Archive December 2015

Vitamin D and Metastatic Colorectal Cancer Survival!

Prospective epidemiologic data suggests higher levels of vitamin D are associated with improved survival in patients with colorectal cancer (CRC), however the relationship between 25(OH)D (vitamin D status) and outcome in metastatic CRC specifically is unknown. Researchers prospectively assessed the association between plasma 25(OH)D and overall survival (OS) in previously untreated metastatic CRC patients enrolled in CALGB 80505, a randomized phase III trial of chemotherapy + bevacizumab, cetuximab, or both, prior to the KRAS WT amendment. Among 1,043 patients, median plasma 25(OH)D was 17.2 ng/mL. Patients in the highest quintile of 25(OH)D had significantly improved overall survival (OS) compared to those in the lowest after adjusting for pathologic and clinical prognostic factors. Increasing concentrations of 25(OH)D were also associated with improved progression-free survival (PFS). Results were consistent across subgroups of patient characteristics, including KRAS status. The researchers concluded that higher concentrations of plasma 25(OH)D are associated with significantly improved survival in metastatic CRC patients treated with chemotherapy and biologics.

Kimmie, Ng, et al. Vitamin D status and survival of metastatic colorectal cancer patients: Results from CALGB/SWOG 80405 (Alliance). 2015 Gastrointestinal Cancers Symposium. J Clin Oncol 33, 2015 (suppl 3; abstr 507)


Niacin for Parkinson’s Disease?

Anecdotal animal and human studies have implicated the symptomatic and neuroprotective roles of niacin in Parkinson’s disease (PD). Niacin has a high affinity for GPR109A, an anti-inflammatory receptor. Researchers hypothesize that GPR109A message and expression are up-regulated in individuals with PD. Niacin is a precursor for NDA-NADH which is needed for dopamine production, therefor niacin may serve three purposes: reduce inflammation through GPR109A-related mechanisms, increase dopamine synthesis in the striatum through NADPH supply, and increase NAD/NADH ratio to boost mitochondrial functions. GPR109A and its agonists are known to exert anti-inflammatory actions in the skin, gut and retina, but these roles are neither anticipated nor established in the central nervous system (CNS). These researchers, for the first time propose the roles of GPR109A and its agonist including niacin in CNS pathology, Moreover they predict that the neuroprotective roles of either niacin or butyrates in CNS occur via GPR109A.

Wakade C, Chong R. A novel treatment target for Parkinson’s disease. J Neurol Sci. 2014 Dec 15;347(1-2):34-8


How to Diagnose Non-Celiac Gluten Sensitivity

Non-Celiac Gluten Sensitivity (NCGS) is a syndrome characterized by intestinal and extra-intestinal symptoms related to the ingestion of gluten-containing food, in subjects that are not affected by either celiac disease (CD) or wheat allergy (WA). Although NCGS is triggered by gluten-containing cereals, the offending dietary protein has not been identified yet, and could include other components such as amylase-trypsin inhibitors (ATIs). Indirect evidence suggests that NCGS is more common than CD. Using a self-administered evaluation incorporating a modified Gastrointestinal Symptom Rating Scale, the patient identifies 1 to 3 main symptoms that are quantitatively assessed using a Numerical Rating Scale ranging from 1 to 10. The double-blind placebo-controlled gluten challenge (8 g/day) includes a one-week challenge followed by a one-week washout of strict gluten free diet (GFD) and by the crossover to the second one-week challenge. The vehicle should contain cooked, homogeneously distributed gluten. A variation of 30% of 1 to 3 main symptoms between the gluten and the placebo challenge should be detected to discriminate a positive from a negative result. Note that NCGS may be transient, therefor gluten tolerance needs to be re-assessed in patients with NCGS.

Carlo Catassi, et al. Diagnosis of Non-Celiac Gluten Sensitivity (NCGS): The Salerno Experts’ Criteria. Nutrients. 2015 June; 7(6): 4966-4977.


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