The Effects of Two Servings of a Thermogenic Supplement on Metabolism, Hemodynamic Variables, and Mood State Outcomes in Young Overweight Adults.

Introduction We examined if acute ingestion of a novel thermogenic supplement influences resting energy expenditure (REE), mood, and hemodynamic function. Methods Forty-six adults completed this randomized, placebo-controlled, double-blind, crossover study. Participants underwent two conditions: placebo (PL) and treatment (TX) containing 300 mg of caffeine and 3 g of acetyl-L-carnitine. REE, systolic blood pressure (SBP), diastolic blood pressure (DBP), heart rate (HR), and mood states were assessed at baseline and 30, 60, and 120 minutes post-ingestion. Data were analyzed using repeated measures analysis of variance. Results A significant condition-by-time interaction was observed for REE. At the 30-, 60-, and 120-minute post-ingestion timepoints, REE was 202 ± 26, 238 ± 40, and 209 ± 29 kcal/d greater in the TX condition compared to PL. No significant differences were observed for SBP and HR but a significant interaction indicated that DBP was elevated at 30 minutes in the TX vs. PL, though values remained within normal ranges. Significant interactions were observed for perceived alertness, concentration, energy, and focus, with increases in TX. Conclusion These data provide evidence that acute consumption of the thermogenic dietary supplement OxyShred (EHPlabs, Salt Lake City, Utah, USA) stimulates increases in REE that are sustained for ≥ two hours, along with increasing perceived alertness, concentration, energy, and focus. Changes in hemodynamic function are minimal and within normal ranges.

The effects of a thermogenic supplement on metabolic and hemodynamic variables and subjective mood states.

BACKGROUND: Thermogenic supplements are widely used in the general population to support attempted fat loss; however, the efficacy and safety of these supplements are questioned. PURPOSE: To determine whether a thermogenic supplement affects metabolic rate, hemodynamic responses, and mood states. METHODS: In a randomized double-blind crossover design, 23 females (22.2 ± 3.5 years; 164.8 ± 6.4 cm; 73.5 ± 6.9 kg) who were moderate caffeine consumers (<150 mg/day) reported to the lab after a 12 h fast for baseline assessments of resting energy expenditure (REE) via indirect calorimetry, heart rate (HR), blood pressure (SBP and DBP), blood variables, and hunger, satiety, and mood states. Thereafter, subjects ingested the assigned treatment (active treatment containing caffeine, micronutrients, and phytochemicals [TR] or placebo [PL]). All variables were reassessed at 30-, 60-, 120-, and 180 min post-ingestion. Subjects repeated the same protocol with ingestion of the opposite treatment on a separate day. All data were analyzed using a 2 × 5 ANOVA with repeated measures and significance was accepted a priori at p < 0.05. RESULTS: In the TR group, mean increases in REE of 121 to 166 kcal/d were observed at 30-, 60-, and 180 min post-ingestion (p < 0.01 for all). PL group mean decreases in REE of 72 to 91 kcal/day were observed at 60-, 120-, and 180 min (p < 0.05 for all). Respiratory quotient decreased at 120 and 180 min in both treatments. Slight increases in SBP of 3-4 mmHg were observed at 30, 120, and 180 min (p < 0.05 for all) post-ingestion of TR, while no effects were observed for DBP. Observed increases in SBP were within normal blood pressure ranges. TR decreased subjective fatigue with no other significant changes in mood states. Glycerol was maintained in TR, while there was a decrease at 30, 60, and 180 min (p < 0.05 for all) post-ingestion of PLA. Free fatty acids increased in TR at 60 and 180 min (p < 0.05) post-ingestion as well as a significant difference between treatments at 30 min post-ingestion indicating greater circulating free fatty acids levels in TR vs. PL (p < 0.01). CONCLUSION: These findings indicate that ingestion of a specific thermogenic supplement formulation produces a sustained increase in metabolic rate and caloric expenditure and reduces fatigue over 3 h without producing adverse hemodynamic responses.

