All terrestrial animals live their lives embedded in the twenty-four-hour light-dark cycle. How does the sleep cycle fit into the larger twenty-four-hour or circadian cycle? The current belief is that a brain-based circadian pacemaker or master clock is synched-up with, or entrained to the twenty-four-hour light-dark cycle such that it sends chemical messages to the rest of the brain that signal changes in the daily light–dark cycle. As light turns to dark and dark turns to light the master clock sends the appropriate chemical messenger into the appropriate brain regions that turn sleep on and off. A homeostatic process linked to the pacemaker region regulates (with the help of pacemaker genes) or influences the amount and timing of sleep, possibly via accumulation of adenosine or some other neuroendocrine or neurochemical substance that signals sleep need and sleep debt. Adenosine accumulates as the individual goes about his waking day and with it the urge to sleep increases until sleep occurs and adenosine levels reset. The circadian pacemaker regulates the release of adenosine and related chemical messengers via its control of the neuroendocrine hypothalamic region that contains the master clock.

How should we study the typical development and expression of sleep patterns in people? The most straightforward way to do so would be to simply observe the development of sleep states in people as those people develop into maturity, reproduce, age, and die. But who, what peoples, should we study in order to get a picture of the typical human pattern?

This chapter examines the neurobehavioural impacts in adults of both starvation (food restriction/cessation) and energy restriction for life extension. Section 8.2 covers animals, finding that restriction causes hippocampal damage and stress responses. Section 8.3 covers humans. Short-term fasting (<1 week) has limited cognitive effects, primarily increasing attention to food. Long-term fasting (weeks-to-years) has been studied naturalistically (e.g., famines, hunger strikes) and in the lab (e.g., Minnesota starvation study). Findings are convergent, with dramatic increases in appetite, low mood and egocentricity. The neural basis of these effects can be studied indirectly in people with anorexia nervosa, although this is complicated by pre-existing brain changes that may dispose to this disease. The impacts of cachexia and aging are also examined, alongside the longer-term impacts of food restriction post-recovery. Part three examines the animal and human energy restriction literature. While lifespan extension can occur in small mammals, the evidence in primates and humans for beneficial effects is equivocal.

This chapter examines acute and chronic dietary neurotoxins. One group of acute neurotoxins are plant alkaloids, with ergot poisoning from rye the most notable. Others include the marine neurotoxins, which cause hundreds of thousands of poisonings from seafood that have ingested toxic diatoms/dinoflagellates (e.g., amnestic shellfish poisoning) and from seafood itself (e.g., fugu). Acute neurotoxins also arise from processing, flavourants (e.g., absinthe) and contaminants (e.g., milk sickness). Chronic neurotoxins are diverse, common and sometimes lethal. Prions are one group, in the form of kuru, and mad cow disease. Another is BMAA found in cycad seeds, leading to parkinsonian-like diseases. Reliance on cassava can be problematic if poorly prepared, alongside many bush foods eaten during famine (e.g., grass pea and lathyrism). Lead, aluminium, arsenic and especially mercury can all be ingested, with some tragic examples (e.g., Minamata). Interactions between neurotoxins, vulnerability from poor nutrition and the link to neurodegenerative diseases are also considered.

This chapter focusses on addiction to food-related drugs and whether food can be thought of as a drug. Section 7.2 considers alcohol, its behavioural effects and how these might arise in the brain. Consequences of chronic use on brain and behaviour are also examined, both for adult neurological sequelae and for foetal brain development. Section 7.3 explores caffeine and theobromine, the former being the world’s most widely used drug. Whether caffeine’s cognitive-behavioural benefits arise from it ameliorating withdrawal in chronic users or whether it has some cognitive enhancing properties in everyone is examined. The biological basis of these cognitive-behavioural effects are also reviewed, including how caffeine may affect striatal dopamine. Section 7.5 examines food addiction. A number of conceptual issues are discussed, namely obesity as an endpoint of addiction, whether there can be addiction to a biological need, and the appropriateness of parallels to substance abuse and behavioural models of addiction.

This chapter concerns neuroprotective diets, and the use of particular diets and dietary components as an intervention. The first section examines the Mediterranean diet, with its beneficial effects – as prevention and intervention – on cognitive performance, mental health and neurodegeneration. The second section explores the DASH (dietary approaches to stop hypertension) diet, which has shown promise across the same set of conditions as the Mediterranean diet, and with probably a similar set of common mechanisms (e.g., reductions in inflammation and oxidative stress, plus benefits to the cardiovascular system). The third section looks at the ketogenic diet and its variants, with its high fat to carbohydrate ratio, originally and successfully developed for paediatric epilepsy, and its more recent use in other conditions (e.g., multiple sclerosis, brain tumours). The final part of the chapter reviews single nutrients, these being either examples of polyphenols or omega-3 fatty acids, with research focussing on mental health, aging and neurodegeneration.

This chapter concerns neuro-cognitive development, from conception through to childhood. Breastfeeding has been studied extensively using cross-sectional methods, finding cognitive benefits. However, after controlling for confounding variables and with better designs, beneficial effects are at best small. Maternal undernutrition can result in adverse neurodevelopmental outcomes (e.g., enhanced risk of schizophrenia). Undernutrition during infancy and early childhood causes stunting – inadequate growth for age. Stunting is common (around 500 million children worldwide) and is linked to multiple cognitive impairments, imposing lifelong costs on the individual. As stunting involves a complex interaction between nutrition, brain and environment, dietary remediation alone may not be that effective. Maternal overnutrition is also associated with adverse neurodevelopmental outcomes, but here it is unclear if this relates to poor diet quality, maternal body fat or socio-economic factors. Finally, there are a wide range of specific nutritional deficiencies that affect neurocognitive development, many having lifelong impacts (e.g., thiamine, folate iron, iodine).

This chapter examines the impacts of consuming a Western-style diet (WS-diet), rich in saturated fat, sugar and salt. Animal and human data convincingly show that a WS-diet causes hippocampal and prefrontal cortical impairment. Determining which component of a WS-diet is responsible is not currently clear. Several mechanisms may underpin these adverse effects on the brain: (1) reductions in neurotrophic factors; (2) neuroinflammation; (3) oxidative stress; (4) increased stress responsivity; (5) selective vulnerabilities in the hippocampal blood-brain barrier; and (6) changes to gut microbiota. The last one is intriguing as gut microbiota changes may impair the gut endothelial barrier allowing gut material to leak into the bloodstream, subsequently affecting the brain. Eating a WS-diet has also been linked to poorer mental health (anxiety/depression), it may exacerbate multiple sclerosis, and increased risk for Alzheimer’s and Parkinson’s disease. Finally, obesity may be a consequence of these adverse neural changes, leading to appetitive dysregulation and overeating.

This chapter explores the acute effects of food intake. The first part (Section 3.2) deals with whole meals. Having breakfast may have some limited cognitive benefits, but confounds (the link between breakfast and socio-economic status) and absence of a theoretical rationale are problematic. There were few consistent effects linked with other meal-types, except lunch, which is linked to drowsiness. The second part (Sections 3.3–3.4) considers the impact of glucose on the brain and its basis, finding acute administration assists hippocampal-dependent learning and memory and executive function, but with no impact on self-control. Section three examines if dietary manipulation of amino acids can be used to affect specific monoamine neurotransmitter systems, via loading or depletion. Tryptophan (serotonin precursor) is best studied, with loading generating fatigue and depletion lowering mood in at-risk individuals. Tyrosine (dopamine precursor) loading has facilitative effects on working memory, but the depletion findings are ambiguous. There is little data on histidine (histamine precursor).