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ARTICLE
The metabolic mind: A role for leptin and ghrelin
in affect and social cognition
Jennifer K. MacCormack | Keely A. Muscatell
University of North Carolina at Chapel Hill
Correspondence
Jennifer MacCormack, Department of
Psychology and Neuroscience, University of
North Carolina at Chapel Hill, 124 Howell
Hall, Chapel Hill, NC 27599.
Email: jkmaccor@unc.edu.
Funding information
Ruth L. Kirschstein National Research Service
Award, Grant/Award Number:
1F31AG055265-01A1
Abstract
Leptin and ghrelin are metabolic hormones central to
energy regulation in the body. Theories of allostasis suggest
that metabolism could matter for more than just food intake
and weight regulation but also ultimately for psychological
processes, such as affect and social cognition. Allostasis is
the process by which the brain monitors ongoing physiolog-
ical states and, in turn, regulates physiology based on
expectations about how a given situation will impact the
self. Motivated by this allostatic perspective, we argue that
leptin and ghrelin may be influenced by and even contribute
to psychological processes such as affect and social cogni-
tion. Specifically, we review literature suggesting that leptin
and ghrelin may be sensitive to social affective signals and
related contexts (e.g., social status, and social threat
vs. support), given that these signals and contexts may rep-
resent access to tangible physical and psychological
resources that support allostasis and metabolic needs. We
then review literature showing that leptin, ghrelin, and asso-
ciated metabolic states may feed into the construction of
social affective states and behaviors (e.g., emotion and risk
taking), in order to motivate behaviors in line with allostatic
needs. We close by offering guidelines for researchers inter-
ested in contributing to this emerging field and highlight
opportunities for future research. We believe that leptin
and ghrelin offer exciting new directions for social and
affective scientists interested in linking the mind, brain,
and body.
DOI: 10.1111/spc3.12496
Soc Personal Psychol Compass. 2019;e12496. wileyonlinelibrary.com/journal/spc3 © 2019 John Wiley & Sons Ltd 1of18
https://doi.org/10.1111/spc3.12496
1|INTRODUCTION
Leptin and ghrelin are metabolic hormones central to energy regulation in the body. Leptin is an adipokine hormone
produced by adipose cells (the body's largest energy reservoir), signaling satiety or energy sufficiency to the brain
(Maffei et al., 1995; Ramsay, 1996). Leptin supports long-term appetite and energy regulation, shifting slowly with
weight gain or loss. For example, in rodents, leptin administration reduces feeding behavior, increases physical activ-
ity, and stimulates the innate and adaptive immune systems, presumably in part because higher leptin indicates that
the body has sufficient energy stores to engage in metabolically costly activities (Bernotiene, Palmer, & Gabay, 2006;
Houseknecht, Baile, Matteri, & Spurlock, 1998). These findings also replicate in humans (e.g., Licinio et al., 2007).
Alternately, ghrelin is a peptide hormone produced by gastrointestinal cells, acting on the central nervous system to
signal hunger or energy depletion (Kojima et al., 1999). Ghrelin supports short-term appetite and is secreted when
the stomach is empty (Cummings et al., 2001, 2004). Animal models show that ghrelin administration increases feed-
ing behavior (Nakazato et al., 2001), and in humans, ghrelin injected into the bloodstream increases self-reported
hunger within approximately 30 min, although ghrelin and hunger are not necessarily coupled in a one-to-one fash-
ion (Wren et al., 2001).
But why should psychologists care about leptin and ghrelin if these hormones are primarily involved in food
intake and energy regulation? Well, a small but growing literature suggests that they may also matter for social affec-
tive processes. At first glance, this idea that metabolic hormones could be influenced by or even contributes to affect
and social cognition may seem counterintuitive. However, perspectives on allostasis (i.e., how the brain monitors and
manages physiology) argue that metabolism is fundamental for psychology (Barrett, Quigley, & Hamilton, 2016;
McEwen & Wingfield, 2003). As such, metabolic hormones leptin and ghrelin may, by extension, be implicated in
people's experiences, perceptions, and behaviors beyond motivations to eat. Below, we briefly discuss allostasis
and how it can guide hypotheses about the role of leptin and ghrelin in social affective processes. Next, we review
literature suggesting that leptin and ghrelin may be sensitive to social affective signals and related contexts
perhaps because these signals and contexts are “metabolically salient.”In other words, social affective signals
(e.g., interpersonal conflict, and social status) and their associated psychology (e.g., perceptions of threat
vs. belonging) may impact leptin and ghrelin because these signals and contexts inform the brain's predictions about
anticipated energy needs. Second, we review literature showing that leptin and ghrelin may also feed into the con-
struction of social affective processes (e.g., mood and risk taking), as a way of motivating behaviors that support
anticipated energy needs. We close by sketching potential mechanisms that could guide future research and offer
practical guidelines for psychologists wishing to incorporate leptin and ghrelin into their own work.
2|THE METABOLIC MIND: A FRAMEWORK CONNECTING LEPTIN,
GHRELIN, AND SOCIAL AFFECTIVE PROCESSES
Energy is a fundamental principle of biological life. In mammalian cells, energy is derived from food and oxygen to
power cellular electrochemical processes (Nicholls & Fergusson, 2013). Metabolism refers to this process of energy
maintenance, including the breakdown of food into energy (measured in kilojoules or calories) and the management
of fat tissue for energy storage. Because the acquisition and use of energy are central to sustain life and reproduce
(Wallace, 2010), theories on allostasis suggest that metabolism should matter for more than just food intake and
weight regulation but also psychological processes, such as affect and social cognition. Allostasis is the active process
by which the brain predicts how past, present, and future life circumstances may impact an organism, in turn coordi-
nating physiological changes (e.g., metabolic, autonomic, neuroendocrine, and immune) to meet actual or anticipated
environmental demands and to support the organism's movement, growth, reproduction, and survival (Kleckner
et al., 2017; McEwen & Stellar, 1993; Picard, McEwen, Epel, & Sandi, 2018; Schulkin, 2011; Sterling & Eyer, 1988).
