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Lactobacillus Bacteria in the Gut Increase Stress Resilience in Mice

Posted on June 3, 2024June 12, 2024 by CNP Staff

A study on mice published in Brain Behavior and Immunity found that Lactobacillus bacteria living in the gut protect against developing anxiety- and depression-like symptoms after stress exposure.
Anxiety- and depression-like symptoms could be induced in mice not exposed to stress by transplanting gut microbiota from stressed mice
Gut Lactobacillus bacteria increased the quantities of the interferon-gamma protein, which reduced neural reactions to stress.

When we notice something really harmful, threatening, or challenging is happening, we experience a series of emotional states that prepare us to deal with that event. We may experience fear or anxiety, but we can also experience rage. If the developments threaten someone we love, our mind will remind us of that love and the need to act to protect that person. In such situations, our bodies will experience stress. The reactions will not be solely psychological, but a series of strong physiological changes will also occur.

What is stress?

Stress is the body’s natural response to perceived threats or challenges. It activates the body’s fight-or-flight response, releasing hormones like cortisol and adrenaline, which prepare the body to react to stressful situations. Short-term stress can be beneficial because it enhances focus and the body’s ability to withstand exertion and hardship. However, chronic stress can lead to various health problems, including anxiety, depression, and cardiovascular issues (McEwen, 2017; Tafet & Bernardini, 2003; Torpy et al., 2007).

Studies have also linked chronic stress with the dysregulation of the immune system. Chronic stress is associated with a state of chronic low-grade inflammation that results in delayed wound healing and increased susceptibility to infectious illnesses (Gouin, 2011). The recent discovery of the microbiota-gut-brain axis (MGBA) has led to a stream of research implicating microorganisms living in the gut in the changes that develop due to chronic stress (Hedrih, 2023; Zhu et al., 2023).

The recent discovery of the MGBA has led to research implicating microorganisms living in the gut in the changes that develop due to chronic stress

The microbiota-gut-brain axis

The microbiota-gut-brain axis is a bidirectional communication pathway linking gut microbiota, i.e., the microorganisms living in the human gastrointestinal tract, with the brain. Through this pathway, gut microbiota can influence brain function and behavior and vice versa. This communication is achieved through mechanisms that are part of the nervous system and immune system, but also through hormones (García-Cabrerizo et al., 2021; Hedrih, 2023; Heiss et al., 2021).

Studies often report finding disruptions in the gut microbiota of individuals experiencing intensive stress or mood disorders (Merchak et al., 2024; Valles-Colomer et al., 2019) (see Figure 1).

Figure 1. Microbiota-gut-brain axis pathway

Studies often report finding disruptions in the gut microbiota of individuals experiencing intensive stress or mood disorders

Very often, there tend to be less Lactobacillus bacteria in the guts of these individuals. Also, studies on animals indicate that gut Lactobacillus bacteria aid stress resistance (Merchak et al., 2024)

The current study

Study author Andrea R. Merchak and her colleagues wanted to explore how completely removing Lactobacillus bacteria from mice’s guts would affect their behavior and specific metabolic processes. They used a set of eight bacterial strains known as the Altered Schaedler Flora to achieve this.

The Altered Schaedler Flora (ASF) consists of two strains of Lactobacillus, two strains of Clostridium, and one strain of Bacteroides, Mucispirillum, Eubacterium, and Pseudoflavonifactor. This set of bacterial species colonizes the guts of mice used in research, revealing the composition of their gut microbiota.

The study was conducted on four different groups of mice: a strain without gut microbiota (germ-free mice), a strain with Altered Schaedler Flora (ASF), a strain with the same flora but without Lactobacillus bacteria, and a group of standard laboratory mice (C57BL/6J).

Transferring gut microbiota from stressed mice to germ-free mice induced depressive- and anxiety-like symptoms

Some of the mice were exposed to unpredictable chronic stress during the experiments. Researchers would restrain them for two hours each day, but at different times, and apply one of three randomly chosen stressors each night—wet bedding, tilted cage, or two cage changes in a day. These mice developed symptoms similar to anxiety and depression in humans. As expected, they also had lower levels of gut Lactobacillus bacteria.

Researchers then transferred these mice’s dirty bedding to germ-free mice’s cages to transfer their gut microbiota. After this, the previously germ-free mice also developed anxiety—and depression-like behaviors, even though they were not exposed to stress. Further analyses revealed that these microbiota from stressed mice suppressed the production of interferon-gamma (IFNγ), an important signaling protein involved in the immune response (see Figure 2).

