The synthetic food dye, Red 40, causes DNA damage, causes colonic inflammation, and impacts the microbiome in mice.

The incidence of colorectal cancer (CRC) among young people has been on the rise for the past four decades and its underlying causes are only just starting to be uncovered. Recent studies suggest that consuming ultra-processed foods and pro-inflammatory diets may be contributing factors. The increase in the use of synthetic food colors in such foods over the past 40 years, including the common synthetic food dye Allura Red AC (Red 40), coincides with the rise of early-onset colorectal cancer (EOCRC). As these ultra-processed foods are particularly appealing to children, there is a growing concern about the impact of synthetic food dyes on the development of CRC. Our study aimed to investigate the effects of Red 40 on DNA damage, the microbiome, and colonic inflammation. Despite a lack of prior research, high levels of human exposure to pro-inflammatory foods containing Red 40 highlight the urgency of exploring this issue. Our results show that Red 40 damages DNA both in vitro and in vivo and that consumption of Red 40 in the presence of a high-fat diet for 10 months leads to dysbiosis and low-grade colonic inflammation in mice. This evidence supports the hypothesis that Red 40 is a dangerous compound that dysregulates key players involved in the development of EOCRC.

Prescribing patterns and outcomes of enoxaparin for anticoagulation of atrial fibrillation.

STUDY OBJECTIVE: To determine prescribing patterns and clinical outcomes of enoxaparin for anticoagulation of atrial fibrillation. DESIGN: Retrospective analysis. SETTING: A 650-bed, tertiary care, community teaching hospital. SUBJECTS: Two hundred thirteen patients who received enoxaparin for thromboprophylaxis during an episode of atrial fibrillation. Intervention. Data collection on demographics, antithrombotic usage, and thrombotic and bleeding episodes from January-June 2001. MEASUREMENTS AND MAIN RESULTS: Patients were characterized as having acute (51.6%) or chronic (48.4%) atrial fibrillation and were categorized according to stroke risk. Three enoxaparin dosing strategies had been prescribed: therapeutic, prophylactic, or adjusted. Prescribed regimens did not reflect stroke risk or type of atrial fibrillation but did reflect the degree of renal impairment. No episodes of stroke occurred with therapeutic enoxaparin dosages, but five strokes occurred among patients receiving prophylactic or adjusted dosages. Bleeding was similar with all dosing strategies in patients with adequate renal function and appeared to be more frequent in those with renal impairment. CONCLUSION: At a single hospital, wide variation in enoxaparin prescribing patterns existed. Further study is necessary to elucidate more fully the appropriate dosing strategy for this agent in the treatment of atrial fibrillation.

Probable case of torsades de pointes induced by fluconazole.

A 25-year-old woman who was hospitalized for worsening endocarditis had a prolonged QT interval at baseline and developed monomorphic ventricular arrhythmias, which were managed successfully with pacing and antiarrhythmic therapy. Several days later, the patient started receiving high-dose fluconazole for fungemia and subsequently experienced episodes of torsades de pointes, a polymorphic ventricular arrhythmia associated with a prolonged QT interval or prominent U wave on the electrocardiogram. The arrhythmia developed in the presence of known risk factors. Clinicians should be aware of these risk factors and other relevant structural similarities with drugs that cause torsades de pointes so that they can recognize patients who may be at risk for fluconazole-associated arrhythmia.