Category: Contributors

Can Experiencing Chronic Discrimination Make Our Brains More Reactive to Food Cues?

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  • A neuroimaging study published in Nature Mental Health found that individuals experiencing high levels of unfair treatment have stronger reactions to food cues in areas of the brain involved in reward processing and self-control.
  • Their willingness to eat unhealthy foods was also increased, particularly for unhealthy sweet foods.
  • These individuals tended to have increased levels of two gut metabolites.

When we suddenly find ourselves in a dangerous situation, our body activates a series of changes that prepare us to fight the source of the danger or flee from it. It will release stress hormones into our bloodstream; the heart will start beating faster, breathing will quicken, and sweating will increase. We will forget about being hungry, sleepy, or tired. This is called the acute stress response. However, the acute stress response is only temporary. As soon as the danger is over, the source of stress no longer threatens us; all the processes will return to normal. But what happens if the danger does not end if the cause of stress continues to threaten our well-being?

Chronic stress


When the state of stress persists and continues for an extended period, we call it chronic stress. In modern society, chronic stress typically arises from enduring circumstances such as work-related pressures, financial difficulties, or strained relationships. It can also be a consequence of more catastrophic events such as life in a warzone, slavery, societal collapse, persecution, or other sources of serious stress (Bezo & Maggi, 2015; de Tubert, 2006; Hedrih et al., 2018; Hedrih & Husremović, 2021).

 

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Chronic stress exposes the body to increased levels of stress hormones, such as cortisol and catecholamines, for prolonged periods. Studies indicate that this can, in turn, lead to detrimental effects on physical and mental health, including an increased risk of heart disease, anxiety disorders, depression, or changes in immune system activity (Adell et al., 1988; Hedrih, 2023; Tafet & Bernardini, 2003; Torpy et al., 2007).

 

Individuals under chronic stress tend to increase their food intake and shift their preferences toward sweet and fatty foods

 

Chronic stress also changes appetite. Individuals under chronic stress tend to increase their food intake and shift their preferences towards sweet and fatty foods. Researchers have come to call such foods “comfort foods” (Dallman et al., 2005).

Chronic stress and discrimination


Discrimination is the unjust or prejudicial treatment of different categories of people, especially on the grounds of race, age, sex, or disability. When a society accepts discriminatory practices, they become an important source of chronic psychosocial stress for exposed individuals. Such experiences can lead to all the adverse consequences related to chronic stress, including changes in appetite. In this way, exposure to discrimination can contribute to stress-related weight gain and obesity (Zhang et al., 2023).

 

Exposure to discrimination can contribute to stress-related weight gain and obesity

 

The current study


Study author Xiaobei Zhang wanted to explore the link between exposure to discrimination and neural reactivity to healthy and unhealthy food cues and certain gut metabolites. Their expectation was that individuals more exposed to discrimination would have different brain activity in areas of the brain processing rewards and self-control when seeing unhealthy foods compared to individuals with lower levels of discrimination experiences. Their second expectation was that levels of specific biochemicals involved in inflammation (glutamate metabolites) would differ in individuals exposed to more discrimination (Zhang et al., 2023).

The procedure


The study participants were 107 healthy individuals recruited from Los Angeles through advertisements and local clinics. 87 of them were women (see Figure 1).

 

%learn about nutrition mental health %The Center for Nutritional Psychology Figure 1. Study Procedure (Zhang et al., 2024)

 

These individuals completed an assessment of chronic exposure to unfair treatment (the Everyday Discrimination scale). This assessment does not target discrimination specifically but captures different chronic experiences of unfair treatment in various domains of everyday life, including discrimination. Based on the scores of this assessment, the study authors divided the participants into two groups: those experiencing high levels of unfair treatment (the high discrimination group) and those experiencing comparatively low levels of such treatments (the low discrimination group).

Participants also underwent functional magnetic resonance imaging while hungry, i.e., after not having eaten for 6 hours. During the imaging, researchers showed participants pictures of different food items and recorded their brains’ reactions to the pictures. At the end of the scan, participants reported their willingness to eat the foods shown. Additionally, participants gave stool samples that allowed the study authors to estimate levels of specific gut metabolites.

 

The brains of individuals exposed to high levels of unfair treatment tend to be more reactive to unhealthy, sweet foods

 

Results showed that the brains of individuals from the high discrimination group were more reactive to unhealthy sweet foods. Regions that showed greater reactivity were the insula, inferior frontal gyrus, lateral orbitofrontal cortex, and frontal operculum cortex. The brains of these individuals also had stronger reactions to unhealthy savory foods in the caudate, putamen, insula, frontal pole, and lateral orbitofrontal cortex. These areas of the brain process emotions, decision-making, reward, and self-control (see Figure 2).

 

%learn about nutrition mental health %The Center for Nutritional Psychology Figure 2. Discrimination and reactivity to sweet foods

 

When unhealthy sweet foods were compared with healthy sweet foods, the high discrimination group had lower food-cue reactivity towards unhealthy sweet foods than the low discrimination group in the ventromedial prefrontal cortex.

The high discrimination group also had increased levels of two metabolites—N-acetylglutamate and N-acetylglutamine. Additionally, these individuals tended to express greater willingness to eat unhealthy foods than the low discrimination group, which was not the case with healthy foods.

Conclusion


The study showed that the brains of individuals experiencing greater levels of unfair treatment in their everyday lives tend to be more reactive to unhealthy, sweet foods. They were also more willing to eat such foods.

 

Experiencing unfair treatment can contribute to increased neural reactivity to unhealthy food cues

 

The study shows that experiencing unfair treatment can contribute to increased neural reactivity to unhealthy food cues. This can, in turn, promote unhealthy eating behaviors, increasing the risk of obesity.

The paper “Discrimination exposure impacts unhealthy processing of food cues: crosstalk between the brain and gut” was authored by Xiaobei Zhang, Hao Wang, Lisa A. Kilpatrick, Tien S. Dong, Gilbert C. Gee, Jennifer S. Labus, Vadim Osadchiy, Hiram Beltran-Sanchez, May C. Wang, Allison Vaughan, and Arpana Gupta.

 

References

 

Adell, A., Garcia-Marquez, C., Armario, A., & Gelpi, E. (1988). Chronic Stress Increases Serotonin and Noradrenaline in Rat Brain and Sensitizes Their Responses to Further Acute Stress. Journal of Neurochemistry, 50(6), 1678–1681. https://doi.org/10.1111/j.1471-4159.1988.tb02462.x

Bezo, B., & Maggi, S. (2015). Living in “survival mode:” Intergenerational transmission of trauma from the Holodomor genocide of 1932-1933 in Ukraine. Social Science and Medicine, 134, 87–94. https://doi.org/10.1016/j.socscimed.2015.04.009

Dallman, M. F., Pecoraro, N. C., & La Fleur, S. E. (2005). Chronic stress and comfort foods: Self-medication and abdominal obesity. Brain, Behavior, and Immunity, 19(4), 275–280. https://doi.org/10.1016/J.BBI.2004.11.004

de Tubert, R. H. (2006). Social trauma: The pathogenic effects of untoward social conditions. International Forum of Psychoanalysis, 15(3), 151–156. https://doi.org/10.1080/08037060500526037

Hedrih, V. (2023). Immune Mechanism Linking Changes in Gut Microorganism and Behavior after Chronic Stress. CNP Articles in Nutritional Psychology. https://www.nutritional-psychology.org/researchers-discover-immune-mechanism-linking-changes-in-gut-microorganisms-and-behavior-after-chronic-stress/

Hedrih, V., & Husremović, D. (2021). Organizational Psychology: Traumatic Traces in Organizations. In A. Hamburger, C. Hancheva, & V. D. Volkan (Eds.), Social Trauma—An Interdisciplinary Textbook (pp. 235–243). Springer Nature Switzerland AG. https://doi.org/10.1007/978-3-030-47817-9

Hedrih, V., Pedović, I., & Pejičić, M. (2018). Attachment in postwar societies of Ex Yugoslavia. In A. Hamburger (Ed.), Trauma, Trust, and Memory: Social Trauma and Reconciliation in Psychoanalysis (pp. 141–151). Routledge.

Tafet, G. E., & Bernardini, R. (2003). Psychoneuroendocrinological links between chronic stress and depression. Progress in Neuro-Psychopharmacology and Biological Psychiatry, 27(6), 893–903. https://doi.org/10.1016/S0278-5846(03)00162-3

Torpy, J. M., Lynm, C., & Glass, R. M. (2007). Chronic Stress and the Heart. JAMA, 298(14), 1722. https://doi.org/10.1001/jama.298.14.1722

Zhang, X., Wang, H., Kilpatrick, L. A., Dong, T. S., Gee, G. C., Labus, J. S., Osadchiy, V., Beltran-Sanchez, H., Wang, M. C., Vaughan, A., & Gupta, A. (2023). Discrimination exposure impacts unhealthy processing of food cues: Crosstalk between the brain and gut. Nature Mental Health, 1(11), 841–852. https://doi.org/10.1038/s44220-023-00134-9

 

 

Can Our Facial Attractiveness Depend on What We Just Ate?

Posted on by CNP Super Admin
  • A study in France published in PLOS One found that facial attractiveness can change depending on what a person eats.
  • Opposite-sex raters evaluated study participants’ facial attractiveness using pictures taken two hours after breakfast.
  • Facial attractiveness of both men and women was reduced after a breakfast rich in carbohydrates.
  • The effects were possible due to an increase in age appearance in women and a decrease in perceived masculinity in males.

We all know that our attractiveness can change depending on the circumstances. For example, when we’re tired or after sleepless nights, we might not appear as attractive as when fresh and well-rested. This difference will primarily reflect on our face, one of the most important parts of the human body for evaluating attractiveness.

Facial attractiveness


Facial attractiveness is a highly valued trait in many cultures. It is often associated with health, youth, and symmetry, which are genetic fitness markers. From an evolutionary perspective, facial attractiveness is thought to signal good genes and reproductive potential, leading individuals to prefer mates with appealing facial features. In various cultures, attractive faces tend to be linked to social status, success, and desirability. They influence mate selection and social interactions (Little, 2021; Rhodes, 2006).

Research suggests that certain universal features, such as clear skin, balanced facial proportions, and symmetry, are consistently rated more attractive across different cultures. However, cultural differences exist, with preferences for specific facial traits varying based on societal norms and environmental factors (Zhan et al., 2021).

Facial beauty is one of the first things we notice when observing someone. Studies show that our brains need just one-tenth of a second to recognize a face and evaluate the aggressiveness and trustworthiness of a person (Shavlokhova et al., 2024; Willis & Todorov, 2006).

The beauty premium


Researchers also discuss the “beauty premium,” the phenomenon where individuals perceived as more attractive tend to receive various advantages in life. These include higher earnings, better job opportunities, and preferential treatment in social situations. This advantage is not limited to employment but can extend to other areas such as education, politics, and legal outcomes (Dossinger et al., 2019).

Researchers suggest that the beauty premium may stem from a combination of factors, including societal biases that associate physical attractiveness with positive traits and the confidence and social skills that attractive individuals may develop as a result of favorable treatment (Borland & Leigh, 2014; Mobius & Rosenblat, 2006).

But does facial beauty depend on what we have just eaten?

The current study


Study author Amandine Visine and her colleagues wanted to investigate whether refined carbohydrate intake affects facial attractiveness in young men and women. They note that Western populations started consuming much more refined carbohydrates in several previous decades than they did in earlier centuries. This shift was associated with various adverse health consequences. Some researchers proposed that it also affected facial attractiveness, but the results were inconclusive (Visine et al., 2024). This study aimed to clarify those effects.

The study procedure


The study participants were 52 males and 52 females, young adults between 20 and 30 years of age, heterosexual, and with four grandparents of European origin. The study authors invited them for breakfast in their lab and asked them to ensure they came on an empty stomach.