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

Mice without Lactobacillus are more susceptible to stress

Study authors exposed some of the ASF mice with and without Lactobacillus bacteria in their guts to mild stress – being restrained in small vials with breathing holes for 3 hours. After this treatment, they analyzed the activity level in their brains during that period (using c-Fos staining after euthanizing the mice). They found that mice without gut Lactobacillus bacteria had increased activity in regions of the brain associated with fear and anxiety (the amygdala and the paraventricular thalamus) compared to mice with these bacteria (see Figure 3).

Figure 3. Link of Lactobacillus with stress

Mice without gut Lactobacillus bacteria had increased activity in regions of the brain associated with fear and anxiety

Interferon-gamma protects against the harmful effects of stress

They conducted another, somewhat different, experiment to verify this finding, and it also confirmed that mice without Lactobacillus bacteria are more susceptible to stress. Finally, the study authors conducted an experiment in which they administered interferon-gamma to one group of mice and antibodies to neutralize interferon-gamma to the other before exposing them to acute stress. Analysis of the brains of these mice showed that mice that received interferon-gamma had lower, while those who received the antibodies for it had higher levels of neural activity in brain regions responsible for fear and anxiety.

Mice without Lactobacillus bacteria are more susceptible to stress

Conclusion

The study showed that Lactobacillus bacteria seem to have a protective effect against developing anxiety—and depression-like symptoms after stress in mice. These bacteria seem to regulate the levels of the signaling protein interferon-gamma, which, in turn, reduces the anxiety—and depression-like effects of stress.

While humans and mice are very different species, they share many physiological similarities. If these findings are confirmed in humans, this might open ways to develop resilience to stress through interventions aimed at gut microbiota and diet.

The paper “Lactobacillus from the Altered Schaedler Flora maintain IFNγ homeostasis to promote behavioral stress resilience” was authored by Andrea R. Merchak, Samuel Wachamo, Lucille C. Brown, Alisha Thakur, Brett Moreau, Ryan M. Brown, Courtney R. Rivet-Noor, Tula Raghavan, and Alban Gaultier.

References

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

Gouin, J.-P. (2011). Chronic Stress, Immune Dysregulation, and Health. American Journal of Lifestyle Medicine, 5(6), 476–485. https://doi.org/10.1177/1559827610395467

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/

Heiss, C. N., Mannerås-Holm, L., Lee, Y. S., Serrano-Lobo, J., Håkansson Gladh, A., Seeley, R. J., Drucker, D. J., Bäckhed, F., & Olofsson, L. E. (2021). The gut microbiota regulates hypothalamic inflammation and leptin sensitivity in Western diet-fed mice via a GLP-1R-dependent mechanism. Cell Reports, 35(8). https://doi.org/10.1016/j.celrep.2021.109163

McEwen, B. S. (2017). Neurobiological and Systemic Effects of Chronic Stress. Chronic Stress, 1. https://doi.org/10.1177/2470547017692328

Merchak, A. R., Wachamo, S., Brown, L. C., Thakur, A., Moreau, B., Brown, R. M., Rivet-Noor, C. R., Raghavan, T., & Gaultier, A. (2024). Lactobacillus from the Altered Schaedler Flora maintain IFNγ homeostasis to promote behavioral stress resilience. Brain, Behavior, and Immunity, 115, 458–469. https://doi.org/10.1016/j.bbi.2023.11.001

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

Valles-Colomer, M., Falony, G., Darzi, Y., Tigchelaar, E. F., Wang, J., Tito, R. Y., Schiweck, C., Kurilshikov, A., Joossens, M., Wijmenga, C., Claes, S., Van Oudenhove, L., Zhernakova, A., Vieira-Silva, S., & Raes, J. (2019). The neuroactive potential of the human gut microbiota in quality of life and depression. Nature Microbiology, 4(4), 623–632. https://doi.org/10.1038/s41564-018-0337-x

Zhu, X., Sakamoto, S., Ishii, C., Smith, M. D., Ito, K., Obayashi, M., Unger, L., Hasegawa, Y., Kurokawa, S., Kishimoto, T., Li, H., Hatano, S., Wang, T. H., Yoshikai, Y., Kano, S. ichi, Fukuda, S., Sanada, K., Calabresi, P. A., & Kamiya, A. (2023). Dectin-1 signaling on colonic γδ T cells promotes psychosocial stress responses. Nature Immunology. https://doi.org/10.1038/s41590-023-01447-8

Adherence to the Nordic Diet Is Associated with Lower Depression, Anxiety, and Stress in Individuals Recovering from COVID-19

Posted on May 27, 2024September 12, 2025 by CNP Staff

A study in Iran published in BMC Nutrition found that individuals adhering to the Nordic diet tended to show lower levels of anxiety, depression, and stress after recovering from COVID-19.
Higher intake of whole grains was associated with lower levels of anxiety, depression and stress.
Individuals with more root vegetables in their diets tended to have better sleep quality.

