Chronic sleep deprivation and seasonality: Implications for the obesity epidemic

Abstract

Sleep duration has progressively fallen over the last 100 years while obesity has increased in the past 30 years. Several studies have reported an association between chronic sleep deprivation and long-term weight gain. Increased energy intake due to sleep loss has been listed as the main mechanism. The consequences of chronic sleep deprivation on energy expenditure have not been fully explored. Sleep, body weight, mood and behavior are subjected to circannual changes. However, in our modern environment seasonal changes in light and ambient temperature are attenuated. Seasonality, defined as cyclic changes in mood and behavior, is a stable personality trait with a strong genetic component. We hypothesize that the attenuation in seasonal changes in the environment may produce negative consequences, especially in individuals more predisposed to seasonality, such as women. Seasonal affective disorder, a condition more common in women and characterized by depressed mood, hypersomnia, weight gain, and carbohydrate craving during the winter, represents an extreme example of seasonality. One of the postulated functions of sleep is energy preservation. Hibernation, a phenomenon characterized by decreased energy expenditure and changes in the state of arousal, may offer useful insight into the mechanisms behind energy preservation during sleep. The goals of this article are to: a) consider the contribution of changes in energy expenditure to the weight gain due to sleep loss; b) review the phenomena of seasonality, hibernation, and their neuroendocrine mechanisms as they relate to sleep, energy expenditure, and body weight regulation.

INTRODUCTION

The past decades have witnessed a marked decrease in sleep time (1, 2). At the same time, obesity, a leading cause of morbidity and mortality in the 21^st century, has been rapidly increasing (3). Although increased food intake and decreased physical activity are often cited as the two ultimate reasons for the obesity epidemic, causative evidence is scanty; we have recently summarized the putative reasons for the surge in weight gain (4). Complex societal and lifestyle changes may have contributed to the decline in sleep duration and the rise in obesity. Sleep time has substantially decreased and sleep quality has worsened in all age groups, but especially in children, whose sleep has decreased by as much as 2 h (5). The reasons are unclear: the advent of artificial light at the beginning of the 1900’s and more recently the proliferation of television, personal computers, and other media, both increasing the number of “productive hours”, may have drastically changed our sleep habits (6).

The epidemiological evidence of an association between short sleep and weight gain has been mounting since the first report in 2004 by Hasler et al., followed shortly by another report by Taheri et al. (7, 8). As of today, over 40 studies describe either an inverse or U-shaped relationship between self-reported sleep and weight gain (9). Based on the seminal studies of Van Cauter et al., acute sleep deprivation reduces insulin sensitivity in healthy lean male volunteers via increased cortisol, cytokines, and other endocrine and immune mechanisms (10). Furthermore, severe sleep deprivation has shown to increase appetite via decreased leptin and increased ghrelin levels (11).

Body weight is the net resultant of energy intake and energy expenditure. The effect of short sleep and sleep disorders on appetite and energy intake is known, but the repercussions of sleep deprivation on energy expenditure have not yet been quantified. This is surprising, as it has long been known that energy expenditure varies across sleep stages (21). Of note, sleep architecture has a substantial genetic component, varies with age, and is affected by many pathological conditions.

Albeit seasonality is considered reductional in humans and even more attenuated in modern humans because of living conditions, sleep, body weight, mood, and behavior, among other parameters still exhibit circannual variations (4). In this review, we will summarize some of the consequences of the mismatch between attenuation in environmental changes across seasons and the biological remnants of seasonality in people’s genes and behavior.

An extreme example of seasonality observed in animals is hibernation, which is characterized by a decrease in energy expenditure and alterations in the state of arousal (12). We will summarize the endocrine and metabolic changes of hibernation, as they may be informative of mechanism(s) of energy preservation during sleep in humans.

To accomplish this goal we review: a) the energy expenditure in the different sleep stages; b) seasonality and the mechanisms of hibernation as they relate to sleep, temperature and body weight regulation.

ENERGY EXPENDITURE DURING SLEEP STAGES: IMPLICATIONS FOR ENERGY BALANCE

One of the functions proposed for sleep is to conserve energy (13). Recently, the amount of energy conserved per night has been estimated by determining the metabolic cost of missing one night of sleep (14). Staying awake for 24 h costs approximately 134 kcal; paying back the sleep debt the following night recovers most, approximately 96 kcal, but not all of the calories expended. This leaves a net loss of 38 kcal, an amount that over time may be of physiological meaning.