In the lab, researchers randomly assigned participants to eat a breakfast containing only unrefined carbohydrates or a breakfast containing only refined carbohydrates. Both breakfasts had 500 calories. Approximately 2 hours after breakfast, the study authors took participants’ photos. On this occasion, participants also completed a dietary habits index. The study authors used these data to calculate participants’ glycemic load, which estimates the impact of food eaten on blood sugar levels. They estimated this parameter and the total energy intake for breakfast, afternoon snacks, and participants’ between-meal food intake.

After this, the study authors recruited independent groups of raters in a public place in Montpellier, France, to rate femininity/masculinity, apparent age, and attractiveness of study participants’ faces using the photos the study authors took. Raters rated the facial attractiveness of participants of the opposite sex. Seventy-seven raters rated apparent age, 150 rated perceived masculinity/femininity, and 252 raters rated attractiveness. Independent of this, the study authors used computer software to produce estimates of the masculinity/femininity of a face based on its morphology (see Figure 1).

 

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Figure 1. Study Procedure (Visine et al., 2024)

 

Eating breakfast comprised of refined carbohydrates reduced facial attractiveness in both men and women
Raters rated the faces of participants who ate breakfast consisting of refined carbohydrates as less attractive than those who ate unrefined carbohydrate breakfast. Raters saw men and women from the refined carbohydrate breakfast group as less attractive.

Regarding chronic food intake, raters saw participants with the highest total energy intake for breakfast as the most attractive. They tended to rate both men and women with higher refined carbohydrate intake between meals as less attractive. Women, but not men, eating more refined carbohydrates for breakfast and for the afternoon snack were seen as less attractive. Raters saw men eating more refined carbohydrates for afternoon snacks as more attractive. Men preferred women with lower breakfast and afternoon snack glycemic load, while women preferred men with a higher afternoon snack glycemic load and a lower energy intake (see Figure 2).

 

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Figure 2. Results of refined vs. unrefined carbohydrate breakfast on attractiveness

 

In general, higher age was associated with lower attractiveness ratings. Physical activity and perceived masculinity/femininity were associated with better attractiveness ratings.

Further analysis showed that it is possible that breakfast contents and dietary habits modified one’s age and masculine/feminine appearance. This, in turn, affected the attractiveness ratings.

Conclusion


The study shows that the immediate contents of a meal and long-term dietary habits can affect one’s attractiveness to individuals of the opposite sex. It also indicated that higher refined carbohydrate consumption reduces perceived attractiveness.

This indicates that to maintain facial beauty, one needs to consider diet, aside from other factors.

The paper “Chronic and immediate refined carbohydrate consumption and facial attractiveness” was authored by Amandine Visine, Valerie Durand, Leonard GuillouI, Michel Raymond, and Claire Berticat.

 

References

Borland, J., & Leigh, A. (2014). Unpacking the Beauty Premium: What Channels Does It Operate Through, and Has It Changed Over Time? Economic Record, 90(288), 17–32. https://doi.org/10.1111/1475-4932.12091

Dossinger, K., Wanberg, C. R., Choi, Y., & Leslie, L. M. (2019). The beauty premium: The role of organizational sponsorship in the relationship between physical attractiveness and early career salaries. Journal of Vocational Behavior, 112, 109–121. https://doi.org/10.1016/j.jvb.2019.01.007

Little, A. C. (2021). Facial Attractiveness. In T. K. Shackelford & V. A. Weekes-Shackelford (Eds.), Encyclopedia of Evolutionary Psychological Science (pp. 2887–2891). Springer International Publishing. https://doi.org/10.1007/978-3-319-19650-3_1881

Mobius, M. M., & Rosenblat, T. S. (2006). Why Beauty Matters. American Economic Review, 96(1), 222–235. https://doi.org/10.1257/000282806776157515

Rhodes, G. (2006). The Evolutionary Psychology of Facial Beauty. Annual Review of Psychology, 57(1), 199–226. https://doi.org/10.1146/annurev.psych.57.102904.190208

Shavlokhova, V., Vollmer, A., Stoll, C., Vollmer, M., Lang, G. M., & Saravi, B. (2024). Assessing the Role of Facial Symmetry and Asymmetry between Partners in Predicting Relationship Duration: A Pilot Deep Learning Analysis of Celebrity Couples. Symmetry, 16(2), 176. https://doi.org/10.3390/sym16020176

Visine, A., Durand, V., Guillou, L., Raymond, M., & Berticat, C. (2024). Chronic and immediate refined carbohydrate consumption and facial attractiveness. PLOS ONE, 19(3), e0298984. https://doi.org/10.1371/journal.pone.0298984

Willis, J., & Todorov, A. (2006). First Impressions: Making Up Your Mind After a 100-Ms Exposure to a Face. Psychological Science, 17(7), 592–598. https://doi.org/10.1111/j.1467-9280.2006.01750.x

Zhan, J., Liu, M., Garrod, O. G. B., Daube, C., Ince, R. A. A., Jack, R. E., & Schyns, P. G. (2021). Modeling individual preferences reveals that face beauty is not universally perceived across cultures. Current Biology, 31(10), 2243-2252.e6. https://doi.org/10.1016/j.cub.2021.03.013

Multivitamin-Multimineral Supplements Might Improve Cognitive Functioning in Elderly Adults

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Multivitamin-multimineral supplements might improve cognitive functioning in elderly adults

 

  • Results of a large study published in the American Journal of Clinical Nutrition reported that taking multivitamin-multimineral supplements for two years somewhat improved cognitive functioning in elderly adults.
  • The most favorable change compared to placebo was in episodic memory, which corresponds to 4.8 years of fewer aging years.
  • The effect on global cognition was more modest and equivalent to reducing cognitive aging by two years.

We are all aware that people of advanced age can often be forgetful, and their memory is no longer what it used to be. Tasks requiring speed and quick reactions are more difficult. Is there a way to prevent this?

Cognition and age


Cognitive changes occur throughout the entire lifespan, starting from infancy and continuing into old age. In early childhood, our cognitive abilities develop rapidly. Language, memory, and problem-solving skills improve quickly, particularly in the earliest years of life. During adolescence and young adulthood, cognitive functions such as processing speed, working memory, and executive functions reach their peak (e.g., R. Siegler, 2024).

However, from the mid-20s to the 30s, subtle declines in processing speed and memory begin. By the time individuals reach their 60s and beyond, more noticeable declines in cognitive functions, such as short-term memory, attention, and executive functions, are visible (e.g., Williams & Kemper, 2010). Despite this, certain cognitive abilities like emotional regulation and some aspects of long-term memory can remain stable or even improve with age (Isaacowitz, 2022) (see Figure 1).

 

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Figure 1. Cognition and age

 

In the 1960s, the famous psychologist Raymond Cattell proposed a theory that differentiated between cognitive abilities that remain stable or even improve as we age and those that decline with age. He called them crystalized and fluid intelligence. Crystallized intelligence refers to the accumulation of knowledge and skills acquired through experience and education, such as vocabulary and general knowledge. Fluid intelligence, on the other hand, encompasses the ability to reason, think abstractly, and solve problems in novel situations. Later studies confirmed that some abilities do not decline until very advanced age and start visibly declining much earlier (e.g., Murman, 2015) (see Figure 2).

 

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Figure 2. Crystallized intelligence vs. fluid intelligence

 

Raymond Cattell proposed a theory that differentiated between cognitive abilities that remain stable or improve as we age and those that decline

 

What causes cognitive decline?


There are many causes of age-related cognitive decline. Some of them are genetic; others have to do with changes that our brain undergoes as we age. Biochemical processes such as oxidative stress contribute, and changes in neurotransmitter levels have a similar effect (Raz & Rodrigue, 2006; Wilson et al., 2010).

Research also indicates that some factors can reduce the rate of cognitive decline and even prevent it in some aspects. These include education, being cognitively active, healthy lifestyle habits, good physical health, and good nutritional choices (Williams & Kemper, 2010).

The current study


Study author Chirag M. Vyas and his colleagues conducted a large-scale longitudinal study on older adults called COSMOS (COcoa Supplement and Multivitamin Outcomes Study). The study explored the effects of cocoa extract (500 mg flavanols) and multivitamin-multimineral supplements (Haleon; Centrum Silver®) on preventing cardiovascular disease and cancer. It also focused on age-related cognitive decline.

The COSMOS study consisted of three parts: an experiment called COSMOS-clinic, involving 573 participants; COSMOS-Mind, a study involving annual telephone-based cognitive assessments for three years (2158 participants); and COSMOS-Web, involving annual computer-based cognitive assessments for three years (2472 participants). 

In this analysis, the study authors focused on COSMOS-clinic. Around 50% of participants in the COSMOS-clinic study were males, and over 50% had post-college education. Their average body mass index was around 27, meaning they were overweight. Around 32% reported taking alcohol daily.

The study procedure


COSMOS-clinic participants were divided into four groups. One group was taking multivitamin-multimineral supplements and cocoa extracts, another was taking cocoa extracts and a placebo instead of multivitamin-multimineral supplements, the third group was taking placebo instead of cocoa extract and (real) multivitamin-multimineral supplements, and the fourth group was taking placebo instead of both substances. The look of placebo capsules was identical to that of capsules containing cocoa extract or multivitamin-multimineral supplements, with the difference that they contained no active ingredients (i.e., did not contain any cocoa extract,  vitamins, and minerals). Around 90-91% of participants reported adhering to the treatment regimen, i.e., taking the assigned pills as required by the study protocol.

Participants completed cognitive assessments at the study authors’ clinic before and after two years of taking their assigned treatments (depending on the group) (see Figure 3).

 

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Figure 3. Study Procedure (Vyas et al., 2024)

 

Multivitamin-multimineral supplements improved episodic memory


Results showed that participants assigned to the groups taking multivitamin-multimineral treatments had a bit better global cognition after two years compared to groups taking placebo. Effects on episodic memory were much better, showing a higher average difference from the placebo group.

When study authors compared these changes to typical changes caused by age, the improvement in episodic memory was equivalent to 4.8 years less aging compared to placebo groups. Effects on global cognition amounted to 2.4 years less aging. This sample did not affect executive functions or attention (see Figure 4).

 

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Figure 4. Results

 

Multivitamin-multimineral supplements improved global cognition across all three studies

 

The study authors also conducted a metanalysis of the results of all three COSMOS studies together. In this analysis, multivitamin-multimineral supplements had a clear positive effect on global cognition and episodic memory in particular.

Looking at the difference’s magnitude, global cognition’s effect amounted to around two years less aging. Results were similar across the three studies.

Conclusion


Results of these studies showed that taking multivitamin-multimineral supplements might slow down the cognitive decline that occurs with aging. The effects were the strongest on episodic memory, while executive functioning and attention were unaffected.

The observed effects are small, but taking supplements is easy and practically does not require changes to daily life habits. This is particularly the case when comparing them to other prospective methods of slowing cognitive decline. This means that this kind of supplement could be a useful addition to programs aimed at preventing age-related cognitive decline.

The paper “Effect of multivitamin-mineral supplementation versus placebo on cognitive function: results from the clinic subcohort of the COcoa Supplement and Multivitamin Outcomes Study (COSMOS) randomized clinical trial and meta-analysis of 3 cognitive studies within COSMOS” was authored by Chirag M Vyas, JoAnn E Manson, Howard D Sesso, Nancy R Cook, Pamela M Rist, Alison Weinberg, Vinayaga Moorthy, Laura D Baker, Mark A Espeland, Lok-Kin Yeung, Adam M Brickman, and Olivia I Okereke.

