Beyond the neo-Darwinist paradigm.

DESCRIPTION: Ever since Darwin, there have been challenges to the claim that the natural selection of small random variations is a sufficient explanation of evolution. Even mainstream evolutionists are now beginning to accept that something more is required. The question is whether this will be merely a few add-ons that leave the paradigm unaltered, or whether the whole framework of explanation, including its application to other disciplines, will be changed.

Evolutionary psychology: a house built on sand.

While Darwinism has contributed much to our understanding of the living world, it has not given us an adequate account of why organisms are the way they are and how they came to be that way. For that we will need all of science, not just a single algorithm. The crucial contribution of Darwinism to biology is that it explains how we can have functional physical traits without a creator. This is less important in psychology because no one is surprised when people behave in ways that work to their advantage. Evolutionary psychology nevertheless follows the Darwinian model. It assumes from the outset that the brain is largely modular and that human nature is made up of a very large number of functionally specialized psychological mechanisms that have been constructed over time by natural selection. How much confidence one should have in its conclusions depends very much on how far one accepts its premises.

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.

Ether-induced segmentation disturbances in Drosophila melanogaster.

Drosophila embryos, exposed to ether between 1 and 4 h after oviposition, develop defects ranging from the complete lack of segmentation to isolated gaps in single segments. Between these extremes are varying extents of incomplete and abnormal segmentation. On the basis of both their temporal and spatial characteristics, five major phenotype classes may be distinguished: headless - unsegmented or incompletely segmented anteriorly; gap - interruptions of segmentation not obviously periodic; alternating segment gaps - interruptions with double segment periodicities; fused segments; and short segments - truncations with single segment periodicities. Many defects resemble known mutant phenotypes. The disturbances in segmentation are predominantly global and frequently accompanied by alterations in segment specification, such that the segments obtained show no resemblance to the normal homologues. These features, together with the distinctive spatiotemporal characteristics of the defects, all point to segmentation as a dynamic process. The regular spacing of the segments and the fact that the entire range of defects is inducible by ether are further consistent with the hypothesis that at least part of the segmentation process may consist of physicochemical reactions coordinated over the whole body. The relationship between our data and data from genetic and other analyses are briefly discussed.