The body needs a wide variety of nutrients to stay healthy. Some are needed in large quantities, and they are called macronutrients, while others are needed in smaller quantities (micronutrients). Still, all of these nutrients are needed for our body to remain healthy. To obtain all the nutrients found in different food items, people establish patterns of eating and drinking we refer to as “diets” (or, in nutritional psychology, “dietary intake patterns”).

The Nordic diet

The Nordic diet is a nutritional approach based on traditional foods commonly consumed in the Nordic countries—Norway, Denmark, Sweden, Finland, and Iceland. It emphasizes a high intake of whole grains, such as barley, rye, and oats; locally sourced fruits and berries, especially those native to the region, like lingonberries and bilberries; and vegetables, particularly root vegetables and cabbages.

The diet also includes a significant amount of fatty fish such as salmon, mackerel, and herring, which provide a healthy dose of omega-3 fatty acids. Lean meats, particularly game meats and free-range livestock, are also part of the diet, though consumed in moderation. Dairy products are included but typically in fermented forms like fermented milk and cheese (Adamsson et al., 2012) (see Figure 1).

Figure 1. Traditional foods common in Nordic countries

Multiple research studies examined the health effects of the Nordic diet and its associations with health outcomes. They tended to report beneficial results, often comparing the Nordic diet with the Mediterranean diet, another food intake pattern known for its health benefits. These studies found the Nordic diet to be beneficial for conditions including low-grade inflammation and cardiovascular health in individuals with high cholesterol, overweight, and high blood pressure (Adamsson et al., 2011; Lankinen et al., 2019; Poulsen et al., 2014).

The Nordic diet has been found to be beneficial for conditions involving low-grade inflammation and cardiovascular health

The 2020 COVID-19 pandemic

The COVID-19 pandemic was a global health crisis caused by the novel coronavirus SARS-CoV-2, which first emerged in late 2019. It led to widespread illness and death across the globe, significantly impacting public health, economies, and daily life. Governments worldwide responded with measures such as lockdowns, travel restrictions, and mask mandates to control the spread of the virus.

The COVID-19 disease, once triggered by the SARS-CoV-2 virus, predominantly affects the respiratory system, typically causing symptoms like coughing, shortness of breath, and pneumonia. However, it can also affect other body systems and lead to a wide range of symptoms, including fever, fatigue, and loss of taste or smell. In severe cases, COVID-19 can cause complications such as acute respiratory distress syndrome, cardiovascular issues, and multi-organ failure (Huang et al., 2020).

A study reported that 35% of COVID-19 patients also have (or develop) moderate or severe psychological symptoms. A review of studies reported that 36% of COVID-19 patients developed anxiety, while 42% showed symptoms of insomnia (Araste et al., 2024).

Thirty-five percent of COVID-19 patients have (or develop) moderate or severe psychological symptoms

The current study

Study author Asie Araste and her colleagues wanted to investigate the association between adherence to the Nordic diet and mental health symptoms in both individuals who recovered from COVID-19 and healthy people.

Study participants were 123 individuals who recovered from COVID-19 within the past 1 month and 123 healthy adults with no history of COVID-19. They were referred to the Qaem Hospital in Mashad, Iran. The average age of participants was 57-60 years. Around 45% of participants were female. The two groups showed differences in dietary patterns and overall energy intake (Araste et al., 2024).

Study participants completed a dietary intake assessment (Food Frequency Questionnaire) and assessments of depression, anxiety, and stress (the DASS scales), sleep quality (the Pittsburgh Sleep Quality Index), insomnia severity (the Insomnia Severity Index), and quality of life (the Short-Form Health Survey, SF-36) (see Figure 2).

Figure 2. Study procedure

Individuals whose diets were closer to the Nordic diet tended to have better mental health indicators

The results of this study indicated that individuals consuming more whole grains tended to have lower anxiety, stress, and depression scores. Those eating more fruits tended to have lower depression scores. Individuals consuming more root vegetables tended to have less pronounced insomnia symptoms and better sleep quality.