 

References

 

Isaacowitz, D. M. (2022). What do we know about aging and emotion regulation? Perspectives on Psychological Science : A Journal of the Association for Psychological Science, 17(6), 1541–1555. https://doi.org/10.1177/17456916211059819

Murman, D. L. (2015). The Impact of Age on Cognition. Seminars in Hearing, 36(3), 111–121. https://doi.org/10.1055/s-0035-1555115

Siegler. (2024). Cognitive Development in Childhood. In R. Biswas-Diener & E. Diener (Eds). Noba textbook series: Psychology. IL: DEF publishers. http://noba.to/8uv4fn9h

Raz, N., & Rodrigue, K. M. (2006). Differential aging of the brain: Patterns, cognitive correlates and modifiers. Neuroscience & Biobehavioral Reviews, 30(6), 730–748. https://doi.org/10.1016/j.neubiorev.2006.07.001

Williams, K., & Kemper, S. (2010). Exploring Interventions to Reduce Cognitive Decline in Aging. Journal of Psychosocial Nursing and Mental Health Services, 48(5), 42–51. https://doi.org/10.3928/02793695-20100331-03

Wilson, R. S., Leurgans, S. E., Boyle, P. A., Schneider, J. A., & Bennett, D. A. (2010). Neurodegenerative basis of age-related cognitive decline. Neurology, 75(12), 1070–1078. https://doi.org/10.1212/WNL.0b013e3181f39adc

 

 

 

Does Lack of Sleep Dysregulate Parts of Our Brain that Control Appetite?

Posted on by CNP Super Admin
  • A study published in Nature Communications sought to identify the brain mechanism through which a lack of sleep increases food desire.
  • They found that a lack of sleep decreases the activity of cortex regions responsible for cognitive processes regarding food intake while increasing the activity of the subcortical amygdala region.
  • Loss of sleep leads to a heightened desire for high-calorie foods.

When lacking sleep, some drink coffee, some try to increase their physical activity to stay awake, and some visit the fridge. Most people have experienced this situation when they couldn’t get enough sleep, accompanied by a desire to eat more food than usual. But does lack of sleep really increase our appetite?

Sleep and appetite


Researchers extensively investigated the link between sleep and the desire to eat. Many found that insufficient sleep is associated with increased food intake. A 2008 meta-analysis of 30 studies found that short sleepers, people spending below-average time asleep, are more likely to be overweight and obese. This association was present in adults and children (Cappuccio et al., 2008). A newer meta-analysis confirmed these findings again, showing that short sleep duration leads to an increased risk of obesity later in life (Bacaro et al., 2020) (see Figure 1).

 

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Figure 1. Sleep and obesity

 

Similarly, newer studies showed that people who eat at night, at the time when they should be sleeping, were more likely to be overweight or obese. They also consumed sugar-sweetened beverages more often and ate fruits and vegetables less often than those not prone to eating at night (Lent et al., 2022). Additionally, individuals suffering from night eating syndrome, a condition in which they tend to eat lots of food at night, have a lower quality of sleep than those without this disorder (Tzischinsky et al., 2021).

One experiment showed that individuals who slept only 4 hours at night ate 22% more calories for breakfast the following day and felt hungrier immediately before breakfast (Brondel et al., 2010)(see Figure 2).

 

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Figure 2. Sleep and food intake behaviors

 

Despite all the evidence that the desire for food and sleep quality are connected, the neural mechanisms that produce this effect remained more or less unknown (Greer et al., 2013).

The current study


Study author Stephanie Greer and her colleagues wanted to identify the neural mechanism through which a lack of sleep increases the desire for food. They wanted to know what changes in the brain when we lack sleep produce this effect.

These authors conducted a neuroimaging study in which they focused on a set of cortical and subcortical regions of the brain that researchers consider crucial for evaluating food stimuli and regulating the desire for food. These areas were the anterior insular cortex, lateral orbital frontal cortex, and anterior cingulate cortex in the brain’s cortex. All of these areas have well-established roles in signaling the value of a food stimulus and regulating how we integrate evaluations of various food features to create preferences for food. Studies have also shown that the functioning of these areas of the cortex is disrupted when an individual lacks sleep (Muzur et al., 2002).

On the subcortical level, they focused on the amygdala and the ventral striatum regions. Previous studies showed that the amygdala is very reactive to food stimuli. Activity in the ventral striatum, on the other hand, very precisely predicts immediate food intake, binge eating, and weight gain (Greer et al., 2013) (see Figure 3).

 

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Figure 3. Neuroimaging study of various brain regions

 

The procedure


The study participants were 23 young adults, the average age of whom was 21. Of these, 13 were females. Their mean body mass index was 23, meaning that, on average, they were normal weight.

Participants completed two experimental sessions. During one session, they spent a night of normal sleep in the study authors’ lab, monitored by polysomnography equipment. The second session was a night without sleep in the same lab, monitored by lab personnel and wrist actigraphy.

Wrist actigraphs are wearable devices that measure movements. Researchers can use them to determine when the wearer is sleeping and when he/she is awake. Polysomnography equipment consists of a set of devices used to record various physiological parameters during sleep. These can include brain waves (EEG), eye movements, muscle activity, heart rate, and breathing patterns. Polysomnography is used to monitor sleep quality and diagnose sleep disorders.

Study participants underwent functional magnetic resonance imaging (fMRI)  the morning after the experimental night (see Figure 4).

 

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Figure 4. Procedure (Greer et al., 2013)

 

Sleep deprivation reduced activity in the studied cortical regions


Results showed that brain activity was reduced after the night without sleep in all three studied areas of the cortex – the anterior cingulate cortex, the lateral orbital frontal cortex, and the anterior insular cortex.

In contrast to the cortical regions, the amygdala region became much more responsive to desirable food items after sleepless nights than when participants slept normally. The ventral striatum activity did not differ between the two experimental nights (see Figure 5).

 

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Figure 5. Increased amygdala responsiveness to desirable food after reduced sleep

 

Sleep deprivation increases the desirability of high-calorie foods


Compared to the night when they normally slept, study participants expressed higher levels of desire for high-calorie foods after the night without sleep. There was no difference between the two nights in how much participants desired low-calorie items. Overall, the increase in desire for specific foods represented a desire to eat an additional 600 calories after the night without sleep. The increase in desire for high-calorie foods was so specific that the increase in the desirability of a specific food item after a night without sleep could be predicted based on its calorie content (see Figure 6).

 

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Figure 6. Sleep deprivation and high-calorie food desirability

 

Conclusion


Overall, the study found that lack of sleep decreases the activity of the cortex areas responsible for cognitive processes regarding food while increasing the activity of the amygdala subcortical region. After a sleepless night, high-calorie food items also became more desirable.

These findings contribute to a better scientific understanding of the neural mechanisms underpinning the link between sleep deprivation and increased desire for food. They very strongly suggest that weight loss and obesity prevention programs should consider sleep quality and include regulating any sleep problems among their goals.

The paper “The impact of sleep deprivation on food desire in the human brain” was authored by Stephanie M. Greer, Andrea N. Goldstein, and Matthew P. Walker.

 

References

 

Bacaro, V., Ballesio, A., Cerolini, S., Vacca, M., Poggiogalle, E., Donini, L. M., Lucidi, F., & Lombardo, C. (2020). Sleep duration and obesity in adulthood: An updated systematic review and meta-analysis. Obesity Research & Clinical Practice, 14(4), 301–309. https://doi.org/10.1016/j.orcp.2020.03.004

Brondel, L., Romer, M. A., Nougues, P. M., Touyarou, P., & Davenne, D. (2010). Acute partial sleep deprivation increases food intake in healthy men. The American Journal of Clinical Nutrition, 91(6), 1550–1559. https://doi.org/10.3945/ajcn.2009.28523

Cappuccio, F. P., Taggart, F. M., Kandala, N.-B., Currie, A., ChB, M., Peile, E., & Miller, M. A. (2008). Meta-Analysis of Short Sleep Duration and Obesity in Children and Adults. 31(5).

Greer, S. M., Goldstein, A. N., & Walker, M. P. (2013). The impact of sleep deprivation on food desire in the human brain. Nature Communications, 4. https://doi.org/10.1038/ncomms3259

Lent, M. R., Atwood, M., Bennett, W. L., Woolf, T. B., Martin, L., Zhao, D., Goheer, A. A., Song, S., McTigue, K. M., Lehmann, H. P., Holzhauer, K., & Coughlin, J. W. (2022). Night eating, weight, and health behaviors in adults participating in the Daily24 study. Eating Behaviors, 45. https://doi.org/10.1016/j.eatbeh.2022.101605

Muzur, A., Pace-Schott, E. F., & Hobson, J. A. (2002). The prefrontal cortex in sleep. Trends in Cognitive Sciences, 6(11), 475–481. https://doi.org/10.1016/S1364-6613(02)01992-7

Tzischinsky, O., Latzer, I. T., Alon, S., & Latzer, Y. (2021). Sleep quality and eating disorder-related psychopathologies in patients with night eating syndrome and binge eating disorders. Journal of Clinical Medicine, 10(19). https://doi.org/10.3390/jcm10194613

Reactions in Our Immune System Can Lead to Behavioral Changes, Including Depression

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An enzyme produced in white blood cells regulates some of the psychological symptoms of depression

 

  • A study on mice published in Nature reported that an enzyme called matrix metalloproteinase 8 (MMP8) regulates the effects of stress on the symptoms of depression.
  • MMP8 was increased in the blood serum of humans with major depressive disorder and mice exposed to chronic stress.
  • Injecting mice with an appropriate dose of MMP8 promoted social avoidance.
  • The results showcase how immune system reactions can affect the brain, leading to profound behavioral changes.

Scientists have studied mental health problems for centuries. However, for most of this time, their focus has solely been on psychological symptoms because the scientific know-how needed to understand the complex biochemical mechanisms underpinning psychology was simply not there until now. Recent advances in biomedical technology allowed modern researchers to start mapping the biochemical mechanisms behind these disorders. One major topic of this type of research is stress-related disorders, such as major depressive disorder.

Major depressive disorder and stress

Major depressive disorder, or MDD, is a serious mental health condition characterized by persistent feelings of sadness, hopelessness, and a lack of interest or pleasure in daily activities, often accompanied by physical symptoms such as changes in appetite or sleep patterns. It is one of the most frequent psychiatric disorders worldwide (Steffen et al., 2020; Weinberger et al., 2018).

Stress likely plays a significant role in the development and exacerbation of major depressive disorder

Studies on mice showed that chronic stress can lead to depression-like symptoms and alterations in the brain’s structure and function, particularly in areas involved in mood regulation, such as the hippocampus, amygdala, and prefrontal cortex (PFC) (Khan et al., 2020). Neuroimaging studies have reported alterations to similar brain areas in humans with depression (Zhang et al., 2018)

Stress can also disrupt the balance of neurotransmitters, like serotonin and norepinephrine, which are crucial for maintaining mood stability (Adell et al., 1988). Furthermore, prolonged stress activates the hypothalamic-pituitary-adrenal axis (HPA axis), leading to elevated cortisol levels. This stress hormone has been linked to depression (Tafet & Bernardini, 2003) (see Figure 1).

 

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Figure 1. Role of stress in major depressive disorder

 

Inflammatory processes and depression

Studies show chronic stress also activates the immune system, the body’s natural defense against bacteria, viruses, and other pathogens. This activation leads to the mobilization of a type of white blood cell called myeloid cells. The organism under stress also increases the concentration of specific signaling proteins called cytokines (such as interleukin-6) in the bloodstream. This initiates and promotes inflammatory reactions in the body (Cathomas et al., 2024) (see Figure 2).

 

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Figure 2. Immune system activation by chronic stress

 

In line with this, studies on humans show that individuals with stress-related mental health conditions such as major depressive disorder display a state of chronic low-grade inflammation characterized by increased concentrations of these pro-inflammatory proteins in the bloodstream (Dowlati et al., 2010)

The current study

Study author Flurin Cathomas and his colleagues wanted to understand better the role of immune system molecules in the development of psychological symptoms of depression. The initial results they obtained focused their attention on the role of the enzyme matrix metalloproteinase 8 (MMP8).

