Long waves of consumption or a unique social generation? Exploring recent declines in youth drinking

Background: There is growing evidence for recent declines in adolescent alcohol use in the Western world. While these changes have been subject to scientific debate, the reasons for this downward trend are not yet understood. Method: We consider broader theoretical framings that might be useful in understanding declines in youth drinking. In particular, we reflect on the historical observations of ‘long waves of alcohol consumption’, the ‘Total Consumption Model’, and the ‘Theory of Social Generations’. Based on this, we explore some of the main hypotheses that are presently discussed as possible explanations for changes in youth drinking. Results: We suggest there may have been a change in the social position of alcohol as a social reaction to the negative effects of alcohol, but also emphasize the importance of changes in technology, social norms, family relationships and gender identity, as well as trends in health, fitness, wellbeing and lifestyle behavior. As a result of the interplay of these factors, the ‘devaluation’ of alcohol and the use of it may have contributed to the decrease in youth drinking. Conclusions: For interrupting the recurrent cycle of the ‘long waves of alcohol consumption’, we need to take advantage of the present change in sentiment and “lock in” these changes by new control measures. The model of change presented here hinges on the assumption that the observed change in the position the present young generation takes on alcohol proceeds through the life course, eventually reducing alcohol use in the whole population

Short-term, but not acute, intake of New Zealand blackcurrant extract improves insulin sensitivity and free-living postprandial glucose excursions in individuals with overweight or obesity

Abstract: Impaired postprandial glucose handling and low-grade systemic inflammation are risk factors for developing insulin resistance in individuals with overweight or obesity. Acute ingestion of anthocyanins improves postprandial glucose responses to a single carbohydrate-rich meal under strictly controlled conditions. Purpose: Examine whether acute and short-term supplementation with anthocyanin-rich New Zealand blackcurrant (NZBC) extract can improve postprandial glucose responses to mixed-macronutrient meals. Methods: Twenty-five overweight (BMI > 25 kg m2) sedentary individuals participated in one of the following double-blinded, randomised controlled trials: (1) ingestion of 600 mg NZBC extract or placebo prior to consumption of a high-carbohydrate, high-fat liquid meal (n = 12); (2) 8-days supplementation with NZBC extract (600 mg day−1) or placebo, with insulin sensitivity and markers of inflammation assessed on day-7, and free-living postprandial glucose (continuous glucose monitoring) assessed on day-8 (n = 13). Results: A single dose of NZBC extract had no effect on 3 h postprandial glucose, insulin or triglyceride responses. However, in response to short-term NZBC extract supplementation insulin sensitivity was improved (+ 22%; P = 0.011), circulating C-reactive protein concentrations decreased (P = 0.008), and free-living postprandial glucose responses to both breakfast and lunch meals were reduced (− 9% and − 8%, respectively; P < 0.05), compared to placebo. Conclusion: These novel results indicate that repeated intake, rather than a single dose of NZBC extract, is required to induce beneficial effects on insulin sensitivity and postprandial glucose handling in individuals with overweight or obesity. Continuous glucose monitoring enabled an effect of NZBC extract to be observed under free-living conditions and highlights the potential of anthocyanin-rich supplements as a viable strategy to reduce insulin resistance

Correlation of gene expression and protein production rate - a system wide study

<p>Abstract</p> <p>Background</p> <p>Growth rate is a major determinant of intracellular function. However its effects can only be properly dissected with technically demanding chemostat cultivations in which it can be controlled. Recent work on <it>Saccharomyces cerevisiae </it>chemostat cultivations provided the first analysis on genome wide effects of growth rate. In this work we study the filamentous fungus <it>Trichoderma reesei </it>(<it>Hypocrea jecorina</it>) that is an industrial protein production host known for its exceptional protein secretion capability. Interestingly, it exhibits a low growth rate protein production phenotype.</p> <p>Results</p> <p>We have used transcriptomics and proteomics to study the effect of growth rate and cell density on protein production in chemostat cultivations of <it>T. reesei</it>. Use of chemostat allowed control of growth rate and exact estimation of the extracellular specific protein production rate (SPPR). We find that major biosynthetic activities are all negatively correlated with SPPR. We also find that expression of many genes of secreted proteins and secondary metabolism, as well as various lineage specific, mostly unknown genes are positively correlated with SPPR. Finally, we enumerate possible regulators and regulatory mechanisms, arising from the data, for this response.</p> <p>Conclusions</p> <p>Based on these results it appears that in low growth rate protein production energy is very efficiently used primarly for protein production. Also, we propose that flux through early glycolysis or the TCA cycle is a more fundamental determining factor than growth rate for low growth rate protein production and we propose a novel eukaryotic response to this i.e. the lineage specific response (LSR).</p

