The dominant concept of intelligence is based on IQ, which is based, in turn, on the concept of the gene. Indeed IQ testing is very largely rooted in that concept. So, if I am trying to change the concept of intelligence in this book (which I am) it’s obvious that we must first tackle the concept of the gene.

The ideology surrounding intelligence has been two-fold. First, it has aimed to convince us that the social order is a consequence of immutable biology – that inequalities and injustices are natural and cannot be eliminated. Second, where problems cannot be ignored, it tells us to look for solutions at the level of the individual rather than the level of society. Undoubtedly, the story has been phenomenally successful. Nearly everyone, across the political spectrum and around the world, accepts it to some extent. A 2020 paper from the Foundation for European Progressive Studies supports that view. It reports a European survey of attitudes of the most affluent individuals to social inequalities. Although hard work and having a supportive family background are mentioned, educational aptitude and being ‘academically bright’ or intelligent are cited as the primary factors.

When people consider intelligence, they will first tend to think of IQ, and scores that distinguish people, one from another. They will also tend to think of those scores as describing something as much part of individuals’ make-up as faces and fingerprints. Today, a psychologist who uses IQ tests and attempts to prove score differences are caused by genetic differences will be described as an ‘expert’ on intelligence. That indicates how influential IQ testing has become, and how much it has become part of society’s general conceptual furniture.

Whether they believe in IQ or not, most people sense that individual differences in intelligence are substantial and at least partly ‘genetic’. The nature–nurture debate about the origins of such differences goes back a long way; at least as far as the philosopher-scientists of Ancient Greece. And most people have probably adopted common-sense views about it for just as long. It is evident today in popular cliches: our genetic blueprints set levels of potential, while nurture determines how much of it is reached; individual differences result from both genes and environments; genes and environments interact to determine individual differences; and so on.

Charles Darwin’s On the Origin of Species is a delightfully sophisticated account of evolution. But the core ideas are not that difficult to understand. Variations in traits in individuals arise by chance, due to what we now think of as mutations in genes. Some of those trait variations are functionally better adapted to part of the environment than others. Individuals so advantaged will tend to survive and leave more offspring. Accordingly, the advantage, and the frequency of the genes causing it, will increase from generation to generation. Conversely, genes causing less advantageous or harmful variations will decrease in frequency. That is natural selection.

So far I have tried to show how intelligence evolved at different levels according to the complexity of the environments faced. We have just seen how the breakthrough to cognitive intelligence emerged from the chatter between neurons in large networks. In this chapter, I show how human evolution involved another, even more stunning, breakthrough in a way not fully appreciated but fully consistent with biological principles. As with intelligent systems generally, it emerged from social interaction at a number of levels, not lucky genetic accidents.

A review of the history and pioneers in the study of thirst and drinking is provided, including the debate between dry mouth and systemic theories. The measurement of thirst and drinking is discussed, including whether water has a taste. Consideration is given of the three main phases of components of drinking, namely, its initiation, maintenance, and termination. The chapter ends with the study of brain mechanisms, and in particular the pivotal role of structures of the lamina terminalis.

Thermolytic responses are required in either high ambient temperatures, when conductive heat loss is low, or during states of increased heat production such as during exercise. Most of the thermolytic responses involve fluid loss, including panting (i.e., tachypnea) and evaporative cooling from skin moistened by sweating or saliva spreading. The relative contribution of these mechanisms is species dependent. In all cases, the principal systemic change produced by the fluid loss is hyperosmolarity, although hypovolemia can also be considerable. Humans and animals usually do not drink sufficient water to replace the lost fluid, resulting in a state of hypohydration. This can be partially mitigated by repeated exposure (i.e., adapation) or by providing electrolytes to drink. Sustained hypohydration and/or elevated core temperature produces loss of physical performance and, in the extreme, can be lethal. Available evidence siuggests that the OVLT and/or MnPO play important roles in detection of heat stress and execution of the thermolytic responses.

In free-feeding animals, including humans, most daily water consumption is prandial, occurring during or soon after meals. In contrast to earlier interpretations, it now appears that this drinking has a systemic basis and is not purely anticipatory. Those systemic changes include small increases in osmolality, especially in hepatic portal regions, or decreased plasma volume with increase in plasma ANG II, and together these may be suprathreshold for initiation of drinking. In addition, release of histamine during eating may promote prandial drinking. Because feeding and thus associated drinking normally have a species-typical nycthemeral rhythm, studies of drinking at different times of day are potentially informative. Despite many studies in this regard, it is not fully clear whether osmotic (and/or volumetric) mechanisms for initiation of drinking and/or termination of drinking have different thresholds at different times of day. Recent work has shown a direct pathway from the suprachiasmatic nucleus (master clock) to the OVLT, which suggests at least the potential for direct clock influences on osmoregulation. I speculate that nycthemeral changes in body temperature may also affect the sensitivity of osmoreceptive and/or other elements of drinking circuitry in the brain.

Mechanisms of water acquisition, including drinking, are quite varied across species, reflecting their evolutionary and ecological histories. Increased osmolality seems to be a near-universal stimulus to water acquisition, but responsiveness to ANG II is considerably more restricted.

Cellular dehydration caused by stimuli such as hypertonic NaCl or mannitol cause a sustained shrinkage of osmosensitive cells, and in osmosensitive neurons this is transduced into a proportional change in firing rate. The basal firing rate of these neurons may encode an effective set point for osmoregulation. In the brain, these osmoreceptors seem to be predominantly in the SFO, MnPO, and OVLT. From selective lesion and other evidence, it appears that these regions act in a synergistic manner, such that optimal drinking and/or AVP secretion occurs when all three of these interconnected regions are functional. Some data suggest that there may be species differences in the details of this integrated functioning of the lamina terminalis.