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Consuming Fat and Sugar (At The Same Time) Promotes Overeating, Study Finds

Posted on February 19, 2024March 4, 2024 by CNP Super Admin

A study on mice published in Cell Metabolism found that gut-brain neural circuits conveying and processing information about the presence of fat and sugar in the gut are separate
Foods that contain both sugar and fats activate both circuits, releasing more dopamine compared to foods of equal caloric value containing only fat
The large amounts of dopamine released in this way create feelings of pleasure that promote overeating on the types of food that caused the release

When we want to find out what a piece of food is like, we can taste or smell it. When we smell something, sensory cells located in a small patch of tissue (olfactory epithelium) at the top of our nasal cavity react to the odorant molecules coming from that piece of food, and the olfactory nerve to carries the information to our brain, allowing us to experience smell. Similarly, when we taste a piece of food, taste buds in our mouth react to it, and specific nerves carry the information to our brain. While we eat, this evaluation of the qualities of food using our sensory organs happens continuously. However, not all of our food sensations come from our external senses. Our body also has sensory cells in the gut that inform the brain about what we eat.

The vagus nerve
After we ingest food through our mouth, it enters the esophagus. It continues towards the stomach and, after that, into the intestine. Food is further digested and broken down into components absorbed into the body as nutrients in these parts of the gastrointestinal system.

There are sensory cells located throughout the gastrointestinal system. The vagus nerve, one of the longest nerves in the body, connects these cells to the brain through a communication pathway called the gut-brain axis. In this way, it conveys sensory information about the state of the intestinal environment, including nutrient levels, gut microbiota activity, and intestinal wall integrity from the gut to the brain. These signals are then integrated into the brainstem, allowing the brain to monitor and respond to gut activity, influencing digestive processes, immune responses, and emotional states. (Bonaz et al., 2018) (see Figure 1).

Figure 1. Role of sensory cells and vagus nerve in the Gut-Brain Axis.

Among other things, the vagus nerve carries information to the brain about the nutritional value of our food. However, scientists so far have not fully understood the intricate details of how this system functions (McDougle et al., 2024).

The obesity pandemic
Recent decades have seen a continued increase in the share of obese individuals throughout the developed world. Many call this the obesity pandemic (Wong et al., 2022). This has motivated many studies into the causes of this pandemic. Results point to an intricate interplay between specific types of nutrients and other substances in the food and the properties of the human central nervous system as important contributing causes of obesity (Wilding, 2001).

Notably, while human brains (and brains of many other species) have a food intake regulation mechanism that determines when we will feel a desire to eat or when we will feel satiated, studies indicate that parts of this mechanism might be malfunctioning in obese individuals (Pujol et al., 2021; Seabrook et al., 2023). Studies indicate that feeding rodents high-fat diets instead of their regular chow can, in time, dysregulate their food intake regulation mechanisms, leading them to eat more calories than they need, resulting in obesity (Ikemoto et al., 1996). In humans, studies have linked the dysregulation of this mechanism with the consumption of foods that are both fatty and sweet (a property rarely found in natural foods) but also to various additives that create addiction-like reactions to foods that contain them (Hedrih, 2023).

The current study
Study author Molly McDougle and her colleagues wanted to explore the neural pathways through which the brain detects the intake of fats and sugars (i.e., fatty and sweet foods). They wanted to know whether the intake of these two types of nutrients triggers the same sensory neurons and whether they engage overlapping or separate neural circuits.

What was known before this study was that a direct infusion of fats or sugars into the gut (of mice) activates the vagus nerve. This, in turn, leads to the release of the neurotransmitter dopamine in the dorsal striatum region of the brain. The dorsal striatum is involved in reward and motivation processing, and dopamine is a key neurotransmitter that signals pleasure and reward (see Figure 2).

Figure 2. Vagal nerve activation from the direct infusion of fats or sugars into the gut

Study procedure
The study was conducted on 70 mice. The mice used in this study were between 6 and 20 weeks of age. Thirty-five mice were male, and 35 were female. They were housed at 22 degrees C and had free access to mouse food.

The study authors performed a series of experiments on these mice. The experiments involved surgical procedures that exposed or cut the vagus nerve and/or exposed the nodose ganglion (a part of the vagus nerve) for further activities. These surgeries also involved the implantation of catheters that allowed researchers to inject fluids directly into the gut of these mice, bypassing the mouth and, thus, taste receptors.

These researchers used 2-photon imaging to study the activity of the nodose ganglion in the mice (while the mice were alive) and of brain areas involved in sensing and processing information about nutrient intake. Two-photon imaging is a fluorescence microscopy technique that allows for deep-tissue, high-resolution imaging of live cells and tissues. It uses two photons of lower energy to excite a fluorophore simultaneously. Fluorophores are special molecules that emit a visible glow when excited by light of a specific wavelength, thus allowing researchers to track and observe different biological processes or structures.

Other experimental procedures included behavioral tests, techniques using light to control neurons that have been genetically modified to express ion channels sensitive to light (optogenetics), sampling extracellular fluid from the dorsal striatum region of the brain to measure the quantities of dopamine (microdialysis) and others. In the end, the study authors harvested and analyzed the brain tissues of these mice (see Figure 3).

Figure 3. Study procedure summary (McDougle et al., 2024).

Fats and sugars are sensed by separate neurons of the vagal nerve
Results showed that fats and sugars increased the activity of neurons in the vagus nerve, but mostly not of the same ones. Neurons comprising the nodose ganglion mostly reacted to the presence of fat or sugars. Very few neurons reacted to both. These neurons reacting to nutrients in the intestine comprised around 17% of the neurons in the nodose ganglion. The nodose ganglion is a cluster of sensory neurons located on the vagus nerve, transmitting visceral sensory information from the body to the brain.

When researchers infused sugar or fat into the guts of mice, the neurons of the nodose ganglion they previously marked increased their frequencies of nerve impulses. Analysis of the neural circuits activated by fats and sugars showed that they differ. They were largely separate. Information about sugar and fats in the gut is carried to the brain through two distinct pathways. These pathways convey information about the type of nutrient in the gut, but they also likely convey information about its concentration (see Figure 4).

Figure 4. Sensing fats and sugars in the gut

The duodenum is the key sensing site for both sugar and fat
Tracing the locations of sensory cells, these neurons led these researchers to discover an extensive network of sensory cells in the duodenum. Almost all sensory cells detecting fats and many of those detecting sugars were located there. The duodenum is the first section of the small intestine, connecting the stomach to the jejunum. It plays a crucial role in the initial phase of digestion by receiving partially digested food from the stomach and digestive enzymes from the pancreas and liver. On the other hand, study authors found that sugar-sensing also happens in the hepatic portal vein, a blood vessel that carries nutrient-rich blood from the gastrointestinal tract and spleen to the liver (see Figure 5).

Figure 5. Detection of fats and sugars by a network of sensory cells in the duodenum

Reinforcement learning based on sugar and fat happens through separate circuits
Experiments where researchers destroyed fat-sensing neurons but left the sugar-sensing ones intact or vice versa indicated that reinforcement learning, a type of learning where a mouse can associate a specific object or sensation with a specific nutrient, can be conducted using only the neurons sensing that specific nutrient. Mice without fat-sensing neurons but with intact sugar-sensing neurons were able to form a preference for a flavor associated with sugar intake.

Mice without fat-sensing neurons but with intact sugar-sensing neurons were able to form a preference for a flavor associated with sugar intake

In the nigrostriatal region of the brain, both information about fat and sugar in the gut led to the release of dopamine (thought to produce the feeling of pleasure and a rewarding experience). However, these nutrients activated parallel and largely separate neuronal populations at each node of the reward circuit in this part of the brain. This means that distinguishable neural circuits are responsible for reinforcement learning for fat and sugar, i.e., for learning to associate stimuli with pleasure caused by the ingestion of sugar and pleasure caused by the ingestion of fat (see Figure 6).

Figure 6. Release of dopamine in response to fat and sugar

Consuming fat and sugar at the same time promotes overeating for pleasure
In another group of experiments, study authors found that when they gave mice a choice between taking solutions of fat, sugar (sucrose), or a mixture of the two nutrients, mice consumed equal amounts of fat or sugar solutions. However, the number of licks of the solution containing both sugar and fats nearly doubled compared to just sugar or just fat alone.

Consuming fat and sugar at the same time promotes overeating for pleasure

Researchers then offered mice a non-nutrient-flavored solution to lick, injecting sugar, fat, or a combination of the two directly into their guts (using the catheters they installed). After training to pair a non-nutritive flavor with a solution, mice again showed a preference for the mixed solution (both sugar and fat), indicating that the preference for this solution is independent of taste. This means that the preference for the sugar and fat combination has to do with sensing those nutrients in the gut and not with their taste in the mouth.

The preference for the sugar and fat combination has to do with sensing those nutrients in the gut and not with their taste in the mouth

Study authors conclude that this is because this mixed solution activates both the brain’s rewarding circuits for fat and sugar, increasing the overall feeling of pleasure. Analysis of the quantity of released dopamine in the dorsal striatum region of the brain found that it is much higher after the injection of the mixed sugar-fat solution than after the injection of a solution with equal caloric value but containing only fat.

This suggests that foods rich in fat and sugar produce higher activation of reward circuits for the same amount of calories than foods containing just one of these two nutrients. This would translate to higher feelings of pleasure after consumption, motivating the individual to consume more food of that type, which could lead to obesity (see Figure 7).

Figure 7. Activation of the brain’s rewarding circuits with combined sugar and fat

Conclusion
The study showed that sensing the presence of sugars and fats in the intestines of mice is achieved through different sets of neurons. The study also found that these two types of nutrients activate parallel but largely separate reward circuits in the brain. Due to this, consuming foods that contain both sugars and fats activates reward circuits in the brain for both of these substances, resulting in a higher release of dopamine and, thus, higher feelings of pleasure, compared to consuming foods of equal caloric value but containing only fats or only sugars. These peculiarities of neural pathways make mice, and possibly humans, more likely to overeat foods rich in fats and sugars driven by feelings of pleasure the simultaneous activation of these two neural pathways creates.

The discovery of these separate mechanisms and understanding of the ways they work can help scientists. Still, people working in nutrition better understand how the properties of certain food items lead to obesity. This can, in sequence, help better plan individual diets and develop policies to help stop the ongoing obesity epidemic.

The paper “Separate gut-brain circuits for fat and sugar reinforcement combine to promote overeating” was authored by Molly McDougle, Alan de Araujo, Arashdeep Singh, Mingxin Yang, Isadora Braga, Vincent Paille, Rebeca Mendez-Hernandez, Macarena Vergara, Lauren N. Woodie, Abhishek Gour, Abhisheak Sharma, Nikhil Urs, Brandon Warren, and Guillaume de Lartigue.

References

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

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

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

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

Pujol, J., Blanco-Hinojo, L., Martínez-Vilavella, G., Deus, J., Pérez-Sola, V., & Sunyer, J. (2021). Dysfunctional Brain Reward System in Child Obesity. Cerebral Cortex, 31, 4376–4385. https://doi.org/10.1093/cercor/bhab092

Seabrook, L. T., Naef, L., Baimel, C., Judge, A. K., Kenney, T., Ellis, M., Tayyab, T., Armstrong, M., Qiao, M., Floresco, S. B., & Borgland, S. L. (2023). Disinhibition of the orbitofrontal cortex biases decision-making in obesity. Nature Neuroscience, 26(1), 92–106. https://doi.org/10.1038/s41593-022-01210-6

Wilding, J. P. H. (2001). Causes of obesity. Practical Diabetes International, 18(8), 288–292. https://doi.org/10.1002/PDI.277

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

Study Identifies Link Between Post-Traumatic Stress Disorder and Gut Microbiome Composition in a Cohort of Women

Posted on February 5, 2024February 14, 2024 by CNP Super Admin

A study published in Nature Mental Health examined the links between post-traumatic stress disorder (PTSD), dietary patterns, and gut microbiome in U.S. nurses
Results showed that nurses with higher PTSD symptom levels tended to eat less plant-based food and more red/processed meat
Microbial processes related to the production of pantothenate and coenzyme A can potentially be protective against PTSD

When we are exposed to distressing events or conditions that overwhelm our ability to cope, our body can produce a severe emotional response, and we experience psychological trauma. We feel that we have lost control of events around us. Our ability to integrate these emotional experiences into the story of our lives is reduced. After experiencing psychological trauma, people often start dividing the subjective timeline of their lives into the time before and the time after the traumatic event. Long-lasting psychological and health consequences may often follow (Hamburger et al., 2021). Among other things, the experience of psychological trauma can lead to the development of a serious mental health disorder called post-traumatic stress disorder or PTSD.

After experiencing psychological trauma, people often start dividing the subjective timeline of their lives into the time before and after the traumatic event

What is post-traumatic stress disorder?
Post-traumatic stress disorder is a mental health condition that can develop in individuals who have experienced or witnessed a traumatic event. Symptoms of PTSD include intrusive thoughts, nightmares, and flashbacks related to the traumatic experience, causing significant distress. Individuals with PTSD may actively avoid reminders of the trauma, experience heightened arousal, and have negative changes in mood and cognition.

Mainstream treatments for PTSD include psychotherapy, particularly cognitive-behavioral psychotherapy, and medications. Studies indicate that these treatments can be effective in reducing PTSD symptoms (see Figure 1). In some individuals, they are very effective (Watts et al., 2013). However, around 20% of patients suffering from PTSD drop out of treatment before symptoms have withdrawn, while up to 60% of individuals undergoing treatment do not respond to it, i.e., experience no reduction of symptoms as a result (Wittmann et al., 2021).

Figure 1. PTSD symptoms and mainstream treatments

For these reasons, researchers are intensely working on new treatment options. They are trying alternative ways to achieve a reduction of symptoms, such as acupuncture (Watts et al., 2013) or psychedelic drugs (Barone et al., 2019). Researchers are also looking at chemicals that could potentially prevent the disorder from forming in the first place if taken immediately after the traumatic event, such as hydrocortisone (Hennessy et al., 2022).

Health impact of PTSD
Individuals suffering from PTSD often suffer from other psychiatric disorders as well. Epidemiological surveys indicate that the vast majority of individuals with PTSD meet the criteria for at least one other disorder, while a substantial percentage have three or more other psychiatric disorders. These most commonly include major depressive disorder, substance use disorder, and anxiety disorders (Brady et al., 2000).

The majority of individuals with PTSD meet the criteria for at least one other disorder, while a substantial percentage have three or more other psychiatric disorders

Individuals with PTSD also have a higher likelihood of various somatic diseases, particularly chronic ones. These include asthma, cardiovascular disease, chronic pain and inflammation, obesity, type 2 diabetes, gastrointestinal disorders, and cognitive decline (Ke et al., 2023).

However, researchers are still looking for mechanisms through which this association between PTSD and somatic disorders is achieved. One promising avenue of research is the study of the gut microbiome, the community of organisms living in the human digestive system. The recent discovery of the microbiota-gut-brain axis, a bidirectional communication pathway through which gut microorganisms affect processes in the brain and vice versa (Carbia et al., 2023; García-Cabrerizo et al., 2021), has made it even more likely that at least a part of the link between PTSD and somatic disorder includes the gut microbiome.