Individuals whose dietary pattern was highly similar to the Nordic Diet (i.e., who showed high adherence to the Nordic diet) tended to have lower symptoms of anxiety, depression, and stress. This association was detected after adjusting for age, education, gender, and energy intake. However, the link between adherence to the Nordic diet and these mental health outcomes was present only in participants who recently recovered from COVID-19. It was absent in the group of healthy participants. There were no associations of adherence to the Nordic diet with sleep quality, insomnia, or quality of life in either of the two groups (see Figure 3).

Figure 3. Nordic diet and mental health

Conclusion

The study showed that individuals eating more whole grains, fruits, and root vegetables tended to have better values of specific mental health indicators. Among individuals who recently recovered from COVID-19, those whose dietary patterns highly resembled the Nordic diet tended to have lower symptoms of stress, anxiety, and depression.

The design of this study does not allow any cause-and-effect conclusions to be drawn. Therefore, it is not possible to say whether adherence to the Nordic diet leads to lower levels of stress, depression, and anxiety symptoms or whether lower levels of these symptoms allow individuals to structure their dietary patterns in a way that highly resembles the Nordic diet. Other possibilities are also open.

However, a balanced diet affording all the necessary macro and micronutrients is a prerequisite for maintaining good physical and mental health. Enroll in NP 150 (Coming Summer 2024) to learn about the mechanisms connecting diet and mental health.

The paper “Adherence to the nordic diet is associated with anxiety, stress, and depression in recovered COVID-19 patients, a case-control study” was authored by Asie Araste, MohammadReza Shadmand Foumani Moghadam, Kimia Mohammadhasani, Mohammad Vahedi Fard, Zahra Khorasanchi, MohammadReza Latifi, Elahe Hasanzadeh, Nasrin Talkhi, Payam Sharifan, Parisa Asadiyan-Sohan, Marjan Khayati Bidokhti, Arezoo Ghassemi, Reza Assaran Darban, Gordon Ferns, and Majid Ghayour-Mobarhan.

References

Adamsson, V., Reumark, A., Cederholm, T., Vessby, B., Risérus, U., & Johansson, G. (2012). What is a healthy Nordic diet? Foods and nutrients in the NORDIET study. Food & Nutrition Research, 56(1), 18189. https://doi.org/10.3402/fnr.v56i0.18189

Adamsson, V., Reumark, A., Fredriksson, I.-B., Hammarström, E., Vessby, B., Johansson, G., & Risérus, U. (2011). Effects of a healthy Nordic diet on cardiovascular risk factors in hypercholesterolaemic subjects: A randomized controlled trial (NORDIET). Journal of Internal Medicine, 269(2), 150–159. https://doi.org/10.1111/j.1365-2796.2010.02290.x

Araste, A., Moghadam, M. R. S. F., Mohammadhasani, K., Fard, M. V., Khorasanchi, Z., Latifi, M., Hasanzadeh, E., Talkhi, N., Sharifan, P., Asadiyan-Sohan, P., Bidokhti, M. K., Ghassemi, A., Darban, R. A., Ferns, G., & Ghayour-Mobarhan, M. (2024). Adherence to the nordic diet is associated with anxiety, stress, and depression in recovered COVID-19 patients, a case-control study. BMC Nutrition, 10(1), 38. https://doi.org/10.1186/s40795-024-00845-x

Huang, C., Wang, Y., Li, X., Ren, L., Zhao, J., Hu, Y., Zhang, L., Fan, G., Xu, J., Gu, X., Cheng, Z., Yu, T., Xia, J., Wei, Y., Wu, W., Xie, X., Yin, W., Li, H., Liu, M., … Cao, B. (2020). Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China. The Lancet, 395(10223), 497–506. https://doi.org/10.1016/S0140-6736(20)30183-5

Lankinen, M., Uusitupa, M., & Schwab, U. (2019). Nordic Diet and Inflammation—A Review of Observational and Intervention Studies. Nutrients, 11(6), 1369. https://doi.org/10.3390/nu11061369

Poulsen, S. K., Due, A., Jordy, A. B., Kiens, B., Stark, K. D., Stender, S., Holst, C., Astrup, A., & Larsen, T. M. (2014). Health effect of the New Nordic Diet in adults with increased waist circumference: A 6-mo randomized controlled trial1234. The American Journal of Clinical Nutrition, 99(1), 35–45. https://doi.org/10.3945/ajcn.113.069393

Do Gut Microbiota Play an Important Role in Regulating Food Intake and Satiety?