A typical night is made of 6–7 cycles of sleep, each lasting approximately 90 min (15). The first cycle begins with Stage 1, which lasts a few minutes and is characterized by a low arousal threshold. Stage 2 has a duration of 10–25 min and is distinguished by increased slow wave sleep activity; Stage 3 and 4, which are also slow wave sleep stages, are characterized by electroencephalogram (EEG) spindles. Rapid eye movement (REM) is a form of deep sleep with a higher arousal threshold. Typically, slow wave sleep predominates in the first third of the night and REM sleep is more common in the remaining of the night. In young adults non-REM (NREM) sleep accounts for 75–80% of total sleep time. Slow wave sleep is maximal in young children but is decreased by 40% by the second decade of life. By the age of 60 slow wave sleep has almost disappeared. Total sleep duration changes also with age: toddler and pre-school children typically sleep 14 hours over the course of the day, in middle childhood sleep duration goes down to 10 h and further decreases during adolescence to 7 h (16).

It has long been known that oxygen consumption, an indirect index of energy expenditure, is lower during sleep than during quiet wake (17). During the night, core temperature decreases by 1 C which translates into a 10% decrease in metabolic rate (18), but metabolic rate may decline by as much as 25–30%, suggesting an additional decrease independent of changes in body temperature (19–22). About ¼ of nighttime reduction in metabolic rate occurs during the initial sleep period (21). REM carries the highest energy expenditure of whole sleep, approximately 1.12 kcal/min, 4% higher than in Stage 2 (1.08 kcal/min) and 8% higher than in Stage 3 and 4 (1.04 kcal/min) (21, 23). Larger differences in energy expenditure in sleep stages are observed in newborns: during REM metabolic rate is 5 cal/kg/24h, 9% greater than during quiet sleep (24). The brain is responsible for most of the energy expenditure during REM sleep: positron emission tomography (PET) studies with deoxyglucose-¹⁸F indicate that the metabolic rate is higher in REM vs NREM sleep, especially in the cingulated area, frontal cortex, thalamus, and visual association areas (25).

Age differences in energy expenditure during sleep should be considered when estimating caloric cost. A polysomnography study reported an average difference of 18 kcal/night in the 40–54 age group vs the 54–61 age group. A study by Diji et al. provides aggregated data of energy expenditure during sleep (26). The mean difference in nighttime energy expenditure between a 25 yr-old and a 50 yr-old was approximately 25 kcal/night, which in theory would result in an accumulation of fat of about 1.2 kg/yr. Past the age of 70, fat accumulation would be even higher, approximately 2 kg/yr (Table 1) (26, 27).

Table 1.

Energy expended during the different sleep stages: implications for fat accumulation during lifespan.

Age (yr)	Sleep time (min)	REM		Stage 2		Stage 3–4		Energy Expenditure	Fat accumulation accounted by age-related sleep changes
		% total sleep	kcal/night	% total sleep	kcal	% total sleep	kcal	kcal/night	kg fat/yr
from (27): only males
40–54	480	19.5	104.8	61.4	318.3	11.2	53.7	476.8	ref
54–61	460	19.1	98.4	64.5	320.4	8.2	39.2	458	0.89
61–70	440	18.4	90.7	65.2	309.8	6.7	30.7	431.2	2.16
>70	420	17.8	83.7	66.5	301.6	5.5	24	409.3	3.19
from (26): males and females
		min/night	kcal/night	min/night	kcal/night	min/night	kcal/night	kcal/night	kg fat/yr
25	433.5	87.9	98.4	198.9	214.8	118.5	123.2	436.4	ref
50	409.9	83.9	94	211.8	228.8	85.3	88.7	411.5	1.18
70	390.4	75	84	204.5	220.8	84.2	87.6	392.4	2.09

In the awake animal, cooling the hypothalamus with a probe inserted in this brain area elicits an increase in energy expenditure (17). The hypothalamic control of body temperature varies during sleep stages: during slow wave sleep the same procedure elicits 50% less increase in metabolic rate than during wake, but during REM sleep cooling the hypothalamus produces no increase in metabolic rate at all. Of note, as a survival strategy against cold environment, animals tend to decrease time spent in REM sleep. The amount of REM sleep in a given night may therefore be “modulated” by ambient temperature. This is evident in neonates; short-term exposure to a cold challenge induces a decrease in REM sleep (28).