Researchers are looking for mechanisms connecting PTSD and somatic disorders -with one promising avenue of research being the gut microbiome

The current study
Study author Shanlin Ke and his colleagues hypothesized that gut microbiome might play a role in PTSD. They note that previous studies have already linked the gut microbiome with various other mental health disorders through the microbiota-gut-brain axis (Hedrih, 2023; Leclercq et al., 2020; Valles-Colomer et al., 2019). Additionally, studies show that the gut microbiome influences the brain region involved in learned fear. Fear is a key feature of PTSD. Gut microbiota depends on food intake, while individuals with PTSD tend to be more prone to eating unhealthy foods (Ke et al., 2023).

Previous studies have already linked the gut microbiome with various other mental health disorders through the microbiota-gut-brain axis (MGBA)

With this in mind, these researchers analyzed data from two studies of female registered nurses in the U.S. in order to systematically examine the associations of trauma exposure and PTSD status with dietary and microbiome data.

The study procedure
Data came from 191 nurses who were part of the NHS-II study. NHS-II is a large longitudinal study of U.S. women with over 100,000 registered nurses that started in 1989. Nurses whose data were analyzed here participated in two substudies – the 2008 PTSD substudy that collected data about trauma exposure and PTSD symptoms and the 2013 mind-body study that, among other things, collected up to four stool samples. Stool samples were collected 48-72 hours apart. This was followed by a second set of collections six months later. Stool samples were analyzed to make inferences about the composition of the gut microbiome.

Of the nurses included in this study, 44 had probable PTSD, 119 were exposed to trauma but did not develop PTSD, and 28 participants had no trauma exposure (see Figure 2).

Figure 2. Study Procedure

No association between PTSD and overall microbiome structure
Statistical analyses showed no associations between overall gut microbiota composition and PTSD status. Gut microbiota diversity was also not associated with PTSD.

However, there were associations between various other factors and the overall microbiome structure. Body mass index, depression, and the use of antidepressants were all associated with the overall composition of gut microbiome species.

Childhood trauma experiences and antidepressant use were associated with the relative abundance of species forming different metabolic pathways. The gut microbiome metabolic pathways refer to types of activities within the gastrointestinal tract that specific species of microorganisms perform.

Individuals with PTSD eat less plant-based food and more red/processed meat
Examination of associations between dietary habits and PTSD revealed that individuals with more pronounced PTSD symptoms tend to eat less plant-based foods and more red/processed meats compared to individuals with lower PTSD symptom levels. The diets of these individuals were less healthy overall.

Individuals with more pronounced PTSD symptoms tend to eat less plant-based foods and more red/processed meats compared to individuals with less PTSD symptoms

Individuals with PTSD symptoms had lower abundances of Eubacterium eligens
After statistical analyses showed no associations between the overall gut microbiome composition and PTSD, these authors examined associations between PTSD symptoms and the abundance of individual species of bacteria. They looked for species of microorganisms that differed in abundance in individuals with different levels of PTSD symptoms. Three species were clearly more abundant in individuals with more PTSD symptoms – Parabacteroides goldsteinii, Barnesiella intestinihominis, and Paraprevotella unclassified. Seven species with the highest negative association with PTSD symptoms, i.e., species less abundant in individuals with more PTSD symptoms, were also identified (Eubacterium eligens, Parabacteroides distasonis, Akkermansia muciniphila, Bacteroides massiliensis, Bifidobacterium longum, Dialister invisus, and Roseburia inulinivorans). These species play diverse roles in the human digestive system, contributing to functions ranging from fermentation of dietary fibers to protection of the gut lining.

Eubacterium eligens (a good bacteria) was less abundant in individuals eating more pies, carbonated beverages with sugars, candy without chocolate, hot dogs, bacon, and processed meats. It tended to be more abundant in individuals eating more vegetables (for example, raw carrot, spinach/collard greens cooked, and yellow squash), fruits (for example, orange and banana), and fish. The abundance of this bacteria was the most strongly associated with PTSD symptoms of all analyzed microorganisms. Eubacterium eligens in the gut synthesize pantothenate and Coenzyme A (see Figure 3).

Figure 3. Microorganisms associated with PTSD

Researchers tested a number of statistical models proposing that specific dietary habits mediate the impact of PTSD symptoms on the abundance of specific species of gut bacteria. These analyses revealed that it is possible that the impact of PTSD symptoms on the abundance of Eubacterium eligens is mediated by the consumption of raw carrots. Similarly, it is possible that Adlercreutzia equolifaciens mediates the link between PTSD symptoms and the intake of dairy-cottage/ricotta cheese.

Conclusion
In summary, the study showed that PTSD symptoms in U.S. nurses are not associated with the overall structure of the gut microbiome, but the abundance of several bacterial species was associated with the severity of PTSD symptoms in spite of this. Additionally, it turned out that participants with PTSD tend to eat less plant-based food and more red/processed meat. Their overall dietary habits tended to be less healthy (see Figure 4).

Figure 4. Research findings (Ke et al., 2023)

The study also established statistical links between PTSD symptoms, dietary habits, and bacteria. Future studies could explore the nature of these links in more detail. Potentially, these could lead to the discovery of ways to affect PTSD symptoms through dietary interventions and modifying the abundance of certain species of gut bacteria. However, the feasibility of such an approach is yet to be established.

The paper “Association of probable post-traumatic stress disorder with dietary pattern and gut microbiome in a cohort of women” was authored by Shanlin Ke, Xu-Wen Wang, Andrew Ratanatharathorn, Tianyi Huang, Andrea L. Roberts, Francine Grodstein, Laura D. Kubzansky, Karestan C. Koenen, and Yang-Yu Liu.

Visit the research category within the Nutritional Psychology Research Library on “Diet, Trauma and PTSD” to learn more about the connection between diet and trauma. To access evidence-based continuing education on the connection between the microbiome and mental health, see the CNP Education page.

References

Barone, W., Beck, J., Mitsunaga-Whitten, M., & Perl, P. (2019). Perceived Benefits of MDMA-Assisted Psychotherapy beyond Symptom Reduction: Qualitative Follow-Up Study of a Clinical Trial for Individuals with Treatment-Resistant PTSD. Journal of Psychoactive Drugs, 51(2), 199–208. https://doi.org/10.1080/02791072.2019.1580805

Brady, K., Killeen, T., Brewerton, T., & Lucerini, S. (2000). Comorbidity of Psychiatric Disorders and Posttraumatic Stress Disorder. Journal of Clinical Psychiatry, 61(suppl 7), 22–32.

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

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

Hamburger, A., Hancheva, C., & Volkan, V. (Eds.). (2021). Social Trauma – An Interdisciplinary Textbook. Springer Nature Switzerland AG. https://doi.org/10.1007/978-3-030-47817-9

Hedrih, V. (2023). 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/

Hennessy, V. E., Troebinger, L., Iskandar, G., Das, R. K., & Kamboj, S. K. (2022). Accelerated forgetting of a trauma-like event in healthy men and women after a single dose of hydrocortisone. Translational Psychiatry, 12(1). https://doi.org/10.1038/s41398-022-02126-2

Ke, S., Wang, X.-W., Ratanatharathorn, A., Huang, T., Roberts, A. L., Grodstein, F., Kubzansky, L. D., Koenen, K. C., & Liu, Y.-Y. (2023). Association of probable post-traumatic stress disorder with dietary pattern and gut microbiome in a cohort of women. Nature Mental Health, 1(11), 900–913. https://doi.org/10.1038/s44220-023-00145-6

Leclercq, S., Le Roy, T., Furgiuele, S., Coste, V., Bindels, L. B., Leyrolle, Q., Neyrinck, A. M., Quoilin, C., Amadieu, C., Petit, G., Dricot, L., Tagliatti, V., Cani, P. D., Verbeke, K., Colet, J. M., Stärkel, P., de Timary, P., & Delzenne, N. M. (2020). Gut Microbiota-Induced Changes in β-Hydroxybutyrate Metabolism Are Linked to Altered Sociability and Depression in Alcohol Use Disorder. Cell Reports, 33(2). https://doi.org/10.1016/J.CELREP.2020.108238

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

Watts, B. V., Schnurr, P. P., Mayo, L., Young-Xu, Y., Weeks, W. B., & Friedman, M. J. (2013). Meta-analysis of the efficacy of treatments for posttraumatic stress disorder. Journal of Clinical Psychiatry, 74(6). https://doi.org/10.4088/JCP.12r08225

Wittmann, L., Muller, J., Morina, N., Maercker, A., & Schnyder, U. (2021). Predicting Treatment Response in Psychotherapy for Postraumatic Stress Disorder: a Pilot Study. Psihologija, 54(1), 1–14. https://doi.org/10.2298/PSI190905007W

Can Symptoms of Alzheimer’s be Transferred to Rats via the Gut Microbiota of Alzheimer’s Patients?

Posted on January 29, 2024February 16, 2024 by CNP Super Admin

A study published in Brain showed that symptoms of Alzheimer’s disease can be transferred to young rats via the gut microbiota of Alzheimer’s patients
Transplantation of these microorganisms into the guts of healthy rats induced cognitive deficits
The deficits resulted from the disruption of adult hippocampal neurogenesis, the capacity of the hippocampus to produce new neurons

Our gut is home to trillions of different microorganisms. These microorganisms sustain themselves using the food we eat and help our digestion process. For example, many food items contain substances called resistant starches. Our digestive system cannot digest these resistant starches, but some bacteria in our gut can. They ferment those types of starches, creating substances called short-chain fatty acids (SCFA) that our bodies can use (Li et al., 2023) (see Figure 1).

Figure 1. Digestion of resistant starch by gut bacteria

Similarly, these bacteria help digest substances like dietary fiber, other complex polysaccharides, lignans, and many others, converting them into substances our body can use as nutrients or that convey various health benefits. However, when pathogenic, unhealthy microorganisms infect our digestive tract, we experience an upset stomach. This includes symptoms such as nausea, vomiting, diarrhea, abdominal pain, and others.

The microbiota-gut-brain axis (MGBA)
This community of microorganisms living in our gut is called the gut microbiota. However, its effects on us go far beyond helping digestion. Gut microbiota can also influence our central nervous system –and be influenced by it. The mechanism through which this bidirectional communication link between gut microbiota and the brain is achieved is called the microbiota-gut-brain axis (MGBA). It is crucial in regulating various physiological and psychological processes (Carbia et al., 2023; García-Cabrerizo et al., 2021).

The Microbiota-Gut-Brain Axis is crucial in regulating various physiological and psychological processes

This bidirectional communication mechanism occurs via several biomolecules, including the hormone cortisol, short-chain fatty acids (SCFAs), and tryptophan. Emerging studies reveal that the gut microbiota produces substances (called ‘signaling molecules’) that can influence the brain’s activity and responses to stress and emotions (more about this can be found in NP 120 Parts I & II). The MGBA is closely tied to the immune system, influencing the body’s inflammatory responses and potentially contributing to neuroinflammation (Zhu et al., 2023) (see Figure 2).

Figure 2. MGBA, bidirectional communication, and signaling molecules

What is Alzheimer’s disease?
Alzheimer’s disease is a progressive neurodegenerative disorder characterized by a decline in cognitive function, memory loss, and changes in behavior. It is the most common form of dementia, affecting primarily older adults. The exact cause of Alzheimer’s disease is not fully understood. Still, it is associated with the accumulation of abnormal protein deposits in the brain, called beta-amyloid plaques and tau tangles. These deposits disrupt communication between nerve cells and eventually lead to their degeneration and death (Grabrucker et al., 2023) (see Figure 3).

Figure 3. Alzheimer’s Disease (AD)

Alzheimer’s disease and adult hippocampal neurogenesis
The hippocampus is a brain area that is particularly vulnerable to Alzheimer’s disease. It plays a crucial role in learning, memory, and emotional regulation. The hippocampus hosts a population of neural stem cells, special undifferentiated cells that can produce new neurons throughout their lifespan. This process of creating new neural cells is called adult hippocampal neurogenesis. It is crucial for cognitive processes like spatial learning, distinguishing between similar events and environments, and emotion regulation (see Figure 4).

Figure 4. Adult hippocampal neurogenesis

Interestingly, hippocampal neurogenesis is impaired in Alzheimer’s even before abnormal protein deposits can be detected in the brain, including in the hippocampus. This indicates that dysfunction of this system is an early indicator that Alzheimer’s disease is developing (Grabrucker et al., 2023).

The hippocampus is a brain area that is particularly vulnerable to Alzheimer’s disease. It plays a crucial role in learning, memory, and emotional regulation

Causes of Alzheimer’s
Genetic factors, such as specific gene mutations, are linked to early-onset Alzheimer’s, while other risk factors include age, family history, and certain lifestyle factors. Despite ongoing research, there is currently no cure for Alzheimer’s disease, and treatment focuses on managing symptoms and improving the quality of life for affected individuals.

However, the recent discovery of the MGBA has opened a new avenue of research demonstrating that this communication pathway is a significant mediator of behavior throughout the lifespan. Studies indicate clear links between gut microbiota composition and behavior (e.g., Leclercq et al., 2020; Valles-Colomer et al., 2019).

Studies indicate clear links between gut microbiota composition and behavior

Recently, links between the MGBA and Alzheimer’s have begun to appear. Studies on mice indicate that transplanting gut microbiota from Alzheimer’s patients into mice can cause adverse cognitive changes in these mice (Kim et al., 2021; Wang et al., 2022) (see Figure 5). But could it also disrupt the adult hippocampal neurogenesis? And would these changes correlate with the level of cognitive impairment of the person the transplanted microbiota came from?

Figure 5. Gut microbiota transplanted from Alzheimer’s patients

The current study
Current studies clearly implicate the gut microbiota in the pathological features of Alzheimer’s disease, but until this particular study, it has remained unclear whether cognitive symptoms in human Alzheimer’s patients and underlying cellular changes (such as the disruption of adult hippocampal neurogenesis) could be transmitted to a healthy organism via the gut microbiota. Study author Stefanie Grabrucker and her colleagues wanted to find out. They also wanted to uncover the mechanism through which this happens.

These authors conducted a study in which they took fecal samples containing gut microbiota from humans suffering from Alzheimer’s disease and transplanted them into the guts of young adult male rats.

Current studies implicate gut microbiota in the pathological features of AD, but until now, it has remained unclear whether cognitive symptoms and underlying cellular changes in human Alzheimer’s patients could be transmitted to a healthy organism via the gut microbiota

The study procedure
Study participants were 69 patients with Alzheimer’s disease, and 64 healthy individuals were included as controls. They were recruited at the IRCCS Centro San Giovanni di Dio Fatebenefratelli, Brescia, Italy. They all underwent clinical assessment for cognitive function and a physical examination. All participants gave blood samples for further analysis. Fifty-four participants with Alzheimer’s disease and 41 healthy participants gave stool samples in a sterile cup at their homes. Researchers processed these samples for transplanting gut microbiota found in feces into rats.

Animals used in the study were male Sprague-Dawley rats aged 11 weeks. They were kept in environmentally controlled conditions at a temperature of 21oC and under a 12-hour light-dark cycle (12 hours in light and 12 hours in the dark).