Posted on May 20, 2024May 24, 2024 by CNP Staff

A review published in the Journal of Physiological Sciences discussed how the human body regulates satiety and food intake.
GLP-1 encourages the development of various advantageous bacteria in the gut, making it easier to produce satiety-related microbial products.
Gut microorganisms that produce short-chain fatty acids stimulate cells in the colon lining to produce GLP-1 and other hormones.
Other types of gut microorganisms produce substances that can affect inflammatory processes in the hypothalamus, disrupting or restoring the functionality of the body’s food intake regulation mechanism.

Living beings need to eat to stay alive. Multiple times daily, processes in our body tell our brain that we need to eat. We feel hunger, prompting us to look for food and eat it. After we have eaten, we feel satiated. This cycle continues as long as we live. But how does this function on the neural and biochemical level?

Hunger and satiety

A complex interaction between the digestive system, the brain, and various hormones regulates hunger and satiety. Satiety is the feeling of being full or satisfied after eating. It’s a physiological state where the body senses that it has consumed enough food. This allows it to regulate how much and how often a person eats. Satiety is influenced by various factors, including the type and volume of food consumed, its nutrient content, and hormonal responses during and after a meal.

When the stomach is empty, the hormone ghrelin is released, which signals the brain to trigger feelings of hunger. After eating, the stomach and intestines produce hormones like glucagon-like peptide-1 (or GLP-1), peptide YY (PYY), and others, signaling the brain to produce feelings of satiety. Leptin, a hormone primarily produced by fat tissue, acts in a similar fashion, signaling the brain to suppress appetite. The more fat tissue there is, the higher the production of leptin (Hedrih, 2023; Stevenson et al., 2023; Swami et al., 2022) (see Figure 1).

Figure 1. Complex interaction between the digestive system, brain, and hormones to regulate hunger and satiety

These hormones act on the hypothalamus, a region of the brain that plays a key role in regulating hunger and satiety. This structure of the brain contains groups of neurons that increase the feeling of satiety, such as the pro-opiomelanocortin (POMC) and cocaine–amphetamine-regulated transcript-containing (CART) neurons, but also those that trigger appetite and eating behaviors—neuropeptide Y (NPY) and agouti-related peptide (AgRP) (Barakat et al., 2024).

AgRP neurons are also known as “hunger neurons” because studies demonstrate that artificially triggering them (in rodents) initiates feeding behavior (Chen et al., 2016) (see Figure 2).

Figure 2. “Hunger and satiety neurons” in the hypothalamus

The sensation of hunger

Hunger is not only a physiological process but also a subjective sensation. This sensation makes us more sensitive to stimuli related to food, pay more attention to food items and to things we learned to associate with food (e.g., restaurant or food brand logos), and be willing to eat (Hedrih, 2023; Lazarus et al., 1953; McKiernan et al., 2008).

Hunger is not only a physiological process but also a subjective sensation

Scientists initially thought that hunger results from decreased levels of nutrients in the body (e.g., lower blood sugar levels, decreased fat contents, empty stomach), but more novel studies indicated that many other conditions can trigger this sensation. These include (but are not limited to) boredom, desire for sensory stimulation, lack of sleep, and chronic stress (Brondel et al., 2010; Hedrih, 2023; Levine & Morley, 1981; McKiernan et al., 2008; Swami et al., 2022). Also, humans and animals can develop eating habits at specific times. These habits make them feel hungry when what they perceive as mealtime arrives (Isherwood et al., 2023) (Nutritional Psychology Research Library, 2024) (see Figure 3).

Figure 3. Factors influencing our sense of hunger

The role of GLP-1 and gut microbiota in satiety

In their review, Ghinwa M. Barakat and her colleagues note that recent discoveries indicate that gut microbiota, the community of microorganisms living in our gut, play an important role in human metabolism. This became particularly evident with the discovery of the microbiota-gut-brain axis, a bidirectional communication pathway that allows gut microbiota to influence processes in the brain and vice versa (Barakat et al., 2024; Bonaz et al., 2018; Heiss et al., 2021).

Recent findings indicate that GLP-1 hormone might be particularly important for gut microbiota’s role in the feeling of satiety. GLP-1 is produced by specialized endocrine cells located in the lining of the small intestine and the colon called L cells. Receptors for this hormone, i.e., proteins on the surface of cells that react with it, are abundant in the hypothalamus, particularly in the arcuate nucleus region. Studies have demonstrated that injections of GLP-1 and medicines that behave like GLP-1 in the body reduce food intake (Barakat et al., 2024; Heiss et al., 2021) (see Figure 4).