MMP8 belongs to the metalloproteinase family, a group of enzymes responsible for breaking down extracellular matrix proteins. MMP8 is primarily produced by neutrophils, a type of myeloid white blood cell that plays a crucial role in the immune system’s response to infection and inflammation. They are derived from myeloid progenitor cells in the bone marrow.

These researchers conducted experiments on 4-7-week-old mice purchased externally or bred in the researchers’ laboratory. In the experiments, the study authors exposed these mice to different types of stressors and conducted different biomedical and surgical procedures. The main type of stress-induced in these mice was chronic social defeat. This was done by exposing them for 5 or 10 minutes to a large, aggressive mouse for ten days. After this treatment, some mice started avoiding other mice, developing social avoidance, a pattern of behaviors comparable to that of depression in humans. Other mice did not. Study authors called the first type of mice “susceptible” mice and the later “resistant” mice. They also used mice not exposed to stress as controls (see Figure 3).

 

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Figure 3. Study Procedure (Cathomas, 2024)

 

Chronic stress upregulates genes producing MMP8 in the bloodstream of susceptible mice

The study authors examined the activity of white blood cells in mice and grouped them into four categories based on their gene activity patterns. They identified a group of genes that were more active in susceptible mice compared to controls. Many of the genes in this group were proteins known to play a role in the process of inflammation. One of the most differentially active genes in the two groups of mice was the one encoding MMP8.

Further analysis showed that this increased activity of MMP8 genes was not found in the brain but only in white blood cells circulating in the bloodstream. Although these MMP8 molecules are produced outside the brain, it turned out that they can still travel to the brain. Chronic stress makes the blood-brain barrier (BBB) in the area of the brain called nucleus accumbens more permeable, allowing MMP8 to enter the brain at that point. Upon entering, they increase the space between cells in this area. A separate experiment showed that increasing the space between cells in the nucleus accumbens leads to more social avoidance in these mice (see Figure 4).

 

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Figure 4. Impact of chronic stress on MMP8 gene activity and BBB permeability

 

Study authors verified these findings in humans and found that individuals with major depressive disorder also have increased concentrations of MMP8 in their bloodstream.

MMP8 regulates social avoidance

When study authors injected MMP8 into mice that were exposed to subthreshold stress (social defeat stress insufficient to produce behavioral changes), these mice also reduced their social interactions (i.e., started displaying social avoidance). To ensure this is the effect of MMP8 (and not of something else), the study authors bred mice genetically altered not to produce it. Exposing these mice to chronic social defeat stress did not result in social avoidance. They even showed higher social interaction and spent less time in the corner than regular mice. This indicated that MMP8 regulates social avoidance behavior in mice (Figure 5).

 

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Figure 5. Link of MMP8 activity with chronic stress

Conclusion

The study showed that chronic stress increases the enzyme matrix metalloproteinase 8 (MMP8) production in myeloid white blood cells in the bloodstream. These enzymes enter the nucleus accumbens region of the brain and increase the space between brain cells, leading to social avoidance in mice (see Figure 6).

 

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Figure 6. Chronic stress increases MMP8

 

Although the study was conducted on mice, similar physiological mechanisms also likely exist in humans. Thanks to this similarity, these findings contribute to the scientific understanding of biochemical mechanisms underpinning psychological reactions to chronic stress and symptoms of disorders such as depression. Understanding the biochemical mechanisms of mental disorders will likely lead to the development of much more effective ways to treat them.

The paper “Circulating myeloid-derived MMP8 in stress susceptibility and depression” was authored by Flurin Cathomas, Hsiao-Yun Lin, Kenny L. Chan, Long Li, Lyonna F. Parise, Johana Alvarez, Romain Durand-de Cuttoli, Antonio V. Aubry, Samer Muhareb, Fiona Desland, Yusuke Shimo, Aarthi Ramakrishnan, Molly Estill, Carmen Ferrer-Pérez, Eric M. Parise, C. Matthias Wilk, Manuella P. Kaster, Jun Wang, Allison Sowa, William G. Janssen, Sara Costi, Adeeb Rahman, Nicolas Fernandez, Matthew Campbell, Filip K. Swirski, Eric J. Nestler, Li Shen, Miriam Mera, James W. Murrough, and Scott J. Russo.

References
Adell, A., Garcia-Marquez, C., Armario, A., & Gelpi, E. (1988). Chronic Stress Increases Serotonin and Noradrenaline in Rat Brain and Sensitizes Their Responses to a Further Acute Stress. Journal of Neurochemistry, 50(6), 1678–1681. https://doi.org/10.1111/j.1471-4159.1988.tb02462.x

Cathomas, F., Lin, H.-Y., Chan, K. L., Li, L., Parise, L. F., Alvarez, J., Durand-de Cuttoli, R., Aubry, A. V., Muhareb, S., Desland, F., Shimo, Y., Ramakrishnan, A., Estill, M., Ferrer-Pérez, C., Parise, E. M., Wilk, C. M., Kaster, M. P., Wang, J., Sowa, A., … Russo, S. J. (2024). Circulating myeloid-derived MMP8 in stress susceptibility and depression. Nature, 626(8001), 1108–1115. https://doi.org/10.1038/s41586-023-07015-2

Dowlati, Y., Herrmann, N., Swardfager, W., Liu, H., Sham, L., Reim, E. K., & Lanctôt, K. L. (2010). A Meta-Analysis of Cytokines in Major Depression. Biological Psychiatry, 67(5), 446–457. https://doi.org/10.1016/j.biopsych.2009.09.033

Khan, A. R., Geiger, L., Wiborg, O., & Czéh, B. (2020). Stress-Induced Morphological, Cellular and Molecular Changes in the Brain—Lessons Learned from the Chronic Mild Stress Model of Depression. Cells, 9(4), 1026. https://doi.org/10.3390/cells9041026

Steffen, A., Thom, J., Jacobi, F., Holstiege, J., & Bätzing, J. (2020). Trends in prevalence of depression in Germany between 2009 and 2017 based on nationwide ambulatory claims data. Journal of Affective Disorders, 271, 239–247. https://doi.org/10.1016/J.JAD.2020.03.082

Tafet, G. E., & Bernardini, R. (2003). Psychoneuroendocrinological links between chronic stress and depression. Progress in Neuro-Psychopharmacology and Biological Psychiatry, 27(6), 893–903. https://doi.org/10.1016/S0278-5846(03)00162-3

Weinberger, A. H., Gbedemah, M., Martinez, A. M., Nash, D., Galea, S., & Goodwin, R. D. (2018). Trends in depression prevalence in the USA from 2005 to 2015: Widening disparities in vulnerable groups. Psychological Medicine, 48(8), 1308–1315. https://doi.org/10.1017/S0033291717002781

Zhang, F.-F., Peng, W., Sweeney, J. A., Jia, Z.-Y., & Gong, Q.-Y. (2018). Brain structure alterations in depression: Psychoradiological evidence. CNS Neuroscience & Therapeutics, 24(11), 994–1003. https://doi.org/10.1111/cns.12835

 

Depressive Individuals Tend To Eat More Sugar

Posted on by CNP Super Admin
  • An analysis of the National Health and Nutrition Examination Survey data published in BMC Psychiatry found an association between sugar intake and depression in U.S. adults.
  • With every 100 grams of additional sugar intake, the prevalence of depression increased by 28%.
  • Results were similar across subgroups by age, sex, education, and other personal characteristics.

Most people know that there is a link between appetite and mood. When stressed, some of us tend to eat more (Dakanalis et al., 2023). A similar thing happens when we do not have enough sleep (Greer et al., 2013). On the other hand, when we are hungry, we tend to become angry and irritable. That is how the term “hangry” came to be (Hedrih, 2023a; Swami et al., 2022). But is there a link between moods or mental health in general and specific foods? For example, do the dietary choices of individuals suffering from depression differ from the dietary choices of individuals who aren’t suffering from depression?

 

Do the dietary choices of individuals with depression differ from the dietary choices of individuals without depression?

 

What is depression?


Depression is a common and serious mental health condition characterized by persistent feelings of sadness, hopelessness, and a lack of interest or pleasure in activities. It can affect a person’s thoughts, behavior, feelings, and sense of well-being, leading to various emotional and physical problems. Symptoms can include changes in appetite, sleep disturbances, fatigue, difficulty concentrating, and even thoughts of death or suicide (see Figure 1).

 

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Figure 1. Symptoms of depression

 

Depression is one of the most prevalent mental health disorders worldwide. The share of depressed individuals has been on the rise in recent decades in many world countries (Steffen et al., 2020; Weinberger et al., 2018). In 2018, the World Health Organization estimated that 4.4% of the global population is affected by it (Zhang et al., 2024). They expect the numbers to rise further in the coming years.

Unfortunately, existing treatments for depression are not very effective. It is estimated that around 30% of individuals suffering from depression do not respond to standard treatments, i.e., these treatments do not result in the withdrawal of depression symptoms (McIntyre et al., 2023). That is why a large number of scientists are working on finding novel ways to diagnose and treat depression. One of the topics that draw interest in this regard is the dietary specificities of people suffering from depression.

 

Around 30% of individuals suffering from depression do not respond to standard treatments

 

Dietary choices and depression


In recent decades, many studies have reported links between symptoms of depression and anxiety and various food choices. A large-scale study found that depressed women tend to drink artificially sweetened beverages and eat ultraprocessed food more than the average person (Hedrih, 2023b; Samuthpongtorn et al., 2023). Another study linked the consumption of fried food with symptoms of anxiety and depression. These researchers conducted an experiment showing that acrylamide, a product of frying foods such as potatoes, can induce anxiety-like symptoms in zebrafish (Wang et al., 2023). 

Similarly, many studies link increased sugar consumption with adverse health outcomes (Huang et al., 2023). But does this include depression?

 

Many studies report links between symptoms of depression and anxiety and various food choices (artificially sweetened beverages and fried foods)

 

The current study


Study author Lu Zhang and her colleagues wanted to explore whether sugar consumption is associated with the severity of depressive symptoms (Zhang et al., 2024). They analyzed data from the National Health and Nutrition Examination Survey database. The National Health and Nutrition Examination Survey is a program of studies conducted by the National Center for Health Statistics (NCHS), part of the Centers for Disease Control and Prevention (CDC), designed to assess the health and nutritional status of adults and children in the United States through interviews and physical examinations.

The study data


Data used in this study came from participants aged 20 or above who provided their survey responses between 2011 and 2018. The study authors used data on the frequency of depressive symptoms (the Patient Health Questionnaire) and dietary sugar intake. Dietary information was collected from participants through two interviews held 3-10 days apart. In these interviews, researchers asked participants to recall all types and amounts of food and beverages they consumed during the 24 hours before the interviews. Dietary sugar intake was calculated from data collected in these interviews.

The study authors also analyzed data on several other participants’ characteristics. These included body mass index, age, total energy intake, education level, race, marital status, physical activity, etc.

This analysis used data from 18,439 participants (see Figure 2).

 

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Figure 2. Study Procedure (Zhang et al., 2024)

 

Older, wealthier, more educated, partnered, and female participants tend to consume the least sugar

 

Results showed that individuals consuming the least sugar daily tended to be older, female, and wealthy. Their overall energy intake was lower; they smoked less and drank more than the average participant. Participants with the highest daily sugar intake tended to be younger, male, and with lower income. They tended to have never smoked and had a higher energy intake than average.

Depressed individuals tended to consume more sugar


There was a clear association between the prevalence of depression and sugar intake. On average, people consumed around 93 grams of sugar per day, but individuals were consuming quite a bit more than that. One-quarter of participants consumed over 140 grams per day. Statistical analyses showed that for every additional 100 grams of daily sugar consumption, the share of participants with depression increased by 28% (see Figure 3).