AN EXTREME MODEL: CONSEQUENCES OF EXTREME SLEEP DEPRIVATION IN ANIMALS

Extreme sleep deprivation in rodents elicits severe weight loss in spite of increased food intake. Seminal studies by Rechtschaffen et al. showed that sleep deprivation for up to 2 weeks, achieved via forced activity, resulted in a distinct syndrome characterized by hyperphagia and increased energy expenditure secondary to massive sympathetic activation (29). The animals gradually became debilitated and hypothermic, developed opportunistic infections and eventually died (29, 30). The main mechanism involved in weight loss secondary to severe sleep deprivation in animals is a massive activation of brown adipose tissue, as indicated by an increase in UCP1 gene expression (31). Selective deprivation of REM sleep for 20 days resulted in a substantial increase in energy expenditure; however, in spite of doubling food consumption animals lost weight. Selective REM sleep deprivation caused an increase in the expression of neuropeptide Y, a strong appetite stimulant, in the arcuate nucleus; the expression of the stress neuropeptide CRH was also increased in the paraventricular nucleus, but its anorexic effect was lost in sleep deprivation (31).

Insomnia is associated with a substantial increase in resting energy expenditure, possibly secondary to sympathetic activation. An 11% increase in energy expenditure was reported in a small group of subjects with insomnia lasting for more than 1 yr (32). Therefore, if sleep loss is secondary to insomnia rather than voluntary, it may induce weight loss rather than weight gain.

SEASONALITY AND ITS CONSEQUENCES ON ENERGY BALANCE, SLEEP, AND BEHAVIOR

Seasonality, a phenomenon characterized by changes in sociability, sleep, mood, behavior, appetite, food preferences and body weight, is considered reductional in humans compared to other species. Genetics account for approximately ⅓ of the variability in seasonality (33). From an evolutionary standpoint seasonality represents an advantage as it allows energy savings at times of food scarcity. Conceivably, there has not been sufficient time to adapt biologically to the large food availability at all times and the attenuation in light and ambient temperature excursions across seasons that characterize our modern societies. Seasonality may therefore become maladaptive in the current environment and individuals more susceptible to it may be at greater risk of weight gain in winter. Seasonality modulates yearly variations in body mass index (BMI), with weight gain secondary to increased preference for carbohydrates (34). Seasonality also influences energy expenditure during seasons, with lower energy expenditure due to limited physical activity levels during the winter (35).

The Seasonal Pattern Assessment Questionnarie (SPAQ) reported that 92% of the individuals from a random household sample in Maryland experienced seasonal changes in mood and behavior (36). Younger women were more likely to have the highest seasonality scores. In a large survey conducted in Norway, higher SPAQ scores were associated with greater BMI, waist/hip ratio, total cholesterol (men only), and lower HDL levels; in addition, women with accentuated seasonality exercised less and smoked more (37). Thus, subjects with accentuated seasonality are more likely to engage in unhealthy behavior during the winter months that may put them at greater risk for cardiovascular morbidity. In addition, these individuals exhibit sleep disturbances such as insomnia, daytime sleepiness, and chronic sleep deprivation (37). Furthermore, they adapt at a slower pace to daylight saving time. Of note, myocardial infarctions are more common during the winter (38). Sleep EEG recordings reveal changes in REM sleep architecture with more REM sleep and less Stage 4 sleep during winter, suggesting an overall higher metabolic rate during sleep compared to non-affected individuals (39).

The amount of REM sleep varies across seasons, with a difference of approximately 16% more REM sleep in winter, a zenith around December-January and a nadir in summer in subtropical climates (40). A similar increase in REM sleep during winter was reported across different latitudes in the US (41), as well as in Japan (39).

Modern societies are characterized by social rituals such as the holiday period between Thanksgiving and New Year’s Eve, which is associated with increased food intake, or the religious festivity of the Ramadan during which food and water intake are denied during the daytime. These rituals are superimposed on the attenuation of seasonality and they are often incongruous with our biological predispositions. As an example, winter has been identified in our genome with food scarcity, rather than the modern abundance. Average weight gain between October and March is approximately 0.5 kg and is not reverted during the following spring or summer (42). Religious fasting has specific health consequences as well. The Islamic Ramadan lasts 28–30 days during which food and drink are prohibited during the daylight hours. This sudden shift in healthy habits has potential consequences for sleep, energy expenditure, and core body temperature (43).

