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Effects of Emotional and Stress Eating on Obesity | by Don Karl Juravin

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Don Juravin at Original Bible Foundation - code2GOD
Don Juravin
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Rouzbeh Motiei-Langroudi
Rouzbeh Motiei-Langroudi
Rouzbeh Motiei-Langroudi
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Waqar Ahmad at The University of Agriculture, Peshawar
Waqar Ahmad
Kelly
Kelly
Kelly
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The world's most comprehensive research about:
Effects of Emotional And Stress Eating
On Obesity
Authors: Don Karl Juravin, Marcus Free MD,
Rouzbeh Motiei-Langroudi MD, Waqar Ahmad,
Kelly Daly
Abstract (research summary)
1. The mechanism in which stress causes overeating is a combination of behavioral
changes in appetite, surges in cortisol and decreases in serotonin stimulating the
brain reward system and resulting in suppressed insulin and increased ghrelin.
This potent combination of hormonal and chemical changes result in the
uncontrollable urge for unhealthy foods when stressed and/or emotional.
2. Stress results in uncontrolled and emotional eating and is associated with
increased consumption of highly palatable foods (Groesz 2012, Oliver 1999),
finally resulting in weight gain (Järvelä-Reijonen 2016).
3. Acute stress leads to consumption of an additional 151 calories per day (Torres
2007), leading to weight gain of up to 330g per week, or 17 kg (37 lbs) per year.
4. Stress stimulates hypothalamic-pituitary-adrenal (HPA) axis, resulting in excess
glucocorticoids (Adam 2007), increased appetite, gluconeogenesis, hyperphagia
and food intake (Gluck 2006).
5. HPA axis stimulation interacts with brain reward pathways to motivate intake of
high calorie food through release of opioids in stressful conditions (Adam 2007).
6. Stress suppresses insulin secretion (Peters 2010) and increases ghrelin levels
(Labarthe 2014) resulting in increased food consumption.
7. Decreased serotonin levels induce stress and stress eating (Capello 2014,
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Markus 2012, Corwin 2011).
8. Green Camellia Sinensis (200mg to 500mg daily) reduces stress eating (Mirza
2013).
9. Ashwagandha root extract (300mg twice daily) reduces stress and stress eating
(Choudhary 2016).
10.Tryptophan reduces stress-induced increase in appetite and stress eating
(Capello 2014, Amer 2004).
Definition
Stress is a condition in which “environmental demands exceed the adaptive capacity
of an organism, resulting in psychological and biological changes which may
increase risk for disease” (Cohen 1997).
Emotional And Stress Eating Related to Obesity
Stress causes emotional and uncontrolled eating and increases food
cravings, resulting in higher intake of sugar and fat leading to
consumption of an additional 151 calories per day. This results in weight
gain of up to 17kg (37 lbs) per year.
● Acute and chronic stress is associated with greater preference for foods rich in
sugar and fat, resulting in weight gain. Acute stress leads to consumption of an
additional 151 calories per day (Torres 2007), leading to weight gain of up to
330g per week, or 17 kg (37 lbs) per year.
● Stress related eating (aka emotional eating, stress eating) causes obesity
(Järvelä-Reijonen 2016).
● Stress results in uncontrolled eating, emotional eating and decreased cognitive
restraint to eating, finally resulting in weight gain (Järvelä-Reijonen 2016).
● Chronic stress is associated with more uncontrolled and emotional eating
(Groesz 2012, Nevanperä 2012), resulting in intake of unhealthy dietary, highly
palatable and high-fat foods and a higher BMI (Konttinen 2010, Nevanperä 2012,
Groesz 2012, Oliver 1999, Barrington 2014).
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● The rewarding aspects of food consumption are regulated by brain circuits.
Stress also contributes substantially to the expression of food reward behaviors
such as cravings for preferred foods resulting in overeating and obesity
(Figlewicz 2015).
● Consumption of sugar increases the activity in brain reward regions and reduces
stress-induced rises in cortisol. Thus, people under stress consume more sugar
to reduce their stress (Tryon 2015).
Emotional And Stress Eating Obesity Mechanism
The mechanism in which stress causes overeating is a combination of
behavioral changes in appetite, surges in cortisol and decreases in
serotonin stimulating the brain reward system and resulting in
suppressed insulin and increased ghrelin. This potent combination of
hormonal and chemical changes result in the uncontrollable urge for
unhealthy foods when stressed and/or emotional.
