From biology to behavior: a cross-disciplinary seminar series surrounding added sugar and low-calorie sweetener consumption.

INTRODUCTION: This report presents a synopsis of a three-part, cross-sector, seminar series held at the George Washington University (GWU) in Washington, DC from February-April, 2018. The overarching goal of the seminar series was to provide a neutral forum for diverse stakeholders to discuss and critically evaluate approaches to address added sugar intake, with a key focus on the role of low-calorie sweeteners (LCS). METHODS: During three seminars, twelve speakers from academic institutions, federal agencies, non-profit organizations, and the food and beverage industries participated in six interactive panel discussions to address: 1) Do Farm Bill Policies Impact Population Sugar Intake? 2) What is the Impact of Sugar-sweetened Beverage (SSB) Taxes on Health and Business? 3) Is Sugar Addictive? 4) Product Reformulation Efforts: Progress, Challenges, and Concerns? 5) Low-calorie Sweeteners: Helpful or Harmful, and 6) Are Novel Sweeteners a Plausible Solution? Discussion of each topic involved brief 15-minute presentations from the speakers, which were followed by a 25-minute panel discussion moderated by GWU faculty members and addressed questions generated by the audience. Sessions were designed to represent opposing views and stimulate meaningful debate. Given the provocative nature of the seminar series, attendee questions were gathered anonymously using Pigeonhole™, an interactive, online, question and answer platform. RESULTS: This report summarizes each presentation and recapitulates key perspectives offered by the speakers and moderators. CONCLUSIONS: The seminar series set the foundation for robust cross-sector dialogue necessary to inform meaningful future research, and ultimately, effective policies for lowering added sugar intakes.

Potentiation of cold-water swim analgesia and hypothermia by clonidine.

The analgesia induced by acute exposure to cold-water swims (CWS) covaries with levels of brain norepinephrine and is reduced by lesions placed in the locus coeruleus. In assessing whether alpha-noradrenergic receptor mechanisms mediated CWS analgesia, the first experiment found that clonidine pretreatment (500, 1000 micrograms/kg) elevated jump thresholds 60 min following injection. While clonidine (1000 micrograms/kg) paired with a 2 degrees C CWS potentiated CWS analgesia in a synergistic manner, additivity of analgesic effects was observed following pairing of clonidine (500 micrograms/kg) with a 2 degrees C CWS and pairing of clonidine (500 and 1000 micrograms/kg) with a 15 degrees C CWS. The second experiment showed that clonidine (500 micrograms/kg) paired with a 2 degrees C CWS enhanced CWS enhanced CWS analgesia on the tail-flick test. The third experiment indicated that while clonidine (500 and 1000 micrograms/kg) or CWS (2 degrees C) each produced hypothermia, pairing of these clonidine doses with CWS enhanced CWS hypothermia. These data are discussed in terms of the possible modulatory role that norepinephrine, and particularly its alpha-noradrenergic receptor subclass, plays in the full expression of CWS analgesia and hypothermia.

Analgesia following intraventricular administration of 2-deoxy-D-glucose.

The glucose analogue, 2-deoxy-D-glucose (2-DG) elicits hyperphagic and analgesic responses in rats. The former response appears to be mediated by central processes since overeating is elicited following intraventricular administration of 2-DG at low (3.5 and 5.0 mg/kg) doses. The present study examined whether flinch-jump threshold would increase 30, 90 and 180 min following intraventricular injections of 2-DG at low (3.5, 5.0 and 10.0 mg/kg) doses and compared these effects with systemically-applied 2-DG doses of 350 and 500 mg/kg. Intraventricular 2-DG administration increased jump thresholds for up to 180 min across all test doses. Flinch thresholds were also increased, but in a manner dissociated from jump thresholds. Animals with cannulae located near, but not in the lateral ventricle, displayed delayed analgesic effects. The magnitude of intraventricular 2-DG analgesia was not at potent as the 100-fold higher systemic injections. It appears that central mechanisms mediated intraventricular 2-DG analgesia at the low dose range since higher, systemic 2-DG doses have previously failed to increase flinch-jump thresholds.