Transplanting gut microbiota from stool samples into rats
Researchers kept rats for two weeks after arrival at the laboratory without any treatment to let them acclimatize. After this period, they added a powerful cocktail of antibiotics to their water for seven consecutive days. This combination of antibiotics consisted of ampicillin (1 g/l), vancomycin (500 mg/l), ciprofloxacin HCL (200 mg/l), and imipenem (250 mg/l). This treatment aimed to deplete rats’ own microbiota so that their digestive system could readily accept the microorganisms to be transplanted from human participants.

After the antibiotic treatment, the study authors randomly allocated the rats into two groups. one was to receive microbiota transplants from Alzheimer’s patients, while the other would receive it from healthy control participants.

They then applied oral gavage of homogenized fecal slurry of human participants (from stool samples) on them for three days. Gavage is a force-feeding method involving inserting a tube into the animal’s esophagus and delivering a measured amount of food directly into the stomach. In this way, study authors transplanted the gut microbiota of human study participants into the guts of these rats (see Figure 6).

Behavior testing and other analyses
Ten days after transplanting the gut microbiota to rats, these researchers conducted a series of behavioral tests on the rats. They conducted the tests during the day (i.e., light cycle), between 9:00 and 19:00. There was a minimum interval of 36 hours between behavioral tests. The tests used were Open Field, Elevated Plus Maze, Modified Spontaneous Location Recognition Test, Novel Object Recognition, Novel Location Recognition, Morris Water Maze, and Forced Swim Test. Their goal was to examine the rats’ cognitive capacity.

Study authors also collected and analyzed fecal samples of the rats during the study. They took blood from their tails ten days after microbiota transplantation for analysis. At the end of the study, the rats were killed, and additional analyses were done on their brain tissue and blood from the trunk (see Figure 6).

Figure 6. Research procedure

Microbiota composition differed between Alzheimer’s patients and controls
Researchers used metagenomics (bacterial 16S rRNA gene sequencing) on participants’ stool samples to estimate the composition of participants’ gut microbiota. Results revealed no differences in microbiota diversity between participants with and without Alzheimer’s.

However, there were differences in the abundances of specific groups of bacterial species. Alzheimer’s patients had a higher abundance of Bacteroides (particularly of various species associated with inflammatory processes) and Desulfovibrio genera of bacteria. They had lower abundances of Clostridium sensu stricto 1 and the short-chain fatty acid butyrate-producing genera Coprococcus.

Further analyses revealed that participants with Alzheimer’s who had better cognitive function and higher mental clarity (assessed using the Mini-Mental State Examination) tended to have higher abundances of Coproccocus bacteria. These individuals tended to have lower abundances of Desulfovibrio and Dialister species of bacteria.

Gut microbiota from Alzheimer’s patients induced cognitive deficits in rats
Analyses of rat stool samples indicated that gut microbiota transplantation was successful. Comparing rats with microbiota from healthy human participants and those from Alzheimer’s patients, study authors noted that the fecal matter of rats with microbiota from Alzheimer’s patients had higher water content. These rats also increased their water intake, and their colon length decreased. There were other structural changes in the colons of these rats as well.

Behavioral tests showed no changes in rats that received microbiota transplants from healthy human participants. On the other hand, rats with microbiota from Alzheimer’s patients showed impaired ability to recognize familiar locations. They also showed impairment in tasks that relied on different types of memory. Study authors note that all of these cognitive functions depend on the normal functioning of hippocampal neurogenesis.

Rats with microbiota from Alzheimer’s patients showed an impaired ability to recognize familiar locations

Hippocampal neurogenesis was reduced in rats with microbiota from Alzheimer’s patients
Direct assessment of hippocampal neurogenesis in rats that received gut microbiota from Alzheimer’s patients showed that hippocampal neurogenesis was indeed disrupted, confirming the study authors’ suspicions. These rats had substantially fewer new neurons than those that received microbiota from healthy human participants.

Serum of patients with Alzheimer’s reduced the capacity of human brain cells to multiply
The study authors then conducted an in vitro experiment on embryonic human hippocampal progenitor cells (undifferentiated cells found in the hippocampus of the brain, obtained from female human fetuses that were medically terminated). After treating these cells with serum (the liquid component of blood that remains after blood coagulation) taken from the two groups of human study participants, researchers noted that the serum from Alzheimer’s patients decreased the capacity of these cells to multiply.

The capacity of these cells to multiply after treatment depended on the human participant serum from which they came. More specifically, the capacity of these cells to multiply tended to be better after treatment with serum from Alzheimer’s patients with better cognitive functions. The prevalence of indicators of neuron development was higher if serum from Alzheimer’s patients with better cognitive function assessments was used.

Conclusion
The study showed that it is possible to transfer symptoms of Alzheimer’s disease to young, healthy rats by using the gut microbiota of humans suffering from Alzheimer’s disease. This transfer induced a number of changes in the digestive tract and disrupted cognitive functions that depend on preserved hippocampal neurogenesis -–the capacity of stem cells in the hippocampus to generate new neurons (see Figure 7).

Figure 7. Transfer of AD symptoms via gut microbiota

These results demonstrate that gut microbiota has a causal role in Alzheimer’s disease and that adult hippocampal neurogenesis is central for cognitive impairments in its course. But most importantly, they indicate that Alzheimer’s disease can potentially be transmitted through the fecal-oral route. These findings will likely lead to new ways to prevent and possibly even treat Alzheimer’s disease very soon.

The paper “Microbiota from Alzheimer’s patients induce deficits in cognition and hippocampal neurogenesis” was authored by Stefanie Grabrucker, Moira Marizzoni, Edina Silajdžić, Nicola Lopizzo, Elisa Mombelli, Sarah Nicolas, Sebastian Dohm-Hansen, Catia Scassellati, Davide Vito Moretti, Melissa Rosa, Karina Hoffmann, John F. Cryan, Olivia F. O’Leary, Jane A. English, Aonghus Lavelle, Cora O’Neill, Sandrine Thuret, Annamaria Cattaneo, and Yvonne M. Nolan.

References

Grabrucker, S., Marizzoni, M., Silajdžić, E., Lopizzo, N., Mombelli, E., Nicolas, S., Dohm-Hansen, S., Scassellati, C., Moretti, D. V., Rosa, M., Hoffmann, K., Cryan, J. F., O’Leary, O. F., English, J. A., Lavelle, A., O’Neill, C., Thuret, S., Cattaneo, A., & Nolan, Y. M. (2023). Microbiota from Alzheimer’s patients induce deficits in cognition and hippocampal neurogenesis. Brain. https://doi.org/10.1093/brain/awad303

Kim, N., Jeon, S. H., Ju, I. G., Gee, M. S., Do, J., Oh, M. S., & Lee, J. K. (2021). Transplantation of gut microbiota derived from Alzheimer’s disease mouse model impairs memory function and neurogenesis in C57BL/6 mice. Brain, Behavior, and Immunity, 98, 357–365. https://doi.org/10.1016/J.BBI.2021.09.002

Li, C., Hu, Y., Li, S., Yi, X., Shao, S., Yu, W., & Li, E. (2023). Biological factors controlling starch digestibility in human digestive system. In Food Science and Human Wellness (Vol. 12, Issue 2, pp. 351–358). KeAi Communications Co. https://doi.org/10.1016/j.fshw.2022.07.037

Wang, F., Gu, Y., Xu, C., Du, K., Zhao, C., Zhao, Y., & Liu, X. (2022). Transplantation of fecal microbiota from APP/PS1 mice and Alzheimer’s disease patients enhanced endoplasmic reticulum stress in the cerebral cortex of wild-type mice. Frontiers in Aging Neuroscience, 14. https://doi.org/10.3389/fnagi.2022.858130

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

Do the Quality and Timing of Your Snacks Affect Your Cardiometabolic Health?

Posted on December 30, 2023January 12, 2024 by CNP Super Admin

A study published in the European Journal of Nutrition found that individuals consuming poor-quality snacks tend to have poorer cardiometabolic health indicators

Individuals snacking late in the evening, after 9 pm, tended to have poorer cardiometabolic health indicators than those not snacking late

The number of consumed snacks per day was not associated with cardiometabolic health indicator levels

Snacking
Snacking is consuming small, often casual, food portions between regular meals. Individuals typically do this to curb hunger, satisfy cravings, ease stress/boredom/nerves, or provide a quick energy boost. Snacks can vary widely in terms of their nutritional content and may range from healthy options like fruits and nuts to less nutritious choices like chips and candy.

A study in the U.S. indicated that 97% of people practiced snacking in 2006. The same study reported that the share of snack calories in the total daily energy intake stood at 24%. This was a substantial increase compared to findings in previous years. Not only did snacking become more widespread, but the energy density of snacks consumed increased (Piernas & Popkin, 2010). This increase in snacking coincided with the worldwide obesity pandemic (Wong et al., 2022).

A study in the U.S. in 2006 indicated that 97% of people practiced snacking and the share of snack calories in their total daily energy was 24%

Cardiometabolic blood markers
When studying the effects of various dietary patterns or differences between groups of individuals practicing different dietary patterns, researchers rely on various indicators of the functioning of study participants’ metabolisms and various physiological parameters to estimate possible links between dietary patterns and health. One very frequently used group of indicators is cardiometabolic blood markers, a group of indicators that can be derived from a blood sample.

Cardiometabolic blood markers are a group of specific substances found in the bloodstream that provide information about an individual’s cardiovascular and metabolic health. These markers include cholesterol levels, particularly low-density lipoprotein (LDL) cholesterol (“bad” cholesterol), which is associated with an increased risk of heart disease when elevated. Additionally, triglycerides (TGs), a type of fat in the blood, and blood glucose levels are important indicators of metabolic health. Elevated markers can signify an increased risk of diabetes, obesity, and heart disease, making them crucial for assessing and managing overall health and wellness (see Figure 1).

Figure 1. Cardiometabolic blood markers and associated health risks

Snacking and health
On the general level, snacking can be beneficial for health. It distributes energy and nutrient intake across multiple occasions in a day. Frequent snacks also present more opportunity for an individual to consume specific nutrients required by the body, thereby completing main meals (Marangoni et al., 2019)

On the general level, snacking can be beneficial for health

However, this largely depends on what the snacks are, i.e., their quality. For example, a recent study showed that snacking on a high-quality snack, i.e., whole almonds for six weeks, improved endothelial function, i.e., the ability of a thin layer of cells lining the inner surface of blood vessels to regulate various physiological processes in the cardiovascular system. These snacks also reduced concentrations of LDL cholesterol (also known as “bad“ cholesterol) in the blood (Dikariyanto et al., 2020).

On the other hand, consuming low-quality snacks, snacks consisting of ultra-processed foods, and foods with poor nutritional values can have opposite effects. Studies have linked frequent consumption of ultra-processed foods to adverse health outcomes (Monteiro et al., 2019; Samuthpongtorn et al., 2023), and it makes little difference whether these foods are perceived as snacks or as the main meals.

Frequent consumption of ultra-processed foods leads to adverse health outcomes

The current study
Study author Kate M. Bermingham and her colleagues wanted to explore the relationship between snacking habits – frequency of snacks, their quality, and timing with cardiometabolic blood markers, body measures, and the gut microbiome. They analyzed data from the ZOE PREDICT 1 study.

ZOE PREDICT 1 was a diet intervention study conducted between June 2018 and May 2019 that examined interactions between diet and cardiometabolic markers. The study participants were 967 healthy individuals from the UK. They were between 18 and 65 years of age. 73% of the participants were females. The study lasted for two weeks. Participants visited the clinic on the first day to take measurements and logged their dietary behavior for the next 13 days.

Participants logged food intake through an app
Researchers running the ZOE PREDICT 1 study trained study participants to accurately record their food intake using photos, product barcodes, portion sizes, and weighing food items on digital scales. Participants used a specially developed app called ZOE to record their food intake data throughout the study. Researchers collected data on the nutrient compositions of food from a nutrient database, while data on the contents of branded food items came from supermarket websites.

Participants reported the meal type (i.e., snack, breakfast, lunch, dinner, or drink), when they had it, and the food items consumed. A meal was when a participant consumed food or drinks separated by at least 30 minutes from a previous occasion. All food and drinks taken within 30 minutes of each other were considered a single meal. Participants consumed standardized meals on multiple study days to allow researchers to test their effects, but data from those days were not included in these analyses (see Figure 2).

Figure 2. Recording data on food consumption

Snacking habits and other data
Study authors considered snacks to be food or drinks consumed between main meals. They could consist of a single or multiple types of foods. However, the study authors did not count drinks of up to 50 kcal (e.g., drinking a glass of water) as snacks (if nothing else was consumed along with those drinks).

From the snacking data, researchers assessed the quality of snacks and inferred typical consumption times. The quality of snacks was related to the level of processing. Poor-quality snacks were ultra-processed, while unprocessed or minimally processed foods were considered high-quality.

Participants reported their hunger levels daily through the ZOE app. They did this at the time of the first logging into the app of the day and at regular intervals later. There were up to 7 hunger ratings per day. Participants also self-reported their general activity levels over the past year (“In the past year, how frequently have you typically engaged in physical exercises that raise your heart rate and last for 20 min at a time?”). They provided stool samples to allow researchers to examine their gut microbiome composition and gave blood samples at the start of the study for measuring cardiometabolic markers.

People who snack have 2.28 snacks per day on average

Results showed that 95% of participants snacked. On average, participants who snacked had 2.28 snacks per day: 19% had one snack per day, 47% had two snacks/day, and 29% had more than 2. The more snacks an individual had, the higher the share of snacks in their total daily energy intake was. Participants with larger shares of sugar and fats in their diets tended to consume more daily snacks, and their snacks tended to be higher in energy. Compared to main meals, snacks had higher shares of fats and sugars but lower protein contents (see Figure 3).

Figure 3. Snacking and snack vs. main meals

Cakes, pies, cereals, and ice cream were snacks with the highest contribution to energy intake
The most popular foods consumed as snacks were drinks (milk, tea, coffee, fruit drinks), candy, cookies and brownies, nuts, seeds and fruits (apples, bananas, citrus fruits), crisps, bread, cheese and butter, cakes and pies, and granola or cereal bars.

However, snacks with the highest contributions to total daily energy intakes were cakes and pies (14% of energy intake), cereals (13%), ice cream and frozen dairy products (12%), donuts and pastries (11%), candies, cookies and brownies (11%), nuts and seeds (11%) and corn snacks, chips and puffs (11%). There were no differences between genders on the average share of energy derived from snacks. The same was true with different age groups and people with different overall physical activity levels (see Figure 4).

Figure 4. Snacks with the highest contributions to total daily energy intake

People who eat better-quality snacks tend to have more favorable cardiometabolic blood marker levels

There were no differences in cardiometabolic blood marker levels between people who ate different numbers of snacks per day, nor between those who ate and those who did not eat snacks. There was also no association between the quantity of energy derived from snacks and cardiometabolic marker levels. Gut microbiota composition was not associated with snacking habits.

