TL;DR: Stress eating is not a failure of willpower — it is a predictable neurobiological response driven by cortisol and the brain’s reward circuitry. When the hypothalamic-pituitary-adrenal (HPA) axis is chronically activated, elevated cortisol increases the salience of calorie-dense foods by amplifying dopamine signalling in the nucleus accumbens. Comfort food genuinely reduces the stress response in the short term, which is precisely why the behaviour is so self-reinforcing. Over time, however, the cycle promotes visceral fat accumulation (which itself produces inflammatory cytokines that impair cognition), disrupts the gut-brain axis, and degrades hippocampal function — the brain region most critical for memory and learning. Breaking the cycle requires addressing both the neurochemistry and the behaviour: cortisol-regulating nutrients (omega-3s, magnesium, vitamin C), complex carbohydrates that support serotonin synthesis without blood sugar crashes, gut microbiome support, mindful eating practices, and proactive meal planning for high-stress periods.

Introduction

Everyone has experienced it. A brutal day at work, a family crisis, financial pressure — and suddenly the pull toward a bag of crisps, a bowl of ice cream, or a drive-through burger feels less like a choice and more like a biological imperative. You know it is not hunger. You know the food will not solve the problem. You eat it anyway, and for a few minutes, the world feels slightly less hostile.

This is not a character flaw. It is your hypothalamic-pituitary-adrenal axis doing exactly what it evolved to do — except in a food environment that evolution never anticipated.

Stress eating sits at the intersection of endocrinology, neuroscience, and nutrition. The mechanisms are now well-characterised: cortisol alters reward processing, shifts metabolic priorities toward energy storage, and creates a genuine (if temporary) neurochemical payoff for consuming calorie-dense food. Understanding these mechanisms is not merely academic. It is the first step toward interventions that address the root biology rather than relying on willpower, which decades of research have shown to be a depletable and unreliable resource.

This article examines the full arc of stress eating — from the initial HPA axis activation to the cognitive consequences of chronic engagement — and provides evidence-based strategies for interrupting the cycle at multiple points.

The HPA Axis: How Stress Becomes a Craving

The Stress Response Cascade

The hypothalamic-pituitary-adrenal (HPA) axis is the body’s central stress response system. When the brain perceives a threat — whether physical, psychological, or social — the hypothalamus releases corticotropin-releasing hormone (CRH), which stimulates the anterior pituitary gland to secrete adrenocorticotropic hormone (ACTH). ACTH travels through the bloodstream to the adrenal cortex, where it triggers the release of cortisol, the primary human stress hormone.

In acute stress, this system is adaptive and essential. Cortisol mobilises glucose from liver glycogen stores, suppresses non-essential functions (digestion, reproduction, immune surveillance), and sharpens attention. The response is self-limiting: cortisol feeds back to the hypothalamus and pituitary to shut down CRH and ACTH release once the threat has passed.

The problem arises when stress is chronic. Modern stressors — job insecurity, financial pressure, relationship conflict, information overload — do not resolve in minutes the way a predator encounter would. The HPA axis remains activated for days, weeks, or months. Cortisol levels stay elevated. And the downstream effects on appetite, food preference, and metabolism become profoundly maladaptive.

Cortisol and Food Preference

Elevated cortisol does not simply increase appetite in a general sense. It specifically shifts food preference toward energy-dense combinations of fat and sugar. Epel and colleagues (2001), in a study published in Psychoneuroendocrinology, demonstrated that women with higher cortisol reactivity to laboratory stressors consumed significantly more calories after the stress exposure — and those extra calories came disproportionately from sweet, high-fat foods.

The mechanism involves cortisol’s interaction with the brain’s reward circuitry. Cortisol enhances the activity of the mesolimbic dopamine pathway — the same circuitry discussed in the context of ultra-processed food addiction. Specifically, cortisol increases dopamine release in the nucleus accumbens in response to palatable food cues, making high-calorie food appear more rewarding during stress than it does under baseline conditions. This has been confirmed by neuroimaging work from Rudenga and Small (2012), published in NeuroImage, showing that stress amplifies striatal responses to food reward cues.