Coordinating physiological changes and enacting behavioral responses to life events each require energy
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expenditure, suggesting that the anticipation and regulation of energy needs are important facets of allostasis. Meta-
bolic messengers like leptin and ghrelin help communicate an organism's energy availability to the brain and in turn
mediate efferent brain-to-body commands in support of states and behaviors that assist with energy intake and reg-
ulation (Ahima & Antwi, 2008; Seeley & York, 2005). Leptin's and ghrelin's role in metabolic signaling suggests that
they may contribute to predictions about the current energy state of the brain and body, guiding how the brain
adjusts states and behaviors in line with expectations about the world.
Affective and social cognitive processes also play an important role in allostasis, as they are viewed as arising
from and contributing to the brain's allostatic predictions. This is in part because all behaviors and even cognitive
functions require metabolic energy beyond our resting energy expenditure (Magistretti & Allaman, 2015), and some
behaviors and situations are more metabolically costly than others (e.g., a stressful job interview or threatening social
altercation vs. relaxing on the sofa with a romantic partner). Furthermore, afferent signals from the body provide
important information about whether or not one has the energy reserves to engage in different behaviors
(e.g., should I seek out new social connections or stay at home to conserve energy? Barrett, Quigley, & Hamilton,
2016; Touroutoglou, Andreano, Adebayo, Lyons, & Barrett, 2019). Thus, leptin and ghrelin could contribute to our
social affective experiences and behaviors in a causal way. Following this idea that the mind is built upon metabolic
motivations, we review early evidence from both animal and human literatures linking leptin and ghrelin to affective
and social cognitive processes.
3|FROM MIND TO BODY: SOCIAL AFFECTIVE IMPACTS ON LEPTIN AND
GHRELIN
Given that efficient allocation and regulation of metabolic energy are crucial for any aspect of an organism's func-
tioning and survival, life events or environmental signals that might impact an organism's allostasis should also impact
metabolic functions, including leptin and ghrelin. For social species like humans, social affective signals may serve as
an additional type of allostatic signal, indicating whether a current or upcoming context or stimulus is safe
vs. threatening and whether there are sufficient physiological resources to respond accordingly. Humans have long
lived in hunter–gatherer bands (Hill et al., 2011), wherein the presence of others (especially close supportive others)
improved chances of survival than did living alone. In this way, social affective signals and contexts, such as whether
an individual is of high or low status, liked or disliked, and socially integrated or isolated may serve as signals about
access to tangible physical and psychological resources that support allostasis and metabolic needs. For example, an
individual living without social support would likely have higher metabolic needs not only because they have to indi-
vidually complete more tasks for daily functioning and survival but also because they may be more susceptible to
physical and psychosocial threats without a buffer of supportive others. In line with this idea, we hypothesize that
leptin and ghrelin, as key metabolic signals, may be sensitive to social affective signals and contexts. For example,
social isolation, threat, and conflict may upregulate ghrelin, as a means of supporting energy intake for active coping.
Below, we explore existing literature relevant to this hypothesis with regard to social isolation and conflict, social sta-
tus, and chronic vs. acute stressors.
3.1 |Social isolation and conflict
Initial work demonstrated that social isolation was associated with higher leptin in men (Häfner et al., 2011). A more
targeted study (Jaremka et al., 2015) investigated whether loneliness increases ghrelin and appetite. Forty-two
women ate standardized meals, with ghrelin sampled before the meal, immediately post-meal, and 2 and 7 hr post-
meal. Women also rated feelings of chronic loneliness and social isolation. Lonelier women had stronger ghrelin
spikes post-meal (during the 2 to 7 hr period) as hunger again increased, but only for leaner participants (computed
at −1SD from sample mean BMI compared to heavier BMI at +1SD). This finding suggests the possibility that, in
MACCORMACK AND MUSCATELL 3of18
leaner women, feelings of loneliness or “threats to belonging”promote greater food intake, with ghrelin as a key
mediator (Jaremka, Lebed, & Sunami, 2018). Experimental rodent work provides stronger causal evidence: Healthy
mice subjected to social isolation showed significant ghrelin increases after one week relative to group-housed con-
trols (Yamada et al., 2015). Social isolation may also interact with diet choices to alter leptin. For example, rats
exposed to chronic social isolation showed an exacerbated effect of high-fat diet on long-term leptin levels
(Toniazzo, Arcego, & Lampert, 2018). This early work suggests that social isolation and loneliness may elicit shifts in
leptin and ghrelin.
Besides social isolation and loneliness, leptin and ghrelin may be sensitive to interpersonal conflicts or distress,
given that such conflicts could signal the onset of threats or changes in support networks that could compromise
allostasis. In one study (Jaremka et al., 2016), 43 married couples ate a standardized meal before completing a marital
problems discussion, during which marital distress was coded. Leptin and ghrelin were assayed before the meal and
again at 2, 4, and 7 hr post-meal. Results showed that greater marital distress in either spouse was associated with
higher post-meal ghrelin (but not leptin); this effect only held for leaner individuals (again, −1SD from sample mean
BMI). This null leptin effect is curious, given that circulating leptin tends to increase by 4–6 hr post-food ingestion
(Havel, Townsend, Chaump, & Teff, 1999). Perhaps leptin is less sensitive to interpersonal conflicts than ghrelin, but
future investigations are needed.