HIBERNATION: IMPLICATIONS FOR ENERGY BALANCE AND SLEEP

It has been proposed that circadian, circannual, and the sleep-wake cycle can be interpreted to reflect an intrinsic metabolic cycle (44). Summarized here are some considerations on hibernation, as they relate to sleep and energy expenditure in humans from an evolutionary perspective (Table 2) (43–53). Hibernation is observed in homoeothermic mammals such as bears and marmots. Characterized by bouts of torpor, a form of temporary decrease in body temperature and metabolism lasting from a few days to a few weeks, hibernation is interrupted by periods of increased energy expenditure: in the marmot one episode of hibernation may last between 6 to 20 days during midwinter, followed by an arousal and then by an euthermic period of 1–2 days (44). During a given winter, there may be between 15 and 20 bouts of hibernation (44). Hibernation reduces energy expenditure by about 20% in bears, but the energy savings are even greater in smaller animals. Cold is not the only change in ambient temperature able to initiate a state of hypometabolism: an equivalent state of shallower torpor, called estivation, is observed in some species in hot climates when ambient conditions become harsh, such as during very dry seasons.

Table 2.

Similarities between the hibernation response in homeothermic mammals and seasonal changes in physiological parameters relevant to sleep and weight regulation in humans.

Seasonal changes in winter months vs summer months	Hibernating homeothermic mammals	Humans
Melatonin	⇓ pineal melatonin over time of hibernation. It might be of importance for duration of hibernation (45)	⇑ length of nocturnal melatonin secretion during winter compared to summer (effect larger in men than women) (46)
Leptin	Transient leptin resistance in November (47)	No changes in summer and winter (48)
Catecholamines	⇓ α1 receptor and ⇑ in α2 receptors during hibernation (49)	⇑ cortisol metabolites during summer (50)
Haptoglobulin	⇑ in plasma during hibernation (51)	⇑ in obese subjects ⇑ in subjects with depression it correlates with insomnia and other vegetative symptoms (52)
State of vigilance	Altered	Conditioning of healthy individuals to extended dark exposure results in biphasic sleep pattern with two main sleep episodes separated by a waking period of 1–3 h (56)
Metabolic rate	Decreased	⇑ energy expenditure in winter (11.5%) vs summer (7.5% p=0.05) after cold-exposure (53)
Food intake	⇓ during the winter	⇑ during the winter due to social and ritual (Holydays Season) eating (43, 44)
Physical activity	⇓ during the winter	⇓ during the winter (53)

Hibernation is centrally driven by mechanisms, which remain largely unknown; complex cellular and molecular changes take place triggered by a drop in environmental temperature coupled with a (yet to be identified) internal clock (54). Protein synthesis, mostly macromolecules, is inhibited and ATP consumption declines. Levels of haptoglobin, an inflammatory marker, increase several fold in winter in bears compared to summer (55). Interestingly, during hibernation mammals become sleep-deprived and must periodically escape torpor to pay their sleep debt (51). Physiological adaptations to hibernation in animals display interesting similarities to the changes observed in obesity or major depression in humans. Levels of haptoglobin increase in obese subjects, as they strongly relate to BMI (56); in subjects with major depression, insomnia and the other vegetative symptoms create a similar increase (57).

SEASONAL AFFECTIVE DISORDER: THE HUMAN EQUIVALENT OF HIBERNATION?

Seasonal affective disorder (SAD), a condition that was described in 1984 by Rosenthal et al., is characterized by anergia, hypersomnia, hyperphagia, craving for carbohydrates, and modest weight gain during the winter (52). SAD has a strong gender preference: 4 out of 5 patients with SAD are women. It is also more common in women during reproductive age. It has been hypothesized that seasonal changes in food intake, libido, and behavior are advantageous, as they would increase reproductive success in women by favoring weight gain in the fall, with weight gain coinciding with the second trimester of pregnancy, when most of the gain has to take place (58). Furthermore, the decreased libido experienced by women during the winter months would discourage intercourse and thus decrease the chances of birth with the following winter approaching, the least conducive time of the year to the survival of neonates.