This is not a conscious process. You do not decide to find ice cream more appealing when stressed. Your neurobiology makes that decision for you, before conscious deliberation has a chance to intervene.

Why the Body Wants Calories Under Stress

From an evolutionary perspective, the cortisol-driven craving for calorie-dense food makes sense. For most of human history, significant stressors were physical — predation, conflict, famine, injury. All of these either demanded immediate energy expenditure or threatened future energy availability. A stress response that motivated caloric intake and directed those calories toward efficient storage (visceral fat) was a survival advantage.

The mismatch is obvious: modern psychological stressors do not burn calories. The energy that cortisol mobilises and that comfort food provides has nowhere to go. It gets stored — preferentially as visceral adipose tissue, due to the high density of glucocorticoid receptors in abdominal fat cells (Bjorntorp, 2001, Obesity Reviews).

Why Comfort Food Actually Works — Temporarily

The persistence of stress eating is not explained by simple habit. Comfort food genuinely reduces the physiological stress response, creating a powerful reinforcement loop.

The Reward System Dampens the Stress Response

Dallman and colleagues (2003), in an influential paper published in the Proceedings of the National Academy of Sciences, demonstrated in rodent models that consumption of palatable food (sucrose and lard) reduced HPA axis activity, lowering CRH expression in the hypothalamus and dampening corticosterone (the rodent equivalent of cortisol) release. The palatable food was, in a real neurochemical sense, medicating the stress response.

Subsequent human research has confirmed the principle. Tryon and colleagues (2013), publishing in Psychoneuroendocrinology, found that women who reported greater chronic stress showed blunted cortisol responses after consuming comfort food — their stress hormone levels came down faster and further than those of women eating neutral food. The comfort food was acting as a pharmacological buffer against the HPA axis.

The Reinforcement Trap

This is what makes stress eating so difficult to extinguish through willpower alone. The behaviour produces a genuine, measurable neurochemical reward — reduced cortisol, increased dopamine, a brief period of subjective relief. The brain learns from this sequence. Next time stress occurs, the memory of relief drives a stronger craving. Each repetition deepens the association.

The cycle looks like this: stress activates the HPA axis, cortisol rises, reward-seeking intensifies, comfort food is consumed, cortisol temporarily drops and dopamine surges, the brain encodes the behaviour as effective, and the next stress exposure triggers a faster and stronger craving. Over weeks and months, the behaviour becomes automatic — a conditioned response that operates below conscious awareness.

Cortisol, Visceral Fat, and the Inflammatory Feedback Loop

Chronic stress eating does not merely add body weight. It preferentially adds visceral adipose tissue — the fat that accumulates around abdominal organs — and this distinction matters enormously for brain health.

Visceral Fat as an Endocrine Organ

Visceral adipose tissue is not inert storage. It is an active endocrine organ that produces pro-inflammatory cytokines, including interleukin-6 (IL-6), tumour necrosis factor-alpha (TNF-alpha), and C-reactive protein (CRP). These cytokines enter systemic circulation and cross the blood-brain barrier, activating microglia and promoting neuroinflammation (Guillemot-Legris and Bhatt, 2019, Progress in Lipid Research).

Neuroinflammation, in turn, impairs hippocampal neurogenesis, degrades synaptic plasticity, and disrupts the prefrontal cortex — producing measurable deficits in memory, executive function, and decision-making. This creates a secondary feedback loop: stress eating increases visceral fat, visceral fat increases neuroinflammation, neuroinflammation impairs the prefrontal cortex (which is responsible for impulse control and long-term planning), and diminished prefrontal function makes resisting stress eating harder.

Cortisol and Hippocampal Damage

The hippocampus — the brain structure most critical for memory consolidation and spatial navigation — is particularly vulnerable to chronic cortisol exposure. It has one of the highest densities of glucocorticoid receptors in the brain, making it disproportionately sensitive to elevated cortisol.

Lupien and colleagues (1998), in a landmark longitudinal study published in Nature Neuroscience, measured cortisol levels and hippocampal volume in older adults over a five-year period. Participants with consistently elevated cortisol showed significant hippocampal atrophy and performed worse on memory tests compared to those with normal cortisol. The reduction in hippocampal volume was proportional to the degree and duration of cortisol elevation.