Emotional and stress eating related to behavioral changes
Stress adaptively changes eating behavior as it increases appetite and
high calorie food intake.
● Adaptation responses to stress change behaviors, including eating behavior,
leading to increased food intake resulting in weight gain (Wardle 2011, Byrne
2002).
● Stress decreases appetite control and increases food intake, emotional eating,
and sedentary behavior, all of which result in weight gain and obesity (Diggins
2015).
Emotional and stress eating anatomical and physiological
aspects
Stress puts the body in a ‘fight or flight’ state, surging cortisol and
increasing bodily needs for high calorie foods. Through interaction with
the brain reward system, stress also causes cravings and emotional
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eating. Stress also decreases serotonin, increases ghrelin and
decreases insulin levels resulting in increased food consumption.
Emotional and stress eating related to increase in cortisol
● Stress stimulates hypothalamic-pituitary-adrenal (HPA) axis, resulting in excess
glucocorticoids which causes obesity (Adam 2007).
● Stress causes an exaggerated cortisol response which leads to uncontrolled
eating (Radin 2016).
● Stress causes elevations in serum cortisol and exaggerated cortisol response,
which increases appetite, gluconeogenesis, hyperphagia and food and fat intake,
finally resulting in weight gain and obesity (Gluck 2006).
Emotional and stress eating related to decrease in serotonin
● Decreased serotonin levels induces stress and changes its related eating
behavior, causing overeating (Capello 2014, Markus 2012, Corwin 2011).
Emotional and stress eating related to opioid system
● HPA axis stimulation interacts with brain reward pathways to motivate intake of
high calorie food, through release of opioids in stressful conditions. This both
decreases stress and stimulates reward pathways, resulting in overeating (Adam
2007).
● Stress increases eating through opioid-mediated increases in cortisol, causing
greater food addiction symptoms and reward-driven eating (Mason 2015).
Emotional and stress eating related to insulin suppression
● Under stressful conditions, the brain suppresses insulin secretion to satisfy its
excessive energy needs during stress, finally resulting in overeating and weight
gain (Peters 2010).
Emotional and stress eating related to increase in ghrelin
● Stress increases ghrelin (hunger hormone) levels, causing overeating and weight
gain (Labarthe 2014).
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Emotional And Stress Eating Related Obesity
Treatment
The mainstem of treatment for stress eating is behavioral therapy,
anti-anxiety and antidepressant drugs, as well as other medications
including Green Camellia Sinensis, tryptophan and Ashwagandha root
extract.
● Green Camellia Sinensis (green tea extract) (200mg to 500mg daily) reduces
stress eating and promotes weight loss through exerting anti-anxiety effects
(Mirza 2013).
● Ashwagandha root extract (300mg twice daily) reduces stress, stress eating and
its related weight gain (Choudhary 2016).
● Tryptophan reduces stress-induced cortisol levels and prevents stress-induced
increase in appetite and stress eating (Capello 2014, Amer 2004).
● Behavioural methods (e.g. Cognitive Behavioral Therapy (CBT), behavioral
therapy and relaxation) help to decrease stress and related stress eating
(Christaki 2013, Amianto 2015).
● Pharmacological treatment of stress with anxiolytic (anxiety-reducing) and
antidepressant drugs helps in stress management and decreases stress eating
(Christaki 2013). Among antidepressants, the most effective group is selective
serotonin reuptake inhibitors (e.g. fluoxetine, sertraline and fluvoxamine)
(Amianto 2015).
● Glutamate-modulating agents like Gabapentin reduce binge and stress eating
and as a result cause weight loss (Amianto 2015).
● Acamprosate, a drug used in alcohol dependence, is associated with
improvements on binge eating and food cravings caused by stress (Amianto
2015).
References
1. Adam, T., Epel, E. (2007). Stress, eating and the reward system. Physiology and Behavior
[online], 91 (4), pp. 449-58. Available from: http://www.ncbi.nlm.nih.gov/pubmed/17543357
[Accessed 19.06.2016].
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2. Amer, A., Breu, J., McDermott, J. (2004). 5-Hydroxy-L-tryptophan suppresses food intake in
food-deprived and stressed rats. Pharmacology Biochemistry and Behavior
[online], 77 (1), pp.
137-43. Available from: http://www.ncbi.nlm.nih.gov/pubmed/14724051 [Accessed 22.06.2016].