3.2 |Social status
Besides social connection, social status may be especially metabolically relevant to allostasis. For social animals, low
status means reduced access to food and mating partners, more frequent aggressions, and altered immune function-
ing (e.g., Sapolsky, 2004; Snyder-Mackler et al., 2016). As such, leptin and ghrelin may be sensitive to social status.
Jarrell et al. (2008) found that female rhesus monkeys who moved to high-status positions showed a boost in leptin,
perhaps indicating that higher-status individuals do not need to build up metabolic reserves thanks to easier food
access. Follow-up studies (Michopoulos, Higgins, Toufexis, & Wilson, 2012; Michopoulos, Loucks, Berga, Rivier, &
Wilson, 2010; Michopoulos & Wilson, 2011) found that dominant female monkeys showed increased leptin and
improved weight maintenance during social threat relative to subordinates, suggesting that leptin may promote more
effective metabolic adaptation to status-related stressors. On the other hand, low-status monkeys showed ghrelin
upregulation in the face of social threat, perhaps to motivate food intake to support coping.
Despite these intriguing primate findings, little work tests the effects of social status on leptin and ghrelin in
humans. One recent study (Sim et al., 2018) examined whether subjective social status impacts ghrelin: Healthy men
(N=48) showed greater circulating ghrelin and lower fullness/satiety ratings after a low subjective social status
manipulation compared to their ghrelin and fullness ratings following a control task. Similarly, inducing low subjective
status leads people to prefer high-calorie foods and consume more calories (Cardel et al., 2016; Cheon & Hong,
2017), although this work did not include assessment of metabolic hormones. Future studies should unpack how
both objective (i.e., socioeconomic status or SES) and subjective social status can alter metabolic signaling, especially
given that altered leptin and ghrelin may contribute to the link between low social status and downstream obesity
and disease.
3.3 |Chronic and acute stress
Ultimately, social isolation, interpersonal conflicts, and low social status can all be understood as types of chronic or
acute social stressors. As such, another pathway for social affective influences on leptin and ghrelin is via the psycho-
logical states and behaviors that such signals and contexts evoke. Within an allostatic framework, environmental
pressures likely signal to the brain that more resources are needed to cope with demands (McEwen & Wingfield,
2010), which could lead to increases in metabolically relevant behaviors such as greater food consumption that can
in turn provide energy for coping. In this way, stress is an already recognized mechanism underlying emotional eating
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(e.g., Tomiyama, Finch, & Cummings, 2015), which occurs when people cope with negative affect and stress by
increasing food intake (i.e., binging) or eating more of certain food types (Macht, 2008; Tomiyama, Finch, &
Cummings, 2015). Indeed, work on emotional eating suggests that leptin and ghrelin may help facilitate stressors'
impacts on feeding behaviors. For example, both emotional and non-emotional eaters show increased circulating
ghrelin after an acute psychosocial stressor (Raspopow, Abizaid, Matheson, & Anisman, 2010). Alternately, lower lep-
tin reactivity after an acute stressor is associated with greater consumption of high-sugar, high-fat “comfort”foods
(Tomiyama et al., 2012). Finally, stress-induced cortisol release appears to stimulate ghrelin (Sinha & Jastreboff,
2013). Together, these findings suggest that stress may alter metabolic behaviors (e.g., eating), as one mechanism
linking stress and obesity, and may do so in part via leptin and ghrelin. Below, we review existing evidence linking
chronic and acute stress to altered leptin and ghrelin.
First, as a type of chronic stressor, greater early life adversity is associated with higher circulating leptin in middle
adulthood, even after controlling for physical activity, diet, and BMI (Joung et al., 2014). Leptin also helps explain the
relation between childhood adversity and higher blood pressure (Crowell et al., 2016). Chronic stress effects may
even be trans-generational. Both rodent and human studies show that chronically stressed mothers bear children
with higher leptin and body weight than do low-stress mothers, with effects for children lasting even into adulthood
(review in Entringer, 2013). But why would individuals with higher adiposity also have greater leptin, if leptin signals
satiety and sufficiency of metabolic resources? One common explanation is leptin resistance. Despite obese individ-
uals having excessive adipose tissue and proportionally high leptin, this higher leptin does not reduce appetite or
support weight loss, suggesting that the brain and body may have become insensitive to leptin signaling (Myers
et al., 2012). More research is needed to unpack links between chronic stress, leptin, and weight gain/obesity.
Beyond chronic stressors such as early life adversity, leptin may also be sensitive to acute stressors. For example,
Brydon et al. (2008) found a small increase in leptin 45 min after an acute stressor (Stroop and speech tasks). How-
ever, a second study using the Trier Social Stress Test (TSST; Tomiyama et al., 2012) found no change in leptin at
50 or 90 min post-stressor. This inconsistency may be due to task differences (e.g., the latter involved greater social
evaluative stress) or because leptin's reactivity to acute stress is a small effect (e.g., as found in the former study).
Given that leptin typically responds to food ingestion within 4–6 hr (Havel, Townsend, Chaump, & Teff, 1999), a lon-
ger measurement window may be necessary. Future work should continue investigating the effects of acute stress
on leptin reactivity in humans.