This finding has been replicated and extended. A meta-analysis by Ouanes and Popp (2019), published in Frontiers in Aging Neuroscience, confirmed the association between chronic cortisol elevation and reduced hippocampal volume, along with impaired episodic memory performance.

Cognitive Consequences of Chronic Stress Eating

The cognitive damage from chronic stress eating operates through multiple overlapping pathways. Understanding them is important because the effects are not merely theoretical — they are measurable and, in many cases, progressive.

Blood Sugar Dysregulation and Cognitive Performance

Diets dominated by refined carbohydrates and added sugar — the hallmark of stress eating — produce repeated blood glucose spikes and crashes. Each crash produces a transient state of neuroglycopenia (insufficient glucose delivery to the brain) that impairs attention, working memory, and processing speed.

Over the longer term, chronic glucose variability promotes insulin resistance, which has been independently associated with cognitive decline. A study by Crane and colleagues (2013), published in the New England Journal of Medicine, found that higher blood glucose levels — even within the non-diabetic range — were associated with increased risk of dementia. The relationship was continuous and graded: every incremental rise in average glucose carried additional risk.

Disrupted Sleep and Cognitive Recovery

Stress eating patterns often extend into evening and nighttime hours, when cortisol-driven cravings coincide with the depletion of daytime self-regulatory resources. Consuming high-sugar, high-fat food close to bedtime disrupts sleep architecture — reducing slow-wave sleep and REM sleep, both of which are essential for memory consolidation and emotional regulation (St-Onge et al., 2016, Journal of Clinical Sleep Medicine).

Poor sleep, in turn, elevates cortisol the following day, intensifies cravings, and further impairs prefrontal cortex function — creating yet another self-reinforcing loop within the broader stress eating cycle.

Reduced BDNF

Brain-derived neurotrophic factor (BDNF) is essential for synaptic plasticity, learning, and the survival of existing neurons. A diet high in saturated fat and refined sugar has been shown to reduce hippocampal BDNF expression in animal models (Molteni et al., 2002, Neuroscience). Cortisol itself suppresses BDNF. The combination of a stress-eating diet and chronically elevated cortisol creates a double assault on the brain’s primary mechanism for maintaining neural adaptability.

The Gut-Brain Axis Under Stress

The gastrointestinal system is sometimes called the “second brain” for good reason: the enteric nervous system contains over 100 million neurons, produces the majority of the body’s serotonin, and communicates bidirectionally with the central nervous system via the vagus nerve, immune signalling, and microbial metabolites. The full scope of this gut-brain axis and how diet shapes it is a critical piece of the stress eating puzzle.

Stress Reshapes the Microbiome

Chronic stress directly alters the composition of the gut microbiome. Bailey and colleagues (2011), publishing in Brain, Behavior, and Immunity, demonstrated that social stress in mice significantly reduced the relative abundance of Bacteroides species and increased inflammatory markers in both the gut and the bloodstream. Similar shifts have been observed in human studies of chronic psychological stress, including work by Karl and colleagues (2018), published in Journal of the International Society of Sports Nutrition, documenting microbiome changes in military trainees undergoing sustained stress.

Comfort Food Compounds the Problem

The foods typically chosen during stress eating — ultra-processed products high in refined sugar, saturated fat, and emulsifiers — further disrupt microbiome composition. Emulsifiers such as carboxymethylcellulose and polysorbate-80, common in processed foods, have been shown to erode the protective mucus layer of the gut, increase intestinal permeability, and promote the translocation of bacterial endotoxins into the bloodstream (Chassaing et al., 2015, Nature). This endotoxemia activates systemic inflammation and, through the pathways described above, impairs brain function.

The combined effect of stress and a stress-eating diet on the gut is synergistic. Stress alone reduces microbial diversity. The resulting diet further depletes beneficial species and feeds pathogenic ones. The inflammatory consequences of both converge on the brain.