 

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Figure 3. Association between depression prevalence and sugar intake

 

Conclusion


The study shows a clear link between dietary sugar consumption and depression. However, the design of the study does not allow us to conclude whether it is the intake of sugar that contributes to depression or whether it is depression that makes individuals consume more sugary drinks and foods. It is also possible that there is some third factor contributing to both depression and the heightened intake of sugar.

Be that as it may, the link between heightened sugar intake and depression is quite clear. However, it is up to future researchers to identify the underlying mechanism and determine whether limiting dietary sugar intake could help improve symptoms in individuals suffering from this disorder.

The paper “Association between dietary sugar intake and depression in US adults: a cross-sectional study using data from the National Health and Nutrition Examination Survey 2011–2018” was authored by Lu Zhang, Haiyang Sun, Zihui Liu, Jiguo Yang, and Yuanxiang Liu.


References

Dakanalis, A., Mentzelou, M., Papadopoulou, S. K., Papandreou, D., Spanoudaki, M., Vasios, G. K., Pavlidou, E., Mantzorou, M., & Giaginis, C. (2023). The Association of Emotional Eating with Overweight/Obesity, Depression, Anxiety/Stress, and Dietary Patterns: A Review of the Current Clinical Evidence. Nutrients, 15(5), 1173. https://doi.org/10.3390/nu15051173

Greer, S. M., Goldstein, A. N., & Walker, M. P. (2013). The impact of sleep deprivation on food desire in the human brain. Nature Communications, 4. https://doi.org/10.1038/ncomms3259

Hedrih, V. (2023a). Food and Mood: Is the Concept of ‘Hangry’ Real? CNP Articles in Nutritional Psychology. https://www.nutritional-psychology.org/food-and-mood-is-the-concept-of-hangry-real/

Hedrih, V. (2023b). Women Consuming Lots of Artificially Sweetened Beverages Might Have a Higher Risk of Depression, Study Finds. CNP Articles in Nutritional Psychology. https://www.nutritional-psychology.org/women-consuming-lots-of-artificially-sweetened-beverages-might-have-a-higher-risk-of-depression-study-finds/

Huang, Y., Chen, Z., Chen, B., Li, J., Yuan, X., Li, J., Wang, W., Dai, T., Chen, H., Wang, Y., Wang, R., Wang, P., Guo, J., Dong, Q., Liu, C., Wei, Q., Cao, D., & Liu, L. (2023). Dietary sugar consumption and health: Umbrella review. BMJ (Clinical Research Ed.), 381, e071609. https://doi.org/10.1136/bmj-2022-071609

McIntyre, R. S., Alsuwaidan, M., Baune, B. T., Berk, M., Demyttenaere, K., Goldberg, J. F., Gorwood, P., Ho, R., Kasper, S., Kennedy, S. H., Ly-Uson, J., Mansur, R. B., McAllister-Williams, R. H., Murrough, J. W., Nemeroff, C. B., Nierenberg, A. A., Rosenblat, J. D., Sanacora, G., Schatzberg, A. F., … Maj, M. (2023). Treatment-resistant depression: Definition, prevalence, detection, management, and investigational interventions. World Psychiatry, 22(3), 394–412. https://doi.org/10.1002/wps.21120

Samuthpongtorn, C., Nguyen, L. H., Okereke, O. I., Wang, D. D., Song, M., Chan, A. T., & Mehta, R. S. (2023). Consumption of Ultraprocessed Food and Risk of Depression. JAMA Network Open, 6(9), e2334770. https://doi.org/10.1001/jamanetworkopen.2023.34770

Steffen, A., Thom, J., Jacobi, F., Holstiege, J., & Bätzing, J. (2020). Trends in prevalence of depression in Germany between 2009 and 2017 based on nationwide ambulatory claims data. Journal of Affective Disorders, 271, 239–247. https://doi.org/10.1016/J.JAD.2020.03.082

Swami, V., Hochstöger, S., Kargl, E., & Stieger, S. (2022). Hangry in the field: An experience sampling study on the impact of hunger on anger, irritability, and affect. PLOS ONE, 17(7), e0269629. https://doi.org/10.1371/JOURNAL.PONE.0269629

Wang, A., Wan, X., Zhuang, P., Jia, W., Ao, Y., Liu, X., Tian, Y., Zhu, L., Huang, Y., Yao, J., Wang, B., Wu, Y., Xu, Z., Wang, J., Yao, W., Jiao, J., & Zhang, Y. (2023). High-fried food consumption impacts anxiety and depression due to lipid metabolism disturbance and neuroinflammation. Proceedings of the National Academy of Sciences of the United States of America, 120(118). https://doi.org/10.1073/pnas.2221097120

Weinberger, A. H., Gbedemah, M., Martinez, A. M., Nash, D., Galea, S., & Goodwin, R. D. (2018). Trends in depression prevalence in the USA from 2005 to 2015: Widening disparities in vulnerable groups. Psychological Medicine, 48(8), 1308–1315. https://doi.org/10.1017/S0033291717002781

Zhang, L., Sun, H., Liu, Z., Yang, J., & Liu, Y. (2024). Association between dietary sugar intake and depression in US adults: A cross-sectional study using data from the National Health and Nutrition Examination Survey 2011–2018. BMC Psychiatry, 24(110), 1–10. https://doi.org/10.1186/s12888-024-05531-7

 

What Makes Us Like or Dislike Specific Foods?

Posted on by CNP Super Admin
  • In an online experiment published in Appetite, participants rated various characteristics of foods, including energy density, level of processing, and carbohydrate-to-fat ratio.
  • Results showed that carbohydrate-to-fat ratio and taste were the primary determinants of food liking and the desire to eat.
  • Contrary to findings from previous studies, the level of processing was not linked to either the desire to eat the food or its taste ratings.

Have you ever wondered what makes us like and want to eat certain foods while disliking others? Most people will say that they like tasty food when asked this question. But what makes some foods tastier than others? Many scientific studies explored this question.

 

What makes some foods tastier than others? 

 

Ultraprocessed foods and obesity


Scientists first studied this question in the context of the obesity pandemic currently plaguing the world (Wong et al., 2022). Their findings showed that many overweight people tend to eat lots of ultraprocessed foods. Ultraprocessed foods have undergone extensive processing and often contain additives to improve their taste and appeal (Monteiro et al., 2019). Researchers found that some components of ultraprocessed foods trigger neural processes similar to those found in various addictions, creating intense desires for those foods (Gearhardt et al., 2023; Hedrih, 2023).

 

Some components of ultraprocessed foods trigger neural processes similar to those found in various addictions, creating intense desires for those foods

 

Fat, carbohydrates, and food reward processing in the brain


Other studies indicate that foods rich in fat and carbohydrates create the strongest activation of the reward processing system in the brain, the system of neural circuits that produces the pleasurable and rewarding feelings we experience when we eat something tasty (see Figure 1).

 

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Figure 1. Activation of the brain’s reward processing system

 

A recent study on mice showed that our brain has separate neural reward circuits for sugars and fats. Due to this, foods that are both fatty and sweet trigger both of these circuits simultaneously resulting in stronger feelings of pleasure than what foods that are just sweet or just fatty could produce (Hedrih, 2024; McDougle et al., 2024). Research has shown for quite some time that feeding mice a fat-rich diet (mouse food already contains carbohydrates) will cause them to overeat and become obese (Ikemoto et al., 1996) (see Figure 2).

 

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Figure 2. Fat and Sugar Mediated Activation of Reward Processing System

 

The current study


Study author Peter J. Rogers and his colleagues wanted to test which characteristics of food contribute to how rewarding the food is for humans (Rogers et al., 2024). They focused on 1) the energy density of food, 2) its level of processing, and 3) the carbohydrate-to-fat ratio (see Figure 3). The energy density of food refers to the amount of energy (calories) in a given weight of food, typically expressed in calories per gram.

 

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Figure 3. Rewarding characteristics of foods 

 

The procedure


The authors recruited 224 adult participants through social media. Participants were required not to be vegetarians or vegans and to be familiar with the food they would be rating. The mean age of participants was 35 years. 62.5% of them were female. 5% of participants were underweight, 53% had a healthy weight, and 43% were overweight or obese.

The study authors divided these participants into three groups. One group would rate a set of food items differing in energy density (32 foods), and the second group would do that for foods differing in the level of processing (24 foods). In contrast, the third group rated foods differing in their carbohydrate-to-fat ratio (see Figure 4).

 

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Figure 4. Study Procedure (Rogers et al., 2024)

 

Participants rated their assigned food set on food reward (how much they desire to eat), liking (how pleasant they think the food tastes in their mouth), sweetness, saltiness, and flavor intensity.

Food items were presented as pictures of a 50-gram portion on a light-beige colored plate. To ensure that participants were somewhat hungry at the time of the study, the authors instructed them not to eat anything for 2 hours before the study. Participants were supposed to imagine taking a bite of the food shown in the picture and tasting it. They would then provide the rating. 

Foods presented in the energy density group included (in increasing order of energy density) fresh apple slices (the lowest energy density), a boiled egg, Edam cheese slices, crisps, and original Pringles (the highest energy density). Foods in the level of processing set included avocado (no processing), Parma ham, and wine gums (a type of gummy candy, the highest level of processing). The carbohydrate-to-fat ratio group included dried apple slices (high share of carbohydrates, little fat), Cornish dairy ice cream (moderate amounts of both fats and carbohydrates), and Frankfurter sausage (high in fats, little carbohydrates).

 

Participants liked very energy-dense foods and medium-processed foods the most

 

Results showed that participants liked and wanted to eat energy-dense foods the most. However, the least liked foods were not those with the lowest energy density but foods with medium energy density levels. The situation with food rewards was the same. Taste intensity tended to increase with energy density. Participants rated the least energy-dense foods as having the least intensive taste.

In the set of foods that differed by the level of processing, participants found processed, but not ultraprocessed foods, to be the most to their liking, the most rewarding, and with the highest taste intensity. Minimally processed foods received the lowest ratings. However, participants found unprocessed foods even more rewarding (i.e., they wanted to eat them more) than medium-processed foods.

 

Participants found processed, but not ultraprocessed foods, to be the most to their liking, the most rewarding, and with the highest taste intensity

 

Foods containing both fats and carbohydrates received the best ratings


In the carbohydrate-to-fat ratio food group, participants found foods containing roughly equal amounts of carbohydrates and fats to be the most to their liking and the most rewarding. Foods consisting solely of carbohydrates or solely of fats tended to receive the worst ratings. Differences in food intensity in this group of food items were less pronounced.

The study authors developed a statistical model to predict food reward and liking and included various food constituents, intensity of taste, and carbohydrate-to-fat ratio. Statistical tests showed that participants liked foods containing roughly equal amounts of fats and carbohydrates, with the most intense taste and low fiber content. They also found such foods the most rewarding (see Figure 5).

 

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Figure 5. Research findings

 

Conclusion


The study showed that people find foods with intensive taste containing roughly equal amounts of fats and carbohydrates the most to their liking and the most rewarding. Contrary to previous studies, participants did not find ultraprocessed foods the most rewarding or like them the most. This shows that in this study, it was not the level of processing that determined how liked and rewarding a food item would be.

These findings can help researchers and health practitioners better understand the psychological values of different food items. This might allow for better diets and improved obesity prevention programs.

The paper “Evidence that carbohydrate-to-fat ratio and taste, but not energy density or NOVA level of processing, are determinants of food liking and food reward” was authored by Peter J. Rogers, Yeliz Vural, Niamh Berridge-Burley, Chloe Butcher, Elin Cawley, Ziwei Gao, Abigail Sutcliffe, Lucy Tinker, Xiting Zeng, Annika N. Flynn, Jeffrey M. Brunstrom, and J.C. Brand-Miller.