The number of snacks in a day and the quantity of energy derived from them were not associated with cardiometabolic blood markers (the quality of snacks was)

However, the quality of snacks was associated with cardiometabolic marker levels. Analysis showed that, on average, individuals who eat lower-quality snacks have higher levels of cardiometabolic markers than those who eat better-quality snacks. More specifically, these individuals had higher triglyceride levels and were more likely to show insulin resistance. They also had higher average levels of self-reported hunger. Participants eating high-quality snacks tended to have lower body weight, body mass index values, and body fat (see Figure 5).

Figure 5. Effect of snack quality on cardiometabolic marker levels

Late-evening snackers had poorer cardiometabolic blood marker levels
Analysis of the time of snack consumption showed that 13% of participants tended to mostly snack before noon (up to 50% of calories from snacks in that period), 39% were afternoon snackers (12 pm – 6 pm), and 31% were evening snackers (after 6 pm). 17% ate snacks equally throughout the day – there was no specific period when they ate more snacks. Additionally, researchers found that 32% of individuals tend to eat snacks (at least one) late in the evening – after 9 p.m. They referred to these individuals as late-evening snackers (see Figure 6).

Figure 6. Snacking times

Statistical analyses showed that late-evening snackers tend to have poorer cardiometabolic marker levels than those who do not snack after 9 p.m. Notably, these individuals had heightened blood glucose and triglyceride levels after meals and higher glycated hemoglobin levels compared to those who ate their snacks during the day. These differences were even higher in late-evening snackers prone to consuming poor-quality snacks (see Figure 7).

Figure 7. Effect of late-evening snacking on cardiometabolic markers

Conclusion
The study showed that the number of snacks eaten throughout the day is not associated with cardiometabolic blood marker levels. The same was the case with the share of energy derived from snacks. However, these health indicators are related to the quality of snacks and the time of day consumed. Consuming poor-quality snacks, particularly late in the evening, was associated with poorer cardiometabolic health indicators.

These findings could be used to inform the general public, as well as metabolic and cardiovascular disease prevention programs, about the possible health effects of snacking habits. Although the study design does not allow any cause-and-effect conclusions to be drawn, i.e., it remains unknown whether changing snacking habits would affect cardiometabolic indicator levels, there is a possibility that simply switching to better-quality snacks and avoiding late-evening snacking might indeed improve cardiometabolic health indicators and reduce the risk of serious metabolic diseases by at least some extent.

The paper “Snack quality and snack timing are associated with cardiometabolic blood markers: the ZOE PREDICT study” was authored by Kate M. Bermingham, Anna May, Francesco Asnicar, Joan Capdevila, Emily R. Leeming, Paul W. Franks, Ana M. Valdes, Jonathan Wolf, George Hadjigeorgiou, Linda M. Delahanty, Nicola Segata, Tim D. Spector, and Sarah E. Berry.

References

Bermingham, K. M., May, A., Asnicar, F., Capdevila, J., Leeming, E. R., Franks, P. W., Valdes, A. M., Wolf, J., Hadjigeorgiou, G., Delahanty, L. M., Segata, N., Spector, T. D., & Berry, S. E. (2023). Snack quality and snack timing are associated with cardiometabolic blood markers: the ZOE PREDICT study. European Journal of Nutrition. https://doi.org/10.1007/s00394-023-03241-6

Dikariyanto, V., Smith, L., Francis, L., Robertson, M., Kusaslan, E., O’Callaghan-Latham, M., Palanche, C., D’Annibale, M., Christodoulou, D., Basty, N., Whitcher, B., Shuaib, H., Charles-Edwards, G., Chowienczyk, P. J., Ellis, P. R., Berry, S. E. E., & Hall, W. L. (2020). Snacking on whole almonds for 6 weeks improves endothelial function and lowers LDL cholesterol but does not affect liver fat and other cardiometabolic risk factors in healthy adults: the ATTIS study, a randomized controlled trial. The American Journal of Clinical Nutrition, 111(6), 1178–1189. https://doi.org/10.1093/AJCN/NQAA100

Marangoni, F., Martini, D., Scaglioni, S., Sculati, M., Donini, L. M., Leonardi, F., Agostoni, C., Castelnuovo, G., Ferrara, N., Ghiselli, A., Giampietro, M., Maffeis, C., Porrini, M., Barbi, B., & Poli, A. (2019). Snacking in nutrition and health. International Journal of Food Sciences and Nutrition, 70(8), 909–923. https://doi.org/10.1080/09637486.2019.1595543

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

Piernas, C., & Popkin, B. M. (2010). Snacking Increased among U.S. Adults between 1977 and 2006, ,. The Journal of Nutrition, 140(2), 325–332. https://doi.org/10.3945/JN.109.112763

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

Intake of Micronutrients May Quicken Recovery From Anxiety and Depressive Symptoms

Posted on December 16, 2023January 12, 2024 by CNP Super Admin

An experimental study published in the Journal of Affective Disorders reports that intake of micronutrients might accelerate the improvement of depression and anxiety symptoms
Symptoms of the group taking micronutrients improved more quickly than those of the placebo group
The effect of the micronutrients was greater in younger participants, men, those from lower socioeconomic groups, and participants who had previously tried psychiatric medication

Everyone occasionally experiences situations in which they feel low, sad, or not interested in doing anything in particular, having difficulty gathering the motivation to perform daily activities. Similarly, we all feel anxious from time to time, particularly before important events, but the outcome of which is uncertain. However, in some individuals, these feelings become so persistent and frequent that they begin to impair their daily functioning. These are conditions that we refer to as depression (or major depressive disorder) and anxiety disorder.

What are depression and anxiety disorders?
Depression is a mental health disorder characterized by persistent feelings of sadness, hopelessness, and a lack of interest or pleasure in activities. Symptoms may include changes in appetite and sleep patterns, fatigue, difficulty concentrating, and thoughts of death or suicide. It significantly impacts a person’s emotional well-being and daily functioning.
Anxiety, on the other hand, is a condition marked by excessive worry, fear, or apprehension about future events. It can manifest in various forms, such as generalized anxiety disorder, panic disorder, social anxiety disorder, or various phobias. Physical symptoms like restlessness, muscle tension, and increased heart rate often accompany anxiety (see Figure 1).

Figure 1. Depression Vs. Anxiety

Epidemiological studies indicate that the number of people suffering from anxiety and depression has been increasing across many world countries in recent decades. Analyses indicate that these increases are likely not solely the consequence of better diagnostics and propose that changes to the way we live our lives might have adverse mental health consequences as well (Baxter et al., 2014; Steffen et al., 2020; Weinberger et al., 2018).

The number of people suffering from anxiety and depression has been increasing across many world countries in recent decades

What causes depression and anxiety disorders?
Researchers currently believe that neither depression nor anxiety have a single cause. Available data indicate that they can stem from various factors, including genetics, imbalances in brain chemistry, trauma, and environmental stressors. Recent studies also linked these disorders to certain dietary habits and changes in gut microbiota (Craiovan, 2015; Hedrih, 2023; Leclercq et al., 2020; Samuthpongtorn et al., 2023; Valles-Colomer et al., 2019).

How are these disorders treated?
Currently, psychiatric medications are an accessible treatment option for many people with depression and anxiety disorders (Blampied et al., 2023). Medications are often combined with psychotherapy. However, the effectiveness of these treatments is far from 100%. In many individuals, standard treatment protocols do not result in the withdrawal of symptoms. They sometimes fail to produce even a reduction of symptoms. This has given rise to concepts such as treatment-resistant depression (Fava, 2003). Also, it motivates researchers to seek alternative treatment options (e.g., Zavaliangos-Petropulu et al., 2023) or additions to the existing protocols that could improve their effectiveness.

Among other things, researchers proposed lifestyle changes and physical exercise as potential ways to improve symptoms of depression and anxiety. However, studies of the effectiveness of such treatments indicate mixed results (Kvam et al., 2016; Serrano Ripoll et al., 2015).

Studies conducted in recent decades identified associations between depression and mental health in general with dietary habits and properties of the gut microbiota (Hedrih, 2023a, 2023b; Leclercq et al., 2020; Valles-Colomer et al., 2019). This opened another possible venue for developing potential mental health disorder treatments – dietary intervention.

The current study
Study author Meredith Blampied and her colleagues wanted to explore the potential of dietary intervention in treating anxiety and depression. They note that poverty of diet is a well-established characteristic of people with these two types of disorders. These researchers considered adding micronutrients to patients’ diets as a promising option for a dietary intervention (Blampied et al., 2023).

Some previous studies already established that dietary interventions might effectively improve mental health symptoms. However, to be truly effective, dietary changes introduced through dietary interventions need to be maintained long-term. This is an issue in many patients (Blampied et al., 2023).

Poverty of diet is a well-established characteristic of people with anxiety and depression

What are micronutrients?
Micronutrients are essential nutrients the body requires in relatively small amounts to maintain proper physiological functions. These include vitamins and minerals, each playing unique roles in supporting various bodily processes. Vitamins such as A, B, C, D, E, and K are organic compounds that contribute to immune support, bone health, and energy metabolism. Minerals, including calcium, iron, zinc, and magnesium, are inorganic elements vital for bone formation, oxygen transport, and enzyme function (see Figure 2).

Figure 2. Impact of micronutrients on Bodily functions

There are several possible mechanisms for how micronutrients might benefit mental health. Some micronutrients are necessary components for the production of neurotransmitters. Other micronutrients help reduce inflammation and oxidative stress or maintain the balance of microbes in the digestive tract. Due to all this, the authors of this study believed that adding a broad spectrum of micronutrients to the diets of individuals suffering from depression or anxiety might lead to a greater reduction of symptoms during treatment (compared to placebo) (Blampied et al., 2023).

There are several possible mechanisms for how micronutrients might benefit mental health

Study participants
Study participants were 150 adults from Canterbury, New Zealand, reporting functionally impairing symptoms of anxiety and/or depression. Functionally impairing symptoms are symptoms that adversely affect their relationships, ability to work and/or engage in meaningful activity, and/or that prevent them from engaging in activities of daily living. Researchers recruited these participants between 2018 and 2020 via referrals from general practitioners and through self-referrals.

Study procedure
The study’s authors divided participants randomly into two groups of equal size. Both groups received pills that they were supposed to take over a ten-week study period. The pills and their packaging looked identical. Researchers sent participants the packages with pills for the study period via courier service. There were 12 pills participants had to consume each day, in three doses, four pills per dose.

However, pills delivered to one group (the micronutrient group) contained essential micronutrients, while those delivered to the other group contained maltodextrin (a carbohydrate derived from starch), fiber acacia gum (a natural thickening agent), and very small amounts of cocoa and riboflavin powders (for flavor) (see Figure 3).

Figure 3. Study Procedure (Blampied et al., 2023)

A full daily dose of micronutrient pills contained vitamins A, C, D, E, B6, B12, thiamin, riboflavin, niacin, biotin, pantothenic acid, calcium, iron, phosphorous, iodine, magnesium, zinc, selenium, copper, manganese, chromium, molybdenum, potassium, and several other ingredients.

Of all the individuals involved in the study procedure, only the pharmacist who prepared the pills had access to the group membership list, i.e., knew which participant was in which group. No one else knew this, including the study participants themselves. This was necessary to ensure that participants in both groups remained uncertain whether they were taking micronutrient capsules or a placebo.

Once per week, participants completed online assessments of depression (the Patient Health Questionnaire – 9 item scale, PHQ-9), anxiety (the Generalized Anxiety Disorder-7 question Scale, GAD-7), and a modified questionnaire used to assess side-effects of antidepressants (the Antidepressant Side-Effect Checklist, ASEC). Additionally, a clinical psychologist monitored the participants’ condition during the trial. This included assessment phone calls at the start and the end of the study and weekly text message reminders to complete the online assessments.

Symptoms improved faster in the micronutrient group
Results showed that anxiety and depression symptom severity decreased in both groups as the study progressed. However, the pace of decrease was faster in the group that consumed micronutrients. This was the case with both symptoms of depression and anxiety (See Figure 4).

Figure 4. Symptoms improved faster in the micronutrient group

To verify that these are the effects of micronutrients (and not, e.g., of participants’ expectations), study authors asked participants to report which group they think they are in. Results showed that 62% of participants in the placebo group and 55% from the micronutrient group believed they were in the placebo group. The small difference in percentages indicated to the researchers that their attempt to not let participants know which group they were in was successful. It also increased the likelihood that the observed differences between groups are the effects of micronutrient supplements (and not some other uncontrolled factor).

Results showed that anxiety and depression symptom severity decreased in both groups as the study progressed. However, the decrease pace was faster in the group that consumed micronutrients

Effects of micronutrients depend on age, previous psychiatric treatments, and socioeconomic status
Further analysis revealed that the effects of micronutrients on depressive symptoms depended on age – younger participants in the micronutrient group showed stronger improvements compared to the placebo group as time progressed.

The effects of micronutrients on depressive symptoms depended on age – younger participants in the micronutrient group showed greater improvements compared to the placebo group as time progressed.

Depression symptoms of participants in the placebo group also improved more quickly if they had not previously tried psychiatric medication. This effect was absent for anxiety symptoms. However, the effects of micronutrient intake on the pace of improvement of both depression and anxiety symptoms were greater in participants who previously used psychiatric medication. In a similar manner, depression symptoms of participants with better socioeconomic status in the placebo group improved more quickly. Still, the effects of micronutrients on the improvement of both types of symptoms were greater in participants with lower socioeconomic status.

Men’s symptoms improved slower than women’s, but micronutrients eliminated the difference
Men showed slower improvement in the placebo condition than women. However, in the micronutrient group, there was no difference in the pace of symptom improvement between men and women. This indicates that micronutrient intake accelerated the pace of symptom improvement in men specifically – men’s response to micronutrient intake was stronger.

By the end of the trial, both groups showed similar levels of improvement
Of participants who entered the study with depression symptom severity that indicated depression disorder, 61% from the micronutrient group and 49% from the placebo group achieved clinically significant symptom improvements by the end of the study.

Of participants who started the study with levels of anxiety symptoms indicating anxiety disorder, 62% from the micronutrient group and 56% from the placebo group achieved clinically significant reductions in symptoms.

In a similar fashion, males and females showed similar levels of improvement by the end of the study, and the same was the case with participants who had and those who had not used psychiatric medications earlier. Clinicians’ assessments of levels of improvement in the two groups indicated similar levels of improvement.

Conclusion
Overall, results showed that micronutrient intake might help existing treatments for anxiety and depression by accelerating the pace of recovery. The effects of this dietary intervention seem to be particularly visible in younger individuals, men, those of low socioeconomic status, and individuals with a previous history of psychiatric medication use.

Overall, results showed that micronutrient intake might help existing treatments for anxiety and depression by accelerating the pace of recovery

While it remains unclear why micronutrients showed greater effects in these categories, an important possibility is that they help alleviate dietary deficiencies in some members of these groups, producing greater overall effects in the group as a whole. This indicates that it might be useful for future depression and anxiety treatment programs, but also programs aimed at prevention, to look at the dietary habits of affected individuals along with their psychological status.

