The human nutritional appetite is said to be a multi-factorial physiological and mental phenomenon that regulates hunger and satiety in response to biological cues (Thom, et al., 2020) to ensure adequate and sufficient metabolic and nutritional needs are met for an organism. Appetite is part of homeostasis, ensuring internal energy and vitamin and mineral dietary input balances that of energy output to keep a constant internal environment regardless of external changes. Stress is a bodily response to a threat (real or perceived) that triggers a complex physiological pathway that as Ans and team write in their 2018 literature review (Ans, et al., 2018) “challenges the body’s ability to maintain homeostasis.” There has been much debate about the effects of stress on appetite, with some evidence suggesting stress increases appetite (Geiker, et al., 2018), and some claiming it decreases appetite (Ans, et al., 2018). Recent research has highlighted how stress impacts mood, pleasure and mental health, gastric motility, key hormone levels, the gut microbiota, sleep, memory, the immune system, and motivation and plays an essential role in eating behaviour and food choice (Oliver, Wardle and Gibson, 2000) and thus appetite regulation (Geiker, et al., 2018). Based on recent evidence, it can be argued that stress both increases and decreases appetite, with the duration of the stressor playing the deciding factor (chronic stress increasing and acute stress decreasing appetite), as well as the individuals ability to leave “fight and flight” mode and return to homeostasis playing a crucial role (an individual in chronic stress can still get appetite inhibition if they have behavioural coping mechanisms to break the chronic period into lots of bursts of acute stress).
What is appetite?
The human appetite has been shown to be regulated by many factors including many complex neurotransmitter and hormonal pathways, kept within limits by the brain homeostatic master, the Hypothalamus which integrates the nervous and endocrine gut-brain systems and signals from the periphery (Ans, et al., 2018). Factors that are said to increase appetite are “orexigenic” signals and those that decrease appetite is “anorexic” signals. Fluctuations in Glucose, the key metabolic ingredient needed for energy, in the blood, are first detected by receptors in the liver, which send signals to the Lateral Hypothalamus (LH) and Paraventricular Nucleus (PVN) (Mangieri, et al., 2018). This is said to trigger the human hunger motivation to search and prepare for and eat food, as, like our cavemen evolutionary ancestor, we eat for energy. The Hypothalamus has also been found to secrete a neuropeptide called Neuropeptide Y (NPY) which is a strong hunger stimulant. An empty stomach is detected by gut distention receptors in the stomach which secrete Ghrelin hormone (Kirchner, Heppner and Tschöp, 2012) the hunger hormone (MacLean, et al., 2017). When Ghrelin increases, the Hypothalamus Arcuate Nucleus (AN) produces more Neuropeptide Y (NPY) and Proopiomelanocortin (POMC) and Cocaine- and Amphetamine-Regulated Transcript (CART) to stimulate feeding. When it is low it secretes Agouti-related peptide (AgRP) to decrease appetite, inhibiting feeding (Montegut, et al. 2021). Oxyntomodulin (OXM), inhibits Ghrelin secretion and suppresses appetite and stimulates Insulin release after carbohydrate intake. When we have consumed sufficient Glucose energy the brain Ventromedial Hypothalamus (VMH), recognizes the raised glycogen (stored glucose) in the liver and triggers satiety. Leptin is found to be released from adipose (fat) cells after food is consumed. Leptin is the satiety hormone, appetite suppressant which decreases Ghrelin, inhibits NPY and AgRP, stimulates POMC and CART and activates the VMH further and feeding stops. Adiponectin is released from adipose tissue, Pancreatic Peptide (PP) and Peptide YY (PYY) from the ilium, colon and rectum and Cholecystokinin (CCK) from (Ahima and Antwi, 2021) the duodenum and jejunum which co-contribute to the inhibition of feeding and energy intake. Low blood sugar has been found to lead to the secretion of Insulin from the pancreas and high blood sugar leads to the secretion of Insulin hormone. Insulin signals the liver and muscle and fat cells to take in Glucose from the blood, decreasing blood sugar (Diabetes.co.uk, 2021). It is said to be supported by Amylin, Gastric-like-peptide 1 (GLP-1) and Gastric-inhibitory-peptide (GIP) in glucose level dependent Insulin secretion causing anti-diabetic effects. Insulin is another powerful hormonal switch for appetite (Austin and Marks, 2009), inhibiting feeding at the VTA and reducing the rewarding Dopaminergic neurotransmitter response to food.
