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Turmeric is the bright yellow root that has been used as a spice, healing remedy, and textile dye. Previous studies have suggested that the most active ingredient in turmeric, curcumin, could reduce serum cholesterol concentration. However, most of these studies were conducted on animals and not many have been done on controlled human trials. This randomized, double-blinded, controlled crossover study evaluates the effects of turmeric on blood cholesterol concentrations including total cholesterol, LDL cholesterol, HLD cholesterol, and triglycerides. In this study, eight healthy participants between the ages of 18 and 45 were randomized to receive either 500mg capsules of turmeric or placebo for a period of three weeks. Following a wash-out period of five weeks, all participants were crossed over to the alternative treatment for another three weeks. After comparing the 3 week treatment and placebo phases, turmeric showed no significant effect on serum lipid concentrations. Furthermore, a slight increase in total cholesterol concentrations was observed following the turmeric phase when compared to the placebo phase.
Curcumin is an active ingredient of Curcuma longa (Turmeric) and is studied extensively for its antioxidant, anti-inflammatory, anti-bacterial, anti-viral, and anti-cancer properties. The purpose of this study was to examine the effects of turmeric on blood glucose and plasma insulin levels. The study utilized a placebo-controlled, randomized cross-over design with participants serving as their own control. Eight glucose tolerant healthy participants completed the full study. Three-weeks washout period was kept in between six-weeks. Prior to the test meal day, participants were asked to eat a bagel with their evening dinner. During the day of the test meal, participants reported to the test site in a rested and fasted state. Participants completed mashed potato meal tests with 500 mg of turmeric powder or placebo mixed in water, followed by 3 weeks of 500 mg turmeric or placebo supplement ingestion at home. During this visit blood glucose finger picks were obtained at fasting, 30, 60, 90, and 120 min post-meal. Blood plasma insulin at fasting and at 30 min after the test meal were also obtained. During week 4, participants reported to the test site in a rested and fasted state where fasting blood glucose finger pricks and blood plasma insulin were measured. During week 5 to 7, participants were given a washout time-period. During week 8, entire process from week 1 to 4 was repeated by interchanging the groups. Compared to placebo, reduction in postprandial blood glucose and insulin response were non-significant after ingestion of turmeric powder. Taking turmeric for 3 weeks had no change in blood glucose and insulin levels. However, taking turmeric powder supplements for 3 weeks, showed a 4.4% reduction in blood glucose. Change in insulin at 30 min were compared with baseline insulin level showing no significant change between placebo and turmeric group. Fasting insulin after 3-weeks consumption of turmeric did not show any significant change, but showed a larger effect size (0.08). Future research is essential to examine the turmeric powder supplement benefits over a long period of time in healthy adults and whether it is beneficial in preventing the occurrence of type 2 diabetes.
Psoriasis is a skin disease that affects millions of individuals. Genetic risk factors for psoriasis include a common deletion of two late cornified envelope (LCE) genes (LCE3B and LCE3C) located within a cluster of genes expressed during epithelial differentiation and skin repair. It was previously discovered that treatment with 1,25-dihydroxyvitamin D3 (1,25D) or analogs thereof can improve psoriasis symptoms in many patients, but the molecular mechanisms for this action are largely unknown. Our laboratory previously showed that 1,25D as well as low affinity ligands for the vitamin D receptor (VDR), such as delphinidin and cyanidin, are capable of upregulating the remaining LCE3A, -3D, and -3E genes to potentially compensate for the loss of LCE3B and -3C in promoting skin repair. In the current study, DHA and curcumin were tested and found to also upregulate LCE3 transcripts in a dose-dependent manner. To investigate other potential target genes for 1,25D and DHA, we tested JunB, for which low or absent expression has been reported to cause or be associated with psoriatic lesions. Our experiments showed a trend for an upregulation of JunB mRNA after DHA treatment, potentially providing benefit for psoriasis patients. Although our hypothesis is that DHA functions as a vitamin D receptor ligand to mediate upregulation of JunB and LCE3 genes, other investigators have assumed that DHA actions in skin are mediated via PPAR isoforms. We therefore utilized a selective ligand for PPAR delta (GW501516) to determine whether PPAR delta, the primary PPAR isoform in keratinocytes, is a mediator of DHA-induced LCE3 gene activation. Although a modest upregulation of LCE3 genes was seen after treatment with GW501516, our findings are still consistent with DHA acting primarily as a VDR ligand. Our results not only provide additional information about the ability of VDR ligands to upregulate specific skin genes with relevance for skin repair, but also may help provide a molecular basis for testing improved treatments for mild to moderate psoriasis.