Archaeology: propaganda of the pyramids.
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Biomedical subjects
Publications and source records attributed to Jared Diamond.
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The largest movements and replacements of human populations since the end of the Ice Ages resulted from the geographically uneven rise of food production around the world. The first farming societies thereby gained great advantages over hunter-gatherer societies. But most of those resulting shifts of populations and languages are complex, controversial, or both. We discuss the main complications and specific examples involving 15 language families. Further progress will depend on interdisciplinary research that combines archaeology, crop and livestock studies, physical anthropology, genetics, and linguistics.
Python intestine responds rapidly to luminal nutrients by increasing mass and upregulating nutrient transport. Candidates for luminal signals triggering those responses include mechanical stimulation, single or several dietary nutrients, and endogenous secretions. To identify signals, we infused into the python's small intestine either a nonnutrient solution (saline) or a single- or multinutrient solution. Python intestine failed to respond trophically or functionally to luminal infusions of saline, glucose, lipid, or bile. Infusion of amino acids and peptides, with or without glucose, induced an intermediate response. Infusion of nutritionally complete liquid formula or natural diet induced full intestinal response. Intact meals triggered full intestinal responses without pancreatic or biliary secretions, whereas direct cephalic and gastric stimulation failed to elicit any response. Hence neither physical stimulation (cephalic, gastric, or intestinal) nor the luminal presence of glucose, lipids, or bile can induce intestinal response; instead, a combination of nutrients is required (even without pancreaticobiliary secretions), the most important being amino acids and peptides. This is understandable because pythons, as carnivores, have a high-protein diet.
Domestication interests us as the most momentous change in Holocene human history. Why did it operate on so few wild species, in so few geographic areas? Why did people adopt it at all, why did they adopt it when they did, and how did it spread? The answers to these questions determined the remaking of the modern world, as farmers spread at the expense of hunter-gatherers and of other farmers.
The field of quantitative evolutionary design uses evolutionary reasoning (in terms of natural selection and ultimate causation) to understand the magnitudes of biological reserve capacities, i.e. excesses of capacities over natural loads. Ratios of capacities to loads, defined as safety factors, fall in the range 1.2-10 for most engineered and biological components, even though engineered safety factors are specified intentionally by humans while biological safety factors arise through natural selection. Familiar examples of engineered safety factors include those of buildings, bridges and elevators (lifts), while biological examples include factors of bones and other structural elements, of enzymes and transporters, and of organ metabolic performances. Safety factors serve to minimize the overlap zone (resulting in performance failure) between the low tail of capacity distributions and the high tail of load distributions. Safety factors increase with coefficients of variation of load and capacity, with capacity deterioration with time, and with cost of failure, and decrease with costs of initial construction, maintenance, operation, and opportunity. Adaptive regulation of many biological systems involves capacity increases with increasing load; several quantitative examples suggest sublinear increases, such that safety factors decrease towards 1.0. Unsolved questions include safety factors of series systems, parallel or branched pathways, elements with multiple functions, enzyme reaction chains, and equilibrium enzymes. The modest sizes of safety factors imply the existence of costs that penalize excess capacities. Those costs are likely to involve wasted energy or space for large or expensive components, but opportunity costs of wasted space at the molecular level for minor components.
Safety factors are defined as ratios of biological capacities to prevailing natural loads. We measured the safety factor of the mouse intestinal brush-border hydrolase maltase in series with the glucose transporter SGLT1, for comparison with previous studies of sucrase and lactase. Dietary maltose loads increased 4-fold from virgin to lactating mice. As in previous studies of intestinal adaptive regulation, that increase in load without change in dietary composition resulted in an increase in maltase and SGLT1 capacities mediated non-specifically by an increase in intestinal mass, without change in maltase or SGLT1 activities per milligram of tissue. Maltase and SGLT1 capacities increased only sublinearly with load during lactation, such that safety factors decreased with load: from 6.5 to 2.4 for maltase, and from 1.1 to 0.5 for SGLT1. The apparently high safety factor for maltase may be related to the multiple natural substrates hydrolysed by the multiple sites of maltase activity. The apparently low safety factor for SGLT1 is made possible by the contribution of hindgut fermentation to carbohydrate digestion. SGLT1 activity is paradoxically higher for mice consuming sucrose than for mice consuming maltose, despite maltose hydrolysis yielding double the glucose load yielded by sucrose hydrolysis, and despite glucose constituting the load upon SGLT1.
Quantitative evolutionary design involves the numerical relationships, evolved through natural selection, of biological capacities to each other and to natural loads. Here we study the relation of nutrient-processing capacities of the intestine and of organs beyond it (such as liver and kidneys) to each other and to natural loads of nutrients normally consumed. To control experimentally the rate of nutrient delivery to organs beyond the intestine, we administered nutrients directly into the veins of rats by the method of total parenteral nutrition (TPN). Control rats consuming the TPN solution by mouth ingested glucose at 42 mmol/day and processed it completely, as gauged by negligible appearance of glucose in urine and feces. Experimental rats receiving TPN were able to process infused glucose completely at rates up to 92 mmol/day. At higher infusion rates, they were unable to process further glucose, as gauged by rises in serum and urinary glucose levels and serum osmolality. At the highest infusion rates, they exhibited diuresis, dehydration, and both decreased weight gain and survival. These symptoms closely resemble the human diabetic condition known as nonketotic hypertonicity. Thus, a rat's body has a safety factor of 2.2 (=92/42) for glucose processing: it can process glucose at a rate 2.2 times its voluntary intake. This safety factor represents apparent excess capacity that may have evolved to process other nutrients converted into glucose, to minimize the risk of loads swamping capacities, to handle suddenly increased nutrient requirements, or to effect rapid mobilization of glucose.