The paper “Efficacy and safety of a vitamin-mineral intervention for symptoms of anxiety and depression in adults: A randomized placebo-controlled trial “NoMAD” was authored by Meredith Blampied, Jason M. Tylianakis, Caroline Bell, Claire Gilbert, and Julia J. Rucklidge.

References
Baxter, A. J., Vos, T., Scott, K. M., Ferrari, A. J., & Whiteford, H. A. (2014). The global burden of anxiety disorders in 2010. Psychological Medicine, 44(11), 2363–2374. https://doi.org/10.1017/S0033291713003243

Blampied, M., Tylianakis, J. M., Bell, C., Gilbert, C., & Rucklidge, J. J. (2023). Efficacy and safety of a vitamin-mineral intervention for symptoms of anxiety and depression in adults: A randomised placebo-controlled trial “NoMAD.” Journal of Affective Disorders, 339, 954–964. https://doi.org/10.1016/j.jad.2023.05.077

Craiovan, P. M. (2015). Burnout, Depression and Quality of Life among the Romanian Employees Working in Non-governmental Organizations. Procedia – Social and Behavioral Sciences, 187, 234–238. https://doi.org/10.1016/j.sbspro.2015.03.044

Fava, M. (2003). Diagnosis and Definition of Treatment-Resistant Depression. Biol Psychiatry, 53, 649–659. https://doi.org/10.1016/S0006-3223(03)00231-2

Hedrih, V. (2023a). The Diet-Mental Health Relationship in Astronaut Performance. In CNP Articles. https://www.nutritional-psychology.org/the-diet-mental-health-relationship-in-astronaut-performance/

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/

Kvam, S., Lykkedrang Kleppe, C., Nordhus, I. H., & Hovland, A. (2016). Exercise as a treatment for depression: A meta-analysis. Journal of Affective Disorders, 202, 67–86. https://doi.org/10.1016/j.jad.2016.03.063

Leclercq, S., Le Roy, T., Furgiuele, S., Coste, V., Bindels, L. B., Leyrolle, Q., Neyrinck, A. M., Quoilin, C., Amadieu, C., Petit, G., Dricot, L., Tagliatti, V., Cani, P. D., Verbeke, K., Colet, J. M., Stärkel, P., de Timary, P., & Delzenne, N. M. (2020). Gut Microbiota-Induced Changes in β-Hydroxybutyrate Metabolism Are Linked to Altered Sociability and Depression in Alcohol Use Disorder. Cell Reports, 33(2). https://doi.org/10.1016/J.CELREP.2020.108238

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

Serrano Ripoll, M. J., Oliván-Blázquez, B., Vicens-Pons, E., Roca, M., Gili, M., Leiva, A., García-Campayo, J., Demarzo, M. P., & García-Toro, M. (2015). Lifestyle change recommendations in major depression: Do they work? Journal of Affective Disorders, 183, 221–228. https://doi.org/10.1016/j.jad.2015.04.059

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

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

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

Zavaliangos-Petropulu, A., McClintock, S. M., Khalil, J., Joshi, S. H., Taraku, B., Al-Sharif, N. B., Espinoza, R. T., & Narr, K. L. (2023). Neurocognitive effects of subanesthetic serial ketamine infusions in treatment-resistant depression. Journal of Affective Disorders, 333, 161–171. https://doi.org/10.1016/j.jad.2023.04.015

Scientists Propose that Ultra-Processed Foods be Classified as Addictive Substances

Posted on November 6, 2023January 12, 2024 by CNP Super Admin

An analysis commissioned by the BMJ argues that ultra-processed foods may be addictive
Behaviors around ultra-processed food may meet the diagnostic criteria for substance use disorder
Classifying ultra-processed foods as addictive might open novel approaches to treating food addiction and policies intended to combat it
Ultra-processed food addiction is estimated to occur in 14% of adults and 12% of children (Gearhardt et al., 2023).

We are all familiar with the devastating consequences resulting from the prolonged use of illicit drugs on an individual. In the beginning, the drugs produce pleasurable feelings by activating the brain’s reward system, and novice drug users experience euphoria, relaxation, or reduced stress. This, in turn, trains their brain to associate drug use with pleasure, reinforcing the desire to use drugs again. However, over time the body develops tolerance for the drug, and the individual needs to increase consumption to achieve the same effect continually. Ultimately, this changes the brain’s chemistry, which then becomes highly fixated on drug-induced pleasures and, consequently, less responsive to natural rewards. The desire for the drug becomes uncontrollable, and if this need is not met with more of the drug, unpleasant and difficult withdrawal symptoms occur. To avoid these symptoms, the drug user prioritizes his/her life to be exclusively focused on cycles of drug intake. This is damaging to both psychological and physical health and, in extreme cases, can lead to death. This development is what is usually referred to as addiction.

What is addiction?
A common definition of addiction is any behavior in which an individual has impaired control with harmful consequences. Individuals who recognize that the behavior is harming them or those they care about but still find themselves unable to stop engaging in that harmful behavior are considered addicted. Because addiction, in a way, violates one’s freedom of choice, it can be considered a disorder of motivation (West, 2001).

In certain types of addiction, an individual may experience withdrawal symptoms when the substance or behavior is not accessible. Withdrawal symptoms can vary depending on the specific substance involved, but common symptoms include anxiety, depression, irritability, nausea, vomiting, sweating, muscle aches, and intense cravings. Addiction can devastate an individual’s health, relationships, and overall well-being, making it a significant public health concern.
Can we become addicted to ultra-processed foods?

Although addictions to illicit drugs and alcohol get the most publicity, scientists have also recognized tobacco smoking addiction, gambling addiction, compulsive shopping addiction, smartphone addiction, internet addiction, exercise addiction, addiction to certain prescribed medications such as stimulants or benzodiazepines (medicines used to treat anxiety, sleep disorders, and seizures), pornography addiction, and many others (e.g., O’Brien, 2005; Rakić-Bajić & Hedrih, 2012; Ting & Chen, 2020) (see Figure 1).

Figure 1. Types of addictions

Many recent studies have supported the notion that individuals can display behaviors that meet the definition of addiction toward specific types of food. These behaviors include binge eating, or the inability to control food intake, strong cravings, and many other well-known characteristics of addictions (Gearhardt et al., 2011, 2023; Weingarten & Elston, 1990). Foods most often associated with food addictions are ultra-processed foods.

What are ultra-processed foods?
Almost all foods are processed to some extent. Humans process food to make it edible, preserve it, destroy harmful microorganisms, improve its taste, and for many other reasons. Some foods are not fit to eat without processing, and others would quickly spoil if left unprocessed. It is important to note that ultra-processed foods are not only processed, they have nutritionally lacking or unhealthy substances added.

Ultra-processed foods are formulations made mostly or entirely from derived substances and various additives with few intact unprocessed or minimally processed food components (Hedrih, 2023; Monteiro et al., 2019)

These foods typically contain artificial additives, preservatives, and flavor enhancers. Additives include dyes, color stabilizers, non-sugar sweeteners, de-foaming, anti-caking or glazing agents, emulsifiers, and humectants, among others. Some processes used in preparing ultra-processed foods, such as hydrogenation, hydrolyzation, or extrusion, are exclusively industrial processes that cannot be performed in a regular kitchen (see Figure 2). (Note: More about ultra-processed foods and their effects on the diet-mental health relationship can be found in NP 110: Introduction to Nutritional Psychology Methods through The Center for Nutritional Psychology).

Figure 2. Elements of ultra-processed foods

Examples of ultra-processed foods include instant noodles, artificial sweeteners, artificially sweetened beverages, sugary cereals, microwaveable meals, reconstituted meat products, sweet and savory packaged snacks, pre-prepared frozen dishes, and soft drinks (see Figure 3).

Figure 3. Examples of ultra-processed foods

Ultra-processed foods are linked to various health problems
Ultra-processed foods are often low in nutritional value, high in calories, packed with various unhealthy ingredients, attractively packaged, and marketed intensely (see Figure 3). They are usually created with the intent of having a durable product that is highly palatable but also highly profitable due to the low cost of ingredients (Hedrih, 2023).
Studies have linked the consumption of ultra-processed foods with various health problems. Research indicates that individuals regularly consuming these foods have a higher risk of obesity, type 2 diabetes, heart disease, certain types of cancer, and depression. (Monteiro et al., 2018; Samuthpongtorn et al., 2023). Despite this, the sales of these foods and their share in the dietary calorie intake are rising, both in high- and middle-income countries (Monteiro et al., 2019).

The analysis
Professor Ashley Gaerhart and her colleagues start their analysis by noting that two reviews of 281 studies from 36 different countries found that 14% of adults and 12% of children show indications of being addicted to food. These levels are similar to shares of the population addicted to tobacco and alcohol. Studies also showed that 50% of people diagnosed with binge eating disorder and 32% of people struggling with obesity who are undergoing bariatric surgery may, indeed, suffer from food addiction (Figure X).

Figure 4. Food addiction statistics

These authors then analyze what might make a food addictive. According to them, not all foods have addictive potential. Research results indicate that foods with high levels of refined carbohydrates or added fats, such as sweets and salty snacks, are the most strongly implicated in addiction behaviors, such as losing control over consumption, excessive intake, and continued use despite negative consequences.

Foods with high levels of refined carbohydrates or added fats, such as sweets and salty snacks, are the most strongly implicated in addiction behaviors

What makes food addictive?
The foods described above are all ultra-processed. Unlike natural foods, they often contain high concentrations of both fats and carbohydrates. This is unlike natural or minimally processed foods with high carbohydrate content but little or no fat (e.g., apples) or high-fat content with little or no carbohydrates (e.g., certain types of fish or meat).

Even in rare cases when natural foods do contain large amounts of both fat and carbohydrates (e.g., almonds), they typically require extensive digestion before the body can use them. For example, almond fat remains encapsulated in cell walls even after chewing, which means it is unavailable to the body at the early stages of digestion. This is important because a natural and minimally processed food item, like almonds, takes a long time to break down, so nutrients will be absorbed only in the lower intestine and, therefore, do not trigger the release of dopamine (a neurotransmitter linked to feelings of reward and pleasure). Conversely, when an ultra-processed food undergoes digestion, it readily breaks down, and nutrients rapidly enter the bloodstream through the upper intestine, thereby triggering dopamine signaling, which ultimately induces feelings of pleasure.

Unlike natural foods, fats and carbohydrates in ultra-processed foods become swiftly available to the body during digestion which affects the pleasure response of the brain, contributing to the addictive nature of these foods. The reward of obtaining both of these micronutrients simultaneously is greater than the effect that either of them, individually, can have. This alters the brain’s reward processing system and triggers the changes, leading to addiction. Various additives found in ultra-processed foods that improve their taste and mouthfeel further strengthen these effects (Figure 5).

Figure 5. Differences in body processing of ultra-processed foods and unprocessed foods

This mechanism is similar to the one determining the addictiveness of drugs. Drugs that act faster also tend to be more addictive. Studies indicate that flavor-enhancing additives in products, such as cigarettes, also increase their addictive potential (see Figure 6).

Figure 6. Relationship between flavor-enhancing additives and addictive potential

But what do the critics say?
Not all scientists agree that food addiction is a real addiction. Unlike alcohol, tobacco, or cocaine, we need food to survive. Craving for food already has a name – hunger. Fats and carbohydrates are macronutrients that are needed to fuel the body in considerable amounts. Can an intense desire to consume substances needed for survival really be considered an addiction?

The authors of this analysis note that there is also the question of the addictive chemical. All other substances are addictions to a specific chemical, but such chemical has not been identified for foods. Substances such as alcohol, nicotine, or illicit drugs activate the brain’s reward system directly, but fat and carbohydrates do not do that.

However, these researchers argue that, although fat and carbohydrates do not activate the brain’s reward system directly, they can still activate it to a magnitude similar to alcohol and nicotine. The presence of an addictive chemical might not be crucial for identifying an addiction, as the authors theorize there are many addictive chemicals with the ability to cause addiction in unknown doses and intake levels.

What should be done?
Based on all this, the authors of this analysis propose that ultra-processed foods be classified as addictive substances. They believe this would increase focus on the culpability of manufacturers of these foods, much like how classifying cigarettes as addictive helped combat smoking.

They believe that research should focus on clearly evaluating how complex features of ultra-processed foods combine to increase their addictive potential. That research can then be used to delineate between addictive and non-addictive foods based on those features. Studies should also focus on fully understanding the mechanisms linking the consumption of these foods to obesity and adverse health outcomes.

Tackling food addiction through policies
Authors of the analysis also believe that governments should combat food addiction in the same way they tackled addiction to cigarettes – through a suite of policies targeting foods with high addiction potential, notably ultra-processed foods. Examples of such policies include special taxes on ultra-processed foods and beverages, mandatory or voluntary front-of-pack or shelf labeling systems, and mandatory or voluntary reformulations of the food supply, particularly focused on banning the use of substances, increasing the addictive effects.

However, the authors also note that the consumption of ultra-processed foods tends to be particularly high in disadvantaged neighborhoods because these foods are inexpensive. There is limited if any, availability of lower-calorie, healthier foods in those areas, and those people consume the higher-calorie, ultra-processed foods instead. In light of this fact, tackling the issue of food addiction should be done with care and in a way that does not create food insecurity.

Additionally, including ultra-processed food addiction diagnosis in clinical care would improve access to support and enable the development of treatments to reduce compulsive patterns of ultra-processed food intake. Drugs already exist that show promise in helping overcome food addiction.

Conclusion
Overall, the analysis makes a strong case for the reality of ultra-processed food addiction. The ongoing obesity pandemic (Wong et al., 2022) makes what they say important. The authors propose that researchers focus on fully understanding the mechanisms through which addictive behaviors toward specific foods occur.

They also propose that policymakers approach legislation on food addiction similarly to nicotine, tobacco, and cigarette addiction – through recognizing ultra-processed food addiction as a disorder, through policies targeting the production and the sale of addictive foods, preventing the use of substances or processes that increase the addictiveness of food items, and other measures. Still, this should be done with care and in a way that does not reduce food security for anyone. Ultra-processed foods are still foods, and people need food to survive.

The analysis paper “Social, clinical, and policy implications of ultra-processed food addiction” was authored by Ashley N. Gearhardt, Nassib B. Bueno, Alexandra G. DiFeliceantonio, Christina A. Roberto, Susana Jimenez-Murcia, and Fernando Fernandez-Aranda.

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

Gearhardt, A. N., Yokum, S., Orr, P. T., Stice, E., Corbin, W. R., & Brownell, K. D. (2011). Neural Correlates of Food Addiction. Archives of General Psychiatry, 68(8), 808–816. https://doi.org/10.1001/ARCHGENPSYCHIATRY.2011.32

Hedrih, V. (2023). 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/

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

Monteiro, C. A., Cannon, G., Moubarac, J. C., Levy, R. B., Louzada, M. L. C., & Jaime, P. C. (2018). The un Decade of Nutrition, the NOVA food classification and the trouble with ultra-processing. Public Health Nutrition, 21(1), 5–17. https://doi.org/10.1017/S1368980017000234

O’brien, C. P. (2005). Benzodiazepine Use, Abuse, and Dependence. J Clin Psychiatry, 66(2).