Patients with SAD studied in the Washington area respond to the approach of winter with an increase of 38 min (equivalent to about 7%) in nocturnal melatonin secretion. Such increase is of physiological meaning; a 30-min increase in melatonin secretion in hibernating species is sufficient to regulate reproductive functions. Healthy people do not usually display a season-related increase in melatonin, but when exposed to long (14-h) vs short (8 h) nights, an experimental model of winter, their nocturnal melatonin profile changes accordingly (59). Decreased retinal sensitivity in patients with SAD may play a pathogenetic role (60). Patients with SAD also exhibit distinct alterations in thermoregulation: during the winter when untreated, their resting metabolic rate was surprisingly higher than in normal controls, while treatment with bright light normalized it (61). A study conducted in Siberia in women with SAD in winter found a 16% lower oxygen consumption rate vs women with non-SAD depression and healthy controls (62). Subjects with SAD exhibit distinct alterations in thermoregulation: for example they have abnormal ultradian oscillations of cranial thermoregulation, as indicated by facial temperature; this is corrected by clinical remission induced by light therapy (63).

Differences in the serotoninergic system in the brain have been reported in this condition. The short allele of the 5HT-transporter linked polymorphism is more prevalent in subjects with seasonal affective disorder (64). Healthy individuals carrying specific polymorphisms experience seasonal alterations in the serotoninergic system in the brain. During the winter, carriers of the short serotonin transporter binding have greater in vivo binding of the serotonin transporter in the putamen, a brain area devoted to motor functions with rich serotoninergic innervation (65).

MELATONIN, BROWN ADIPOSE TISSUE, AND β CELL: A NEW ENDOCRINE LOOP? IMPLICATIONS FOR ENERGY BALANCE AND INSULIN SENSITIVITY

Melatonin is a hormone produced at night by the pineal gland (Fig. 1). Via the retino-hypothalamic pathway, daylight exercises a tonic inhibitory control on N-acetylserotonin O-methyltransferase, the enzyme controlling the rate-limiting step of melatonin synthesis. Recent findings suggest that melatonin can stimulate brown adipose tissue, thus providing a mechanism of increased energy expenditure (66). In addition, melatonin modulates seasonal changes in fat mass of Siberian hamsters by increasing lypolisis via the branch of the sympathetic system innervating the white adipose tissue. Administration of melatonin to rats leads to weight loss (67). This effect applies to other mammals as well; for example, a common method in factory farms is to extend artificial light from 8 to 16 h to fatten cattle.

Fig. 1.

The pineal-adipose tissue-β cell endocrine loop. A new endocrine axis? Melatonin is synthesized in the pineal gland starting from the aminoacid L-tryptophan that is converted to serotonin. Serotonin in turn is converted to N-acetyl-5-hydroxytryptamine by the rate limiting enzyme arylalkylamine N-acetyltransferase (AA-NAT) to N-acetyl 5-hydroxytryptamine and finally converted to melatonin. Melatonin is under a constant inhibitory effect exercised by daylight. Via the retino-hypothalamic trait light inhibits melatonin production. In darkness melatonin is produced by the pineal gland and rises in plasma. Melatonin receptors type 1 (MT-1) and 2 (MT-2) are G-protein coupled receptors. They are present in the brown adipose tissue (BAT), in the white adipose tissue (WAT), where they exert a stimulatory role, and in the β cell of the pancreas where they have an inhibitory role. Via these receptors the rise in melatonin in darkness can stimulate heat production from the BAT and expend energy, induce lypolisis from the WAT and decrease insulin production during the night from the beta cell in the pancreas. To close this loop insulin receptors are present on the pinealocyte. Not indicated in the figure, MT receptors are present both in the central nervous system (CNS) and in the periphery. In the CNS they are present in the suprachiasmatic nucleus, retina, cerebellum, and hippocampus. In the periphery they are represented in the skin, cardiovascular system, the reproductive system, and the immune system where they modulate the immune response.

