Abstract The aim of this study was to analyse the association between plain water intake and glycated Hb (HbA1c) in the National Diet and Nutrition Survey (2008–2012) rolling survey. These data included diet (4-d diaries) and HbA1c (fasted blood sample) measures of 456 men and 579 women aged 44 ( sd 18) years with full information on covariates of interest (age, ethnicity, BMI, smoking status, education, other beverage intake, energy intake and fibre). Data were analysed using sex-stratified linear and logistic regressions modelling the associations of cups per d (240 ml) of plain water with HbA1c, and odds of HbA1c≥5·5 %, respectively. Substitution analyses modelled the replacement of sugar-sweetened beverages, fruit juice and artificially sweetened beverages with plain water. After adjustment, 1 cup/d of plain water was associated with a −0·04 % lower HbA1c (95 % CI −0·07, −0·02) in men. In logistic regression, men had a 22 % (95 % CI 10, 32 %) reduced odds of HbA1c≥5·5 %/cup per d of plain water. There was no evidence of an association with either HbA1c or odds of HbA1c≥5·5 % in women. None of the substitution models was associated with a change in odds of HbA1c≥5·5 %. Plain water intake was associated with lower HbA1c in men but not in women. Substituting water for specific beverages was not associated with a reduced odds of HbA1c≥5·5 %, suggesting that the addition of water is the more pertinent factor. Future trials should test whether the relationships between water intake and HbA1c is causal as this could be a cost-effective and simple health intervention.
The aim of this study was to explore the longitudinal association between reported baseline water intake and incidence of coronary artery disease (CAD) and type 2 diabetes in the Malmö Diet and Cancer Cohort (n = 25,369). Using cox proportional hazards models, we separately modelled the effect of plain and total (all water, including from food) water on CAD and type 2 diabetes risk, whilst adjusting for age, sex, diet collection method, season, smoking status, alcohol intake, physical activity, education level, energy intake, energy misreporting, body mass index, hypertension, lipid lowering medication, apolipoprotein A, apolipoprotein B, and dietary variables. Sensitivity analyses were run to assess validity. After adjustment, no association was found between tertiles of plain or total water intake and type 2 diabetes risk. For CAD, no association was found comparing moderate to low intake tertiles from plain or total water, however, risk of CAD increased by 12% (95% CI 1.03, 1.21) when comparing high to low intake tertiles of plain water, and by 17% (95% CI 1.07, 1.27) for high versus low tertiles of total water. Sensitivity analyses were largely in agreement. Overall, baseline water intake was not associated with future type 2 diabetes risk, whilst CAD risk was higher with higher water intakes. Our findings are discordant with prevailing literature suggesting higher water intakes should reduce cardiometabolic risk. These findings may be an artefact of limitations within the study, but future research is needed to understand if there is a causal underpinning.
Authors rely on a range of devices and techniques to attract and maintain the interest of readers, and to convince them of the merits of the author's point of view. However, when writing a scientific article, authors must use these 'persuasive communication devices' carefully. In particular, they must be explicit about the limitations of their work, avoid obfuscation, and resist the temptation to oversell their results. Here we discuss a list of persuasive communication devices and we encourage authors, as well as reviewers and editors, to think carefully about their use.
Gluco-regulatory diseases, such as type 2 diabetes are currently a key public health priority. Public health messages have started to include the addition of water in their dietary guidelines. Such guidelines however are not based on causal evidence pertaining to the health effects of increased water intake, but rather more heavily based upon non-causal or mechanistic data. One line of thinking linking fluid intake and health is that hypohydration induces elevated blood concentrations of arginine vasopressin (AVP). Research in the 1970s and 1980s implicated AVP in gluco-regulation, supported by observational evidence. This important area of research subsequently appeared to stop until this century during which interest in hypertonic saline infusion studies, animal AVP receptor knockout models, dietary and genetic associations, and human interventions manipulating hydration status have resurged. This narrative review briefly describes and critically evaluates the usefulness of the current AVP-gluco-regulatory research. We offer suggestions on how to test the independent gluco-regulatory effects of body mass reductions versus elevated circulating AVP concentrations, such as investigating hydration manipulations using 3,4-Methylenedioxymethamphetamine. Whilst much research is still needed before making firm conclusions, the current evidence suggests that although AVP may only be partially implicated in gluco-regulation; more ecologically valid models using human participants suggests this effect is independent of hydration status. The key implication of this hypothesis if confirmed in future research is that manipulating hydration status to reduce circulating AVP concentrations may not be an effective method to improve gluco-regulatory health.
This dataset provides the data collected for a trial investigating the role of hydration status on glycaemic regulation in healthy adults (n = 16; n = 8 male). To our knowledge, the effect of hydration status on glycemia has never been causally investigated in healthy adults. Therefore, the goal was to explore how acute hypohydration impacts blood sugar control in healthy adults. The trial was a randomised crossover trial, with each trial arm lasting 5 days. The first 3 days were lifestyle monitoring, day 4 was a dehydration/rehydration day (including lifestyle monitoring), and day 5 was the full trial day. The trial arms were hypohydrated (HYPO), or rehydrated (RE).
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