Stress states have been found to impact key metabolic needs regulated by hormones and neuropeptide and impact our mood, desire for hedonic addictive substances, impulsivity, and our food choices, and thus vastly impact appetite. Stress thus plays an essential role in malnutrition and maladaptive eating disorders from anorexia to obesity and so inhibition of chronic stress or short-term activation of the stress response, could be a novel therapy in the treatment of this (primarily western world) malnutrition (Ans, et al., 2018).
The Stress Response
A stressor (a stressful experience or even something simple which stresses the body like exercise or infection), causes physical and emotional changes which can take a person out of homeostasis. The adaptive stress response attempts to feedback and re-establish homeostasis, essential for innate survival. Some stress is necessary. We rely on Cortisol, Adrenaline, and Insulin from the stress response for our biological rhythms, to get us up in the morning and motivate us to hunt, gather, eat, mate, reproduce and work etcetera. However, as Chika Nakamura and team (Nakamura, et al., 2020) write in their 2020 paper investigating the effects in the brain of stress on appetite “an excessive and/ or prolonged stress response can lead to behavioural and somatic pathological conditions” including “changes in diet and appetite” (Xie, et al., 2021). The acute biological stress mechanism has been shown to focus on the flight, fright or freeze mechanism involving the HPA axis with the Hypothalamus, Pituitary and Adrenal glands and the key catecholamine neurotransmitters and hormones Cortisol and Adrenaline as well as many other factors (Herman, et al., 2020). In response to stressor stimuli (real or perceived), human bodies respond in a similar way to our caveman ancestor brains in response to a tiger, we prepare to either fight the threat, run from the threat or hide from the threat. This mechanism involves the detection of stimuli by receptors, processing the threat in the brain Prefrontal Cortex (PFC) and limbic system, primarily Amygdala and Hippocampus, based on memories and previous experiences and learnings and innate survival cues. This has been found to initiate a signal transduction pathway leading to the brain Hypothalamus secreting CRH (Corticotrophin Releasing Hormone), which (You and Your Hormones, 2021) signals the pituitary gland to secrete Adrenocorticotrophic Hormone (ATCH), in turn leading to the secretion of Cortisol from the Adrenal glands. Adrenaline increases via activation of the sympathetic branch of the (SMS) autonomic nervous system (MacLean, et al., 2018). Cortisol turns off all non-essential biological mechanisms, including the immune system and inhibits the production of many key hormones (Ranabir and Reetu, 2011), to focus on defense from threat and works with Adrenaline to prepare us for instant activity, together widening our pupils so we can see the threat better, making us more alert with increased blood flow to the muscles and therefore increasing respiration and energy production rate and taking (Lewis, 2016) blood flow away from the digestive system (Yaribeygi, et al., 2017).
As a result of the acute stress response, studies show that the heart and breathing rate and blood pressure increase and energy levels increase (and so are more active and have more energy to exercise more) and experience sleep disturbances (and subsequent fatigue), impaired concentration and restlessness, tight muscles (and subsequent aches and pains as muscles fatigue), get ill more easily, gastrointestinal disturbances, amenorrhea and reduced libido, mood changes and decreased appetite. Research by Stengel and Tache show that the acute stress response effects appetite as it effects the gastrointestinal tract via its effects on gastric emptying, fluid secretion and colonic motility (Stengel and Tache, 2009) which can cause nausea, diarrhea or constipation and abdominal pain. Blood flow is diverted from the gastrointestinal tract to the muscles and digestion is slowed, increasing the sense of satiety. Thus, there is much evidence to support the idea that short-term acute stress can decrease appetite and induce weight loss. As Armghan Ans and team write in their 2018 appetite and stress review, “a general assumption can be made that acute or repeated restraint stress results in decreased food intake resulting in stress-induced anorexia,” (Ans, et al., 2018). This weight loss can cause terrible consequences in the elderly and sick and can induce pro-anorexic pathways, causing terrible effects on the heart, kidneys, bones and immune system.
On the other hand, if the stress is prolonged over a chronic period, it has been found to create an energy deficit, suppressing key appetite satiety signals and inducing appetite, playing a role in nutritional surplus in conditions such as obesity. Acute stress (or chronic stress broken into acute stress chunks by effective stress management techniques), stimulates Insulin secretion from the pancreas which has an appetite suppressant effect. However, chronically activated glucocorticoids can trigger Insulin resistance, (Ranabir and Reetu, 2021) which may result in chronic stress-induced high blood sugar (hyperglycemia), (Sominsky and Spencer, 2014), increased energy and activity, insomnia and then an energy low and fatigue.
