To investigate current advice given to insulin-treated diabetic patients undertaking international flights crossing time-zones, we have conducted a survey of UK physicians running diabetic clinics. Consultants were asked to give the general advice they would give to travellers on twice-daily short- and intermediate-acting insulins in four different flight situations: westward London to New York (morning and evening departures) and eastward Manchester to Singapore (morning and evening departures). Response rate was poor (37%). Six percent of replies were unhelpful (e.g. 'ring the BDA', 'carry on as usual'), and 14% liable to cause hypoglycaemia. Thirteen percent advocated change to a 'basal-bolus' system of insulin administration. The rest used variants of additional insulin for westward flights and reduced flights eastward. There was great variation in advice, and many regimens were excessively complicated. We recommend simple individualized advice, without attempts at over-zealous glycaemic control during travel. Local arrival and departure times may fit in easily with insulin and meals at standard times before and after flying, and little or no dosage alteration may be needed.
Summary: In experiments on 8 healthy young male volunteers, the ingestion of a large meal was found to cause plasma osmolality to rise from 288.8 + 0.8 (mean + s.e. mean) to 295.6 + 0.9 mmol/kg at 4 hours (P <0.001). There was an accompanying rise in plasma sodium (Na) from 141.9 + 0.8 to 144.6 + 0.8 mmol/l, also at 4 hours (P < 0.01), but little change in other plasma electrolytes. Serum total amino acids rose slightly, non-esterified fatty acid fell minimally and changes in blood glucose concentrations were unremarkable. Thirst was experienced at plasma osmolality of 294.8 + 0.7 mmol/kg. Repeating the experiment either without food, or with the salt content of the meal only, was without effect on plasma Na, other solutes or osmolality. Postprandial hypersomolality and hypernatraemia is probably due to movement of water from the vascular compartment to the gut, or into cells. Plasma osmolality is best measured in the fasting state.
IntroductionIn health, plasma osmolality is tightly controlled by well-defined homeostatic mechanisms (Baylis 1983). We postulated, however, that absorption of solutes produced within the gastrointestinal tract after large meals, by digestion of food, might increase plasma osmolality. This paper reports our investigation of this hypothesis. Relative hyperosmolality after meals was confirmed, but it appeared to be due to net loss of water from the extracellular fluid (ECF), rather than the addition of absorbed exogenous 'osmoles' to the ECF.
We describe a 24-year-old short, obese girl who has bizarre episodic neurological abnormalities related to hyperosmolality due to hypernatraemia. Investigation of osmoregulation by water loading and infusion of hypertonic saline revealed (i) hypodipsia with thirst onset raised to plasma osmolality of 332 mmol/kg and (ii) elevation of the threshold for vasopressin release (plasma osmolality 320 mmol/kg) but normal slope of the plasma vasopressin-plasma osmolality curve. Baroregulated vasopressin release was also grossly subnormal. Other hypothalamo-pituitary investigations showed deficiencies of releasing hormones for gonadotrophins and growth hormone, but prolactin response to combined hypoglycaemia and TRH was blunted She demonstrated other anomalies including hyperlipoproteinaemia and defective lymph drainage of the legs. Skull X-rays, together with computerized tomography and nuclear magnetic resonance scans of the hypothalamo-pituitary region and the rest of the brain were normal. We believe that this is the first case of essential hypernatraemia documented with direct evidence of resetting of the osmostat.
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