Figure 4. GLP-1 hormone stimulates the feelings of satiety

Recent studies on mice indicated that Liraglutide, a substance commonly used to treat diabetes and obesity, mimics the effects of GLP-1 and can also affect the gut microbiota composition. High levels of GLP-1 or substances that act like it seems to help enrich microbiota strains more abundant in lean individuals and reduce the abundance of strains of microorganisms more common in obese individuals. For example, these injections increased the amounts of Akkermansia muciniphila, a species known to be more present in the gut when an individual loses weight and in lean individuals. On the other hand, it reduces the amount of Proteobacteria, which is more abundant in obese individuals.

Gut microbiota participate in satiety hormone regulation

Studies also indicate that gut microbiota might participate in regulating the release of satiety hormones. The authors of this review point to several studies indicating that some short-chain fatty acids (SFCAs) produced by gut bacteria increase the production and release of GLP-1 into the bloodstream. If more gut bacteria produce these substances, the digestive system lining will produce more GLP-1, sending a stronger satiety signal to the brain.

This effect is achieved through specific receptors on the intestine’s GLP-1-producing cells, which react to short-chain fatty acids, such as acetate, propionate, and butyrate, produced by gut bacteria (see Figure 5).

Figure 5. Role of gut microbiota in regulating satiety hormone secretions

Gut microbiota affect inflammatory processes

Another way in which gut microbiota can affect satiety is by affecting the inflammatory processes in the hypothalamus. Specific species of gut microorganisms can produce substances that increase inflammatory processes in the hypothalamus. This reduces its ability to regulate appetite (e.g., through reducing sensitivity to leptin). These types of bacteria tend to be more abundant in the guts of obese individuals. Studies on mice indicated that this could be countered by introducing bacteria into the gut that have the opposite effect, such as Lactobacillus rhamnosus, Lactobacillus acidophilus, and Bifidobacterium bifidum. Research results indicate that these bacteria restore sensitivity to leptin, thus helping reduce excessive weight (see Figure 6).

Figure 6. Role of gut microbiota in leptin sensitivity

Conclusion

The review discusses the various mechanisms through which the body regulates food intake and satiety. It points to the important role gut microorganisms play in this system and how it can be affected by gut microbiota.

The presented findings potentially open a new avenue of research to look for methods to prevent and treat obesity by influencing the gut microbiome. Future discoveries may lead to a new group of obesity treatments based on probiotics, devise ways to detect developing obesity, and allow effective prevention.

The paper “Satiety: a gut–brain–relationship” was authored by Ghinwa M. Barakat, Wiam Ramadan, Ghaith Assi, and Noura B. El Khoury.

For more information on mechanisms influencing dietary intake and food satiety, enroll in NP 150: Mechanisms in the Diet-Mental Health Relationship (DMHR). Find NP 150 and other courses in the DMHR through The world’s leader in nutritional psychology education here.

References

Barakat, G. M., Ramadan, W., Assi, G., & Khoury, N. B. E. (2024). Satiety: A gut–brain–relationship. The Journal of Physiological Sciences, 74(1), 11. https://doi.org/10.1186/s12576-024-00904-9

Bonaz, B., Bazin, T., & Pellissier, S. (2018). The vagus nerve at the interface of the microbiota-gut-brain axis. Frontiers in Neuroscience, 12(FEB). https://doi.org/10.3389/fnins.2018.00049

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

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

Hedrih, V. (2023). 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/

Isherwood, C. M., van der Veen, D. R., Hassanin, H., Skene, D. J., & Johnston, J. D. (2023). Human glucose rhythms and subjective hunger anticipate meal timing. Current Biology, 33(7), 1321-1326.e3. https://doi.org/10.1016/j.cub.2023.02.005

Lazarus, R. S., Yousem, H., & Arenberg, D. (1953). Hunger and Perception. Journal of Personality, 21(3), 312–328. https://doi.org/10.1111/J.1467-6494.1953.TB01774.X

Levine, A. S., & Morley, J. E. (1981). Stress-induced eating in rats. American Journal of Physiology – Regulatory, Integrative and Comparative Physiology, 241(1), R72–R76.