Rakić-Bajić, G., & Hedrih, V. (2012). Prekomjerna upotreba interneta, zadovoljstvo životom i osobine ličnosti [Excessive use of the internet, life satisfaction and personality factors]. Suvremena Psihologija, 15(1), 119–131.

Ting, C. H., & Chen, Y. Y. (2020). Smartphone addiction. Adolescent Addiction: Epidemiology, Assessment, and Treatment, 215–240. https://doi.org/10.1016/B978-0-12-818626-8.00008-6

Weingarten, H. P., & Elston, D. (1990). The phenomenology of food cravings. Appetite, 15(3), 231–246. https://doi.org/10.1016/0195-6663(90)90023-2

West, R. (2001). Theories of addiction. Addiction, 96(1), 3–13. https://doi.org/10.1046/J.1360-0443.2001.96131.X

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

Women Consuming Lots of Artificially Sweetened Beverages Might Have a Higher Risk of Depression, Study Finds

Posted on October 13, 2023November 13, 2023 by CNP Super Admin

What is food processing?
Almost all foods are processed to some extent (Monteiro et al., 2019). Humans process food to preserve it so that it would not spoil, to make it edible, to destroy harmful microorganisms or chemical compounds, to improve its taste, and for many other reasons.

Many foods are not edible unless processed. For example, cassava, a root vegetable that is one of the staple foods in many parts of the world, contains large amounts of cyanogenic glycosides. If consumed raw, these compounds can release the poison cyanide. Thorough processing, which involves peeling, soaking, and cooking, is necessary to make cassava safe to eat. This thorough processing turns a poisonous plant into an important source of nutrients for humans.

Many foods are not edible unless processed

Other types of food would readily spoil without processing. For example, left on their own, meat, fish, and many fruits and vegetables would spoil very quickly in most environments. However, drying, curing, and canning allow us to preserve these foods for long periods, ensuring food is available throughout the year. Food processing such as this is crucial for creating a stable and dependable human food supply. Due to all this, it is not helpful to be critical of food processing in general. Food processing is necessary.

It is worth noting, however, that the way humans process foods – even the same food – can vary significantly depending on various factors, for example, the setting. Processing food at home (e.g., cooking a meal) differs from processing food on an industrial level (e.g., preparing the same meal industrially for mass distribution). The latter involves specific manufacturing techniques and often uses additives (e.g., colorants, flavor enhancers, preservatives, pesticides, etc.) even in relatively unprocessed foods.

With regard to food processing, researchers have developed classifications of various food items

The NOVA food classification system
With regard to processing, researchers have developed various classifications of food items. One very popular classification is the NOVA classification system (Monteiro et al., 2018), which groups foods into four categories according to the extent and purpose of processing they undergo.

The NOVA system categories are (see Figure 1):

Group 1. Unprocessed or minimally processed foods – natural foods altered only by processes that include removing inedible or unwanted parts and preparation for storage (e.g., vacuum-packaging, drying, pasteurization, refrigeration, freezing, roasting…)
Group 2. Processed culinary ingredients – derived from group 1 foods and processed to make durable products suitable for kitchens to prepare, season, and cook group 1 foods. These processes include milling, grinding, refining, pressing, and drying. Examples are oils, butter, sugar, and salt.
Group 3. Processed foods – created by adding salt, oil, sugar, or other substances from group 2 to group 1 foods. Examples include bottled vegetables, canned fish, fruits in syrup, cheeses, and freshly made bread.
Group 4. Ultra-processed foods (UPFs) are formulations made mostly or entirely from substances derived from foods and additives with little if any, intact group 1 food (Monteiro et al., 2018).

Figure 1. Nova food classification system and examples of foods in each class

Why are ultra-processed foods special?
Ultra-processed foods (UPFs) are heavily processed before consumption. They typically contain numerous artificial additives, preservatives, and flavor enhancers. These additives include dyes, color stabilizers, non-sugar sweeteners, de-foaming, anti-caking or glazing agents, emulsifiers, humectants, and many others. Some processes used in preparing these foods, such as hydrogenation, hydrolyzation, or extrusion, are exclusively industrial processes that cannot be performed in a regular kitchen (see Figure 2).

Figure 2. Elements in ultra-processed foods

Ultra-processed foods are often low in nutritional value, high in calories, and packed with unhealthy ingredients like refined sugars, trans fats, and excessive sodium. Examples of ultra-processed foods include instant noodles, artificial sweeteners, artificially sweetened beverages, sugary cereals, microwaveable meals, reconstituted meat products, sweet and savory packaged snacks, pre-prepared frozen dishes, and soft drinks. The overall purpose of ultra-processing is to create a durable product that is highly palatable but also highly profitable due to the low cost of ingredients. Ultra-processed foods usually have attractive packaging and are marketed intensely (see Figure 3).

Figure 3. Characteristics of ultra-processed foods

Ultra-processed foods and health risks
One of the concerning aspects of ultra-processed foods is their link to various health problems. Studies have linked the regular consumption of these foods with a higher risk of obesity, type 2 diabetes, heart disease, and certain types of cancer. Ultra-processed foods often lack essential nutrients like fiber, vitamins, and minerals important for overall health.

Despite these health risks, over half of the dietary energy consumed by individuals from high-income countries such as the USA, Canada, or the UK comes from ultra-processed foods. In middle-income countries such as Brazil, Mexico, and Chile, the share of dietary calories from ultra-processed foods is estimated to be between 20% and 33%. Additionally, the sales of these foods are growing by about 1% per year in high-income countries and up to 10% per year in middle-income countries (Monteiro et al., 2019) (see Figure 4).

Figure 4. Consumption of UPFs by Country.

Over half of the dietary energy consumed by individuals from high-income countries such as the USA, Canada, or the UK comes from ultra-processed foods

The current study
Study author Chatpol Samuthpongtorn and his colleagues wanted to examine whether consuming ultra-processed foods might be associated with the risk of depression. They were aware of findings linking the consumption of ultra-processed foods with many different diseases. Still, they noted that many studies that reported these findings relied only on short-term dietary data and could not account for various factors that could have influenced the results. They also wanted to know if any specific ultra-processed foods are linked to depression and whether the timing of ultra-processed food consumption might play a role.

The study participants were 31,712 females in the Nurses’ Health Study II conducted between 2003 and 2017. Participants were between 42 and 62 years old at the start of the study.

Are any specific ultra-processed foods linked to depression, and does the timing of ultra-processed food consumption play a role?

The procedure
Participants completed a food frequency questionnaire based on the NOVA classification every four years. This questionnaire asked participants to report how often they consumed various foods from the four NOVA categories. The part about ultra-processed foods included questions about the frequencies of consuming ultra-processed grain foods, sweet snacks, ready-to-eat meals, fats and sauces, ultra-processed dairy products, savory snacks, processed meat, beverages, and artificial sweeteners.

Participants reported whether they were diagnosed with depression and whether they consumed antidepressants regularly. Researchers also collected data on participants’ ages, total caloric intake, body mass index, physical activity, smoking status, menopausal hormone therapy, alcohol consumption, chronic diseases, marital status, family income, and other characteristics (see Figure 5).

Figure 5. Food Frequency Questionnaire (FFQ) every four years, and participant reports

Individuals eating more ultra-processed foods had higher body weight, smoked more, and were in poorer health

Participants who reported eating ultra-processed foods most frequently had greater body mass index, smoked more often, and suffered from diseases like diabetes, hypertension, and dyslipidemia compared to those who reported eating ultra-processed foods less often. These individuals were also less likely to exercise regularly.

Dyslipidemia is a medical condition characterized by abnormal levels of lipids (fats) in the blood, typically involving elevated cholesterol and/or triglycerides, which can increase the risk of cardiovascular diseases.

Individuals frequently consuming ultra-processed foods were more often depressive
Depending on the definition of depression used, there were 2122 (using the stricter definition) or 4840 (using the broader definition) participants suffering from depression in the study. In both cases, participants who ate ultra-processed foods most frequently (the top 20% of the sample with the highest ultra-processed food consumption) were more likely to suffer from depression compared to those who ate the ultra-processed foods the least often (the bottom 20% on ultra-processed food consumption).

Participants who ate ultra-processed foods most frequently were more likely to suffer from depression than those who ate ultra-processed foods least often

Depending on the definition of depression, the top consumers of ultra-processed foods had a 34% or 49% higher likelihood of depression compared to participants who consumed these types of food the least. This finding held when study authors considered various other factors and calculated the association between ultra-processed food consumption at one point and depression four years later (see Figure 6).

Figure 6. Research findings

The top consumers of ultra-processed foods had a higher likelihood of depression than participants who consumed these types of food the least

Sweetened beverages and artificial sweeteners are the ultra-processed foods most strongly linked with depression
Next, the study authors explored which ultra-processed foods are most linked with depression. Are all types of ultra-processed foods equally associated with depression, or is the high consumption of some specific types of ultra-processed foods linked with a higher likelihood of depression?

Analyses showed that only high consumption of artificially sweetened beverages and artificial sweeteners is associated with an increased likelihood of depression. These findings, however, don’t necessarily imply that all other UPFs consumed in the longitudinal study are exempt from having undesired effects on psychological well-being.

Analyses showed that only high consumption of artificially sweetened beverages and artificial sweeteners is associated with an increased likelihood of depression

Additional analyses indicated that individuals who reduced their intake of ultra-processed foods by at least three servings per day were at a lower risk of depression compared to individuals with a relatively stable intake of these foods in each four-year period.

Conclusion
Overall, the study results suggest that frequent intake of ultra-processed foods is associated with an increased risk of depression. This is particularly the case with high intake of artificially sweetened beverages and artificial sweeteners. While the nature of this association remains unknown, the large number of participants involved in this study and the fact that the association held across multiple years makes these findings particularly strong.

Given the current increase in the number of people suffering from depression in many world countries (e.g., Steffen et al., 2020; Weinberger et al., 2018) and also the increase in ultra-processed foods consumption (Monteiro et al., 2019; Samuthpongtorn et al., 2023), these findings could be used to inform policymakers and the general public about the importance of healthy food choices and how seemingly innocuous dietary decisions may have long-lasting health consequences.

The paper “Consumption of Ultraprocessed Food and Risk of Depression” was authored by Chatpol Samuthpongtorn, Long H. Nguyen, Olivia I. Okereke, Dong D. Wang, Mingyang Song, Andrew T. Chan, and Raaj S. Mehta.

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

Monteiro, C. A., Cannon, G., Moubarac, J. C., Levy, R. B., Louzada, M. L. C., & Jaime, P. C. (2018). The un Decade of Nutrition, the NOVA food classification and the trouble with ultra-processing. Public Health Nutrition, 21(1), 5–17. https://doi.org/10.1017/S1368980017000234

Steffen, A., Thom, J., Jacobi, F., Holstiege, J., & Bätzing, J. (2020). Trends in the 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

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

Gut Microbiota Play Crucial Role in Mediating Effects of Western Diet

Posted on August 8, 2023August 22, 2023 by CNP Super Admin

Introduction

The past several decades have seen the rise of an obesity pandemic that is ongoing worldwide. While obese individuals were quite rare just a century ago, 2015-2018 estimates for the U.S. state that more than two-thirds of the adult population is overweight or obese (Wong et al., 2022). Determining the causes of this increase in obesity rates has attracted much research attention. Studies have revealed a complex interplay between diet components, environmental factors, and previously unknown psychological and physiological mechanisms resulting in overeating and obesity in the long term. These novel studies on the intersection of nutrition and psychology are part of a developing field of science called nutritional psychology (The Center for Nutritional Psychology, 2023) (see Figure 1).

Figure 1. Diet, environment, psychological, and physiological factors in nutritional psychology

There is a complex interplay between diet, environmental factors, and psychological and physiological mechanisms resulting in overeating and obesity

Gut microbiota and the microbiota-gut-brain axis

The human gut microbiome consists of trillions of microorganisms that live in the human intestinal tract. These microorganisms play a key role in digesting the food we eat. However, their influence extends beyond the gut, encompassing crucial roles in metabolic regulation, body weight maintenance, and immune system modulation.

This growing body of evidence suggests that these gut microorganisms also profoundly impact brain functions, mood, cognition, and emotional well-being (Zhu et al., 2023). This topic is explored in continuing education curricula within nutritional psychology — particularly how the gut microbiota and the gut-brain axis interconnect with the diet-mental health relationship to influence psychological functioning and experience, shedding light on its potential therapeutic implications for mental health outcomes.

This growing body of evidence suggests that gut microorganisms profoundly impact brain functions, mood, cognition, and emotional well-being

Scientists have recently discovered a communication pathway connecting the gut microbiome and the brain. This pathway is called the microbiota-gut-brain axis. It is based on small proteins called cytokines and a number of other biomolecules, including the hormone cortisol, short-chain fatty acids (SCFAs), tryptophan, and others.

The Western diet

The Western diet is a modern dietary pattern prevalent in Western societies, characterized by a high intake of processed and hyperpalatable foods with increased contents of fat, sugary snacks, and refined grains. It typically includes low consumption of fruits, vegetables, unprocessed-high-quality proteins, nuts, and seeds. This diet’s excessive reliance on added sugars and unhealthy fats has been linked to an increased risk of obesity, metabolic syndrome, and various chronic diseases.

Studies have indicated that feeding mice a Western diet causes inflammation in the region of the brain called the hypothalamus (Heiss et al., 2021; Thaler et al., 2013). Inflammation of the hypothalamus damages the neurons and leads to the formation of scars made of glial cells. This is called gliosis. Inflammation of the hypothalamus often happens before a mouse starts gaining weight. Due to this, scientists believe it might cause weight gain by causing leptin resistance.

Studies have indicated that feeding mice a Western diet causes inflammation of the region of the brain called the hypothalamus

Leptin and leptin resistance

Leptin is a hormone produced by fat cells during eating. It regulates appetite and body weight and is produced in proportion to the amount of fat in the body. Leptin concentrations inform the brain of how much fat is stored. Increased leptin concentrations (normally caused by an abundance of body fat) “tell” the brain to decrease food intake and increase energy expenditure.

Leptin is a hormone produced by fat cells that regulate appetite and body weight

Factors such as chronic inflammation or eating high-fat diets (HFDs) may cause the body to be less receptive to leptin. This is called leptin resistance. Leptin resistance results in disrupted appetite and energy regulation, i.e., the brain does not reduce food intake in spite of the abundance of body fat. This can contribute to obesity and cause difficulty controlling body weight (Thaler et al., 2013) (see Figure 2).

Figure 2. Normal leptin cycle versus leptin resistance.

Gliosis, leptin resistance, and gut microbiota

Microglia are a type of immune cell in the central nervous system that helps protect and maintain the brain and spinal cord by detecting and responding to potential threats or damage. Studies have shown that activation of microglia cells that happens during inflammation of the hypothalamus might be causing leptin resistance. Removing these microglia cells from the hypothalamus has improved sensitivity to leptin. Improved sensitivity to leptin allows the brain to recognize when enough fat is stored in the body and reduce food intake.