Changes in the hepatic copper conent after treatment with foreign compounds

The effects of dimercaprol, CaNa2EDTA, D-penicillamine, diethyldithiocarbamate, disulfiram, pyrazole and phenobarbital on the hepatic copper content were studied. Adult male albino rats were given these compounds subcutaneously or intragastrically for 4 or 7 days, and the copper content in the hepatic crude homogenate was measured with an atomic absorption spectrophotometer. The metal chelating compounds dimercaprol, D-penicillamine and diethyldithiocarbamate only slightly decreased the level of copper in the liver. CaNa2 EDTA caused no change in the copper content. A slight decrease was found also after phenobarbital treatment. On the contrary, disulfiram and pyrazole increased the copper content 3- and 2-fold, respectively. It is suggested that the accumulation of copper in the liver is due to the cholestatic action of disulfiram and pyrazole.Arch Toxicol Supp

Increase of hepatic and serum aldehyde dehydrogenase activity after TCDD treatment

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), a contaminant of some herbicides, is an extremely potent enzyme inducer. Male albino rats of two genetically different substrains developed for the inducibility (RR) and noninducibility (rr) of aldehyde dehydrogenase by phenobarbital were given TCDD 80 microgram/kg as a single dose 6 days before analysis. rr-Animals having no induction of the hepatic soluble high-Km aldehyde dehydrogenase by phenobarbital showed an approximate 25-fold increase in activity after TCDD treatment. The increase in aldehyde dehydrogenase activity could be detected only when measured with a millimolar substrate concentration. The aldehyde dehydrogenase activity in serum was increased 3-fold after TCDD administration in both substrains.Arch Toxicol Supp

Responses of the D-glucuronic acid pathway in rat tissues to treatment with tetrachlorodibenzodioxin

1. 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) was administered to rats to study its effects on the enzyme activities of the D-glucuronic acid pathway in the liver, small intestine and kidney. 2. The UDP-glucuronosyl transferase activity of male albino rats given TCDD (80 mug/kg, one dose, i.p.) 6 days before killing was significantly increased in all tissues examined, and UDP-glucuronic acid pyrophosphatase activity was markedly decreased in the liver. D-Glucuronolactone and L-gulonate dehydrogenase activities in the liver and small intestine were slightly decreased after TCDD treatment. 3. The activities of UDP-glucose dehydrogenase and beta-glucuronidase were unchanged. 4. The 24 h urinary excretion of L-ascorbic acid was enhanced 8-fold, although no difference was detected in the excretion of D-glucaric acid between the control and experimental animals. 5. These results suggest an increased capacity for glucuronide conjugation after treatment with TCDD. 6. The lack of increase in the urinary excretion of D-glucaric acid further challenges its use as a reliable indicator of enhanced drug metabolism.Xenobiotic

Chelating agents and hepatic drug metabolism in the rat

Arch Int Pharmacodyn The

Modifications of drug metabolism by disulfiram and diethyldithiocarbamate. II. D-Glucuronic acid pathway

Hepatic enzymes connected with the formation and metabolism of free D-glucuronic acid were affected in rats after treatment with disulfiram or diethyldithiocarbamate (300 mg/kg, intragastrically, per day, 4 X). The activities of UDPglucose dehydrogenase, UDPglucuronic acid pyrophosphatase, UDPglucuronosyltransferase and L-gulonate dehydrogenase were enhanced, while those of glucose-6-phosphate dehydrogenase, beta-glucuronidase and D-glucuronolactone dehydrogenase were inhibited. These changes were more pronounced with disulfiram than diethyldithiocarbamate. Treatment with phenobarbital (80 mg/kg, i.p., per day, 4 X) enhanced UDP glucuronosyl-transferase, but brought about different effects on the other enzymes. Concurrent administration of phenobarbital with disulfiram or diethyldithiocarbamate led to potentiation or antagonism of the primary effects of each compound when given alone. The results suggest that activation of the D-glucuronic acid pathway may proceed in various ways, and that it is not necessarily followed by a simultaneous induction of the microsomal mixed-function oxygenase activity.Chem Biol Interac