The sleep disturbances caused by stress are hugely important for appetite. A lack of sleep can increase Ghrelin hormone secretion (Abizaid, 2019) and cause Leptin resistance, making it harder to recognize the sensation of satiety (Berger and Polotsky, 2018). This sleep loss is fine if short term, with sleep compensation once the stressor has passed, but if chronic can hugely affect homeostasis and appetite. As sleep (Russell and Lightman, 2019) is needed for memory storage, impulse control and mood regulation (with insomnia said to contribute to mood disorders from anxiety to depression), a lack of sleep contributes to poor impulse control and mood. It also suppresses the immune system and if prolonged over a long period of time, absence of sleep is detected by the brain as a threat to homeostasis, and so can trigger a stress response itself. Chronic stress can cause insomnia and trigger a stress feedback loop, further increasing the lack of sleep and potentially increasing appetite.
The suppression of the immune system if prolonged has also been found to increase susceptibility to disease, causing immunosuppression (Dhabhar, 2009). When suffering from an illness, the bodies energy is prioritized to fight the infection and so can become easily fatigued and suffer low mood and reduced appetite (as like with stress, energy is focused away from the digestive system and so gastric motility slows) which can also cause energy deficits. Thus, chronic stress, via its effects on the immune system, can also indirectly increase appetite for more orexigenic foods.
Other factors to consider
Stress has also been suggested to affect appetite because of its inhibitory affect on the production of the gonadotrophins and gonadal steroid hormones (Whirledge and Cidlowski, 2010). Under normal homeostatic conditions, the Hypothalamus has been shown to secrete GnRH (Gonadotropin-Releasing Hormone) which leads to the secretion of LH and FSH from the pituitary gland. In the testes the LH leads to testosterone release. In the ovary, the FSH triggers the release of the follicle and Oestrogen production whilst LH helps control the egg maturation and release. In stress, for, as Whirledge and Cidlowski write, the “preservation of self” (to focus on defensive protection from stressor the same way our caveman ancestors defended against threat), the body inhibits reproductive behaviour ((Whirledge and Cidlowski, 2010). This can cause hypogonadotropic hypogonadism with decreased Oestrogen and Testosterone production, amenorrhea, impotence, poor libido, and infertility. This is often also seen in female-athletes triad where extreme sports and low body fat to muscle ratio, reduces oestrogen and progesterone inhibits menstruation and in male bodybuilders where the increased muscle and low body fat ratio reduces Testosterone secretion, taking people out of homeostasis and inducing a body stress response. As Oestrogen and Testosterone are said to play a role in appetite, energy expenditure, sleep and mood regulation, prolonged absence of these key hormones affect appetite (Robinson, Dinulescu and Cone, 2000). Oestrogen has been found to decrease appetite, seen acutely with fluctuations in appetite throughout the menstrual cycle. The reduced Oestrogen on day 28 of the menstrual cycle (if the egg has not been fertilised in intercourse and the lining and egg are shed) in menstruation has been found to cause an increased appetite and conversely the Oestrogen peak for ovulation on day 10 to 17 of the cycle is said to decreased appetite. Also, women in menopause often gain weight due to decreased Oestrogen levels. Thus, it has been shown that dysregulated Oestrogen in stress can cause anxiety, poor stress tolerance (Hirschberg, 2012) and increased appetite(Dragano, Milbank and López, 2020), creating stress negative feedback loops where stress reduces hormone levels and low hormone levels increase stress, linking to chronic anxiety.
Stress also causes dysbiosis of the gut microbiota, a phenomenon extensively analyzed in recent years. The gut-microflora, the layer of non-pathogenic microorganisms which line and protect the GI tract, help boost the immune system, produce B and K vitamins (which boost energy metabolism, vitality, and mood) and produce Serotonin, Dopamine, Noradrenaline and GABA neurotransmitters, playing a vital role in mood (the so-called Gut-Brain-axis), decision making, impulse control and stress modulation. The microbiota and the gut and brain exchange information via the Vagus Nerve (VN) and autonomic nervous system. Stress causes dysbiosis where it inhibits the VN (Bonaz, Bazin and Pellisier, 2018) and so reduces the gastrointestinal tract microbiota diversity. Stressors increase the permeability of the gut membrane which can impair the function of the intestinal barrier and permit substances to gain access to brain areas that regulate cognition and emotional responses such as those linked closely to the regulation of mood impacting neurotransmitters such as Serotonin and Dopamine (Yarandi, et al., 2016). Overall, it has been suggested that a healthy flora helps promote satiety, via its illness preventing, vitality promoting, mood stabilising effects, and therefore both acute and chronic stress have been reported to increase appetite via disruption of this key flora balance (Heijnen, et al., 2016).