Studies have shown that the activation of microglia cells that happens during inflammation of the hypothalamus might be causing leptin resistance

Intriguingly, according to the scientific evidence presented in our recent NP 120 course, it has been discovered that the gut microbiota plays a significant role in regulating the development and maturation of microglia cells and influencing their function. Although the mechanism of this action remains unknown, it has led scientists to believe there might be a link between hypothalamus inflammation and gut microbiota (Heiss et al., 2021) (see Figure 3).

Figure 3. Link of Gut Microbiota in regulating development and maturation of microglia cells

There might be a link between hypothalamus inflammation and gut microbiota (Heiss et al., 2021)

The current study

Study author Christina N. Heiss and her colleagues wanted to know whether mice that lack gut microbiota are protected against diet-induced inflammation of the hypothalamus. They noted previous studies’ results showing mice with depleted gut microbiota and those treated with antibiotics to be protected from diet-induced obesity.

In other words, they noted that mice that consume a Western diet, a diet that normally leads to obesity in mice, do not become obese if microbiota are not present in their guts. This might be because the absence of microbiota prevents inflammation of the hypothalamus, which would, in turn, prevent leptin resistance from developing. If this is the case, the mechanism for preventing overeating based on leptin would remain intact, preventing mice from becoming obese. Alternatively, it could be that, without microbiota, the guts of mice could not digest complex nutrients from the food they eat, thus substantially reducing the amount of nutrition they can derive from food. In this case, obesity would be avoided because their bodies cannot use their food. But which of these is the case?

The procedure

The study authors used three groups of male mice, 10-13 weeks old – conventionally raised mice, germ-free mice, and antibiotic-fed mice. They used several genetic groups of mice, including a strain of genetically engineered mice that allow for controlled and regulated manipulation of specific genes in specific tissues (Tamoxifen-inducible Cre mice).

In the scope of the experiments, researchers fed mice either a chow diet or a Western diet. Western diet was given for either 2 days, 1 week, or 4 weeks, depending on the experiment conducted in the scope of the study.

The chow diet for mice is a nutritionally balanced and standardized diet formulated to provide essential nutrients required for the health and growth of laboratory mice. It typically consists of a combination of proteins, carbohydrates, fats, vitamins, and minerals in pellet or block form. The Western diet used in this study was high in fat and sucrose, with 40% of calories coming from fat.

All food for mice was sterilized, i.e., underwent procedures that killed all microorganisms in the food before mice ate it. The chow diet was sterilized in an autoclave, which uses high pressure and steam to kill microorganisms. The Western diet food was irradiated, i.e., radiation was used to kill microorganisms.

The mice

Conventionally raised mice were laboratory mice kept in regular conditions and fed a normal diet for laboratory mice. They have normal gut microbiota.

Germ-free mice are created through techniques that ensure they do not acquire gut microbiota from birth through their entire lifetimes. They are typically born using cesarean section deliveries of pregnant mice in a sterile environment. This is done to prevent the transfer of microbes during birth. After that, they are kept in specialized sterile isolation spaces called isolators or bubbles that maintain a controlled germ-free environment.

These isolators provide filtered air, sterile food, and autoclaved water to prevent microbial contamination. Researchers raising these mice take special care to maintain strict barrier measures, including specialized clothing and equipment, to prevent the unintentional introduction of microorganisms. They regularly monitor these mice’s bodily fluids and tissues through special techniques to ensure the absence of any detectable microorganisms. Germ-free mice are typically leaner than conventionally raised mice and, consequently, have lower leptin levels in circulation.

Antibiotic-fed mice in this study had 1g of ampicillin and 0.5g of neomycin added per liter of their drinking water. Ampicillin and neomycin are antibiotics. Researchers kept the drinking water with antibiotics added in bottles protected from light. They prepared a new solution every second day. Researchers started giving this water with antibiotics to mice three days before changing their regular diet to a Western diet.

Mice without gut microbiota are protected from diet-induced inflammation of the hypothalamus

Results showed that conventionally raised mice fed a Western diet for 1 week developed gliosis in the hypothalamus. Inflammation indicators were increased in these mice in the part of the hypothalamus called the arcuate nucleus compared to conventionally raised mice fed regular mice food (chow) (see Figure 4).

Figure 4. Conventionally raised mice fed a Western diet developed gliosis in the hypothalamus

When researchers examined germ-free mice and mice whose gut microbiota were depleted using antibiotic treatment (antibiotic-fed mice), results showed that these mice also showed no increase in inflammation indicators or the proliferation of microglia cells after eating a Western diet for a week.

Gliosis in the hypothalamus leads to greater gain in body weight and fat mass

The study authors also wanted to know whether gliosis in the hypothalamus caused by a Western diet leads, in turn, to increased body weight and fat mass accumulation in mice. To test that, they fed conventionally raised mice and antibiotic-fed mice a Western diet for 4 weeks.

Results showed that conventionally raised mice fed a Western diet gained more body weight and fat mass than antibiotic-fed mice. Compared to antibiotic-fed mice, they also had increased hypothalamus inflammation indicators and increased numbers of a specific type of microglia cells (iba1-positive microglia).

There was no association between the number of microglia in the arcuate nucleus region of the hypothalamus and changes in body weight or fat mass at the end of the 4 weeks. However, fat mass and the relative increase in fat mass during the study were associated with the number of a specific type of glial cells called astrocytes.

Further analysis showed that germ-free and antibiotic-fed mice are more sensitive to leptin than conventionally raised mice. When researchers gave them leptin injections, the first two types of mice reduced their food intake more than conventionally raised mice did.

Glucagon-like-peptide 1 (GLP-1) seems to be crucial for protection against diet-induced inflammation of the hypothalamus

Germ-free and antibiotic-fed mice had higher levels of the hormone called glucagon-like peptide 1 (GLP-1) when they were fed a regular diet. This hormone secreted in the small intestine’s intestinal lining cells (L cells) is important in regulating blood sugar levels. It also helps reduce inflammation and protect neurons.

Study authors believed it might also be crucial for the protection from inflammation of the hypothalamus induced by the Western diet. After mice were fed a Western diet for a week, antibiotic-treated and germ-free mice had higher levels of GLP-1 than conventionally raised mice. These mice did not gain weight or develop hypothalamic inflammation after this diet. However, when researchers measured these same things in antibiotic-fed and germ-free mice whose GLP-1 signaling pathway was disabled, they also gained weight and developed inflammation, similar to conventionally raised mice. This indicated that the functional signaling path of GLP-1 is crucial for countering the inflammation of the hypothalamus induced by a Western diet.

Just a week on a Western diet led to inflammation of the hypothalamus that, in turn, disrupted the body’s mechanism for regulating food intake

Conclusion

These findings in mice show that gut microbiota changes how the organism, of mice in this case, reacts to a Western diet. When gut microbiota was intact, just a week on a Western diet led to inflammation of the hypothalamus that, in turn, disrupted the body’s mechanism for regulating food intake. However, when gut microbiota was depleted or absent, this inflammation did not happen, provided that the signaling pathway of one specific hormone (GLP-1) was intact.

While the study was done on mice, similar physiological mechanisms exist in humans. Due to this, these findings on mice help scientists better understand how and through which physiological mechanisms changes in the human diet that occurred in the last century disrupted food intake regulation in the human body leading to the current obesity pandemic.

The paper “The gut microbiota regulates hypothalamic inflammation and leptin sensitivity in Western diet-fed mice via a GLP-1R-dependent mechanism” was authored by Christina N. Heiss, Louise Manneras-Holm, Ying Shiuan Lee, Julia Serrano-Lobo, Anna Hakansson Gladh, Randy J. Seeley, Daniel J. Drucker, Fredrik Backhed, and Louise E. Olofsson.

References

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

Thaler, J. P., Guyenet, S. J., Dorfman, M. D., Wisse, B. E., & Schwartz, M. W. (2013). Hypothalamic inflammation: Marker or mechanism of obesity pathogenesis? Diabetes, 62(8), 2629–2634. https://doi.org/10.2337/DB12-1605

The Center for Nutritional Psychology. (2023). What is Nutritional Psychology? https://www.nutritional-psychology.org/what-is-nutritional-psychology/

Food and Mood: Is the Concept of ‘Hangry’ Real?

Posted on July 31, 2023January 10, 2024 by CNP Staff

A recent study conducted in Austria used the method of experience sampling to examine the links between hunger and mood. Researchers asked participants to report their hunger and mood five times per day. Results showed that participants reported greater anger, irritability, and decreased pleasure when hungry (Swami et al., 2022). The study was published in Plos One.

Hunger and satiety exert a very powerful influence on one’s behavior.

Nutritional psychology, as explored by The Center for Nutritional Psychology, focuses on the links between diet, psychological states, and mental health. While the significance of this research topic is widely acknowledged, it remains a relatively new field of study, with crucial findings likely to emerge in the future.

What is hunger?

From a physiological point of view, hunger is a complex biological process that primarily revolves around regulating blood glucose levels and releasing hormones that control appetite and satiety. When we eat food, our bodies break down carbohydrates into glucose, which is the primary energy source for cells. As we go without food, our blood glucose levels gradually decline.

The two key hormones involved in hunger regulation are ghrelin and leptin. Ghrelin, produced by the stomach, signals the brain to stimulate appetite when the stomach is empty. Before meals, ghrelin levels increase, and they decrease after eating. Leptin functions as an appetite suppressor and is produced by fat cells, so when body fat decreases, leptin levels drop (see Figure 1).

Figure 1. Two key hormones involved in hunger regulation are Ghrelin and Leptin

Finally, the brain integrates the input received from hormones and sensory organs (e.g., sight or smell of food) to produce the feeling of hunger or satiety. This integration of signals happens in the hypothalamus region of the brain.

The sensation of hunger

Apart from being the result of a complex physiological process, hunger is also a subjective sensation. This sensation serves to motivate the individual to seek food and ingest it. In turn, this ensures that the nutritional needs of the organism are met (McKiernan et al., 2008). When an individual feels hungry, they become more sensitive to stimuli associated with food (e.g., Lazarus et al., 1953). Individuals will pay increased attention to food items and things they have learned to associate with food (e.g., logos of restaurants or food brands, places and people they have learned to associate with food, etc.).

However, decreased levels of nutrients in the body are not the only thing that can lead to the sensation of hunger. Studies show that humans and other species of animals can eat when bored, desire sensory stimulation (McKiernan et al., 2008), or are under stress (Levine & Morley, 1981). They also learn to expect food at certain times or at certain places. Studies indicate that under regular circumstances, human daily rhythms of biological processes (circadian rhythms) are synchronized with a pattern of three meals per day. However, the body can also adapt and learn to expect meals at different times of the day. This expectation can trigger hunger at a particular time and various physiological processes preparing the body for food intake (Isherwood et al., 2023) (see Figure 2).

Figure 2. Some sources of hunger

Being “hangry” – hungry and angry

Hunger affects the behavior of both humans and animals. Observations of non-human animals show that food deprivation increases their motivation to engage in escalated and persistent aggression to acquire food. It is well-known among keepers of various animals that the animals are the most dangerous when hungry.

Studies in humans link the sensation of hunger with feelings of restlessness, nervousness, irritability, and behavioral difficulties in children. Low blood glucose levels, known to trigger the sensation of hunger, are associated with increased impulsivity, anger, and aggression (Swami et al., 2022). Studies applying the concept of ego depletion suggest that the human capacity for self-regulation and active volition is limited (Baumeister et al., 1998) and that when one is hungry, negative, high-arousal emotions are more likely to occur. This is because individuals may struggle to exercise self-regulation and self-control when their blood glucose is low (Swami et al., 2022).

Studies in humans link the sensation of hunger with feelings of restlessness, nervousness, irritability, and behavioral difficulties in children.

These findings and casual observations have given rise to the term “hangry.” A combination of “hungry” and “angry,” hangry signifies a state in which one experiences both hunger and anger due to hunger.

Coined from hungry and angry, the term “hangry” indicates a state in which one is hungry but is also angry because of hunger.

The current study

Viren Swami, the study author, and his colleagues aimed to investigate the state of being “hangry” in a natural setting more systematically.

They wanted to know the extent to which daily experiences of hunger are associated with negative emotional outcomes. They reasoned that if the sensation of hunger is indeed linked to anger and other negative emotions, this must be the case in everyday life and not only in laboratory experiments.

To examine this link, they conducted an experience sampling study in which a group of study participants reported on their daily experiences of hunger and anger over a 3-week period. Understanding that anger might not be the only emotion connected to hunger, the study authors asked participants to report on irritability, pleasure, and arousal. They expected that hunger would be associated with greater anger, irritability, and arousal but lower feelings of pleasure.

What is experience sampling?

Experience sampling (Figure 3), or ecological momentary assessment, involves collecting real-time participant data throughout their daily lives. Participants are prompted multiple times daily to report on their experiences, emotions, behaviors, or thoughts using electronic devices such as smartphones or specialized wearable devices. This method gives researchers insights into individuals’ subjective experiences in their natural settings. This approach minimizes issues related to recalling events after much time has passed, a common problem encountered in traditional research methods relying on recalling past events. Experience sampling allows for a more nuanced understanding of how various factors fluctuate over time and under different circumstances.

Figure 3. Experience sampling process

The procedure

The study initially involved 121 participants; however, it required them to respond to surveys five times daily, every day, for three weeks, resulting in a total of 105 surveys to be completed by each participant. This workload proved overwhelming for many, with only 39 participants successfully completing all 105 surveys. Seventy-six participants managed to complete at least one survey per day.

Participants were, on average, 30 years old. Their ages ranged between 18 and 60 years. 69% were from Austria, followed by Germany (20%), Switzerland, and other countries. The vast majority of the participants were women (81%). 44% lived alone, 19% were married, and 36% were in a relationship. They had an average of 14 years of education.

Daily surveys

In the survey, participants indicated on a scale of 0 to 100 how hungry they were (“How hungry are you at the moment?”), their irritability (“How irritable do you feel at the moment?”), and how angry they felt at that moment. In addition, they rated their emotional state (“How pleasant do you find your current state?”), and arousal level (“What is your current arousal level?”). They also reported the time since their last meal (“When was your last meal? [______ hours ago]”.

Participants completed the surveys using their smartphones through the ESMira software package. After installing ESMira and registering for participation in the study, participants provided their demographic data. Of the five daily surveys, study authors set three to be at fixed time points during the day, before the three main meals – at 8:00, 12:00, and 18:00. At these time points, participants received an in-app notification to complete the survey. The remaining two surveys were random, one between 9:00 and 11:00 in the morning and the other between 13:00 and 17:00 (in the afternoon) (see Figure 4).

Figure 4. Daily survey procedure

Other measures

After the three-week period of the study, participants completed the final questionnaire, in which they provided their demographic data once again. It also contained assessments of four aspects of dietary behavior – restrictive eating (e.g., “I consciously eat less so as not to gain weight”), two aspects of emotionally-induced eating behavior, with clear emotions (e.g., “When I am irritated, I have the desire to eat”) and unclear emotions (e.g., “I always want to eat something when I have nothing to do”), and externally determined eating behavior (e.g., “I eat more than usual when I see others eating”).

The final questionnaire also contained assessments of dispositional anger (the Anger subscale from the Buss and Perry Aggression Questionnaire, BPAQ) and eating motivation (the Eating Motivation Survey consists of the question “Why do you eat what you eat?” followed by 15 different motivations that the participant has to rate).