Similar to leptin, ghrelin may change in response to both chronic and acute stressors—although given its acute
time-course, it may be especially sensitive to acute stress. Consistent with this, several studies in both humans and
rodents have examined acute stress-related ghrelin reactivity. For example, as noted earlier, Raspopow, Abizaid,
Matheson, and Anisman (2010) found that both emotional and non-emotional eaters (N=48) show ghrelin increases
within 30 min after the TSST relative to baseline. Similarly, in a sample of overweight women (N=28), ghrelin
increased in response to a stressful cold pressor task (Geliebter, Carnell, & Gluck, 2013). In another study
(Monteleone et al., 2012), both women diagnosed with bulimia nervosa and healthy controls showed significant
increases in ghrelin after the TSST relative to baseline. However, in healthy women, ghrelin peaked 25 min post-
stressor and rapidly returned to baseline; women with bulimia showed elevated ghrelin as late as 60 min post-
stressor, suggesting that acute stress effects on ghrelin's peak and recovery could vary depending on population.
Further converging evidence finds that acute stress alters ghrelin in rats relative to sham stress (e.g., Kristenssson
et al., 2006). Beyond acute stress, some rodent work suggests that ghrelin is sensitive to chronic stress (Ochi et al.,
2008; Patterson et al., 2010). In humans, early life adversity may affect ghrelin: For example, Pakistani adolescents
who experienced terrorist attack-related trauma in childhood showed a nearly two-fold elevation in ghrelin relative
to adolescents without a trauma history (Yousufzai et al., 2018). Together, findings suggest that stress (particularly
acute stressors) can increase ghrelin, perhaps in part to motivate greater energy intake for active coping efforts that
are metabolically demanding.
Relatedly, daily life stressors (which can encompass both chronic stressors such as financial worries and acute
stressors such as a recent interpersonal altercation) may also impact metabolic hormones. Jaremka et al. (2014)
MACCORMACK AND MUSCATELL 5of18
recruited 50 women to complete three laboratory visits each two or more weeks apart. During each visit, women
fasted before eating a standardized meal, with blood samples for leptin and ghrelin collected 45 min post-meal. They
also completed the self-reported Daily Inventory of Stressful Events. Results revealed that, even when controlling
for BMI, women reporting more social stressors showed elevated ghrelin and reduced leptin profiles post-meal rela-
tive to women reporting fewer social stressors. Non-social stressors did not relate to leptin and ghrelin. The elevated
ghrelin and reduced leptin post-meal suggest that socially stressed women may feel hungrier and less satiated sooner
after eating than women with fewer social stressors. This suggests that social stress may be particularly metabolically
taxing (above and beyond other types of stressors), lending additional support to the hypothesis that leptin and
ghrelin may be sensitive to social affective signals and contexts.
3.4 |Future questions
Despite an initial literature suggesting that social affective signals and contexts influence leptin and ghrelin, more
work is needed to replicate and extend these findings. For example, future studies could clarify the mechanisms
linking acute stress to ghrelin reactivity, including the neural, autonomic, glucocorticoid, and immune processes that
may mediate effects of acute stress on ghrelin. Similarly, researchers could experimentally manipulate stress
appraisals (e.g., wherein a stressor is perceived to be a challenge vs. threat; Jamieson, Hangen, Lee, & Yeager, 2018)
to determine if these evoke different metabolic profiles. Another idea is to manipulate social support during a stress-
ful task—with the prediction that social support could buffer against stress effects on leptin and ghrelin. Beyond
stress, future work could test whether the social isolation findings reviewed above extend to acute social exclusion
paradigms like Cyberball (Williams & Jarvis, 2006), consistent with the idea that social exclusion should have
allostatic implications for metabolism and safety. Altogether, future work is needed to verify these speculations and
establish the boundary conditions by which social affective signals and contexts modulate leptin and ghrelin.
In sum, there appears to be initial support for the idea that leptin and ghrelin may be sensitive to social affective
signals and contexts. It is also possible that leptin and ghrelin may “bottom-up”contribute to affect and social cogni-
tion, motivating behaviors in line with allostatic needs. We explore this possibility next.
4|FROM BODY TO MIND: LEPTIN AND GHRELIN MAY CONTRIBUTE TO
AFFECT AND SOCIAL COGNITION
Across animals, the brain anticipates energy demands (Kim, Seeley, & Sandoval, 2018; Seeley & York, 2005), in turn
orchestrating physiological and motivational changes to meet those demands, including with the help of metabolic
hormones leptin and ghrelin. For example, during important life events that require intense energy use like migration,
hibernation, puberty, and pregnancy, both human and animal feeding behaviors increase to intake energy, while
weight status, via adipose tissue, signals how much energy is set aside for anticipated demands, e.g., a winter famine
(reviews in Kaplan & Gangestad, 2005; McEwen & Wingfield, 2003). As such, the brain includes receptors for meta-
bolic chemicals from the periphery to signal how much effort or risk is required to meet anticipated energy needs
and guide behaviors in a “bottom-up”fashion.
Accordingly, leptin and ghrelin receptors are widely distributed throughout the brain, especially in the hypothala-
mus and other subcortical limbic structures (reviews in Ferrini, Salio, Lossi, & Merighi, 2009; Howick, Griffin, Cryan, &
Schellekens, 2017; Myers, Münzberg, Leinninger, & Leshan, 2009). For example, there are extensive leptin receptors
in key reward regions like the ventral tegmental area and substantia nigra (Elmquist, Bjorbaek, Ahima, Flier, & Saper,
1998; Hommel et al., 2006), and animal models show that ghrelin is a crucial mediator in brain phasic dopamine sig-
naling, especially in nucleus accumbens and ventral striatum dopamine receptors (Abizaid, 2009). These patterns of
receptor distribution suggest that leptin and ghrelin may play a role in motivating reward seeking more generally.