McKiernan, F., Houchins, J. A., & Mattes, R. D. (2008). Relationships between human thirst, hunger, drinking, and feeding. Physiology & Behavior, 94(5), 700. https://doi.org/10.1016/J.PHYSBEH.2008.04.007

Nutritional Psychology Research Library (NPRL). (n.d.). The Center for Nutritional Psychology. Retrieved May 1, 2024, from https://www.nutritional-psychology.org/np-research-library/

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

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

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

Posted on May 6, 2024May 3, 2024 by CNP Staff

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).

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).

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).

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., & 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.

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

Lonely Women Tend To Show More Maladaptive Eating Behaviors, Study Finds

Posted on April 29, 2024May 9, 2024 by CNP Staff

A neuroimaging study published in JAMA Network Open found that women who feel lonely tend to show more maladaptive social behaviors.
These women also had higher fat mass percentage, lower diet quality, and poorer mental health.
fMRI scans showed altered brain responses to food cues in several regions.

Humans are social creatures. Because of this, relationships with other people play a central role in every individual’s life. They provide a sense of belonging, meaning, intimate connections, and emotional support we all need. Babies and children need interactions with other humans to survive. Without contact with others and its benefits, many basic cognitive capacities will not develop at all. Even in newborns, deprivation of human contact is a strong source of distress. Because of all this, social relationships are crucial to everyone’s mental and physical health and well-being (Christensson et al., 1995; Singer, 2018).

However, many individuals cannot establish or maintain a fulfilling network of interpersonal connections for different reasons. When this happens, we talk about perceived social isolation and the feeling of loneliness.

What is loneliness?
Loneliness or perceived social isolation is a subjective feeling of social isolation, disconnection, or being alone, regardless of the amount of social contact one has. The person experiencing loneliness feels empty and sad and longs for companionship. Loneliness can be a temporary state or a chronic condition. In the long run, it can have significant negative impacts on both mental and physical health, including increased risks of depression, anxiety, and cardiovascular disease (Park et al., 2020; Zhang et al., 2024).

It is important to distinguish between loneliness and solitude (i.e., being alone)

It is important to distinguish between loneliness and solitude (i.e., being alone). A person can be alone without feeling lonely. Oftentimes, solitude can be a positive and enriching experience. In contrast, the very nature of loneliness is that it is a negative experience. Still, while some people choose solitude as their preferred lifestyle, in most cases, solitude is imposed on an individual – by the death of loved ones, illness, changes to the social environment, and various other adverse processes and events (Singer, 2018).

Consequences of loneliness

Studies show that loneliness or perceived social isolation is associated with various adverse physical and mental health outcomes. Mentally, loneliness is associated with an increased risk of depression, anxiety, and cognitive decline, as well as a higher likelihood of experiencing stress and low self-esteem. Physically, it can lead to a weakened immune system, making one more susceptible to infections and diseases (Hawkley & Cacioppo, 2003; Park et al., 2020).

Studies have also linked loneliness to an increased risk of early death and chronic conditions such as cardiovascular diseases and atherosclerosis. Studies during the recent COVID-19 pandemic indicated that loneliness may also be associated with increased obesity, unhealthy eating habits, and cognitive decline (Zhang et al., 2024).

The current study

Study author Xiaobei Zhang and her colleagues wanted to investigate the association between loneliness (i.e., perceived social isolation) and the brain’s reactivity to food cues, eating behaviors, and mental health symptoms. They note emerging evidence indicates that the “lonely brain” may contribute to obesity, i.e., lonely individuals might show differences in brain functioning that lead to obesity.

These authors expected these changes in brain functioning would be more pronounced in individuals with worse mental health outcomes and maladaptive eating behaviors. A part of the explanation for this link might be that sugary foods help alleviate psychological pain associated with perceived social isolation. This might make individuals experiencing this type of pain more sensitive to cues for such foods.

Sugary foods help alleviate psychological pain associated with perceived social isolation

The procedure

The study participants were 93 women from Los Angeles, with an average age of 25. These women completed an assessment of loneliness (the Perceived Isolation Scale). The study authors used this score to divide them into two groups: high perceived social isolation and low perceived social isolation.

The “lonely brain” may contribute to obesity

Study participants also completed assessments of their eating behaviors (food cravings, reward-based eating, maladaptive eating behaviors, and food addiction symptoms). Researchers took their height and weight measures. Participants underwent a bioelectrical impedance analysis, allowing researchers to evaluate their body composition and functional magnetic resonance imaging of their brains. During imaging, participants viewed pictures of various foods (food cue task), allowing study authors to record their brains’ reactions to pictures of food (food cues) (see Figure 1).

