Did a workplace sugar-sweetened beverage sales ban reduce anxiety-related sugar-sweetened beverage consumption during the COVID-19 pandemic?

OBJECTIVE: Workplace sugar-sweetened beverage (SSB) sales bans can reduce SSB consumption. Because stress and anxiety can promote sugar consumption, we examined whether anxiety among hospital employees during the COVID-19 pandemic was associated with changes in SSB consumption and explored whether this relationship varied by exposure to a workplace SSB sales ban. DESIGN: In a prospective, controlled trial of workplace SSB sales bans, we examined self-reported anxiety (generalised anxiety disorder-7) and self-reported SSB consumption (fluid ounces/d) before (July 2019) and during (May 2020) the COVID-19 pandemic. SETTING: Hospital sites in two conditions (four with SSB sales bans and three without sales bans) in Northern California. PARTICIPANTS: We sampled 580 participants (hospital employees) from a larger trial of sales bans; all were regular consumers of SSB (minimum 3/week at main trial enrollment). This subsample was chosen based on having appropriately timed data for our study questions. RESULTS: Across conditions, participants reduced SSB consumption over the study period. However, participants with higher pandemic-era anxiety scores experienced smaller reductions in SSB consumption after 9 months compared with those with lower anxiety scores (ß = 0·65, P < 0·05). When the sample was disaggregated by sales ban condition, this relationship held for participants in the control group (access to SSB at work, ß = 0·82, P < 0·05), but not for those exposed to an SSB sales ban (ß = 0·42, P = 0·25). CONCLUSIONS: SSB sales bans likely reduce SSB consumption through multiple pathways; buffering stress-related consumption may be one mechanism.

Controlled trial of a workplace sales ban on sugar-sweetened beverages.

OBJECTIVE: To examine the effectiveness of a workplace sugar-sweetened beverage (SSB) sales ban on reducing SSB consumption in employees, including those with cardiometabolic disease risk factors. DESIGN: A controlled trial of ethnically diverse, full-time employees who consumed SSB heavily (sales ban n 315; control n 342). Outcomes included standardised measures of change in SSB consumption in the workplace (primary) and at home between baseline and 6 months post-sales ban. SETTING: Sutter Health, a large non-profit healthcare delivery system in Northern California. PARTICIPANTS: Full-time employees at Sutter Health screened for heavy SSB consumption. RESULTS: Participants were 66·1 % non-White. On average, participants consumed 34·7 ounces (about 1 litre) of SSB per d, and the majority had an elevated baseline BMI (mean = 29·5). In adjusted regression analyses, those exposed to a workplace SSB sales ban for 6 months consumed 2·7 (95 % CI -4·9, -0·5) fewer ounces of SSB per d while at work, and 4·3 (95 % CI -8·4, -0·2) fewer total ounces per d, compared to controls. Sales ban participants with an elevated BMI or waist circumference had greater post-intervention reductions in workplace SSB consumption. CONCLUSIONS: Workplace sales bans can reduce SSB consumption in ethnically diverse employee populations, including those at higher risk for cardiometabolic disease.

Copper-Binding Domain Variation in a Novel Murine Lysyl Oxidase Model Produces Structurally Inferior Aortic Elastic Fibers Whose Failure Is Modified by Age, Sex, and Blood Pressure.

Lysyl oxidase (LOX) is a copper-binding enzyme that cross-links elastin and collagen. The dominant LOX variation contributes to familial thoracic aortic aneurysm. Previously reported murine Lox mutants had a mild phenotype and did not dilate without drug-induced provocation. Here, we present a new, more severe mutant, Loxb2b370.2Clo (c.G854T; p.Cys285Phe), whose mutation falls just N-terminal to the copper-binding domain. Unlike the other mutants, the C285F Lox protein was stably produced/secreted, and male C57Bl/6J Lox+/C285F mice exhibit increased systolic blood pressure (BP; p < 0.05) and reduced caliber aortas (p < 0.01 at 100mmHg) at 3 months that independently dilate by 6 months (p < 0.0001). Multimodal imaging reveals markedly irregular elastic sheets in the mutant (p = 2.8 × 10−8 for breaks by histology) that become increasingly disrupted with age (p < 0.05) and breeding into a high BP background (p = 6.8 × 10−4). Aortic dilation was amplified in males vs. females (p < 0.0001 at 100mmHg) and ameliorated by castration. The transcriptome of young Lox mutants showed alteration in dexamethasone (p = 9.83 × 10−30) and TGFß-responsive genes (p = 7.42 × 10−29), and aortas from older C57Bl/6J Lox+/C285F mice showed both enhanced susceptibility to elastase (p < 0.01 by ANOVA) and increased deposition of aggrecan (p < 0.05). These findings suggest that the secreted Lox+/C285F mutants produce dysfunctional elastic fibers that show increased susceptibility to proteolytic damage. Over time, the progressive weakening of the connective tissue, modified by sex and blood pressure, leads to worsening aortic disease.

Inhibition of NOX1 Mitigates Blood Pressure Increases in Elastin Insufficiency.

Elastin (ELN) insufficiency leads to the cardiovascular hallmarks of the contiguous gene deletion disorder, Williams-Beuren syndrome, including hypertension and vascular stiffness. Previous studies showed that Williams-Beuren syndrome deletions, which extended to include the NCF1 gene, were associated with lower blood pressure (BP) and reduced vascular stiffness. NCF1 encodes for p47phox, the regulatory component of the NOX1 NADPH oxidase complex that generates reactive oxygen species (ROS) in the vascular wall. Dihydroethidium and 8-hydroxyguanosine staining of mouse aortas confirmed that Eln heterozygotes (Eln+/- ) had greater ROS levels than the wild-types (Eln+/+ ), a finding that was negated in vessels cultured without hemodynamic stressors. To analyze the Nox effect on ELN insufficiency, we used both genetic and chemical manipulations. Both Ncf1 haploinsufficiency (Ncf1+/- ) and Nox1 insufficiency (Nox1-/y ) decreased oxidative stress and systolic BP in Eln+/- without modifying vascular structure. Chronic treatment with apocynin, a p47phox inhibitor, lowered systolic BP in Eln+/- , but had no impact on Eln+/+ controls. In vivo dosing with phenylephrine (PE) produced an augmented BP response in Eln+/- relative to Eln+/+ , and genetic modifications or drug-based interventions that lower Nox1 expression reduced the hypercontractile response to PE in Eln+/- mice to Eln+/+ levels. These results indicate that the mechanical and structural differences caused by ELN insufficiency leading to oscillatory flow can perpetuate oxidative stress conditions, which are linked to hypertension, and that by lowering the Nox1-mediated capacity for vascular ROS production, BP differences can be normalized.