Specifically, there are receptors for leptin and ghrelin in regions that regulate more than just hunger and satiety,
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responding to multiple types of reward and risk, including non-food-related rewards and risks (see meta-analyses:
Krain, Wilson, Arbuckle, Castellanos, & Milham, 2006; Liu, Hairston, Schrier, & Fan, 2011; Sescousse, Caldú, Segura, &
Dreher, 2013). As such, although leptin and ghrelin at their core help regulate metabolism, we suggest that they may
do so in part by supporting domain-general states and behaviors in service of energy regulation, such as affective
states, social cognition, and behaviors. We explore this possibility below.
4.1 |Affect
Affective states involve feelings of pleasure–displeasure (valence) and activation-quiescence (arousal) and are
thought to be fundamentally motivating for behavior. In line with this idea, we suggest that leptin and ghrelin may
contribute to the generation of affect, as such affect would help motivate behaviors for energy intake and mainte-
nance (Chuang & Zigman, 2010; Zarouna, Wozniak, & Papachristou, 2015). More specifically, the affective dimen-
sions of metabolic states likely not only reinforce future appetitive behaviors as is already suggested (Dagher, 2009),
but these feelings could also serve as an allostatic “barometer”(Duncan & Barrett, 2007)—helping organisms identify
when metabolic energy is low (e.g., feeling hungry and tired) vs. sufficient or in surplus (e.g., feeling full and ener-
gized). In line with this hypothesis, the theory of constructed emotion suggests that moods (longer lasting affective
states) and emotions (more transient states) reflect the brain's interoceptive predictions about an individual's ongoing
allostasis (Barrett, 2017). Affective changes in valence and arousal likely reflect an integration of metabolic, immune,
cardiovascular, and autonomic afferent signals into conscious awareness (Barrett & Bliss-Moreau, 2009;
MacCormack & Lindquist, 2017). As such, feeling anxious or depressed, and angry or sad, may similarly reflect more
chronic or acute signals about anticipated energy supply and demand. If leptin and ghrelin indeed play a domain-
general affective role, then it is important to demonstrate that they do so even when food is not necessarily
involved.
Some early evidence in nonhuman rodent models supports this possibility. For example, leptin administration
in rodents increases self-stimulating behaviors beyond food (e.g., pressing a lever that stimulates an implanted
electrode), likely via interaction with dopaminergic systems (Carr, 2002; Fulton, Woodside, & Shizgal, 2000). A
growing body of evidence in both rodents and humans implicates ghrelin and its receptors in drug-related
reward responses (e.g., Wenthur et al., 2019; Zallar et al., 2019; see also Morris, Voon, & Leggio, 2018, for
review). For example, in humans, individuals with higher fasting ghrelin appear to be more reward sensitive and
report experiencing more intense, longer lasting subjective effects in response to intravenous alcohol administra-
tion relative to saline placebo (Ralevski et al., 2017, 2018; this work used ethanol rather than alcohol ingestion,
which contains carbohydrates, in order to disentangle the pleasure induced by ethanol from alcohol's caloric
value). In the context of addiction wherein reward is highly conditioned, blocking ghrelin receptors in rodent
brains can reduce the craving component of nicotine-dependence and alcoholism (review in Panagopoulos &
Ralevski, 2014). Similarly, leptin and ghrelin—via their interactions with other systems such as the immune and
autonomic nervous systems, may further potentiate rewarding vs. aversive states and help generate subjective
arousal. For example, peripheral leptin administration in rats and mice subjected to thermal pain leads to greater
nociceptive pain sensitivity than placebo controls (Kutlu et al., 2003), perhaps given that leptin is a pro-
inflammatory mediator (Bernotiene, Palmer, & Gabay, 2006) and may exacerbate the pain associated with
injury-induced inflammation. On the other hand, ghrelin administration in rodents and humans mediates the
release of several arousal-associated hormones like cortisol and adrenaline (Mihalache et al., 2016). Further,
peripheral ghrelin administration in humans elicits reports of highly aroused, unpleasant feelings and can
increase sympathetic muscle activation during a stressor relative to placebo saline, suggesting that ghrelin may
increase physiological and subjective arousal, alertness, tension, and action readiness even in contexts where
food intake is not the primary outcome (Garin, Burns, Kaul, & Cappola, 2013; Lambert et al., 2011).
Beyond acute emotion experiences, leptin and ghrelin may also be implicated in the etiology of chronic mood
states. A recent meta-analysis showed that individuals with major depression have lower levels of leptin (Cao et al.,
MACCORMACK AND MUSCATELL 7of18
2018), although findings were correlational, leaving the causal relation unclear. Similarly, leptin administration in
rodents exerts antidepressant effects, wherein leptin performs as well as fluoxetine at reducing depressive symptoms
(Liu et al., 2010). Ghrelin, on the other hand, is implicated in anxiety. For example, both central and peripheral admin-
istration of ghrelin in mice produces behaviors consistent with anxiety (Asakawa et al., 2001; Carlini et al., 2002).
Thus, it appears that leptin and ghrelin may contribute to psychopathologies like depression and anxiety, although
both clinical trials and experimental work in humans are greatly needed.