3. Amianto, F., Ottone, L., Abbate Daga, G., et al. (2015). Binge-eating disorder diagnosis and
treatment: a recap in front of DSM-5. BMC Psychiatry
[online], 15, pp. 70. Available from:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4397811/ [Accessed 20.06.2016].
4. Barrington, W., Beresford, S., McGregor, B., et al. (2014). Perceived stress and eating behaviors
by sex, obesity status, and stress vulnerability: findings from the vitamins and lifestyle (VITAL)
study. Journal of the Academy of Nutrition and Dietetics
[online], 114 (11), pp. 1791-9. Available
from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4229482/ [Accessed 17.06.2016].
5. Byrne, S. (2002). Psychological aspects of weight maintenance and relapse in obesity.
Journal of Psychosomatic Research
[online], 53 (5), pp. 1029-36. Available from:
http://www.ncbi.nlm.nih.gov/pubmed/12445592 [Accessed 17.06.2016].
6. Capello, A., Markus, C. (2014). Effect of sub chronic tryptophan supplementation on
stress-induced cortisol and appetite in subjects differing in 5-HTTLPR genotype and trait
neuroticism. Psychoneuroendocrinology
[online], 45, pp. 96-107. Available
from:http://www.ncbi.nlm.nih.gov/pubmed/24845181 [Accessed 22.06.2016].
7. Choudhary, D., Bhattacharyya, S., Joshi, K. (2016). Body weight management in adults under
chronic stress through treatment with Ashwagandha root extract: A double-blind, randomized,
placebo-controlled trial. Journal Of Evidence Based Complementary Alternative Medicine
[online],
not published yet. Available from: http://www.ncbi.nlm.nih.gov/pubmed/27055824 [Accessed
20.06.2016].
8. Christaki, E., Kokkinos, A., Costarelli, V., et al. (2013). Stress management can facilitate weight
loss in Greek overweight and obese women: a pilot study. Journal of Human Nutrition and
Dietetics
[online], 26, pp. 132-9. Available from: http://www.ncbi.nlm.nih.gov/pubmed/23627835
[Accessed 20.06.2016].
9. Cohen, S., Kessler, R., Gordon, U. (1997). Strategies for measuring stress in studies of
psychiatric and physical disorders. In: Measuring stress: A guide for health and social scientists,
Oxford University Press
[online], pp. 3-26. Available from:
https://global.oup.com/academic/product/measuring-stress-9780195121209?cc=us&lang=en&
[Accessed 17.06.2016].
10. Corwin, R., Avena, N., Boggiano, M. (2011). Feeding and reward: perspectives from three rat
models of binge eating. Physiology and Behavior
[online], 104 (1), pp. 87-97. Available from:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3132131/ [Accessed 22.06.2016].
11. Diggins, A., Woods-Giscombe, C., Waters, S. (2015). The association of perceived stress,
contextualized stress, and emotional eating with body mass index in college-aged Black women.
Eating Behavior
[online], 19, pp. 188-92. Available from:
http://www.ncbi.nlm.nih.gov/pubmed/26496005 [Accessed 19.06.2016].
12. Figlewicz, D. (2015). Modulation of Food Reward by Endocrine and Environmental Factors:
Update and Perspective. Psychosomatic Medicine
[online], 77 (6), pp. 664-70. Available from:
http://www.ncbi.nlm.nih.gov/pubmed/25738439 [Accessed 19.06.2016].
13. Gluck, M. (2006). Stress response and binge eating disorder. Appetite
[online], 46 (1), pp. 26-30.
Available from: http://www.ncbi.nlm.nih.gov/pubmed/16260065 [Accessed 19.06.2016].
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14. Groesz, L., McCoy, S., Carl, J., et al. (2012). What is eating you? Stress and the drive to eat,
Appetite
[online], 58 (2), pp. 717-21. Available from:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3740553/ [Accessed 17.06.2016].
15. Järvelä-Reijonen, E., Karhunen, L., Sairanen, E., et al. (2016). High perceived stress is
associated with unfavorable eating behavior in overweight and obese Finns of working age.
Appetite
[online], 103, pp. 249-58. Available from: http://www.ncbi.nlm.nih.gov/pubmed/27108837
[Accessed 17.06.2016].
16. Konttinen, H., Männistö, S., Sarlio-Lähteenkorva, S., et al. (2010). Emotional eating, depressive
symptoms and self-reported food consumption. A population-based study. Appetite
[online], 54
(3), pp. 473-9. Available from: https://www.ncbi.nlm.nih.gov/pubmed/20138944 [Accessed
17.06.2016].