Serotonin and the Gut

Approximately 95 percent of the body’s serotonin is produced in the gut. Chronic stress and a disrupted microbiome impair serotonin production at this site, contributing to the anxiety and low mood that perpetuate stress eating. While gut-derived serotonin does not cross the blood-brain barrier directly, it modulates vagal signalling and influences tryptophan availability for central serotonin synthesis (Yano et al., 2015, Cell).

Foods That Help Regulate Cortisol

Dietary intervention can target the stress eating cycle at its hormonal root. Several nutrients have evidence for modulating HPA axis activity, reducing cortisol, or buffering the brain against cortisol’s negative effects.

Omega-3 Fatty Acids

EPA and DHA, the long-chain omega-3 fatty acids found in fatty fish, have been shown to reduce cortisol reactivity to psychological stress. Delarue and colleagues (2003), in a study published in Diabetes & Metabolism, found that three weeks of fish oil supplementation (7.2 g per day of combined EPA and DHA) significantly attenuated cortisol and epinephrine responses to a standardised mental stress test. A more recent meta-analysis by Madison and colleagues (2021), published in Molecular Psychiatry, confirmed that omega-3 supplementation reduced both anxiety symptoms and cortisol levels, with stronger effects at higher doses.

Sources: salmon, sardines, mackerel, anchovies, herring. For those who do not eat fish, algal oil supplements provide DHA and some EPA.

Magnesium

Magnesium is directly involved in HPA axis regulation. It acts as a natural antagonist of the NMDA receptor, dampens excitatory neurotransmission, and modulates cortisol release. Subclinical magnesium deficiency — which is estimated to affect 50 to 80 percent of the population in Western countries (DiNicolantonio et al., 2018, Open Heart) — has been associated with exaggerated stress responses and elevated cortisol.

Boyle and colleagues (2017), in a randomised controlled trial published in Nutrients, found that magnesium supplementation (248 mg per day) significantly reduced subjective stress in adults with low magnesium status. The effect was particularly pronounced for individuals reporting high baseline stress.

Sources: pumpkin seeds, spinach, dark chocolate, almonds, avocado, black beans.

Vitamin C

Vitamin C is concentrated in the adrenal glands at levels 50 to 100 times higher than in the bloodstream, reflecting its critical role in cortisol synthesis and regulation. Paradoxically, high-dose vitamin C supplementation appears to dampen the cortisol response to stress. Peters and colleagues (2001), publishing in the Annals of the New York Academy of Sciences, showed that 1,500 mg per day of vitamin C reduced cortisol levels and subjective stress responses in marathon runners.

Brody and colleagues (2002), in a randomised controlled trial published in Psychopharmacology, found that high-dose vitamin C (3,000 mg per day) reduced blood pressure reactivity and subjective stress during a public speaking and mental arithmetic challenge, along with faster cortisol recovery.

Sources: bell peppers, kiwifruit, strawberries, broccoli, citrus fruits.

Complex Carbohydrates and Serotonin

Complex carbohydrates support serotonin synthesis through an insulin-mediated mechanism: carbohydrate consumption triggers insulin release, which drives competing amino acids (branched-chain amino acids) into muscle tissue, leaving a higher proportion of tryptophan available to cross the blood-brain barrier. Tryptophan is then converted to serotonin in the raphe nuclei.

This is the neurochemical basis for the calming effect of carbohydrate-rich foods — and it explains why people instinctively reach for starches and sweets when stressed. The key distinction is between complex carbohydrates (which produce a sustained, moderate serotonin-supporting effect) and refined sugars (which produce a spike-and-crash pattern that worsens mood and cravings).

Whole-food sources that support this pathway without blood sugar disruption include oats, sweet potatoes, brown rice, quinoa, and legumes. Pairing them with protein and healthy fat slows glucose absorption further.

Fermented Foods for Gut Resilience

Given the gut-brain axis disruption caused by chronic stress, actively supporting microbiome diversity is a legitimate stress-management strategy. Tillisch and colleagues (2013), in a study published in Gastroenterology, demonstrated that regular consumption of fermented dairy containing probiotics altered brain activity in regions governing emotion processing. Selhub and colleagues (2014), writing in the Journal of Physiological Anthropology, reviewed the evidence for fermented food consumption as a mediator between diet and mental health, noting that traditional diets high in fermented foods were consistently associated with lower rates of anxiety and depression.