Altogether, these early findings are consistent with our hypothesis that leptin and ghrelin may support the con-
struction of broader affective processes beyond just food-related reward and motivation. However, most research in
this area has been conducted in nonhuman animals, and significant efforts are needed to replicate and extend find-
ings in humans. Given that affective states can motivate behavior, leptin's and ghrelin's effects on reward, arousal,
and mood may exist in part because these states arguably motivate an organism to engage in behaviors that support
metabolic needs. We next discuss evidence that metabolic states and leptin/ghrelin can impact risk taking, impulsiv-
ity, and aggression.
4.2 |Risk taking, impulsivity, and aggression
Cross-species studies suggest that when hungry or under nutritional stress, small animals with high metabolic
rates tend to choose a “risk-prone”strategy. For example, frogs and fish in the fasted state are more likely to
forage outside typical ranges into riskier (more variable) predator- or competitor-laden zones (Carlson, New-
man, & Langkilde, 2015; Damsgird & Dill, 1998; Godin & Crossman, 1994). On the other hand, in large-bodied
omnivores like chimpanzees, energy deficits (e.g., hunger and malnourishment) may elicit divergent risk behav-
iors. For example, an observational study over 14 years (Gilby & Wrangham, 2007) found that chimpanzees
were more likely to adopt risk-prone foraging behaviors (e.g., hunting red colobus monkeys) when nutrients
were abundant but more likely to adopt risk-averse foraging strategies (e.g., feeding on plants) when environ-
mental resources were scarce. This supports the notion that metabolic states may facilitate either risk-prone or
risk-averse behaviors, depending on broader scarcity vs. abundance in the surrounding environment. As humans
are also large omnivores, leptin and especially ghrelin may play a similar contextualized role in risk assessment
and decision making, an idea explored below.
Symmonds, Emmanuel, Drew, Batterham, and Dolan (2010) examined risky economic decisions in healthy-
weight men. In different randomized sessions (14 hr post-fasting vs. immediately after eating a controlled meal
vs. 1 hr after eating a meal), males (N=24) completed a lottery choice task with leptin and ghrelin assayed
each session. Results demonstrated that participants were most risk averse for about 1 hr post-meal, associated
with significant declines in ghrelin—suggesting that higher ghrelin could support risk taking in a metabolically
depleted state but that declining ghrelin, as a signal of nutrient intake, may temporarily induce risk aversion as
the body digests food. However, higher baseline leptin was also correlated with riskier choices post-meal rela-
tive to fasting, suggesting that although ghrelin declines may temporarily induce risk aversion, individuals' prior
leptin status could moderate these effects. Similarly, Levy and colleagues (2013) found that fasted participants
were more risk tolerant, not just in the context of food and water but also in monetary decisions, providing
converging evidence that these metabolic effects on risk are not limited to food. However, here, ghrelin and
leptin were not measured, so more work is needed to examine if metabolic hormones mediate the link between
hunger and risk-seeking behaviors in food vs. non-food domains.
Given the relevance of impulsivity for risk taking, some studies have also begun examining associations
between metabolic hormones on trait impulsivity; for example, initial work shows a positive correlation between
higher fasting ghrelin and dimensions of impulsivity in humans (e.g., Ralevski et al., 2018). Experimental rodent
work further suggests that centrally administered ghrelin injection increases impulsive behavior in rats on behav-
ioral impulsivity measures such as the go/no-go task (Anderberg et al., 2016). Future work should clarify the
impacts of leptin and ghrelin on risk taking and related behavioral tendencies such as impulsivity across
8of18 MACCORMACK AND MUSCATELL
different time-courses (e.g., when hungry vs. immediately after eating) and contexts, especially in humans. For
example, high- vs. low-resource contexts may support divergent risk-prone vs. risk-averse behaviors in humans
that are mediated in part by leptin and ghrelin signaling.
Related to ghrelin's impact on risk taking and relation to impulsivity, there is also the possibility that it
could, in some contexts, motivate aggressive behaviors, consistent with predation and competition for resources.
To our knowledge, only one study has yet explored this possibility. Specifically, when the ghrelin-inhibiting
enzyme butyrylcholinesterase is knocked out in mice, fighting and other aggressive behaviors significantly
increase, mirrored by significant increases in circulating ghrelin (Chen et al., 2015). Given that hunger and low
blood sugar (including manipulation thereof) are associated with aggressive behaviors in humans (e.g., Benton,
1988; Bushman, DeWall, Pond, & Hanus, 2014), ghrelin as a more proximal hunger mediator may also play a
role in human aggression, although this speculation remains untested. Finally, most work examining effects of
metabolic hormones on risk taking and aggression focus on ghrelin, limiting our knowledge of the role of leptin
in these processes.
4.3 |Future questions
In sum, preliminary evidence suggests that both leptin and ghrelin may contribute to affect, risk taking, impulsivity,
and perhaps aggression. Future work should use experimental manipulations to test these causal connections more
rigorously in humans. Of note, metabolic contributions to social cognition and behavior remain underexplored,
although we believe that leptin's and ghrelin's importance for reward, emotion, risk taking, and aggression suggests
that they should also matter for social cognitive processes like prejudice, empathy, and person perception. For exam-
ple, in interpersonal contexts, leptin and ghrelin may shape motivations to meet strangers or initiate new relation-
ships, contingent on metabolic state. Leptin, a key signal for pubertal onset (Sanchez-Garrido & Tena-Sempere,
2013), may also be implicated in adolescent risk behaviors. Finally, given that resource sharing vs. competition is
metabolically relevant, individuals' metabolic states, alongside leptin and ghrelin as central metabolic signals, may
shape in-group/out-group biases, especially under conditions of scarcity vs. abundance. These ideas remain untested
in the literature but may be worth pursuing in future.