17. Labarthe, A., Fiquet, O., Hassouna, R., et al. (2014). Ghrelin-Derived Peptides: A Link between
Appetite/Reward, GH Axis, and Psychiatric Disorders? Frontiers in Endocrinology (Lausanne)
[online], 5, pp. 163. Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4209873/
[Accessed 19.06.2016].
18. Markus, C., Verschoor, E., Smeets, T. (2012). Differential effect of the 5-HTT gene-linked
polymorphic region on emotional eating during stress exposure following tryptophan challenge.
Journal of Nutrition and Biochemistry
[online], 23 (4), pp. 410-6. Available from:
http://www.ncbi.nlm.nih.gov/pubmed/21658929 [Accessed 22.06.2016].
19. Mason, A., Lustig, R., Brown, R., et al. (2015). Acute responses to opioidergic blockade as a
biomarker of hedonic eating among obese women enrolled in a mindfulness-based weight loss
intervention trial. Appetite
[online], 91, pp. 311-20. Available from:
http://www.ncbi.nlm.nih.gov/pubmed/25931433 [Accessed 19.06.2016].
20. Mirza, B., Ikram, H., Bilgrami, S., et al. (2013). Neurochemical and behavioral effects of green tea
(Camellia sinensis): a model study. PakIstanian Journal of Pharmacological Sciences
[online], 26
(3), pp. 511-6. Available from: http://www.ncbi.nlm.nih.gov/pubmed/23625424 [Accessed
20.06.2016].
21. Nevanperä, N., Hopsu, L., Kuosma, E. (2012). Occupational burnout, eating behavior, and weight
among working women. The American Journal of Clinical Nutrition
[online], 95 (4), pp. 934-43.
Available from: http://ajcn.nutrition.org/content/95/4/934.long [Accessed 17.06.2016].
22. Oliver, G., Wardle, J. (1999). Perceived effects of stress on food choice. Physiology and Behavior
[online], 66 (3), pp. 511-515. Available from: http://www.ncbi.nlm.nih.gov/pubmed/10357442
[Accessed 17.06.2016].
23. Peters, A. (2011). The selfish brain: Competition for energy resources. American Journal of
Human Biology
[online], 23 (1), pp. 29-34. Available from:
http://www.ncbi.nlm.nih.gov/pubmed/21080380 [Accessed 19.06.2016].
24. Radin, R., Shomaker, L., Kelly, N., et al. (2016). Cortisol response to an induction of negative
affect among adolescents with and without loss of control eating. PediatrIc Obesity
[online], not
published yet. Available from: http://www.ncbi.nlm.nih.gov/pubmed/26667312 [Accessed
19.06.2016].
25. Torres, S., Nowson, C. (2007). Relationship between stress, eating behavior, and obesity.
Nutrition
[online], 23 (11-12), pp. 887-94. Available from:
http://www.ncbi.nlm.nih.gov/pubmed/17869482 [Accessed 19.06.2016].
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26. Tryon, M., Stanhope, K., Epel, E., et al. (2015). Excessive Sugar Consumption May Be a Difficult
Habit to Break: A View From the Brain and Body. Journal of Clinical Endocrinology and
Metabolism
[online], 100 (6), pp. 2239-47. Available from:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4454811/ [Accessed 19.06.2016].
27. Wardle, J., Steptoe, A., Oliver, G. Et al. (2000). Stress, dietary restraint and food intake. Journal
of Psychosomatic Research
[online], 48 (2), pp. 195–202. Available from:
https://www.ncbi.nlm.nih.gov/pubmed/10719137 [Accessed 17.06.2016].
Footnote
This research was sponsored by Don Karl Juravin and Must Cure Obesity Co. Florida,
2,000.
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Points For The Public:
1. The mechanism in which stress causes overeating is a combination of behavioral
changes in appetite, surges in cortisol and decreases in serotonin stimulating the
brain reward system and resulting in suppressed insulin and increased ghrelin.