As mentioned, one of the best described effects of sleep deprivation is insulin resistance. Recent evidence suggests that melatonin may be one of the endocrine mediators; both melatonin receptor-1 and melatonin receptor-2 are present on the β cells where they inhibit insulin secretion via cAMP and cGMP, respectively; conversely, insulin receptors are present on the pinealocytes. Furthermore, removal of the melatonin Type 1 receptor induces insulin resistance and melatonin administration restores glucose homeostasis (68) in insulin-resistant mice fed a high-fat diet (69). A common variant in MTNR1B is associated with increased risk of diabetes (70). Teleologically, the inhibitory effect of melatonin at night on insulin secretion would allow the β cells to rest, thus preventing burn-out of pancreatic islets over the long-term. The presence of this “hardware” system suggests the existence of a pineal-pancreas classical endocrine loop with negative feed-back mechanisms (Fig. 1).

DISCUSSION

It has been hypothesized that chronic sleep deprivation causes weight gain mostly because of increased appetite and food intake. As illustrated in this review, this picture may be more complex than originally thought. The consequences of chronic sleep deprivation on energy expenditure have not been adequately explored. Energy expenditure during sleep is a function of sleep architecture, with REM sleep having the highest energy cost. As the quota of REM sleep rapidly declines after the 2^nd and 3^rd decades of life, the energy expended during sleep declines accordingly. This is consistent with the epidemiological observation that weight gain secondary to sleep loss is dependent on the subjects’ age; it is mostly observed in children, who have the highest proportion of REM sleep, declines in young adults, and almost disappears after the 5^th decade. Of note, as mentioned sleep loss per se carries a caloric cost, which is at variance – albeit not incompatible – with the concept that chronic sleep deprivation causes weight gain. Given this complexity, we suggest that the effects of chronic sleep deprivation on body weight are likely to be based on the net effects of various factors, rather than been solely due to increased appetite and food intake. Sleep architecture, mood, levels of melatonin at night, and the amount of brown adipose tissue have high inter-individual variability. Thus, the net effect of chronic sleep deprivation on body weight may be variable based on genetic susceptibility, cultural influences, and other factors.

Melatonin stimulates brown adipose tissue while inhibiting insulin production from the β cell: by doing so, melatonin may control body weight via changes in body temperature and energy expenditure whereas, by inhibiting insulin production at night, may favor β cell rest. We suggest that prolonging our days with artificial light may favor obesity by inhibiting melatonin production, thus silencing the brown adipose tissue, and may also impair insulin production in the long-term by prematurely exhausting the β cell. Interestingly, brown adipose may be inducible in adults in health and disease, as suggested by its appearance in patients with pheocromocytoma (71).

By tonically inhibiting melatonin production, excessive exposure to artificial light and attenuation of seasonality per se may contribute to obesity and decreased insulin sensitivity – energy, instead of being dissipated as heat, accumulates as fat. Experiments conducted in the dark on awake subjects (likely, not an unusual condition for our ancestors, especially during the winter) and their counterpart, studying sleeping subjects in daytime light may help dissecting out the effects of melatonin per se vs the effects of sleep on energy metabolism. Since rodents are active in the dark when they also feed they may not represent a good model for the effects of melatonin on metabolism in people. Changes in sleep architecture secondary to aging or induced by depression with subsequent alterations in REM sleep may have a clinical impact on body weight.

The observation that the pathological destruction of the pineal gland in patients causes weight gain suggests that the melatonin-brown fat connection may play an important role in obesity. Future clinical trials of light therapy in patients with SAD should incorporate measurements of adiposity. The effect of melatonin supplementation on body weight, especially in elderly subjects with decreased melatonin production should be tested in clinical trials. Understanding the intimate mechanisms of hibernation may be quite informative: in spite of becoming obese and insulin resistant in the fall, hibernators seem to be spared some of the negative consequences of obesity such as cardiovascular events and a pro-inflammatory state. Studies examining weight changes in people subjected to light manipulation or melatonin administration are needed.

In summary, we have provided several examples of situations in which there is a mismatch between our current culturally-modified modern environment and our genome. Contemporary humans with SAD exhibit during the winter a phenotype reminiscent of the winter preparations our ancestors may have experienced. The behavior associated with SAD may have lost in modern life its evolutionary advantage to become a handicap. By analogy, the “thrifty” genotype, described in Pima Indians and other populations, in modern times is associated with severe obesity and a high prevalence of diabetes (4). Feeding patters currently associated with festivities are often seasonally incongruous to our genome. We conclude that public health interventions to combat the sleep and obesity epidemics would benefit from approaches and strategies taking into account, rather than ignoring, our evolutionary background.