 

References

Gearhardt, A. N., Bueno, N. B., DiFeliceantonio, A. G., Roberto, C. A., Jiménez-Murcia, S., & Fernandez-Aranda, F. (2023). Social, clinical, and policy implications of ultra-processed food addiction. BMJ, e075354. https://doi.org/10.1136/bmj-2023-075354

Hedrih, V. (2023). Scientists Propose that Ultra-Processed Foods be Classified as Addictive Substances. CNP Articles in Nutritional Psychology. https://www.nutritional-psychology.org/scientists-propose-that-ultra-processed-foods-be-classified-as-addictive-substances/

Hedrih, V. (2024, February 19). Consuming Fat and Sugar (At The Same Time) Promotes Overeating, Study Finds. CNP Articles in Nutritional Psychology. https://www.nutritional-psychology.org/16563-2/

Ikemoto, S., Takahashi, M., Tsunoda, N., Maruyama, K., Itakura, H., & Ezaki, O. (1996). High-fat diet-induced hyperglycemia and obesity in mice: Differential effects of dietary oils. Metabolism, 45(12), 1539–1546. https://doi.org/10.1016/S0026-0495(96)90185-7

McDougle, M., de Araujo, A., Singh, A., Yang, M., Braga, I., Paille, V., Mendez-Hernandez, R., Vergara, M., Woodie, L. N., Gour, A., Sharma, A., Urs, N., Warren, B., & de Lartigue, G. (2024). Separate gut-brain circuits for fat and sugar reinforcement combine to promote overeating. Cell Metabolism. https://doi.org/10.1016/j.cmet.2023.12.014

Monteiro, C. A., Cannon, G., Levy, R. B., Moubarac, J. C., Louzada, M. L. C., Rauber, F., Khandpur, N., Cediel, G., Neri, D., Martinez-Steele, E., Baraldi, L. G., & Jaime, P. C. (2019). Ultra-processed foods: What they are and how to identify them. Public Health Nutrition, 22(5), 936–941. https://doi.org/10.1017/S1368980018003762

Rogers, P. J., Vural, Y., Berridge-Burley, N., Butcher, C., Cawley, E., Gao, Z., Sutcliffe, A., Tinker, L., Zeng, X., Flynn, A. N., Brunstrom, J. M., & Brand-Miller, J. C. (2024). Evidence that carbohydrate-to-fat ratio and taste, but not energy density or NOVA level of processing, are determinants of food liking and food reward. Appetite, 193, 107124. https://doi.org/10.1016/j.appet.2023.107124

Wong, M. C., Mccarthy, C., Fearnbach, N., Yang, S., Shepherd, J., & Heymsfield, S. B. (2022). Emergence of the obesity epidemic: 6-decade visualization with humanoid avatars. The American Journal of Clinical Nutrition, 115(4), 1189–1193. https://doi.org/10.1093/AJCN/NQAC005

 

 

Can Social Anxiety From Humans be Transmitted to Mice?

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  • A study published in PNAS: Neuroscience explored whether social anxiety can be transmitted from humans to mice via gut microbiota
  • Mice receiving gut microbiota from human participants with social anxiety disorder became more sensitive to social fear
  • While the nonsocial behaviors of these mice remained normal, biochemical changes linked to higher levels of social fear were also detected

What is social anxiety?

Social anxiety is a common human condition characterized by an intense fear of being evaluated by others in social situations (Morrison & Heimberg, 2013). People with social anxiety constantly worry about acting in a way that will be embarrassing or humiliating. They may even avoid social situations to prevent embarrassment. This fear can interfere with daily activities, work, and relationships. It can also lead to physical symptoms such as sweating, trembling, or a rapid heartbeat. If social anxiety reaches the level of severity where it impairs everyday functioning, it becomes a social anxiety disorder or social phobia.
Studies of brain activity link social anxiety with the hyperactivity of the amygdala region of the brain (Phan et al., 2006), a region involved in processing emotions, and with abnormalities in neural networks that use neurotransmitters serotonin and dopamine (e.g., Wee et al., 2008). However, the causes of these changes remain unknown (see Figure 1).

 

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Figure 1. Social anxiety Characteristics and brain

 

The microbiota-gut-brain axis and social anxiety

The recent discovery of the microbiota-gut-brain axis (MGBA), a bidirectional pathway through which microorganisms residing in our gut can affect processes in the brain and vice versa, showed that microbiota changes can affect different biochemical processes in the brain. Study after study on the microbiota-gut-brain axis shows that gut microbiota composition is linked to various mental health symptoms, that it can regulate reward processing in the brain, craving, certain aspects of social cognition, and binge drinking (Carbia et al., 2023; García-Cabrerizo et al., 2021; V. Hedrih, 2023). Transplanting microbiota from patients with Alzheimer’s disease into rats makes rats develop cognitive impairments (Grabrucker et al., 2023; Hedrih, 2024) (see Figure 2).

 

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Figure 2. Microbiota composition linked to various mental health symptoms

 

Transplanting microbiota from humans with Alzheimer’s disease into rats makes rats develop cognitive impairments

 

The current study

Recent research findings also show that the gut microbiota composition of individuals with social anxiety disorder differs from that of healthy humans. This made the author of this study, Nathaniel L. Ritz, and his colleagues wonder whether gut microbiota might have a causal role in the development of social anxiety. To test this, they conducted a study in which they transplanted the gut microbiota of individuals with social anxiety disorder and healthy individuals into the guts of mice (Ritz et al., 2024).

Study procedure

The study involved 12 human participants: 6 diagnosed with social anxiety disorder (SAD) and six healthy individuals without psychiatric history. The study authors selected the social anxiety group from participants of a previous study on the links between social anxiety and gut microbiota composition. Healthy participants came from University College Cork in Ireland. Both groups provided stool samples needed for transplantation into mice.
The study authors transplanted gut microbiota from the feces of human participants into the guts of 72 male mice. The mice were eight weeks old at the start of the study. They were acclimatized for two weeks and kept in a 12-hour light-dark cycle with free access to standard mouse food and water. Researchers then depleted mice’s gut microbiota using a strong cocktail of antibiotics (ampicillin, vancomycin, imipenem) to prepare them for human microbiota. Each mouse received microbiota from a randomly chosen human participant.
Stool samples from human participants were diluted, filtered, and inserted into the mice’s guts via oral gavage for three consecutive days. Oral gavage is a procedure where researchers use a syringe with a feeding tube to directly insert contents into the guts of mice through their mouths. Half of the mice received microbiota from individuals with social anxiety disorder, while the other half received it from healthy participants.
The study authors waited ten days after the transplantation procedure and then conducted a series of behavioral tests on the mice. They also collected stool samples of mice and conducted different biochemical analyses (see Figure 3).

 

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Figure 3. Study procedure (Ritz et al., 2023)

 

Gut microbiota from individuals with social anxiety differed in composition
Results showed differences in the gut microbiota composition between mice transplanted with microbiota from healthy participants and those from participants with social anxiety disorder. They differed in the abundance of three bacterial species – Bacteroides nordii, Bacteroides cellulosiyticus, and Phocaeicola massiliensi.

Gut microbiota from humans with social anxiety disorder induced social fear sensitivity in mice
Mice with microbiota from social anxiety disorder participants showed reduced social interactions in behavioral tests. However, their non-social exploratory behaviors did not differ from those of mice that received microbiota from healthy human participants. Based on this, the study authors concluded that transplantation of gut microbiota from humans with social anxiety disorder induced greater social fear sensitivity in these mice.

Biochemical changes also indicated heightened susceptibility to social fear
Mice that received gut microbiota from humans with social anxiety disorder had reduced levels of the hormone corticosterone. Corticosterone is a steroid hormone the adrenal cortex produces, primarily regulating stress responses, energy metabolism, immune reactions, and electrolyte balance.

They also showed reduced levels of oxytocin in a specific region of the brain (the bed nucleus of the stria terminalis) and lower activity of genes related to this neurotransmitter in other brain regions (the medial amygdala and the prefrontal cortex) (see Figure 4). Oxytocin is a hormone and neurotransmitter often called the “love hormone” due to its role in social bonding, sexual reproduction, childbirth, and maternal behaviors. Thus, its reduced levels and production make a mouse more susceptible to social fear and less motivated for social interactions.

 

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Figure 4. Effects of microbiota transfer from humans with social anxiety disorder

 

Conclusion

The study showed that it is possible to induce social fear sensitivity in mice by transplanting gut microbiota from humans with social anxiety disorder (i.e., highly sensitive to social fear). These results confirm that gut microorganisms can play a causal role in the development of social fear. If future studies show that changes to gut microbiota can also reduce social anxiety (instead of increasing it), it may open the possibility of developing ways to treat social anxiety using tailor-made probiotics.

 

It’s possible to induce social fear sensitivity in mice by transplanting gut microbiota from humans with social anxiety disorder

 

The paper “Social anxiety disorder-associated gut microbiota increases social fear” was authored by Nathaniel L. Ritz, Marta Brocka, Mary I. Butler, Caitlin S. M. Cowan, Camila Barrera-Bugueño, Christopher J. R. Turkingtona, Lorraine A. Draper, Thomaz F. S. Bastiaanssen, Valentine Turpin, Lorena Morales, David Campos, Cassandra E. Gheorghe, Anna Ratsika, Virat Sharma, Anna V. Golubeva, Maria R. Aburto, Andrey N. Shkoporov, Gerard M. Moloney, Colin Hill, Gerard Clarke, David A. Slattery, Timothy G. Dinan, and John F. Cryan.

 

References
Carbia, C., Bastiaanssen, T. F. S., Iannone, F., García-cabrerizo, R., Boscaini, S., Berding, K., Strain, C. R., Clarke, G., Stanton, C., Dinan, T. G., & Cryan, J. F. (2023). The Microbiome-Gut-Brain axis regulates social cognition & craving in young binge drinkers. eBioMedicine, 89, 104442. https://doi.org/10.1016/j.ebiom.2023.104442

García-Cabrerizo, R., Carbia, C., O´Riordan, K. J., Schellekens, H., & Cryan, J. F. (2021). Microbiota-gut-brain axis as a regulator of reward processes. Journal of Neurochemistry, 157(5), 1495–1524. https://doi.org/10.1111/JNC.15284

Grabrucker, S., Marizzoni, M., Silajdžić, E., Lopizzo, N., Mombelli, E., Nicolas, S., Dohm-Hansen, S., Scassellati, C., Moretti, D. V., Rosa, M., Hoffmann, K.,

Cryan, J. F., O’Leary, O. F., English, J. A., Lavelle, A., O’Neill, C., Thuret, S., Cattaneo, A., & Nolan, Y. M. (2023). Microbiota from Alzheimer’s patients induce deficits in cognition and hippocampal neurogenesis. Brain. https://doi.org/10.1093/brain/awad303

Hedrih, V. (2023, September 2). Gut Microbiota’s Role in Mental Health: The Positives and Negatives. CNP Articles in Nutritional Psychology. https://www.nutritional-psychology.org/how-your-gut-microbiota-is-linked-to-both-positive-and-negative-aspects-of-mental-health/

Hedrih, V. (2024, January 29). Can Symptoms of Alzheimer’s be Transferred to Rats via the Gut Microbiota of Alzheimer’s Patients? CNP Articles in Nutritional Psychology. https://www.nutritional-psychology.org/can-symptoms-of-alzheimers-be-transferred-to-rats-via-the-gut-microbiota-of-alzheimers-patients/

Morrison, A., & Heimberg, R. (2013). Social Anxiety and Social Anxiety Disorder. Annual Review of Clinical Psychology, 9, 249–274. https://doi.org/10.1146/annurev-clinpsy-050212-185631

Phan, K. L., Fitzgerald, D., Nathan, P., & Tancer, M. (2006). Association between Amygdala Hyperactivity to Harsh Faces and Severity of Social Anxiety in Generalized Social Phobia. Biological Psychiatry, 59, 424–429. https://doi.org/10.1016/j.biopsych.2005.08.012

Ritz, N. L., Brocka, M., Butler, M. I., Cowan, C. S. M., Barrera-Bugueño, C., Turkington, C. J. R., Draper, L. A., Bastiaanssen, T. F. S., Turpin, V., Morales, L., Campos, D., Gheorghe, C. E., Ratsika, A., Sharma, V., Golubeva, A. V., Aburto, M. R., Shkoporov, A. N., Moloney, G. M., Hill, C., … Cryan, J. F. (2024). Social anxiety disorder-associated gut microbiota increases social fear. Proceedings of the National Academy of Sciences, 121(1), e2308706120. https://doi.org/10.1073/pnas.2308706120

Wee, N. J. van der, Veen, J. F. van, Stevens, H., Vliet, I. M. van, Rijk, P. P. van, & Westenberg, H. G. (2008). Increased Serotonin and Dopamine Transporter Binding in Psychotropic Medication–Naïve Patients with Generalized Social Anxiety Disorder Shown by 123I-β-(4-Iodophenyl)-Tropane SPECT. Journal of Nuclear Medicine, 49(5), 757–763. https://doi.org/10.2967/jnumed.107.045518

Researchers Identify Neural Pathways Transmitting Anti-Inflammatory Effects of Hunger

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  • A series of experiments on mice published in Cell Reports found that hunger reduces inflammatory responses after an injury.
  • The anti-inflammatory effects of hunger were more robust than those of non-steroidal anti-inflammatory drugs.
  • AgRP neurons projecting to the paraventricular nucleus of the brain’s hypothalamus region mediate the majority of hunger’s anti-inflammatory effects.

