Human-level brains are frighteningly expensive; as Nick Bostrom says, humanity may well be the stupidest possible technological species. "Metabolic costs and evolutionary implications of human brain development", Kuzawa et al 2014 http://www.pnas.org/content/early/2014/08/21/1323099111 : fulltext https://pdf.yt/d/Op8q2FdapabChlPU / https://dl.dropboxusercontent.com/u/243666993/2014-kuzawa.pdf (media: http://www.sciencedaily.com/releases/2014/08/140825152558.htm )

"The metabolic costs of brain development are thought to explain the evolution of humans’ exceptionally slow and protracted childhood growth; however, the costs of the human brain during development are unknown. We used existing PET and MRI data to calculate brain glucose use from birth to adulthood. We find that the brain’s metabolic requirements peak in childhood, when it uses glucose at a rate equivalent to 66% of the body’s resting metabolism and 43% of the body’s daily energy requirement, and that brain glucose demand relates inversely to body growth from infancy to puberty. Our findings support the hypothesis that the unusually high costs of human brain development require a compensatory slowing of childhood body growth.

The high energetic costs of human brain development have been hypothesized to explain distinctive human traits, including exceptionally slow and protracted preadult growth. Although widely assumed to constrain life-history evolution, the metabolic requirements of the growing human brain are unknown. We combined previously collected PET and MRI data to calculate the human brain’s glucose use from birth to adulthood, which we compare with body growth rate. We evaluate the strength of brain–body metabolic trade-offs using the ratios of brain glucose uptake to the body’s resting metabolic rate (RMR) and daily energy requirements (DER) expressed in glucose-gram equivalents (glucose_rmr% and glucose_der% ). We find that glucose_rmr% and glucose_der% do not peak at birth (52.5% and 59.8% of RMR, or 35.4% and 38.7% of DER, for males and females, respectively), when relative brain size is largest, but rather in childhood (66.3% and 65.0% of RMR and 43.3% and 43.8% of DER). Body-weight growth (dw/dt) and both glucose rmr% and glucose der% are strongly, inversely related: soon after birth, increases in brain glucose demand are accompanied by proportionate decreases in dw/dt. Ages of peak brain glucose demand and lowest dw/dt co-occur and subsequent developmental declines in brain metabolism are matched by proportionate increases in dw/dt until puberty. The finding that human brain glucose demands peak during childhood, and evidence that brain metabolism and body growth rate covary inversely across development, support the hypothesis that the high costs of human brain development require compensatory slowing of body growth rate.

Although most primates grow slower than other mammals (7), human childhood and juvenile growth stand out as unusually slow even by primate and great ape standards, during which it proceeds at a pace more typical of reptiles than of mammals (8, 9). In humans, a sizeable percentage of preadult growth is deferred until the pubertal growth spurt, when growth rate markedly increases and adult size is achieved (1).
Many hypotheses have been proposed to explain this slow and prolonged preadult life-stage, with most pointing to the extra time and energy required for human learning and brain development (5, 10–12).

Because of its large size, the human brain has unusually high energy costs (15, 20, 21), which are particularly elevated compared with the body’s metabolic budget early in the life cycle (18, 22). It has been estimated that the human brain accounts for between 44% and 87% of resting metabolic rate (RMR) during infancy, childhood, and adolescence (23–25), suggesting strong trade-offs with other functions.

The only previous attempt to derive a growth curve for brain metabolism that we are aware of assumed that the mass-specific metabolic rate of the brain, measured using the N 2 O method (24), is stable at adult-like levels across development (25, 31). Using this method, it was estimated that the brain accounts for 87% of RMR at birth, and that this fraction then steadily declines as the brain-to-body mass ratio decreases with age (25). This finding, if correct, would not support the hypothesis that ages of slowest body growth, in childhood, coincide with ages of peak brain metabolic requirements. In contrast with the assumption that the per-gram brain metabolic rate is stable with age, PET studies show that glucose uptake in the cerebral cortex is more than twice as high during early- to midchildhood than in adulthood (32). This dynamism reflects the additional energetic costs associated with overproliferation of neuronal processes and synapses before activity-dependent pruning in late childhood and adolescence (33, 34), along with aerobic glycolysis, which is thought to rise in support of synaptic growth (27–29). In contrast, at birth, before extensive postnatal synaptic proliferation and the corresponding rise in aerobic glycolysis, PET-derived glucose uptake is 20–30% lower than in adults (32).

To quantify the metabolic costs of the human brain, in this study we used a unique, previously collected age series of PET measures of brain glucose uptake spanning birth to adulthood (32), along with existing MRI volumetric data (36), to calculate the brain’s total glucose use from birth to adulthood, which we compare with body growth rate. We estimate total brain glucose uptake by age (inclusive of all oxidative and nonoxidative functions), which we compare with two measures of whole-body energy expenditure: RMR, reflecting maintenance functions only, and daily energy requirements (DER), reflecting the combination of maintenance, activity, and growth.