5|METHODOLOGICAL CONSIDERATIONS
Although our understanding of the relation between psychological processes and leptin/ghrelin is nascent, the above
evidence foreshadows exciting directions for future research. For psychologists wishing to adopt leptin and ghrelin
measurements or manipulations, below, we offer key methodological considerations. Key considerations are summa-
rized in Figure 1.
5.1 |Time-course
As noted throughout, leptin and ghrelin have different time-courses, such that leptin is more stable across multiple
days (except for a few hours after a meal: Klok, Jakobsdottir, & Drent, 2007) and less sensitive to single acute events
like missing a night of sleep (Pan & Kastin, 2014). Ghrelin, on the other hand, is highly sensitive to food intake from
the previous 12–24 hr (Spiegel, Tasali, Leproult, Scherberg, & Van Cauter, 2011) and is inversely related to the num-
ber of hours slept the previous night (Taheri, Lin, Austin, Young, & Mignot, 2004). Further, both leptin and ghrelin
have diurnal rhythms tied to sleep and meals. Leptin peaks during sleep and reaches its nadir upon awakening (Shea,
Hilton, Orlova, Ayers, & Mantzoros, 2005), while ghrelin increases from midnight to dawn, appearing to peak mid-
morning if no breakfast is eaten (Cummings et al., 2001). We also note that just as there are individual differences in
fasting or baseline glucose levels, similar individual differences can be observed for other metabolic markers such as
MACCORMACK AND MUSCATELL 9of18
ghrelin (e.g., Ralevski et al., 2017). In light of these temporal and within-subject dynamics, researchers (1) should con-
sider whether the psychological phenomenon of interest is acute or chronic, (2) should assay or administer the hor-
mones at the same time of day across participants (or control for time of day in analyses), (3) should always
incorporate fasting or a standardized meal into the laboratory paradigm, (4) should include within-subject measures
whenever possible (e.g., measure baseline and “reactivity”; use a randomized crossover design), and (5) should assess
the last 24 hrs of sleep and food history for possible inclusion as covariates.
5.2 |Key covariates
Body composition, sex, and age all predict variation in leptin and ghrelin functioning. Much work demonstrates that
body composition extremes (obesity and eating disorders) alter leptin and ghrelin (Cui, López, & Rahmouni, 2017;
Monteleone & Maj, 2013). As such, researchers should use healthy-weight samples unless interested in comparing
effects across populations. Body composition matters most for leptin, given that leptin is proportional to adipose tis-
sue, and thus some metric (e.g., BMI and body fat percentage) should be included as a statistical covariate in ana-
lyses. Sex is another key moderator. For example, leptin and ghrelin vary across the menstrual cycle
(e.g., Dafopoulos, Sourlas, Kallitsaris, Pournaras, & Messinis, 2009), suggesting that sex and menses stage be used as
statistical covariates. Finally, leptin and ghrelin change with age and often mark, even facilitate, critical changes
across major life thresholds, like pubertal onset, fertility, and menopause (Garcia-Galiano, Allen, & Elias, 2014;
Tena-Sempere, 2013). Leptin accumulates and ghrelin declines with age, partially underlying age-related shifts in
appetite and weight status (Mishra et al., 2015; Nass et al., 2014). Studies with leptin and ghrelin should consider
developmental stage when forming hypotheses.
FIGURE 1 Methodological considerations for integrating leptin and ghrelin into study designs
10 of 18 MACCORMACK AND MUSCATELL
5.3 |Manipulation vs. measurement
Manipulation is the strongest approach to investigate leptin and ghrelin impacts on the brain and behavior, affording
inferences about causality. Due to ghrelin's acute nature, it is typical to administer a single subcutaneous injection of
FIGURE 2 Leptin's and ghrelin's bidirectional relations with social affective processes are likely mediated via the
brain, autonomic, and immune system pathways, including interactions between these systems. For example, if
leptin or ghrelin alters inflammation, subsequent inflammation-mediated effects of leptin and ghrelin may also be
observed in the brain and autonomic nervous system. It is important to remember that cross-system relations with
leptin/ghrelin are dynamic, with ghrelin responding more quickly on acute timescales and leptin over chronic
timescales. Furthermore, leptin and ghrelin can also affect each other. Finally, it is important to note that the
relations depicted herein develop and occur within the context of broader environmental factors. For example,
maternal and prenatal health, early life adversity, environmental pollutants, socioeconomic status, food insecurity
and broader nutrition, weight and disease status, age, and lifestyle factors (e.g., smoking and exercise) likely also
influence the bidirectional relations between leptin, ghrelin, and social affective processes
MACCORMACK AND MUSCATELL 11 of 18
ghrelin 15–30 min before measuring the outcome of interest (Garin, Burns, Kaul, & Cappola, 2013). On the other
hand, due to leptin's chronic nature, some studies administer leptin in small doses via subcutaneous injection over a
set time period (e.g., two weeks and one month). Measurement, on the other hand, is useful in cross-sectional designs
or instances where researchers care about leptin and ghrelin as outcomes. It is crucial to note that the time-courses
within which leptin and ghrelin respond to psychological events and tasks are still largely unknown. For example,
Brydon et al. (2008) found that leptin reacted to acute stress within 45 min (but this did not replicate in Tomiyama
et al., 2012, even after 90 min). Other work reviewed herein found that ghrelin reacted to acute stress within 30 min.