This potent combination of hormonal and chemical changes result in the
uncontrollable urge for unhealthy foods when stressed or emotional
2. Stress results in uncontrolled eating and is associated with increased
consumption of highly palatable foods
3. Acute stress leads to consumption of an additional 151 calories per day, leading
to weight gain of up to 330g per week, or 17 kg (37 lbs) per year
4. Green Camellia Sinensis (200mg to 500mg daily) reduces stress eating
5. Ashwagandha root extract (300mg twice daily) reduces stress and stress eating
6. Tryptophan reduces stress-induced increase in appetite and stress eating

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Body Weight Management in Adults Under Chronic Stress Through Treatment With Ashwagandha Root Extract: A Double-Blind, Randomized, Placebo-Controlled Trial
Article
Full-text available
  • Jan 2017
  • Compl Health Pract Rev
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Binge-eating disorder diagnosis and treatment: A recap in front of DSM-5
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Excessive Sugar Consumption May Be a Difficult Habit to Break: A View From the Brain and Body
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Sugar overconsumption and chronic stress are growing health concerns because they both may increase the risk for obesity and its related diseases. Rodent studies suggest that sugar consumption may activate a glucocorticoid-metabolic-brain-negative feedback pathway, which may turn off the stress response and thereby reinforce habitual sugar overconsumption. The objective of the study was to test our hypothesized glucocorticoid-metabolic-brain model in women consuming beverages sweetened with either aspartame of sucrose. This was a parallel-arm, double-masked diet intervention study. The study was conducted at the University of California, Davis, Clinical and Translational Science Center's Clinical Research Center and the University of California, Davis, Medical Center Imaging Research Center. Nineteen women (age range 18-40 y) with a body mass index (range 20-34 kg/m(2)) who were a subgroup from a National Institutes of Health-funded investigation of 188 participants assigned to eight experimental groups. The intervention consisted of sucrose- or aspartame-sweetened beverage consumption three times per day for 2 weeks. Salivary cortisol and regional brain responses to the Montreal Imaging Stress Task were measured. Compared with aspartame, sucrose consumption was associated with significantly higher activity in the left hippocampus (P = .001). Sucrose, but not aspartame, consumption associated with reduced (P = .024) stress-induced cortisol. The sucrose group also had a lower reactivity to naltrexone, significantly (P = .041) lower nausea, and a trend (P = .080) toward lower cortisol. These experimental findings support a metabolic-brain-negative feedback pathway that is affected by sugar and may make some people under stress more hooked on sugar and possibly more vulnerable to obesity and its related conditions.
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The association of perceived stress, C006Fntextualized stress, and emotional eating with body mass index in college-aged black women
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A growing body of literature supports the association between adverse stress experiences and health inequities, including obesity, among African American/Black women. Adverse stress experiences can contribute to poor appetite regulation, increased food intake, emotional eating, binge eating, and sedentary behavior, all of which can contribute to weight gain and obesity. Most research studies concerning the effect of psychological stress on eating behaviors have not examined the unique stress experience, body composition, and eating behaviors of African American/Black women. Even fewer studies have examined these constructs among Black female college students, who have an increased prevalence of overweight and obesity compared to their counterparts. Therefore, the aim of the current study is to examine the associations among emotional eating, perceived stress, contextualized stress, and BMI in African American female college students. All participants identified as African American or Black (N=99). The mean age of the sample was 19.4years (SD=1.80). A statistically significant eating behavior patterns×perceived stress interaction was evident for body mass index (BMI) (β=0.036, S.E.=.0118, p<.01). In addition, a statistically significant eating behavior patterns×contextualized stress interaction was observed for BMI (β=0.007, S.E.=.0027, p=.015). Findings from this study demonstrate that the stress experience interacts with emotional eating to influence BMI. Based on these findings, culturally relevant interventions that target the unique stress experience and eating behavior patterns of young African American women are warranted.
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  • Apr 2015
  • APPETITE
There are currently no commonly used or easily accessible 'biomarkers' of hedonic eating. Physiologic responses to acute opioidergic blockade, indexed by cortisol changes and nausea, may represent indirect functional measures of opioid-mediated hedonic eating drive and predict weight loss following a mindfulness-based intervention for stress eating. In the current study, we tested whether cortisol and nausea responses induced by oral ingestion of an opioidergic antagonist (naltrexone) correlated with weight and self-report measures of hedonic eating and predicted changes in these measures following a mindfulness-based weight loss intervention. Obese women (N=88; age=46.7±13.2 years; BMI=35.8±3.8) elected to complete an optional sub-study prior to a 5.5-month weight loss intervention with or without mindfulness training. On two separate days, participants ingested naltrexone and placebo pills, collected saliva samples, and reported nausea levels. Supporting previous findings, naltrexone-induced cortisol increases were associated with greater hedonic eating (greater food addiction symptoms and reward-driven eating) and less mindful eating. Among participants with larger cortisol increases (+1 SD above mean), mindfulness participants (relative to control participants) reported greater reductions in food addiction symptoms, b=-0.95, SE(b)=0.40, 95% CI [-1.74, -0.15], p=.021. Naltrexone-induced nausea was marginally associated with reward-based eating. Among participants who endorsed naltrexone-induced nausea (n=38), mindfulness participants (relative to control participants) reported greater reductions in food addiction symptoms, b=-1.00, 95% CI [-1.85, -0.77], p=.024, and trended toward reduced reward-based eating, binge eating, and weight, post-intervention. Single assessments of naltrexone-induced cortisol increases and nausea responses may be useful time- and cost-effective biological markers to identify obese individuals with greater opioid-mediated hedonic eating drive who may benefit from weight loss interventions with adjuvant mindfulness training that targets hedonic eating. Copyright © 2015. Published by Elsevier Ltd.
