying diet-CRC associations, and a lack of validation in non-European populations.

    Conclusion

    In conclusion, the study reveals several SNPs showing suggestive interactions with dietary intake, particularly significant interactions between EPDR1 and total fish consumption affecting CRC- risk.

    The findings point to various biological and functional pathways potentially underlying the association and highlight the need for further investigation through experimental studies.

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  • Flavonol-rich diet linked to lower mortality and disease risk, study shows

    Flavonol-rich diet linked to lower mortality and disease risk, study shows

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    In a recent prospective cohort study published in the journal Scientific Reports, researchers investigated the association between flavonol intake and cause-specific and all-cause mortality risk in adults in the United States. They found that an elevated dietary intake of flavonol is associated with a lower risk of all-cause mortality as well as Alzheimer’s disease (AD), cancer, and cardiovascular disease (CVD)-related mortality risk.

    Study: Flavonol-rich diet linked to lower mortality and disease risk, study shows. Image Credit: sematadesign / ShutterstockStudy: Flavonol-rich diet linked to lower mortality and disease risk, study shows. Image Credit: sematadesign / Shutterstock

    Background

    Flavonoids are biologically active polyphenolic compounds found in various plant-based foods. Among the six subclasses of flavonoids, flavonols are the most prevalent and active. Primary flavonols like quercetin, kaempferol, myricetin, and isorhamnetin are abundant in tea, onions, and berries. The consumption of flavonoids is known to potentially enhance endothelial function, maintain nitric oxide status, and influence biological processes relevant to lipid metabolism, platelet function, inflammation, oxidative stress, and blood pressure. Additionally, flavonoids are also known to exhibit anti-tumor effects by targeting key molecules and pathways, leading to apoptosis and inhibiting cell growth and metastasis.

    However, the relationship between flavonol intake and mortality risk has not been studied thoroughly so far. Therefore, using data from the National Health and Nutrition Examination Survey (NHANES) database, researchers in the present study explored the relationship between flavonol intake (total flavonol, kaempferol, myricetin, isorhamnetin, and quercetin), all-cause mortality risk, and cause-specific mortality risk (AD, CVD, cancer, and diabetes mellitus (DM)).

    About the study

    The study included 11,679 individuals aged≥ 20 who completed questionnaires, in-person assessments, and laboratory tests. The exclusion criteria were lack of flavonol intake and missing basic and demographic information. Flavonol intake data for the present study were derived from the US Department of Agriculture Survey Food and Beverage Flavonoid Values database (2003–2004). Detailed dietary interviews were conducted to capture information on foods and beverages consumed in the preceding 24 hours. The precise amounts of total flavonols were estimated in various foods, and the daily flavonol intake of participants was calculated.

    For mortality analysis, data from the National Death Index file and the 2019 Public Access Link mortality dataset were used. Mortality was categorized by causes such as cancer, CVD, DM, AD, and other causes, as per the International Statistical Classification of Diseases and Related Health Problems 10 (ICD-10) codes. Follow-up was conducted from the interview date to either the date of death or the study’s conclusion on December 31, 2019. Participants were stratified based on sociodemographic variables, including age, sex, race/ethnicity, marital status, education level, poverty ratio, alcohol consumption, body mass index (BMI), disease history, and the presence of various health conditions. Statistical analysis involved the use of Cox regression, Fine and Gray competing risks regression models, hazard ratios (HR), chi-square tests, and sensitivity analyses.

    Results and discussion

    Participants with the highest total flavonol intake tended to be male, younger, Non-Hispanic White, married, educated, above the poverty line, alcohol consumers, with BMI 18.5–30.0 kg/m2 and had a history of DM, hypertension, hyperlipidemia, congestive heart failure, coronary heart disease, angina, heart attack, and stroke. Increasing total flavonol intake showed a declining trend in all-cause mortality as well as AD, cancer, and CVD-specific mortality (p < 0.05 for all). Similar decreasing trends were observed for isorhamnetin, kaempferol, and quercetin intakes across various mortality categories, while myricetin intake exhibited a decreasing trend in AD mortality.

    While higher age was associated with a significant increase in all-cause mortality, female gender was found to be significantly linked to a lower risk of all-cause mortality. Conversely, a history of diseases was significantly associated with a higher risk of all-cause mortality.

    Further, higher total flavonol intake, particularly isorhamnetin, kaempferol, myricetin, and quercetin, was found to be associated with a reduced risk of all-cause and mortality owing to AD, CVD, cancer, and other causes. However, no correlation was found between flavonol intake and DM-specific mortality (p>0.05). The findings from the subgroup and sensitivity analyses aligned with the study’s main findings.

    Although the study is strengthened by its use of a multiple confounder-adjusted competing risks model to address competing risks of death, the study is limited by missing flavonol intake data, potential lack of generalizability, lack of data on primary food sources and dietary patterns, and the lack of exclusion of micronutrient supplement intake.

    Conclusion

    In conclusion, the present study establishes an association between dietary flavonol intake and overall mortality as well as cancer, AD, and CVD-specific mortality risk in US adults. The findings suggest that flavonol intake could be employed as an independent and reliable predictor of disease survival, offering patients the potential for health- and risk-management through dietary modifications.

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