'Favourable' IL28B polymorphisms are associated with a marked increase in baseline viral load in hepatitis C virus subtype 3a infection and do not predict a sustained virological response after 24 weeks of therapy.

IL28B host genetic make-up is known to play a critical role in the outcome of genotype 1 hepatitis C virus (HCV) infection in the context of both primary infection and therapy. However, the role of IL28B in subtype 3a infection remains unclear, and has not yet been assessed in the UK population where subtype 3a is dominant. In this study, we evaluated the role of the IL28B single-nucleotide polymorphism rs8099917 in 201 patients recruited from two well-defined cohorts (from Nottingham and Oxford), treated with the standard-of-care therapy of pegylated interferon and ribavirin for 24 weeks. We showed that the 'favourable' IL28B gene was associated with a rapid virological response to therapy at 4 weeks (P<0.0001), but not with a sustained virological response to therapy. The median viral load at baseline, before therapy, was markedly increased in people with the 'favourable' IL28B genotype [median viral load for the TT allele, 925,961 IU ml(-1) (range 2200-21,116,965 IU ml(-1)), and for the GT or GG allele, 260,284 IU ml(-1) (range 740-7,560,000 IU ml(-1)); P = 0.0010]. Our results suggest that the host genetic response plays an important role in early viral clearance of subtype 3a virus from the blood. However, significant reservoirs of infection must persist, as viral relapse is common, even in those with the favourable host genotype.

Novel adenovirus-based vaccines induce broad and sustained T cell responses to HCV in man.

Currently, no vaccine exists for hepatitis C virus (HCV), a major pathogen thought to infect 170 million people globally. Many studies suggest that host T cell responses are critical for spontaneous resolution of disease, and preclinical studies have indicated a requirement for T cells in protection against challenge. We aimed to elicit HCV-specific T cells with the potential for protection using a recombinant adenoviral vector strategy in a phase 1 study of healthy human volunteers. Two adenoviral vectors expressing NS proteins from HCV genotype 1B were constructed based on rare serotypes [human adenovirus 6 (Ad6) and chimpanzee adenovirus 3 (ChAd3)]. Both vectors primed T cell responses against HCV proteins; these T cell responses targeted multiple proteins and were capable of recognizing heterologous strains (genotypes 1A and 3A). HCV-specific T cells consisted of both CD4+ and CD8+ T cell subsets; secreted interleukin-2, interferon-γ, and tumor necrosis factor-α; and could be sustained for at least a year after boosting with the heterologous adenoviral vector. Studies using major histocompatibility complex peptide tetramers revealed long-lived central and effector memory pools that retained polyfunctionality and proliferative capacity. These data indicate that an adenoviral vector strategy can induce sustained T cell responses of a magnitude and quality associated with protective immunity and open the way for studies of prophylactic and therapeutic vaccines for HCV.

Genomic analysis of hepatitis B virus reveals antigen state and genotype as sources of evolutionary rate variation.

Hepatitis B virus (HBV) genomes are small, semi-double-stranded DNA circular genomes that contain alternating overlapping reading frames and replicate through an RNA intermediary phase. This complex biology has presented a challenge to estimating an evolutionary rate for HBV, leading to difficulties resolving the evolutionary and epidemiological history of the virus. Here, we re-examine rates of HBV evolution using a novel data set of 112 within-host, transmission history (pedigree) and among-host genomes isolated over 20 years from the indigenous peoples of the South Pacific, combined with 313 previously published HBV genomes. We employ Bayesian phylogenetic approaches to examine several potential causes and consequences of evolutionary rate variation in HBV. Our results reveal rate variation both between genotypes and across the genome, as well as strikingly slower rates when genomes are sampled in the Hepatitis B e antigen positive state, compared to the e antigen negative state. This Hepatitis B e antigen rate variation was found to be largely attributable to changes during the course of infection in the preCore and Core genes and their regulatory elements.