As described elsewhere (32, 67), glucose uptake was measured by one of the authors (H.T.C.) using PET in 36 individuals, including 7 healthy young adult volunteers (ages 19–30 y; mean 24.4 y; five males, two females) and 29 children (age range: birth to 15.5 y). The lCMRGlc values in the 29 children were compared with those of the seven healthy young adult volunteers, whose detailed neurological and psychological examinations disclosed no abnormalities.

In males and females, respectively, total brain glucose uptake is the equivalent of 52.5% and 59.8% of RMR at birth, drops to 37.5 and 40.8% of RMR in the first half-year, then rises to a lifetime peak of 66.3% and 65.0% of RMR by 4.2–4.4 y (Fig. 1 C and D and SI Appendix, Fig. S6). Although the brain accounted for a smaller fraction of DER, the pattern of glucose consumption relative to DER was very similar to that for RMR (Fig. 1 C and D): glucose_der% accounted for the equivalent of 35.4% and 38.7% of DER at birth, declined to 24.7% and 26.8% by 7 mo, before rising to peak levels of 43.3% at 3.8 y (males) and 43.8% at 4 y (females). Adult glucose_rmr% was 19.1% and 24.0% whereas glucose_der% was 10.9% and 15.0% in males and females, respectively.

Our findings agree with past estimates indicating that the brain dominates the body’s metabolism during early life (31). However, our PET-based calculations reveal that the magnitude of brain glucose uptake, both in absolute terms and relative to the body’s metabolic budget, does not peak at birth but rather in childhood, when the glucose used by the brain comprises the equivalent of 66% of the body’s RMR, and roughly 43% of total expenditure. These findings are in broad agreement with past clinical work showing that the body’s mass-specific glucose production rates are highest in childhood, and tightly linked with the brain’s metabolic needs (40).

Pontzer et al. (43) recently showed that humans and other primates have reduced TEEs [total energy expenditures] for their body sizes, despite having basal metabolic rates (BMRs) consistent with those of other mammals. The authors conclude that a reduced rate of energy throughput helps explain some shared features of primate life histories, including slower growth compared with other mammals. Pontzer et al. speculate that high brain energy needs might account for the fact that primate BMRs are not similarly reduced, but they also note extensive life-history variation among primates that traces to differences in allocation priorities. Our findings complement these data and implicate the high energy and substrate requirements of the brain, especially during the ages of most rapid development and learning, as a likely cause of life-history differences between humans and other closely related primates, such as chimpanzees.

Our findings also lead to the prediction that a slowing of preadult growth and increase in brain metabolism coevolved in the course of human evolution. Estimates of body growth from fragmentary and limited fossil hominin remains can be complicated; nonetheless, current data on hominin dental emergence, enamel growth rate, and skeletal growth suggest that a more extended period between weaning and sexual maturity began to appear at least 1.5 million y ago in Homo erectus (45). Data on dental eruption point to coevolution between brain expansion and maturational delay (45, 46), with a fully modern pattern of delayed physical growth not emerging until the origin of anatomically modern humans (47, 48). Although these findings are generally consistent with the hypothesis that brain expansion has set the pace for changes in body-size growth in the hominin lineage, our results underscore the challenges of interpreting the strength of metabolic trade-offs related to human brain evolution from data on the cranial capacity of fossils alone (e.g., ref. 14). In the modern human sample evaluated here, an average gram of brain tissue at 4 y uses more than 2.5-times the glucose of a gram of brain at birth (see data in SI Appendix, Tables S1 and S2). Absolute brain glucose requirements peak at ∼5 y, several years before final brain size is achieved, and adult brain glucose requirements are only half those at age 5 y. This uncoupling of the energetic requirements of the brain from brain size reflects developmental dynamics in substrate-intensive processes related to neural plasticity and learning, which are not preserved in fossil samples. In this context, it is notable that, despite having similar cranial capacities, dental eruption data suggest that Neanderthals grew more rapidly than modern humans (48).

It has been noted that the high and inflexible glucose requirements of the developing human brain make it susceptible to impairment from nutritional shortfall (18). Despite this finding, we find that peak brain glucose uptake occurs after the age of complete weaning from breast milk in most human societies (4), and when the energetic buffer of body fat stores are near their lifetime nadir (18). In light of this finding, it seems likely that the evolution of human encephalization required cultural or social strategies to buffer the energy intake of dependent offspring. Rudimentary hunting and gathering economies appeared with the emergence of the genus Homo and are believed to have been important in supporting early brain expansion (49–51). A shift to calorically dense and easily digested foods, and greater food sharing among social groups, would have increased the nutritional quality and stability of the diet (14, 15, 20). Although direct evidence for childcare strategies are not preserved in the fossil record, recent comparative analyses suggest that cooperative care in raising and provisioning young was likely important in achieving levels of encephalization seen in Homo sapiens (52, 53). A system in which extended social networks provisioned food for children, combined with shifts to calorically dense and easily digested foods procured through hunting (14, 15), would have allowed the costs of human brain development to be widely distributed and also buffered against shortfall. This shift in the social context of human child rearing, occurring together with a protracted postnatal development of cortical connectivity (54, 55), likely created new opportunities for imitative learning and cumulative, intergenerational development of cultural traditions to become central features of the human adaptive complex (56, 57)."