This secondary data analysis addressed gaps in knowledge about effects of chronic water intake. Longitudinal data from the Adapt Study were used to describe effects of prescribing a sustained increase in water intake relative to baseline, for 4 weeks, on multiple indices of total body water (TBW) flux, regulation, distribution, and volume in five healthy, free‐living, young men, with mean total water intake initially below 2 L/day. Indices were measured weekly. Within‐person fixed effect models tested for significant changes in indices over time and associations between changes in indices. Agreement between indices was described. Mixed models tested if baseline between‐person differences in hydration indices modified changes in indices over time. Body water flux: The half‐life of water in the body decreased significantly. Body water regulation: Serum osmolality decreased significantly. Urine anti‐diuretic hormone, sodium, potassium, and osmolality decreased significantly. Plasma aldosterone and serum sodium increased significantly. Body water distribution: No significant changes were observed. Body water volume: Saliva osmolality decreased significantly. Body weight increased significantly by a mean ± SEM of 1.8% ± 0.5% from baseline over 4 weeks. Changes in indices were significantly inter‐correlated. Agreement between indices changed over 4 weeks. Baseline saliva osmolality significantly modified responses to chronic water intake. The results motivate hypotheses for future studies: Chronic TBW deficit occurs in healthy individuals under daily life conditions and increases chronic disease risk; Sustained higher water intake restores TBW through gradual isotonic retention of potassium and/or sodium; Saliva osmolality is a sensitive and specific index of chronic hydration status.

Biomarkers of chronic cell hydration status are needed to determine whether chronic hyperosmotic stress increases chronic disease risk in population-representative samples. In vitro, cells adapt to chronic hyperosmotic stress by upregulating protein breakdown to counter the osmotic gradient with higher intracellular amino acid concentrations. If cells are subsequently exposed to hypo-osmotic conditions, the adaptation results in excess cell swelling and/or efflux of free amino acids. This study explored whether increased red blood cell (RBC) swelling and/or plasma or urine amino acid concentrations after hypo-osmotic challenge might be informative about relative chronic hyperosmotic stress in free-living men. Five healthy men (20–25 years) with baseline total water intake below 2 L/day participated in an 8-week clinical study: four 2-week periods in a U-shaped A-B-C-A design. Intake of drinking water was increased by +0.8 ± 0.3 L/day in period 2, and +1.5 ± 0.3 L/day in period 3, and returned to baseline intake (0.4 ± 0.2 L/day) in period 4. Each week, fasting blood and urine were collected after a 750 mL bolus of drinking water, following overnight water restriction. The periods of higher water intake were associated with significant decreases in RBC deformability (index of cell swelling), plasma histidine, urine arginine, and urine glutamic acid. After 4 weeks of higher water intake, four out of five participants had ½ maximal RBC deformability below 400 mmol/kg; plasma histidine below 100 μmol/L; and/or undetectable urine arginine and urine glutamic acid concentrations. Work is warranted to pursue RBC deformability and amino acid concentrations after hypo-osmotic challenge as possible biomarkers of chronic cell hydration.

Caloric beverages may promote weight gain by simultaneously increasing total energy intake and limiting fat oxidation. During moderate intensity exercise, caloric beverage intake depresses fat oxidation by 25% or more. This randomized crossover study describes the impact of having a caloric beverage with a typical meal on fat oxidation under resting conditions. On 2 separate days, healthy normal-weight adolescents (n = 7) and adults (n = 10) consumed the same breakfast with either orange juice or drinking water and sat at rest for 3 h after breakfast. The meal paired with orange juice was 882 kJ (210 kcal) higher than the meal paired with drinking water. Both meals contained the same amount of fat (12 g). For both age groups, both meals resulted in a net positive energy balance 150 min after breakfast. Resting fat oxidation 150 min after breakfast was significantly lower after breakfast with orange juice, however. The results suggest that, independent of a state of energy excess, when individuals have a caloric beverage instead of drinking water with a meal, they are less likely to oxidize the amount of fat consumed in the meal before their next meal.

Plasma procainamide levels achieved by oral procainamide treatment were studied in patients with recent myocardial infarction or ischaemia. Procainamide therapy was started after intravenous lignocaine had been used to control ventricular arrhythmias in the acute phase. A i g loading dose did not provoke toxicity and achieved 4-hour levels in or near the therapeutic range in 79 per cent ofpatients. Some patients with cardiac failure absorbed oral procainamide very slowly. A maintenance regimen of 375 mg 4 hourlyfailed to maintain effective procainamide levels in 73 per cent of patients. On a dosage of 500 mg 4 hourly 36 per cent had ineffective levels before each dose. Measurement of procainamide levels is desirable during treatment, since the variation between patients given a standard dosage is considerable and unpredictable. To maintain adequate procainamide levels frequent doses are necessary but inconvenient.

Eleven affected members of a New Zealand family carrying the high oxygen affinity haemoglobin Heathrow are described. The detection of high oxygen affinity abnormal haemoglobins may be difficult as haemoglobin and red cell mass may both fall within the normal range and no abnormality may be detected on haemoglobin electrophoresis or by haemoglobin stability tests. The importance of oxygen affinity studies to establish the diagnosis is emphasized.