Participants rarely skipped dinner

Analysis of the responses to the final questionnaire (see Figure 5) showed that some participants often skipped meals, but not all equally. 58% reported that they usually have breakfast, 78% usually had lunch, and 84% usually had dinner. 48% snacked between main meals. 9% reported getting up at night to eat. 88% declared that their eating habits during the study were the same as usual.

53% of the participants paid close attention to maintaining a healthy diet, either very often or always, and 55% paid attention to the sensation of hunger. The main motivation for eating was hunger and because participants liked the meal. 23% of participants stated they knew when they were full and then stopped eating. 63% reported that from time to time, they would continue to eat even though they were aware that they were full. 13% said they eat when stressed, upset, angry, or bored. Less than 5% reported that they do not feel when they are full and that they orient themselves based on the size of the meal.

Figure 5. Survey Report

When hungry, participants were more often angry, irritable and felt less pleasure

The results demonstrated a strong association between hunger and heightened feelings of anger, irritability, and reduced pleasure. Surprisingly, researchers also observed that participants with higher levels of dispositional anger tended to report higher levels of hunger.

Dispositional anger is a general tendency of an individual to experience anger more frequently and intensely across various situations. In contrast, the feeling of anger refers to a temporary and transient experience of anger.

The link of hunger with irritability, anger, and lower feeling of pleasure persisted even after participants’ sex, age, body mass index, dietary behavior, and dispositional anger were considered (see Figure 6).

Figure 6. Hunger and emotions

Contrary to the study authors’ expectations, hunger was not associated with arousal.

Conclusion

Overall, the study suggests that the experience of being hangry is real. When study participants were hungry, they also tended to experience greater anger, irritability, and less pleasure. This happened in their natural environments while they were living their lives as usual, not in an artificial laboratory environment. It was also not a one-time occurrence – the findings resulted from 105 surveys taken five times daily across three weeks.

These results have important implications for understanding everyday experiences of emotions. They also help practitioners to effectively prevent interpersonal conflicts while ensuring productive behaviors and good relationships. Although the design of this study does not allow for cause-and-effect conclusions to be made, i.e., to conclude that hunger causes anger or vice versa, simply designing school or work schedules to ensure no one goes hungry could help prevent numerous interpersonal problems. Allocating sufficient time and opportunities to eat and reduce prolonged periods of hunger is an important tool for improving everyone’s well-being.

On an individual level, labeling one’s affective state as being “hangry” could allow individuals to make sense of that experience. This is very important as, unlike some other negative states, hunger can be easily resolved by simply eating something.

The paper “Hangry in the field: An experience sampling study on the impact of hunger on anger, irritability, and affect” was authored by Viren Swami, Samantha Hochstoeger, Erik Kargl, and Stefan Stieger.

References

Baumeister, R. F., Bratslavsky, E., Muraven, M., & Tice, D. M. (1998). Ego depletion: Is the active self a limited resource? Journal of Personality and Social Psychology, 74(5), 1252–1265. https://doi.org/10.1037/0022-3514.74.5.1252

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

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

The Center for Nutritional Psychology. (2023). What is Nutritional Psychology? https://www.nutritional-psychology.org/what-is-nutritional-psychology/

Is Food Tastier When Consumed in Aesthetically Pleasing Environments?

Posted on June 12, 2023November 9, 2023 by CNP Super Admin

Editor’s Note: The study of nutritional psychology (NP) involves exploring the influence of diet on psychological, cognitive, behavioral, perceptual, interoceptive, and psychosocial functioning and mental health. It also includes the reverse —which is exploring how our psychological, behavioral, and psychosocial states and mental health influence our dietary intake.

In fact, the study of NP involves exploring and asking questions about the many aspects of the diet-mental health relationship (DMHR). For example, how does our dietary intake pattern affect how we perform tasks? (aka the “Diet-Performance Relationship”). And, how does the look or smell of food influence our desire to eat it? (i.e., the “Diet-Sensory-Perceptual Relationship”).

In this CNP Article, we explore how our environment influences our eating. In particular, we learn about how the aesthetics of an environment can influence our perception and desire to eat the food served in the environment. In nutritional psychology, we call this the Diet-Environment Relationship—the ‘DER.’

Introduction

Although food trucks or “dives” often serve great food that can rival good restaurants in taste, the environment in which foods are consumed can affect people’s perceptions of the food. In this study by Wu et al. (2022), two experiments conducted in China reported that food served in an aesthetically pleasing environment was found to smell better, taste better, and look better than in a less aesthetically pleasing environment. One experiment reported these results using photographs of places and foods, and another confirmed them with actual food. Participants found food they consumed in a nicely decorated room better smelling and tasting than in a less aesthetically pleasing room. They also expressed a greater desire to eat again in a nicer environment (Wu et al., 2022). The study was published in Appetite.

Participants found the food they consumed in a nicely decorated room better smelling and tasting than in a less aesthetically pleasing room.

Food is much more than a collection of nutrients

Humans need food to survive. Food provides human bodies with the energy needed to carry out various functions, such as breathing, circulating blood, and maintaining body temperature. Food is also a source of essential nutrients, such as vitamins and minerals, that our bodies need to function properly.

Food is much more than a collection of nutrients.

However, the value of food does not stop there. Food also provides us with pleasure and enjoyment. Eating is often a social and cultural activity that brings people together and provides comfort and satisfaction. Sharing meals with family and friends is a common way to strengthen relationships and build connections with others.

This sharing of meals with others is a focal point of various cultural customs worldwide. Dining rooms in people’s homes, restaurants, taverns, cafeterias, diners, barbecue parties, and other similar dedicated places and types of social events exist because food consumption and meal sharing are central parts of human culture. Their value goes far beyond the nutritional function of food.

Even in activities like space exploration missions, researchers soon realized that providing nutritious food is not enough and that food must also provide psychosocial comfort. “Ideal food cannot ensure psychosocial comfort, while a grandma-style pie can,” experts in the area wrote (Bychkov et al., 2021).

“Ideal food cannot ensure psychosocial comfort, while a grandma-style pie can,” experts in the area wrote (Bychkov et al., 2021).

The importance of beauty and aesthetics

Beauty and aesthetics, in general, are important to us. We are naturally drawn to things that are visually appealing or pleasing to our senses, and experiencing beauty can give us a sense of pleasure, satisfaction, and joy. This can help reduce stress and anxiety, improve our mood, and enhance our overall well-being.

For example, a recent study has shown that people become happier when they view beautiful images of nature, thus improving their subjective well-being (Xie et al., 2022). Another study has shown that women prefer more attractive men as long-term partners over men with favorable personal traits, despite consciously considering personal traits like ambition and intelligence more important for a partner to have (Li et al., 2023).

Aesthetic preferences (i.e., what one considers beautiful) are so important to us that individuals consider them part of their personal identity. A recent study has shown that when a person’s aesthetic preferences, such as preferences for music or art, change, that person tends to consider that his/her entire identity has changed. Researchers are now talking about an aesthetic self, an aspect of the human person that they believe to be at least as important for our identity as our moral values are (Fingerhut et al., 2021).

Researchers are now talking about an aesthetic self, an aspect of the human person that they believe to be at least as important for our identity as our moral values are.

The current study

Study author Chenjing Wu from the South China Normal University and her colleagues wanted to know whether the beauty of the environment affects the perception of the food we eat. They notice that, in everyday life, people often choose restaurants because of how they look, i.e., because they like the restaurant environment despite there being restaurants with tastier food. The reverse is also the case in that people can avoid particularly bad-looking restaurants even when such restaurants serve tasty food.

People often choose restaurants because of how they look, i.e., because they like the restaurant environment despite there being restaurants with tastier food.

It is well-known that individuals use data about their environment to form judgments. For example, studies have shown that the smell of the environment, lighting, and color affect the perception of food. When identical food is served in different places (e.g., laboratory, restaurant, cafeteria), perception of that food can vary across different places. In a well-known study, researchers served the same food to participants in different settings, ranging from 4-star restaurants to an army training camp and a freshman’s buffet. They found that food received much better evaluation when served in 4-star restaurants than in an army training camp or a freshman’s buffet (Edwards et al., 2003).

The smell of the environment, lighting, and color affect the perception of food.

Procedure Experiment 1

Participants in the first experiment were 132 college students who were divided into two groups. One group was shown a picture of the interior of a nice-looking restaurant (high aesthetic value condition). In contrast, the other was shown a picture of the interior of a poor-looking restaurant (low aesthetic value condition). They were asked to imagine being in that place and rate their emotions about it on a scale from negative to positive, as shown in Figure 1.

Figure 1. Experiment 1

Participants were then shown pictures of 29 different foods. They were asked to rate the beauty of the food based on its looks, expected smell, and expected taste. The task was in Chinese, in which sentence constructions with the word beautiful typically describe both look, smell, and taste. So, although the request looks unusual in English, it was appropriate in the Chinese language. Participants were also asked to rate the desire to eat that food item and to evaluate the aesthetic value of the environment.

Researchers ran one more variant of this experiment on another group of 149 students. In this variant, instead of pictures of restaurant interiors, one group of participants was shown a picture of a beautiful natural landscape (high aesthetic value condition). At the same time, the other viewed a picture of the interior of a ruined building (low aesthetic value condition) (see Figure 2).

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Figure 2. Natural landscape (high aesthetic value) vs. ruined building (low aesthetic value)(not the actual pictures used in the experiment)

Experiment 2

Researchers ran the second experiment with real environments and a real food item. The participants were 81 college students. Researchers decorated a table in their laboratory with covers and flowers for a high aesthetic environment. The low aesthetic environment was the same laboratory table without decorations.

Participants entered the laboratory with a decorated or undecorated table in it, depending on the group they were assigned to. They were then asked to report their emotions about the environment, as in experiment 1. Before entering the laboratory, all participants rated their hunger (see Figure 3).

Figure 3. Experiment 2

They were then set at the table and given a wrapped bar of dark chocolate. Participants first rated the look of the wrapped chocolate bar, its smell, and how much they would like to eat it. They were then instructed to eat the chocolate. Afterward, they rated how tasty it was and how much they would like to eat another one. Finally, they rated the aesthetic value of their environment (a laboratory with a decorated table or a laboratory without decorations).

The food looked better and was expected to smell and taste better in more beautiful environments

In experiment 1, participants who viewed pictures of a more beautiful environment and imagined themselves in it rated the food they saw in the pictures as better looking. They also reported expecting the food to smell and taste better on average compared to the group that evaluated the same food after viewing a less beautiful environment. On average, participants who imagined the more beautiful environment reported a greater desire to eat the food they were presented with.

Participants who imagined the more beautiful environment reported a greater desire to eat the food they were presented with.

The differences in how presented food items were rated were much greater in the second variant of the experiment (a beautiful natural landscape vs. a ruined building) than in the first variant of the experiment (two restaurants, of which one is nicer looking).

Participants who viewed a more beautiful environment also reported feeling better and rated that environment as more aesthetically pleasing. This confirmed the researchers’ expectations about how participants would perceive the environments.

The better the person feels, the better smelling and tasting the food is

In experiment 2, participants from the two groups rated the wrapped chocolate bar as looking equally nice. However, participants who inspected the chocolate bar while sitting at the decorated laboratory table (high aesthetics environment) tended to report that it smelled better than those who were inspecting it while sitting at an undecorated table. Participants sitting at a decorated table also reported a greater desire to eat it.

After eating the chocolate bar, participants from the high aesthetics condition group (i.e., sitting at the decorated table) tended to rate its taste better than participants from the other group. They also expressed a greater desire to eat another chocolate bar.

Differences in ratings provided by the two groups were similar in size to those obtained in the first experiment (two imagined restaurants and imagined food). However, it should be considered that a decorated table in a laboratory is still visibly a table in a laboratory. Hence, the differences between the two environments in experiment 2 were limited.

Further analysis revealed a clear association between the participant’s emotions and the food evaluation. Participants who reported more positive emotions about the environment tended to evaluate the food they were presented with (or asked to imagine) as looking, tasting, and smelling better. They also tended to report a greater desire to eat the food.

Participants who reported more positive emotions about the environment tended to evaluate the food they were presented with as looking, tasting, and smelling better.

Conclusion

The study showed that the aesthetic value of the environment affects the perception of food. Food is perceived as tastier, better smelling, and, in certain conditions, better looking in more aesthetically pleasing environments that elicit more positive emotions. The desire to eat the food is also greater in a better-smelling environment. This refers to the desire to eat the food at hand again in the same environment.

The implications of the findings are quite straightforward – food offered and sold in more aesthetically pleasing environments will be perceived as better by the consumers. They will also have a greater desire to eat it. The findings imply that restaurant managers should pay great attention to the aesthetic qualities of their customers’ environment, not solely to food preparation.

The paper “Does a beautiful environment make food better – The effect of environmental aesthetics on food perception and eating intention” was authored by Chenjing Wu, Hongyan Zhu, Chuangbing Huang, Xiaoling Liang, Kaili Zhao, Siyue Zhang, Mingcheng He, Wei Zhang, and Xianyou He.

More evidence-based information on the Diet-Environment Relationship can be found in the Nutritional Psychology Research Library (NPRL). The Diet and Sensory Perceptual Relationship (DSPR) included within nutritional psychology also involves studies in this area.

References

Bychkov, A., Reshetnikova, P., Bychkova, E., Podgorbunskikh, E., & Koptev, V. (2021). The current state and future trends of space nutrition from a perspective of astronauts’ physiology. International Journal of Gastronomy and Food Science, 24, 100324. https://doi.org/10.1016/J.IJGFS.2021.100324

Edwards, J. S. A., Meiselman, H. L., Edwards, A., & Lesher, L. (2003). The influence of eating location on the acceptability of identically prepared foods. Food Quality and Preference, 14(8), 647–652. https://doi.org/10.1016/S0950-3293(02)00189-1

Fingerhut, J., Gomez-Lavin, J., Winklmayr, C., & Prinz, J. J. (2021). The Aesthetic Self. The Importance of Aesthetic Taste in Music and Art for Our Perceived Identity. Frontiers in Psychology, 11, 1–18. https://doi.org/10.3389/FPSYG.2020.577703

Li, W., Zhu, H., Zhao, K., Zhu, H., Wang, X., & He, X. (2023). Good performance-high attractiveness effect: an empirical study on the association between athletes’ rankings and their facial attractiveness. International Journal of Sport and Exercise Psychology. https://doi.org/10.1080/1612197X.2023.2181846

Wu, C., Zhu, H., Huang, C., Liang, X., Zhao, K., Zhang, S., He, M., Zhang, W., & He, X. (2022). Does a beautiful environment make food better – The effect of environmental aesthetics on food perception and eating intention. Appetite, 175(April), 106076. https://doi.org/10.1016/j.appet.2022.106076

Xie, R., Qiu, C., & Qiu, G. (2022). Finding Beautiful and Happy Images for Mental Health and Well-Being Applications. Lecture Notes in Computer Science, 13536 LNCS, 704–717. https://doi.org/10.1007/978-3-031-18913-5_54

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