It is not possible to understand dreams unless we become familiar with the whole terrain of dreams. We have discussed ordinary run-of-the-mill dreams that are associated with both REM and NREM sleep states. But there is a very large variety of dream types reported by people. To build an adequate understanding of dreams and a testable theory of dreams, we therefore need to marshal all of the salient facts concerning dreams, and those facts must include the chracteristics of a wide variety of dream types. Scientists who study dreams agree that dreams vary substantially in terms of their content and formal phenomenologic features. For example, children’s dreams are very different from adult’s dreams, and men’s dreams differ substantially from women’s dreams. There are nightmares, “big” or emotionally significant dreams, lucid dreams, shared or mutual dreams, twin dreams (dreams reported by twins), “spiritual” dreams, precognitive or prophetic dreams, visitation dreams (where deceased loved ones appear in a dream), and many other types. Dreams also vary by historical period: Dreams of the ancient Greeks and Romans are different than dreams of people in the Rennaissance period of European history. Dreams also vary by culture: Dreams of people living in traditional socieities are very different from the dreams of modernized peoples. Similarly, dreams of people living in Islamic cultures differ from the dreams of people living in cultures where other religions predominate and so on. All of this should be pretty obvious, but dream variation is an understudied topic in the field of sleep and dream studies. While the variation in dream content and types has been documented, there is little discussion of the theoretical importance of that variation. The fundamental theoretical importance of dream variation, I will argue, is that it suggests that dream function is probably multiple. Dreams do not have only one function. No one theory can account for the huge variation in dream conent. The evident fact that there are multiple dream types is also consistent with the idea that dreams are products of the social brain and function, at least in part, to shape, alter, influence, or manipulate social relationships. Now that is NOT all that dreams do. It is likely that dreams transcend mundane social functions in multiple ways, but we simply do not know enough about these suprarational functions of dreams to comment upon them intelligently. I urge further research on so-called anomalous phenomena and dreams, but I focus here on the available empirical data we have on hand.

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).