Sources: yoghurt, kefir, sauerkraut, kimchi, miso, tempeh.

Breaking the Cycle: Practical Strategies

Understanding the neuroscience of stress eating is necessary but not sufficient. The biology must be met with practical strategies that interrupt the cycle at multiple points.

Mindful Eating

Mindful eating — the practice of attending to the sensory experience of food, eating without distraction, and pausing to assess hunger and satiety cues — directly targets the automatic, conditioned nature of stress eating. A randomised controlled trial by Daubenmier and colleagues (2016), published in Obesity, found that a mindful eating intervention significantly reduced cortisol levels, abdominal fat, and binge eating in overweight women compared to a waitlist control.

The practice does not require meditation experience. It can be as simple as: before eating, pause for 30 seconds and ask whether you are physically hungry or emotionally triggered. If the answer is emotional, acknowledge it without judgment, and decide whether eating is the most effective response available.

Proactive Meal Planning for High-Stress Periods

One of the most reliable predictors of stress eating is the absence of accessible, prepared whole food at the moment when cravings peak. Decision-making capacity is a finite resource that chronic stress depletes. When cortisol is elevated and the prefrontal cortex is fatigued, the path of least resistance determines behaviour.

Meal planning and preparation during low-stress periods removes the decision from the stress moment. Concrete tactics include: batch-cooking proteins and grains on weekends, keeping pre-washed vegetables and hummus in the refrigerator, stocking nuts, seeds, and dark chocolate as default snacks, and having frozen meals made from whole ingredients available as alternatives to ordering takeaway.

Stress Reduction as Dietary Intervention

Addressing cortisol directly — rather than only managing its downstream food cravings — is arguably the most effective intervention. Exercise is the most evidence-supported cortisol-lowering behaviour, with both acute and chronic effects on HPA axis regulation. A meta-analysis by Beserra and colleagues (2018), published in Frontiers in Physiology, found that regular aerobic exercise significantly reduced resting cortisol levels over time.

Even brief interventions have measurable effects. A study by Perciavalle and colleagues (2017), published in Neural Plasticity, demonstrated that 10 minutes of diaphragmatic breathing significantly reduced salivary cortisol in healthy adults. The vagal stimulation from deep breathing directly opposes sympathetic activation and HPA axis output.

Addressing Sleep

Sleep deprivation amplifies cortisol, intensifies cravings, and impairs the prefrontal cortical function needed to resist them. Spiegel and colleagues (1999), publishing in The Lancet, demonstrated that restricting sleep to four hours per night for six days increased evening cortisol by 37 percent and elevated glucose and insulin levels to pre-diabetic ranges. Prioritising sleep hygiene — consistent sleep and wake times, limiting screen exposure before bed, and avoiding calorie-dense food in the two hours before sleep — addresses the stress eating cycle at one of its most potent amplification points.

Practical Takeaway

  1. Recognise that stress eating is neurobiological, not moral. Cortisol-driven cravings are a predictable outcome of HPA axis activation in a food environment saturated with calorie-dense options. Understanding this removes shame and creates space for effective intervention.

  2. Front-load cortisol-regulating nutrients. Prioritise omega-3-rich fish two to three times per week, magnesium-rich foods daily (pumpkin seeds, spinach, dark chocolate, almonds), and vitamin C-rich produce at every meal. These nutrients directly modulate HPA axis output.

  3. Use complex carbohydrates strategically. When you feel the pull toward sugar or starch, choose oats, sweet potatoes, or legumes. They support serotonin synthesis through the same insulin-mediated mechanism as refined sugar, but without the crash-and-craving cycle.

  4. Prepare for stress before it arrives. Batch-cook meals during calm periods. Stock your environment with whole-food snacks. Remove ultra-processed food from immediate access. When cortisol is high, you will eat whatever is most available — make that default option a good one.