Whether these timeframes replicate with other psychological paradigms is less clear but could serve as initial esti-
mates. Early investigations should sample multiple timepoints to map the response trajectory of leptin and ghrelin to
social affective events. Finally, blood assay is the most common and reliable assessment of leptin and ghrelin, but
researchers are actively developing other techniques using saliva, urine, and even breastmilk, suggesting that other
measures may become available in time. Ultimately, a combination of manipulation and measurement will provide the
most systematic evidence for bidirectional paths between psychology (e.g., stress, out-group biases, and risk taking)
and leptin/ghrelin.
6|CONCLUSION: MAPPING THE METABOLIC MIND
In sum, the mind is likely metabolic, making predictions about anticipated energy demands and creating feelings, per-
ceptions, and behaviors accordingly. As such, metabolic hormones leptin and ghrelin may be implicated in people's
social affective experiences, perceptions, and behaviors beyond motivations to eat. Yet much more work is needed
to clarify leptin's and ghrelin's relation with affect and social cognition. To close, we suggest three pathways as prom-
ising targets for future research, bridging leptin and ghrelin to the mind and behavior (Figure 2). First, leptin and
ghrelin work closely with the immune system (Bernotiene, Palmer, & Gabay, 2006; Chowen & Argente, 2017). The
immune system is already implicated in well-being, mood disorders, and even social cognition (Gassen & Hill, 2019;
Slavich & Irwin, 2014). Future studies could, for example, assess how leptin and inflammation interact in the context
of poor social support, low SES, or situations of chronic discrimination. Second, leptin's and ghrelin's relation with
the autonomic nervous system remains underexplored, with small samples and mixed findings. For example, ghrelin
shows mixed impacts on heart rate, heart rate variability, blood pressure, and sympathetic nerve activation (Lambert
et al., 2011; Matsumura, Tsuchihashi, Fujii, Abe, & Iida, 2002; Soeki et al., 2014). Future work could systematically
test the autonomic impacts of ghrelin, with implications for acute stress and the construction of emotions like anger.
Recent experiments confirm that hunger can indeed induce negative affective feelings and perceptions (e.g., feeling
“hangry”; MacCormack & Lindquist, 2018)—but it would be valuable to determine whether and how leptin and
ghrelin might help mediate these affective consequences of hunger. Finally, given that leptin and ghrelin have distrib-
uted receptors throughout the brain, both hormones may feed into neural representations of affect and social cogni-
tive processes. For example, ghrelin administration predicts greater functional activation in limbic regions like the
amygdala, anterior insula, ventral striatum, and orbitofrontal cortex (Malik, McGlone, Bedrossian, & Dagher, 2008),
hinting at possible implications for ghrelin in the neural representation of affect, pain, interoception, and mentalizing.
We look forward to future investigations further revealing how leptin and ghrelin may matter for affect and social
cognition.
ACKNOWLEDGEMENTS
We are grateful to Carolina Social Neuroscience and Health lab members Gabriella Alvarez, Samantha Brosso,
Monica Gaudier-Diaz, Tatum Jolink, Carrington Merritt, and Becky Salomon for their feedback on earlier manuscript
drafts and to Kristen Lindquist for constructive comments. This work was supported by a Ruth L. Kirschstein
12 of 18 MACCORMACK AND MUSCATELL
National Research Service Award predoctoral fellowship to J. K. M. (1F31AG055265-01A1) from the National Insti-
tute on Aging.
ORCID
Jennifer K. MacCormack https://orcid.org/0000-0002-1199-0121
Keely A. Muscatell https://orcid.org/0000-0002-7893-5565
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AUTHOR BIOGRAPHIES
Jennifer K. MacCormack is currently a doctoral student in the Department of Psychology and Neuroscience at
the University of North Carolina at Chapel Hill where she works with Dr. Kristen Lindquist in the Carolina
Affective Science Laboratory and Dr. Keely Muscatell in the Carolina Social Neuroscience and Health Laboratory.
Broadly, her work integrates methods from social psychology, psychophysiology, and social affective neurosci-
ence to investigate the role of allostasis and interoception in emotion and social cognition across the life span.
Her research is supported by a Ruth L. Kirschstein National Research Service Award Individual Predoctoral Fel-
lowship from the National Institute on Aging. Jennifer obtained her BA in Psychology from North Carolina State
University and her MA at UNC on the psychological mechanisms behind feeling hangry.
Keely A. Muscatell is currently an assistant professor in the Department of Psychology and Neuroscience at the
University of North Carolina at Chapel Hill, where she is also a member of the Lineberger Comprehensive Cancer
Center. Dr. Muscatell is the director of the Carolina Social Neuroscience and Health Laboratory, where together
with her team of students and trainees she conducts research examining the bidirectional links between social
experiences (e.g., stress, discrimination, and subordination) and health, with a particular emphasis on health dis-
parities. Her work incorporates methods from social psychology, social and affective neuroscience, and psycho-
neuroimmunology to investigate these issues. Dr. Muscatell holds a BA in Psychology and Spanish from the
University of Oregon and a PhD in Psychology from UCLA. She also completed post-doctoral training at UCSF
and UC Berkeley.
How to cite this article: MacCormack JK, Muscatell KA. The metabolic mind: A role for leptin and ghrelin in
affect and social cognition. Soc Personal Psychol Compass. 2019;e12496. https://doi.org/10.1111/spc3.
12496
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