People need food to survive. Severe malnutrition causes the body to break down its own tissues to meet energy needs. The body first utilizes the stored fat, but if starvation continues, it eventually uses muscle mass to fulfill its nutritional needs. Prolonged starvation impairs vital functions and leads to organ failure, weakened immune response, and severe hormonal imbalances (Sidiropoulos, 2007). Cognitive functions also deteriorate. But what happens when people restrict their food intake only for limited periods?

Restricted food intake
While the consequences of a chronic lack of food are dire, cultures worldwide have long believed that restricted food intake for limited periods of time can produce beneficial psychological and physiological consequences.

The practice of fasting, or abstaining from all or some kinds of food or drink for a specific period of time, is an important part of almost all major religions. Religions practice fasting as a means of spiritual discipline, self-reflection, and expressing devotion or penitence. It is often seen as a way to cleanse the body and mind, allowing for deeper religious or spiritual contemplation and connection with the divine or higher power.

 

Cultures worldwide have long believed that restricted food intake for limited periods of time can produce beneficial psychological and physiological consequences

 

Research studies show that restricted food intake for a limited period leads to complex physiological changes in the central and peripheral nervous systems. These changes can inhibit inflammation by preventing the activation of inflammasomes, multi-protein complexes that activate an inflammatory response. Additionally, restricted food intake reduces the production and release of pro-inflammatory cytokines, a group of signaling proteins secreted by immune cells that promote inflammation (Klima et al., 2023). On the psychological side, however, restrained eating can increase the feeling of hunger and food craving (Dicker-Oren et al., 2022).

Restricted food intake for a limited period can inhibit inflammation by preventing the activation of inflammasomes, multi-protein complexes that activate an inflammatory response, and reduce the production and release of pro-inflammatory cytokines 

While inflammation is an adaptive response, helping the body fight off infection or facilitating the repair of damaged tissue, long-term inflammation can become maladaptive and impair basic actions necessary for survival. It is also the cause or a contributing factor to many diseases and adverse medical conditions.

 

On the psychological side, however, restrained eating can increase the feeling of hunger and food craving (Dicker-Oren et al., 2022)

 

Agouti-related peptide (AgRP) neurons – hunger neurons
An important part of the neural circuits that react to restricted food intake are agouti-related peptide neurons, or AgRP neurons for short. Often referred to as “hunger neurons,” they are a specific type of neuron located in the brain’s arcuate nucleus of the hypothalamus region. These neurons play a critical role in regulating feeding behavior and energy homeostasis. AgRP neurons produce neuropeptides, including agouti-related peptide (AgRP) and neuropeptide Y (NPY), which are potent stimulators of appetite (Sternson & Atasoy, 2014) (see Figure 1).

 

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Figure 1. Role of AgRP neurons

 

The activity of AgRP neurons increases food intake and reduces energy expenditure, leading to weight gain. They are part of a complex neural network that responds to various signals related to energy status, such as hormones indicating hunger (ghrelin) or satiety (leptin and insulin). In conditions of energy deficit, such as fasting, AgRP neurons are stimulated, promoting hunger and encouraging food-seeking behavior (Atasoy et al., 2012; Chen et al., 2016).

 

“Hunger neurons” (AgRP) are a specific type of neuron located in the brain’s arcuate nucleus of the hypothalamus region and play a critical role in regulating feeding behavior and energy homeostasis

 

This system is crucial for survival, ensuring that energy intake is increased when energy stores are low. However, dysregulation of AgRP neurons and the pathways they influence can contribute to eating disorders and obesity (see Figure 2).

 

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Figure 2. Dysregulation of AgRP neurons

 

The current study
Study author Michelle L. Klima and her colleagues wanted to map the neural pathways from the brain to the periphery that convey the anti-inflammatory effects of food deprivation. They note that it is likely that hunger circuits (AgRP neurons) in the central nervous system play a role in this because previous studies have shown that manipulations of gene expressions in these neurons can influence immune responses (Klima et al., 2023).

They conducted a series of experiments on mice. The mice used in this study were male and female, kept in group housing, and at least eight weeks old.

Hunger reduces inflammation in response to irritants
In the first experiment, study authors injected either formalin, complete Freund’s adjuvant (CFA), or a saline solution into the paws of these mice. Formalin and CFA are strong irritants that cause an inflammatory reaction and swelling of the paw. The saline solution injection was a control procedure. It is not expected to produce an inflammatory response, so the researchers use it as a reference for comparison with the reactions caused by the injections of the other two substances.

In the experiment, the study authors had two groups of mice – 8 mice that were kept without food for 24 hours before the experiment, i.e., hungry, and another eight that had free access to food. Some mice were injected with irritants and others with a saline solution within the two groups.

Results showed that the paws of mice injected with irritants developed strong inflammation, visibly increasing in size. However, this inflammatory reaction was attenuated by approximately 50% in hungry mice compared to mice fed normally. Female mice had stronger paw inflammation after the CFA injection than male mice, but the inflammation reduction effects of hunger were similar in both sexes.

Concentrations of inflammatory cytokine tumor necrosis factor-alpha, an indicator of inflammation, were much lower in hungry mice, confirming that hunger had a strong anti-inflammatory effect. Researchers also compared the anti-inflammatory effects of hunger with the effects of non-steroidal anti-inflammatory drugs ketoprofen and ketorolac. They found that hunger reduced paw inflammation 20% more than these two drugs (see Figure 3).

 

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Figure 3. Experimental procedure and results 

 

Anti-inflammatory effects of hunger go from the brain through the vagus nerve
In their next experiment, study authors disabled the vagus nerve of the mice either by cutting it below the diaphragm or by injecting chemicals to disable parts of this nerve.

The vagus nerve extends from the brainstem to the abdomen, innervating various organs. It is crucial in the parasympathetic nervous system, responsible for the body’s rest and digest functions. The vagus nerve helps regulate heart rate, digestion, and respiratory rate but is also involved in inflammatory responses. It also conveys sensory information from the internal organs to the brain.

Results showed that the anti-inflammatory effects of hunger were suppressed when the vagus nerve was disabled in this way. This happened both when the nerve was physically cut and when chemicals were used.

Further experimentation showed that the anti-inflammatory effect is suppressed only when neurons going from the brain to the periphery (efferent neurons) are destroyed or disabled. Destroying or disabling neurons that carry information from the periphery to the brain (afferent neurons) did not affect the anti-inflammatory effects of hunger. This told researchers that the anti-inflammatory effects of hunger go from the brain through the vagus nerve to other areas of the body (see Figure 4).

 

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Figure 4. Link of vagus nerve ablation with anti-inflammatory effects of hunger 

 

Activation of AgRP neurons reduces inflammation
Next, the study authors looked for neural circuits in the brain that trigger the anti-inflammatory response to hunger. Knowing that AgRP neurons are activated by hunger, they first looked at them. These researchers genetically modified the AgRP neurons in a group of mice to be activated by specific chemicals or light.

Results showed an anti-inflammatory response followed when they artificially activated these neurons without restricting food to mice. Paws of mice in which study authors artificially activated AgRP neurons showed a much less intense inflammatory reaction after an irritant (CFA) injection than mice from the control group that ate normally and whose AgRp neurons were not artificially activated. The anti-inflammatory reaction caused by the activation of AgRP neurons was rapid, taking less than 1 hour for the reduction in multiple indicators of inflammation in the paw to become visible (see Figure 5).

 

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Figure 5. Central neural circuits that mediate the anti-inflammatory response to hunger

 

The study authors further sought to identify which AgRP neurons specifically activated the anti-inflammatory response. To do this, they activated specific groups of AgRP neurons one by one artificially in normally fed mice. They found that the anti-inflammatory action of AgRP neurons is distributed over two nodes – one projecting to the paraventricular hypothalamic nucleus and the other to the parabrachial nucleus regions of the brain. The magnitude of the anti-inflammatory effect of the first one was larger, mediating the bulk of the anti-inflammatory effects of these neurons.

Conclusions
Through a series of experiments on mice, this study showed that hunger produces an anti-inflammatory effect stronger than the effects of non-steroid anti-inflammatory medications such as ketoprofen and ketorolac. It showed that the bulk of the anti-inflammatory effect is mediated by hunger neurons, i.e., Agouti-related peptide (AgRP) neurons in the arcuate nucleus in the brain’s hypothalamus region. Even artificially triggering the activity of these neurons when a mouse is not hungry causes a rapid anti-inflammatory response.

These findings improve scientific understanding of the neural pathways of inflammation and can help healthcare researchers develop better ways to treat inflammation. Many diseases, from autoimmune diseases to skin disorders, are caused or aggravated by maladaptive immune responses of the body. Finding ways to better modulate or control the body’s immune response may be key to developing more effective treatments for them.

The paper “Anti-inflammatory effects of hunger are transmitted to the periphery via projection-specific AgRP circuits” was authored by Michelle L. Klima, Kayla A. Kruger, Nitsan Goldstein, Santiago Pulido, Aloysius Y.T. Low, Charles-Antoine Assenmacher, Amber L. Alhadeff, and J. Nicholas Betle.

 

References

Atasoy, D., Betley, J. N., Su, H. H., & Sternson, S. M. (2012). Deconstruction of a neural circuit for hunger. Nature, 488(7410), 172–177. https://doi.org/10.1038/nature11270

Chen, Y., Lin, Y.-C., Zimmerman, C. A., Essner, R. A., & Knight, Z. A. (2016). Hunger neurons drive feeding through a sustained, positive reinforcement signal. ELife, 5, e18640. https://doi.org/10.7554/eLife.18640.001

Dicker-Oren, S. D., Gelkopf, M., & Greene, T. (2022). The dynamic network associations of food craving, restrained eating, hunger and negative emotions. Appetite, 175(March), 106019. https://doi.org/10.1016/j.appet.2022.106019

Klima, M. L., Kruger, K. A., Goldstein, N., Pulido, S., Low, A. Y. T., Assenmacher, C. A., Alhadeff, A. L., & Betley, J. N. (2023). Anti-inflammatory effects of hunger are transmitted to the periphery via projection-specific AgRP circuits. Cell Reports, 42(11). https://doi.org/10.1016/j.celrep.2023.113338

Sidiropoulos, M. (2007). Anorexia Nervosa: The physiological consequences of starvation and the need for primary prevention efforts. CASE PRESENTATION. McGill Journal of Medicine, 10(1), 20–25.