  5. Practise the 30-second pause. Before eating in response to a stressor, pause and identify whether the drive is physical hunger or emotional. This interruption — brief as it is — engages prefrontal cortex circuits that can modulate the automatic reward-seeking response.

  6. Support your gut microbiome. Include fermented foods daily (yoghurt, kefir, kimchi, sauerkraut) and high-fibre vegetables. Stress and stress-eating diets both deplete beneficial gut bacteria, and restoring them supports serotonin production and reduces neuroinflammation.

  7. Address cortisol directly through movement and breathing. Even 10 minutes of walking or diaphragmatic breathing can measurably reduce cortisol. Regular aerobic exercise recalibrates HPA axis sensitivity over time, reducing the magnitude of cortisol spikes in response to future stressors.

  8. Protect sleep as a metabolic priority. Sleep deprivation amplifies every component of the stress eating cycle. Consistent sleep timing and avoiding food within two hours of bed are among the highest-yield interventions available.

Frequently Asked Questions

Is stress eating the same as binge eating disorder?

No, though they can overlap. Stress eating refers to the cortisol-driven increase in appetite and preference for calorie-dense food that occurs during periods of psychological stress. It is a normal physiological response that becomes problematic when chronic. Binge eating disorder (BED) is a clinical diagnosis characterised by recurrent episodes of eating large quantities of food in a discrete period, accompanied by a sense of loss of control, distress, and the absence of compensatory behaviours (such as purging). While chronic stress is a common trigger for binge episodes in people with BED, most stress eaters do not meet the diagnostic criteria for the disorder. If stress eating feels compulsive, involves consuming objectively large amounts of food, and causes significant distress, clinical evaluation is warranted.

Can supplements replace dietary strategies for managing stress eating?

Supplements can address specific nutrient gaps — particularly magnesium, omega-3s, and vitamin D — but they cannot replicate the full spectrum of benefits provided by a whole-food dietary pattern. The anti-stress effects of diet operate through multiple concurrent mechanisms: blood sugar stabilisation, microbiome support, anti-inflammatory signalling, and serotonin precursor supply. No supplement stack addresses all of these simultaneously. Furthermore, supplements do not address the behavioural and environmental components of stress eating. They are best used to fill specific, identified deficiencies within the context of an overall dietary strategy.

How long does it take to break a stress eating habit?

The timeline depends on what is being changed. The acute neurochemical benefits of dietary improvement — better blood sugar regulation, reduced cortisol reactivity from omega-3 and magnesium intake — can begin within one to two weeks. Meaningful shifts in gut microbiome composition typically require four to eight weeks of sustained dietary change. The behavioural conditioning underlying stress eating — the automatic association between stress cues and food-seeking — generally takes longer to extinguish, on the order of two to three months of consistent practice with alternative responses. The key insight from habit research is that stress eating habits are not erased; they are overwritten by new, competing habits that must be practised consistently until they become the default.

Does exercise actually reduce stress eating, or does it just burn off the calories?

Exercise reduces stress eating through mechanisms that go far beyond caloric expenditure. It directly lowers cortisol levels (acutely and chronically), increases BDNF expression in the hippocampus, improves insulin sensitivity, and enhances prefrontal cortex function — all of which address root drivers of the stress eating cycle. Exercise also increases endocannabinoid and endorphin signalling, producing a natural mood boost that partially substitutes for the reward that comfort food provides. The evidence suggests that regular exercisers have lower cortisol reactivity to psychological stressors (Beserra et al., 2018), meaning they experience less intense cravings in the first place.

Are some people genetically predisposed to stress eating?

Yes. Genetic variation in the glucocorticoid receptor gene (NR3C1), the serotonin transporter gene (SLC6A4), and the dopamine D2 receptor gene (DRD2) all influence individual susceptibility to stress eating. Some people have HPA axes that produce more cortisol in response to the same stressor, reward systems that are more responsive to food cues, or serotonin systems that recover more slowly — all of which increase the probability of stress eating. However, genetic predisposition is not determinism. The dietary and behavioural strategies described in this article are effective precisely because they target the downstream mechanisms through which genetic vulnerability is expressed.

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