Figure 2. Study Procedure

The brains of lonelier women showed greater reactivity to food cues

Results showed that the high social isolation group had greater reactivity to food cues (pictures of food) in the inferior parietal lobule of the brain than the low social isolation group. When viewing sweet foods, the high social isolation group had higher reactivity in the inferior parietal lobule, inferior frontal gyrus, and lateral occipital cortex. The high social isolation group had lower reactivity for savory foods in the brain’s central precuneus and dorsolateral prefrontal cortex regions.

The brains of women with poorer mental health were more reactive to food cues

Participants with maladaptive eating behaviors and poorer mental health tended to show higher neural reactivity to food cues, regardless of the type of food shown. The brains of women with higher body fat percentages also tended to be more reactive to food cues.

Study authors tested a statistical model proposing that brain reactivity mediates the association between loneliness (i.e., perceived social isolation) and food cravings, reward-based eating, and overall maladaptive eating behaviors. Results showed that such a relationship between these factors is indeed possible. Reward-based eating is a behavior driven by the desire for pleasure or positive emotional response associated with consuming certain foods, often high in sugar or fat, rather than eating in response to hunger or nutritional needs.

This model proposed that it is possible that loneliness leads to increased brain reactivity to sweet foods. This increased reactivity, in turn, leads to higher body fat mass percentage (see Figure 2).

Figure 2. Results and proposed models

Conclusion

Overall, the study showed that the brains of women who perceive high levels of social isolation, i.e., feel very lonely and are highly reactive to food cues. This increased reactivity may lead to maladaptive eating behaviors and obesity. This indicates that alleviating and preventing social isolation may, at the same time, contribute to preventing obesity. Similarly, obesity prevention programs would benefit from considering loneliness and fulfilling social connections as important contributing factors.

The study shows that the brains of women who perceive high levels of social isolation, i.e., feel very lonely, are highly reactive to food cues

The paper “Social Isolation, Brain Food Cue Processing, Eating Behaviors, and Mental Health Symptoms” was authored by Xiaobei Zhang, Soumya Ravichandran, Gilbert C. Gee, Tien S. Dong, Hiram Beltrán-Sánchez, May C. Wang, Lisa A. Kilpatrick, Jennifer S. Labus, Allison Vaughan, and Arpana Gupta.

References

Christensson, K., Cabrera, T., Christensson, E., Uvnäs–Moberg, K., & Winberg, J. (1995). Separation distress call in the human neonate in the absence of maternal body contact. Acta Paediatrica, 84(5), 468–473. https://doi.org/10.1111/j.1651-2227.1995.tb13676.x

Hawkley, L. C., & Cacioppo, J. T. (2003). Loneliness and pathways to disease. Brain, Behavior, and Immunity, 17(1, Supplement), 98–105. https://doi.org/10.1016/S0889-1591(02)00073-9

Park, C., Majeed, A., Gill, H., Tamura, J., Ho, R. C., Mansur, R. B., Nasri, F., Lee, Y., Rosenblat, J. D., Wong, E., & McIntyre, R. S. (2020). The Effect of Loneliness on Distinct Health Outcomes: A Comprehensive Review and Meta-Analysis. Psychiatry Research, 294, 113514. https://doi.org/10.1016/j.psychres.2020.113514

Singer, C. (2018). Health Effects of Social Isolation and Loneliness. Journal of Aging and Care, 28(1), 4–8.

Zhang, X., Ravichandran, S., Gee, G. C., Dong, T. S., Beltrán-Sánchez, H., Wang, M. C., Kilpatrick, L. A., Labus, J. S., Vaughan, A., & Gupta, A. (2024). Social Isolation, Brain Food Cue Processing, Eating Behaviors, and Mental Health Symptoms. JAMA Network Open, 7(4), e244855. https://doi.org/10.1001/jamanetworkopen.2024.4855

Can Our Facial Attractiveness Depend on What We Just Ate?

Posted on April 22, 2024April 29, 2024 by CNP Staff

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).

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).

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

Posted on April 15, 2024April 24, 2024 by CNP Staff

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).

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).

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).

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).

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 April 8, 2024April 10, 2024 by CNP Staff

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).

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).

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).

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).

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).

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).

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

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

Posted on April 1, 2024April 9, 2024 by CNP Staff

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).

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).

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).

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).

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).

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).

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 March 26, 2024January 23, 2025 by CNP Staff

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).

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).

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).

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

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