The correlations within groups and the similarities between them suggest that physical activity in children is under central biological regulation. There are implications both for public health planners and for the potentially novel signalling pathways involved.

It seems likely that type 1 and type 2 diabetes lie at different points of the same spectrum, separated by the misunderstanding that one belongs to childhood and the other to adulthood. The spectrum is that of tempo--the rate at which beta cell function is lost over time. A combination of beta cell up-regulation (insulin demand, largely determined by obesity) and the genetically-determined immune response to it ('autoimmunity') determines tempo, ranging from slow to fast with every variant in between. There is good evidence that people who go on to develop type 1 (fast) diabetes are, like those who develop type 2 (slow diabetes), insulin resistant, and overwhelming evidence that body mass plays a key role. The prevention of type 1 diabetes may lie in weight restriction from an early age.

Autoaggression and autoimmune attack are established vernacular in the literature of autoimmune disease, and reflect the popular view that autoimmunity is a disease of immune dysregulation in which the immune system inappropriately attacks healthy tissues. The aim of this article is to focus attention on an alternative, indeed opposite, view--that autoimmunity represents the response to a primary lesion in the target tissue, rather than its cause, and that like alloimmunity, autoimmunity is physiological appropriate and protective. The cell death and tissue damage which results is characteristic of an immune response programmed to eliminate immunogen, remove detritus and isolate the lesion.

No abstract

The influence of a β-adrenergic blocker on the thermic effect of feeding (TEF) a meal was investigated in 7 healthy male volunteers. Metabolic rate (MR) was measured before and for 180 min after the consumption of 2.0 MJ ‘Ensure’ (Abbott Laboratories, Queensbor-ough, Kent, UK); there were 14, 33 and 53% of energy from protein, fat and carbohydrate, respectively. On one occasion propranolol (ICI pic, Macclesfield, Ches., UK) was administered intravenously at 0.1 mg/kg body weight at meal feeding. On the second occasion a similar volume of saline was infused. Serial blood samples (10 ml) were collected before and at 30-min intervals for 180 min after meal feeding. Mean ( ± SD) resting MR was 104 (13) and 116 (11) kJ/kg and MR increased by 12.8% and 10.8% after the test meal with and without propranolol, respectively. These differences were not significant. The postprandial changes in serum glucose and triiodothyronine were similar in the two trials. The magnitude of the rise of serum insulin was similar in the two trials, but the pattern was not. β-Adrenergenic blockade resulted in an early peak in insulin output at 30 min compared with 60 min for the control trial. We conclude that propranolol had no influence on TEF in this study.