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Perceived Stress and Eating Behaviors by Sex, Obesity Status, and Stress Vulnerability: Findings from the Vitamins and Lifestyle (VITAL) Study
Article
  • May 2014
Stress has been associated with eating patterns in human studies with differences due to the type and duration of stressor, type of food, and individual susceptibility factors. Laboratory and smaller epidemiological studies have reported stress-associated preferences for foods high in sugar and fat; associations have been found more consistently among women and people who are obese. Larger studies are needed to sufficiently test these relationships. The aim of this study was to evaluate associations between self-reported amount of stress and dietary nutrient intakes (percentage energy from fat, carbohydrates, added sugar) and dietary behaviors (number of eating occasions and servings of fruits and vegetables, high-fat snacks, fast-food items, and sweetened drinks) by sex, obesity status, and stress vulnerability. Linear regression was used to estimate associations of perceived stress with eating patterns among 65,235 older adults while adjusting for demographic factors, body mass index, physical activity, alcohol intake, number of comorbidities, and other relevant covariates. Higher perceived stress was associated with greater intake of energy from fat, high-fat snacks, and fast-food items as well as lower intake of energy from carbohydrates (all P for trend ≤0.002). Among those with high perceived stress vulnerability, perceived stress was associated with fewer eating occasions (P for interaction <0.0001). Although associations were small, significant relationships were found for perceived stress arising from everyday experiences among an older, mostly white population. These findings have public health implications and suggest that stress may be important to consider in programs promoting healthy eating.
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Effect of sub chronic tryptophan supplementation on stress-induced cortisol and appetite in subjects differing in 5-HTTLPR genotype and trait neuroticism
Article
  • Jul 2014
  • PSYCHONEUROENDOCRINO
Stress or negative affect often increases preference for, and intake of, palatable snack foods and this may be influenced by cognitive and genetic factors related to stress and 5-HT vulnerability. The short (S) compared to the long (L) allele of the 5-HT transporter linked polymorphic region (5-HTTLPR) has been associated i) with decreased 5-HT transporter function and availability and hence, with 5-HT vulnerability, and ii) with greater stress-responsiveness. Stress-proneness is furthermore promoted by cognitive stress-vulnerability, a key feature of trait neuroticism. Brain 5-HT function can be manipulated by dietary administration of its amino acid precursor tryptophan (Trp), and the beneficial effects of dietary Trp on stress experience and emotional eating may be greatest following repeated administration in both stress- and 5-HT-vulnerable subjects. The aim was to examine the influence of repeated Trp administration on stress responsiveness and emotional eating in homozygous 5-HTTLPR S-allele (N = 60) and L-allele (N = 58) carriers with high and low neuroticism. Following seven days of Trp or PLC intake, mood, cortisol and appetite were assessed before and after exposure to acute stress and snack intake and preference were measured post-stress. It was hypothesised that Trp would reduce stress experience and emotional eating particularly in S-allele carriers with high neuroticism. Results revealed Trp treatment caused a clear reduction in stress-induced cortisol levels in S/S-allele carriers exclusively, and prevented a stress-induced increase in appetite only in S/S-allele carriers with high trait neuroticism. The findings reveal an advantageous effect of sub chronic Trp treatment on stress experience and appetite depending on stress and (genetic) serotonergic vulnerability.
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Linked Research

Effects of Emotional And Stress Eating On Obesity (advance research and conclusions)
Article
July 2016
Don Juravin · Rouzbeh Motiei-Langroudi · Waqar Ahmad · Kelly · Kelly Daly