Evolution of cooperation: cooperation defeats defection in the cornfield model.

"Cooperation" defines any behavior that enhances the fitness of a group (e.g. a community or species), but which, by its nature, can be exploited by selfish individuals, meaning, firstly, that selfish individuals derive an advantage from exploitation which is greater than the average advantage that accrues to unselfish individuals. Secondly, exploitation has no intrinsic fitness value except in the presence of the "cooperative behavior". The mathematics is described by the simple Prisoner's Dilemma Game (PDG). It has previously been shown that koinophilia (the avoidance of sexual mates displaying unusual or atypical phenotypic features, such as mutations) stabilizes any inherited strategy in the simple or iterated PDG, meaning that it cannot be displaced by rare forms of alternative behavior which arise through mutation or occasional migration. In the present model equal numbers of cooperators and defectors (in the simple PDG) were randomly spread in a two-dimensional "cornfield" with uniformly distributed resources. Every individual was koinophilic, and interacted (sexually and in the PDG tournaments) only with individuals from within its immediate neighborhood. This model therefore tested whether cooperation can outcompete defection or selfishness in a straight, initially equally matched, evolutionary battle. The results show that in the absence of koinophilia cooperation was rapidly driven to extinction. With koinophilia there was a very rapid loss of cooperators in the first few generations, but thereafter cooperation slowly spread, ultimately eliminating defection completely. This result was critically dependent on sampling effects of neighborhoods. Small samples (resulting from low population densities or small neighborhood sizes) increase the probability that a chance neighborhood comes to consist predominantly of cooperators. A sexual preference for the most common phenotype in the neighborhood then makes that phenotype more common still. Once this occurs cooperation's spread becomes almost inevitable.

A reappraisal of the blood glucose homeostat which comprehensively explains the type 2 diabetes mellitus-syndrome X complex.

Blood glucose concentrations are unaffected by exercise despite very high rates of glucose flux. The plasma ionised calcium levels are even more tightly controlled after meals and during lactation. This implies 'integral control'. However, pairs of integral counterregulatory controllers (e.g. insulin and glucagon, or calcitonin and parathyroid hormone) cannot operate on the same controlled variable, unless there is some form of mutual inhibition. Flip-flop functional coupling between pancreatic alpha- and beta-cells via gap junctions may provide such a mechanism. Secretion of a common inhibitory chromogranin by the parathyroids and the thyroidal C-cells provides another. Here we describe how the insulin:glucagon flip-flop controller can be complemented by growth hormone, despite both being integral controllers. Homeostatic conflict is prevented by somatostatin-28 secretion from both the hypothalamus and the pancreatic islets. Our synthesis of the information pertaining to the glucose homeostat that has accumulated in the literature predicts that disruption of the flip-flop mechanism by the accumulation of amyloid in the pancreatic islets in type 2 diabetes mellitus will lead to hyperglucagonaemia, hyperinsulinaemia, insulin resistance, glucose intolerance and impaired insulin responsiveness to elevated blood glucose levels. It explains syndrome X (or metabolic syndrome) as incipient type 2 diabetes in which the glucose control system, while impaired, can still maintain blood glucose at the desired level. It also explains why it is characterised by high plasma insulin levels and low plasma growth hormone levels, despite normoglycaemia, and how this leads to central obesity, dyslipidaemia and cardiovascular disease in both syndrome X and type 2 diabetes.