Size matters?

A recent paper [1] from Gideon Nave and colleagues answers an old question: yes, brain size in humans is associated with some indications of intelligence, but only to a tiny degree. Association is not causality, so this finding does not imply that inflating your brain makes you smarter, nor does it suggest that the headache you get when reading, say, one of my papers, is because your brain is starting to burst as its neurones multiply prodigiously.

The study shows what can be done with the massive amounts of data that are now becoming widely available. It is definitive; with data from more than 13,000 individuals, brain size accounts for only about 2% of the variation in ‘fluid intelligence’ [2] between individuals. It’s a rigorous study, discussed sensibly and with due caution;– I’m glad it was done, as strong evidence of the unimportance of things is often much more useful than weak evidence of their importance.

That there should be some relationship between brain size and intelligence is one that fits our experience with, for example, chocolate, that more is better. Pigeons with their tiny brains are obviously stupid, right? (Although they can find their way home when abandoned hundreds of miles away while I can get lost after going to the corner shop.)

So the lack of any conspicuous relationship between brain size and intelligence should give us pause for thought. Why, exactly, do we have big brains?

Brain size generally scales with body size across vertebrate species. We happen to be off that scale with our brains, a point I will come to, but the first question seems to be, why do bigger animals need bigger brains? It’s not easy to answer. Large animals live longer, they need brains that are robust enough to survive the random insults of a long and interesting life, so perhaps they start with enough neurones that we can afford to lose a lot on the way.

But we don’t lose that many neurones, at least not until we are past reproductive senescence unless we overindulge in alcohol – and maybe not even then [3].

While we have bigger brains than might be expected from the general scaling of brain size with body weight, this is not true of all the brain. It’s true of the neocortex, the part that spreads around the brain like one of those fungi that you find yourself sitting next to in deciduous woodland. For the most part, the rest of the brain, including, for instance, the hypothalamus, is just the size you’d expect it to be.

Even so, why exactly do we need a hypothalamus that is bigger than that of, say, a rat?

The human hypothalamus is about 40 times bigger than a rat hypothalamus – in line with the general relationship between body size and brain size. Now a part of the hypothalamus produces hormones that are released into small blood vessels that supply the pituitary gland. The pituitary gland of a human is about 40 times bigger than that of a rat, so might be presumed to need about 40 times as much of the hypothalamic hormones.

So far so good, but why does the pituitary gland need to be 40 times bigger in a human than in a rat? Well, it produces hormones that are secreted into the blood to affect other organs and tissues throughout the body. Obviously we need a bigger pituitary, because the blood volume of a human is much more than a rat.

But the blood volume of a human is much greater than that of a rat. It’s not 40 times greater, but more like 400 times greater.

So the human pituitary and hypothalamus are nowhere near as big as we might expect. But all physiological systems are complex systems with multiple feedback mechanisms, and there are points in these systems that are adaptable. Two things can happen to compensate for a level of hormone secretion that is low: the sensitivity of the target tissues to that hormone can be increased, for example by increasing the expression of hormone receptors, or the concentration of hormone in blood can be raised by reducing the rate at which it is degraded.

Take a particular case – the hormones oxytocin and vasopressin. These are made in the hypothalamus, in neurons that project to the pituitary gland from where they are secreted into the blood. Plasma levels of these hormones (as measured by properly validated methods) are much lower in humans than in rats, as would be expected from the larger blood volumes and from the fact that half-lives of these hormones are similar in rats and humans. To compensate for this, the sensitivity of the peripheral target tissues to these hormones is very much greater in humans.

OK, so far so good, biology is taking care of itself. But what about the brain? The brain is a target for oxytocin and vasopressin too. The oxytocin and vasopressin neurones don’t only project to the pituitary; many parts of the brain contain some fibres that contain oxytocin or vasopressin, including the cortex, that disproportionately enlarged territory.

In 2013, Eleftheria Pissadaki and Paul Bolam asked the interesting question of why it is that only humans get Parkinson’s Disease. Many of the symptoms of this disease are associated with degeneration of dopamine neurons in the substantia nigra (4), so why are these neurons so susceptible to dying? Pissadaki and Bolam noted that, in the rat, each of these neurons makes an unusually large number of connections to neurons in another part of the brain – the striatum. Whereas a “typical” neuron might make 10,000 connections with striatal neurons, these dopamine neurons make ten times as many, about 100,000. This, it might be expected, imposes a considerable metabolic strain on them.

In the human, the striatum has expanded in volume in parallel with the cortex, but the substantia nigra, like the hypothalamus, has remained at the expected size for body size. Accordingly, each of these human dopamine neurons make not 100,000 synaptic contacts in the striatum but ten times, as many, at least a million. Pissadaki and Bolam suggested that this might push these neurons to the edge of metabolic viability.

So, in many things a human is very much like a rat; it has a very similar genome, and the structure and functions of much of the brain are also remarkably similar.

Bigger brains have to do some things differently because, well, because they are bigger.

We don’t really know if bigger brains are better, we assume they are; we assume that they make us more intelligent than other animals, even if we can’t quite explain quite how. We think that brain size has increased as a result of selection for intelligence. But perhaps our brains grew large as the peacock’s tail grew large – by sexual selection – for the ability to sing and compose love letters. Perhaps our ‘intellectual’ abilities to do things like long division sums just came along for the ride. So perhaps, did other things, like susceptibility to Parkinson’s Disease and Alzheimer’s.

We are good at being humans, just as pigeons are good at being pigeons, peacocks at being peacocks, whales at being whales, and ants at being ants. Pigeons can’t write or speak to tell us how clever they really are, or maybe they are too clever to think it worth the effort.

Author: Gareth Leng | 18.04.2020


1 Nave G, Jung WH, Karlsson Linnér R, Kable JW, Koellinger PD. Are Bigger Brains Smarter? Evidence From a Large-Scale Preregistered Study. Psychol Sci. 2019;30:43–54. doi:10.1177/0956797618808470

2 See

3 See and

4 Pissadaki EK, Bolam JP. The energy cost of action potential propagation in dopamine neurons: clues to susceptibility in Parkinson's disease. Front Comput Neurosci. 2013 Mar 18;7:13.