Sternson, S. M., & Atasoy, D. (2014). Agouti-related protein neuron circuits that regulate appetite. Neuroendocrinology, 100, 95–102. https://doi.org/10.1159/000369072

 

Frequent Consumption of Fried Foods is Associated With a Slightly Higher Risk of Depression and Anxiety

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  • A study of UK Biobank data published in PNAS reported that frequent consumption of fried food increased the risk of anxiety by 12% and the risk of depression by 7%.
  • Fried potato consumption was specifically associated with a somewhat increased risk of depression and anxiety symptoms.
  • An experiment on zebrafish confirmed that chronic exposure to acrylamide, a substance created when food is fried, creates anxiety-like symptoms in these fish.

The consolidation of research in the diet-mental health relationship within nutritional psychology has shown that our food choices and patterns can influence our moods and state of mind, and our moods and state of mind can influence our food choices and patterns (NPRL). People tend to eat when stressed or bored (Dicker-Oren et al., 2022; Stevenson et al., 2023). They can also feel angry when hungry (called hanger), in which one experiences anger due to hunger (Hedrih, 2023a).

 

Food choices and patterns can influence our moods and state of mind, which can influence our food choices and patterns

 

But could our dietary choices be associated with serious mental health disorders? Disorders like anxiety or depression?

Depression and anxiety
Depression and anxiety are two of the most frequent mental health disorders. Depression is characterized by persistently low mood and a lack of interest or pleasure in activities. A depressed individual will often feel sad, hopeless, and with little energy. This can lead to adverse changes in appetite and sleep patterns, but sometimes also thoughts of suicide.

Anxiety, on the other hand, is a condition marked by persistent and excessive worry that interferes with daily activities. It is typically accompanied by physical symptoms like restlessness, fatigue, difficulty concentrating, irritability, muscle tension, and sleep disturbances. While both conditions involve emotional distress, depression primarily affects mood and motivation, whereas anxiety is centered around fear and nervousness (see Figure 1).

 

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Figure 1. Characteristics of and differences between depression and anxiety

 

Studies indicate that the share of individuals suffering from depression has been increasing both in the U.S. and globally in the past decades (Steffen et al., 2020; Weinberger et al., 2018). Anxiety and depression often occur together. Estimates state that the number of people suffering from anxiety increased after the global COVID-19 pandemic by 26% (Wang et al., 2023).

 

The number of people suffering from anxiety increased after the global COVID-19 pandemic by 26% (Wang et al., 2023)

 

Diet and mental health
While the precise causes of anxiety and depression are unknown, a great number of genetic, biological, environmental, and psychological factors have been found to play a role in their development. Recent studies have also linked certain dietary habits, such as the consumption of ultra-processed foods or sweetened beverages, to increased depression risks (Hedrih, 2023b; Samuthpongtorn et al., 2023).

Other researchers bring into focus the so-called Western diet, a diet based on fried and processed foods, refined grains, sugary products, and beer, as a dietary pattern associated with an increased risk of depression and anxiety (Wang et al., 2023). Within this diet, researchers single out fried food as particularly contributing to these adverse links with mental health.

 

The Western diet is a dietary pattern associated with an increased risk of depression and anxiety

 

Fried food and health
Frying is a method of food preparation that people widely use at home and in restaurants. However, the process of frying changes the nutrient composition of the food and can produce various hazardous compounds. One such substance is acrylamide. Acrylamide is created during the process of frying foods that are rich in carbohydrates, such as potatoes. Acrylamide is known to be toxic for neurons in higher concentrations. Studies have linked its prolonged intake to an increased risk of cardiovascular disease, neurological disorders, obesity, metabolic syndrome, and depression.

 

The process of frying changes the food’s nutrient composition and can produce various hazardous compounds 

 

The current study
Study author Anli Wang and her colleagues wanted to examine the association between the intake of a substance found in fried food called acrylamide and depression and anxiety in a large sample from the general population. Acrylamide is a substance found in fried food.

These authors expected that high consumption of fried food and, consequently, higher intake of acrylamide would be associated with more severe symptoms of anxiety and depression. Ingested acrylamide would lead to abnormal levels of lipids, such as cholesterol and triglycerides, in the blood and inflammation. This would, in turn, impact the likelihood that depression or anxiety would develop (see Figure 2).

 

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Figure 2. Effects of acrylamide ingested from fried foods

 

In this study, the authors analyzed human data from the UK Biobank and conducted an experiment on zebrafish.

The UK Biobank
The UK Biobank is a large-scale biomedical database and research resource containing in-depth genetic and health information from half a million UK participants. The project, which began in 2006 and is ongoing, aims to improve the prevention, diagnosis, and treatment of a wide range of serious and life-threatening illnesses.

UK Biobank participants provided blood, urine, and saliva samples and detailed health and lifestyle information, which researchers worldwide can access to conduct health-related research. Many valuable scientific discoveries and insights have come from this database, and new studies using UK Biobank data are continuously being published.

For this study, researchers analyzed data from 140,728 individuals from the UK Biobank. Of these, during the 11.3 years of follow-up, 8,294 had symptoms of anxiety, and 12,735 had depression symptoms (see Figure 3).

 

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Figure 3. Study procedure

 

The Zebrafish experimentI
n addition to analyzing the UK Biobank data, the researchers conducted an experiment on zebrafish. This experiment exposed zebrafish groups to different acrylamide concentrations for 180 days. After the exposure period, they conducted a series of tests to evaluate anxiety-like symptoms in these fish. At the end of the experiment, they killed the fish and harvested their brains to analyze tissue changes.

Zebrafish are a small, freshwater fish species extensively used in biomedical research due to their genetic similarity to humans, transparent embryos that allow easy observation of developmental processes, and rapid reproduction.

These researchers looked for specific symptoms in zebrafish exposed to acrylamide –specifically thigmotaxis and scototaxis. Scototaxis is a tendency of fish to prefer darker areas over lighter ones in their environment. Thigmotaxis is a preference for staying close to physical objects or walls in their aquarium. In research, both of these tendencies are indications that the fish is experiencing anxiety-like conditions and that it is under stress. The more pronounced they are, the higher the anxiety-like conditions in the fish are.

 

UK Biobank People consuming fried food more often had somewhat higher risks of depression and anxiety

 

Results from the UK Biobank showed that individuals consuming at least one fried meal per day were more likely to be younger, male, and active smokers than those consuming fried food less often. After taking into account the age and sex of participants, statistical analyses showed that individuals consuming fried food more often were somewhat more likely to have anxiety and depression symptoms.

Notably, individuals consuming fried food were 12% more likely to have anxiety symptoms and 7% more likely to have symptoms of depression. Results of looking at specific food types highlighted fried potatoes and fried white meat. Consumption of each of these foods was associated with a 4% higher risk of anxiety and a 7% higher risk of depression. However, after adjusting for various other factors, the link with fried white meat consumption disappeared, but the one with fried potato consumption remained (see Figure 4).

 

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Figure 4. Fried food consumption and depression and anxiety symptoms 

 

Individuals consuming fried food were 12% more likely to have anxiety symptoms and 7% more likely to have symptoms of depression

 

Zebrafish exposed to acrylamide developed behaviors indicative of stress and anxiety
The experiment on zebrafish showed that fish chronically exposed to acrylamide in a concentration of 0.5 mM decreased in body mass and length. Fish exposed to even lower concentrations of acrylamide (0.125-0.5 mM) showed signs of scototaxis. They spent more time in the dark zones than zebrafish without this exposure. The time the fish spent in the dark zones was associated with the concentration of acrylamide used.

Other behavioral comparisons between zebrafish exposed to acrylamide and those in the control group also confirmed the finding about anxiety-like symptoms in fish exposed to this substance. Analysis of tissues of zebrafish showed that exposure to acrylamide disturbed their lipid metabolism and initiated an inflammatory response, which, in turn, likely led to the observed behavioral changes (see Figure 5).

 

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Figure 5. Behavioral changes and physical changes in Zebrafish exposed to acrylamide

 

Conclusion
An analysis of UK Biobank data showed that individuals frequently consuming fried food have a slightly higher risk of having depression or anxiety symptoms. An experiment on zebrafish confirmed that chronic exposure to acrylamide, a substance created when food rich in carbohydrates is fried, might cause this link. Exposure to acrylamide can disturb the metabolism of lipids and initiate an inflammatory response that may, in turn, contribute to the development of anxiety and depression symptoms. 

 

Chronic exposure to acrylamide, a substance created when food rich in carbohydrates is fried, might cause this link

 

These findings contribute to a better scientific understanding of the diet-mental health relationship (DMHR). They may help individuals and mental health practitioners prevent or better treat anxiety and depression conditions by modifying their diet. The insights brought by this study may also allow for the creation of better menus and meal plans in the hospitality industry and various institutional food services.

The paper “High fried food consumption impacts anxiety and depression due to lipid metabolism disturbance and neuroinflammation” was authored by Anli Wang, Xuzhi Wan, Pan Zhuang, Wei Jia, Yang Ao, Xiaohui Liu, Yimei Tian, Li Zhu, Yingyu Huang, Jianxin Yao, Binjie Wang, Yuanzhao Wu , Zhongshi Xu, Jiye Wang, Weixuan Yao, Jingjing Jiao, and Yu Zhang.

 

References

Dicker-Oren, S. D., Gelkopf, M., & Greene, T. (2022). The dynamic network associations of food craving, restrained eating, hunger and negative emotions. Appetite, 175(March), 106019. https://doi.org/10.1016/j.appet.2022.106019

Hedrih, V. (2023a). Food and Mood: Is the Concept of ‘Hangry’ Real? CNP Articles in Nutritional Psychology.
https://www.nutritional-psychology.org/food-and-mood-is-the-concept-of-hangry-real/

Hedrih, V. (2023b). Women Consuming Lots of Artificially Sweetened Beverages Might Have a Higher Risk of Depression, Study Finds. CNP Articles in Nutritional Psychology. https://www.nutritional-psychology.org/women-consuming-lots-of-artificially-sweetened-beverages-might-have-a-higher-risk-of-depression-study-finds/

Samuthpongtorn, C., Nguyen, L. H., Okereke, O. I., Wang, D. D., Song, M., Chan, A. T., & Mehta, R. S. (2023). Consumption of Ultraprocessed Food and Risk of Depression. JAMA Network Open, 6(9), e2334770. https://doi.org/10.1001/jamanetworkopen.2023.34770

Steffen, A., Thom, J., Jacobi, F., Holstiege, J., & Bätzing, J. (2020). Trends in prevalence of depression in Germany between 2009 and 2017 based on nationwide ambulatory claims data. Journal of Affective Disorders, 271, 239–247. https://doi.org/10.1016/J.JAD.2020.03.082

Stevenson, R. J., Bartlett, J., Wright, M., Hughes, A., Hill, B. J., Saluja, S., & Francis, H. M. (2023). The development of interoceptive hunger signals. Developmental Psychobiology, 65(2), 1–11. https://doi.org/10.1002/dev.22374

Wang, A., Wan, X., Zhuang, P., Jia, W., Ao, Y., Liu, X., Tian, Y., Zhu, L., Huang, Y., Yao, J., Wang, B., Wu, Y., Xu, Z., Wang, J., Yao, W., Jiao, J., & Zhang, Y. (2023). High-fried food consumption impacts anxiety and depression due to lipid metabolism disturbance and neuroinflammation. Proceedings of the National Academy of Sciences of the United States of America, 120(118). https://doi.org/10.1073/pnas.2221097120

Weinberger, A. H., Gbedemah, M., Martinez, A. M., Nash, D., Galea, S., & Goodwin, R. D. (2018). Trends in depression prevalence in the USA from 2005 to 2015: widening disparities in vulnerable groups. Psychological Medicine, 48(8), 1308–1315. https://doi.org/10.1017/S0033291717002781

 

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