Exercise also plays a role in appetite, as it potentiates satiety signals. There is a delicate balance with exercise, between exercising enough that you induce Ghrelin and suppress appetite, and not exercising too much that you increase physical fatigue and decrease blood sugar sufficiently that causes compensatory increased appetite induced food consumption. Stress, both long and short term, affect our ability and motivation to exercise and therefore impacts our appetite.
Low blood sugar, illness, chronic sleeplessness, and chronic stress also affect Serotonin, Oxytocin and Dopamine neurotransmitters and our emotional state. As Serotonin and Dopamine regulate mood, emotions and appetite (Ikemoto and Panksepp, 1999), reinforcing pleasure from food and contributing to behavioural, psychological, mood and feeling, hedonic craving induced feeding and reward-mediated memory-driven repeated consumption when the levels of these key neurohormones and neurotransmitters are disturbed and out of homeostasis, it can further dysregulate appetite. It has been suggested low Serotonin (Miller, 2019) and low Dopamine increases appetite (Romer et al., 2019) (and so potentially high Serotonin and high Dopamine could decrease appetite). Energy deficit (often seen in dieting behaviour) can trigger the brain to respond by increasing appetite for more high glycemic index foods, such as high carbohydrate foods, and can cause low moods which can cause a Dopamine deficit which can increase the desire for more hedonic (pleasure-inducing) high sugar and fat foods and drinks which increase Dopamine and the reward and pleasure response (MacLean, et al. 2018). This can lead to binge eating and overeating to fill this Dopamine deficit.
Food choices also impact appetite with different environmental (the food and nutrient availability around you and ability to access financially or home grow), biological and psychological states found to affect food choices and different food choices affecting appetite. High carbohydrate, high sugar diets have been suggested to increase appetite by increasing blood sugar, stimulating Insulin which converts Glucose to Glycogen causing low blood sugar, increasing energy need and craving (Chandler-Laney et al., 2014). Specifically, research from Parvaresh Rizi and team found a low dietary fat and protein, but high carbohydrate (Santos-Hernandez, et al. 2018) meal increases post-meal Ghrelin, GLP;1 and PYY, increasing appetite (Parvaresh Rizi, et al., 2018). High protein diets have also themselves been found to directly decrease Ghrelin, induce CCK and GLP-1 and induce satiation. High fat (Beglinger and Degen, 2004) diets have been suggested to reduce food craving via induction of CCK which suppresses appetite (Little, Horowitz and Feinle-Bisset). High Fibre diets also are said to increase satiation (Barber, et al., 2020) and increase the gut microbiota also. High carbohydrate but high fibre foods, such as bananas, apples, whole grains, blackberries, potatoes, rice, wholewheat pasta and more (Dhingra, et al., 2012), additionally may help reduce blood sugar spikes and falls, and maintain constant blood sugar (maintaining energy balance), to control blood sugar and keep mood and appetite stable (Barber, et al., 2020). As stress affects the rationality of our Pre-Frontal Cortex decision making ability and shifts us to becoming less logical (Armsten, et al. 2009), more Amygdala emotion driven caveman “survivor mode,” it therefore affects our food decisions, emotions and mood and appetite.
Food for thought?
Other things to think about with stress and appetite behaviour is individuality and learned experience. Some people have learned coping mechanisms (often from parents, upbringing, learned experiences) which help them to bring their brains out of chronic flight and flight mode. An individual in this state may experience long-term chronic stress as lots of prolonged periods of acute stress, thus inhibiting appetite for a sustained time. Therefore, our ability to cope with stress and shift our “flight and fight” sympathetic response to “rest and digest” parasympathetic nervous system may also impact our stress response and appetite.
Genetics also play a role in appetite, though less than previously thought. (Ans, et al. 2018). Additionally, self-awareness of states that affect appetite, from illness to tiredness, thirst (often people can confuse physical hunger (McKiernan, Houchins, J, and Mattes, 2008) and thirst and inadequate hydration can induce appetite), menstruation, alcohol, knowledge and availability of healthier food choices, emotional states and so on, also affects our response to appetite. A food “meal plan” routine, with meals and snacks at certain times each day regardless of external factors and cues, helps regulate our innate internal appetite rhythms with Insulin and blood sugar and energy levels and our sleep patterns, and maintain a sustained energy balance (with no surplus or deficit or homeostatic feedback loops) and keep a constant homeostatic appetite regardless of external or internal stressors.
The effect of stress on appetite is far from a linear relationship. There are many individual biopsychosocial factors to consider, all of which conspire together to contribute to human nutritional appetite. What is clear, however, that stress takes us out of homeostasis and inhibits the ability to regulate key hormones, neurotransmitters and neuropeptides, and therefore the forefront of any nutritional and appetite linked disorder or disease treatment should be the restoration of this key homeostasis.
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