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The Effect of Diet on Mental Health

AHA Publisher — Fri, 08 Apr 2022 07:00:04 +0000

Dr. Liji Thomas, MD via News Medical – The brain controls and regulates most of the body’s vital functions, conscious or not. For this reason, it is essential that the brain receives a steady supply of fuel and oxygen. The fuel is obtained by metabolizing nutrients made available in the bloodstream, originating in the digested food. The brain consumes 20% of the daily intake of calories, that is, about 400 (out of 2000) calories a day. Structurally, about 60% of the brain is fat, comprising of high cholesterol and polyunsaturated fatty acids (PUFAs). Thus, the food one eats is directly linked to brain structure and function, and thus affects the working of the mind. Many studies have found that diets that are too rich in refined sugars are toxic to brain functioning because the high content of simple sugars stresses the pancreas and induces insulin resistance. The high sugar levels with compensatory insulin responses stimulate the counter-reactive surge of autonomic neurotransmitters like cortisol and glucagon. These are known to produce increased anxiety, hunger and irritability. Moreover, they induce inflammatory and oxidative stress. This has been linked to an exacerbation of symptoms of depression and other mood disorders. These findings have led to the emerging field of nutritional psychiatry that traces relationships between food, feelings, gut microbiota, and human behavior. Deficiency Disorders and Mood The deficiency of nutrients like cobalamine, folate and zinc is known to be associated with symptoms of depression and dementia, cognitive decline and irritability. Both overeating and food insecurity are associated with mood and anxiety disorders. Mental illness is ranked among the largest contributors to the global health burden, especially depression, which accounts for the major chunk of disability in the more developed countries, especially in the age group of 15-44 years. Therefore, it is crucial to explore nutritional strategies to ameliorate these conditions. Not only do people eat differently when anxious or depressed, but these changes may occur in either direction. Conversely, depression may be the result, at least partly, of poor eating habits, or may become worsened by the inability of the patient to stop eating comfort foods and choose a healthy diet. Such inability may be financial, psychological, or iatrogenic. Serotonin and the Gut Serotonin is a monoamine neurotransmitter that helps to control sleep and appetite, inhibit pain, and to regulate mood. About 95% of the serotonin is produced in the gut, which is rich in neurons – the enteric plexus contains a hundred million nerve cells. Thus, the gut is intimately involved in emotional regulation, pain perception, and vital physiological functions. Interestingly, the function of these neurons and their secretion of serotonin, and other neurotransmitters, is closely regulated by the metabolic byproducts of the trillion or so bacteria that comprise the gut microbiome. These bacteria ensure epithelial barrier integrity for the intestine, preventing the entry of bacterial toxins and pathogens into the systemic circulation. They also prevent the spread of inflammation beyond the gut lumen, enhance nutrient absorption, and activate gut-brain neural pathways – the gut-brain axis. Monoamine neurotransmitters are synthesized from amino acids in a process that is mediated by mineral-dependent cofactors. Both folate and vitamin B12 are essential for the methylation that occurs during these synthetic processes, also regulating the formation of homocysteine – a metabolite that is strongly linked to cardiovascular risk and depression. Dietary Fats and Brain Functioning Anti-inflammatory fats such as omega-3 fatty acids (FAs) are known to be essential components of neuronal cell membranes, and also play a role in many vital neural processes such as neurotransmission, gene expression, neurogenesis and neuronal survival. They are also known to have antioxidant properties. Omega-3 FAs are used to treat a number of psychological disorders, including attention-deficit hyperactivity disorder (ADHD), depression, bipolar depression and post-traumatic stress disorder (PTSD). A high omega-6 proportion is linked to a higher incidence of these conditions, especially the first two. The standard Western diet is rich in omega-6 but low in omega-3 FAs, primarily because of the consumption of refined flours and sugars, and highly processed foods, and low amounts of seafood (including fish) and grass-fed beef. Some studies have confirmed that diets that are richer in healthier carbohydrates and fats, and lower in refined and highly processed foods, such as the Japanese and Mediterranean diets, are linked to a reduction in the incidence of depression by anywhere between a quarter to over a third, compared to the standard American diet. Inflammation and the Diet Inflammation of the nervous system is also important in the pathogenesis of mental illness, and this is also linked to the diet. Many biomarkers of inflammation, such as C-reactive protein (CRP) and tumor necrosis factor alpha (TNF-α) were associated with a dietary pattern that was linked to a higher risk of depression over the next decade or so. This pattern included high simple sugars (sweetened drinks and refined flours), red meat and margarine (saturated fats), and little green or yellow vegetables, coffee, wine, or olive oil, which are all features of the stereotypical Western diet. The high content of vegetables, fruits, grains, and seafood, with less dairy and meat content, and no refined foods, of the Mediterranean and Japanese diets, compares very favorably with the Western diet. The former uses small amounts of red wine and cheese or yogurt in the daily diet. The mechanism is thought to be via the brain-derived neurotrophic factor or BDNF. This important molecule is implicated in the plasticity and survival of neurons, and neurogenesis. It is reduced in many mental health conditions including depression, PTSD and schizophrenia, and is affected by many antidepressants that are commonly prescribed. Not only so, but the former presents many of the fruits and vegetables in fermented form, which provides probiotics protecting the gut by enhancing the content of health-promoting gut microbes and reducing or preventing inflammation throughout the body. Thus, including more foods with omega-3 FAs in the diet when on inflammation-inducing medications, not only prevents inflammatory changes but also prevents the induction of depression in such individuals, according to recent, admittedly early, work. Again, the Mediterranean diet promotes gut microbes that produce anti-inflammatory metabolites. Of course, depressive tendencies or stressors may prevent the beneficial effects of healthy food from manifesting themselves as reduced inflammation or improved mood. Secondly, only some depressed individuals show this inflammatory tendency, which may mean that diet plays this role in only a proportion of people, perhaps with other inflammatory conditions or due to constitutional factors. Conclusion Many experts would recommend that people pay attention to the relationship between their diet and the foods they eat over a month or at least two weeks. If they could reduce or eliminate processed foods and sugars for this period of time, before bringing back these foods one by one, it would be instructive to notice how they feel. Better eating strategies are essential to promote mental health and recovery from mental illness. It was over 2,000 years ago that the famous Greek physician Hippocrates said, “Let thy food be thy medicine and thy medicine be thy food.” Not only does the Mediterranean (and similar) diet affect the availability of the basic building blocks of the brain and neurotransmitters, including myelin, the neuronal membrane, and monoamine neurotransmitters, but it modulates key chemicals like BDNF to alter neuroplasticity, mutes system inflammation, and determines the health and state of the gut microbiome. Many such traditional diets are known to include mostly nutritious whole foods without much processing. The role of a dietary specialist in helping patients with mentally ill-health to choose approaches that promote the ability to take care of oneself and enhance one’s health is very important and should be encouraged. As one set of authors comment, “This message supports the idea that creating environments and developing measures that promote healthy, nutritious diets, while decreasing the consumption of highly processed and refined “junk” foods may provide benefits even beyond the well known effects on physical health, including improved psychological wellbeing.” To read the original article click here.

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Study Pinpoints Specific Areas of the Brain Where Serotonin Promotes Patience

AHA Publisher — Mon, 07 Dec 2020 08:00:01 +0000

Okinawa Institute of Science and Technology (OIST) Graduate University via News-Medical Net – We’ve all been there. Whether we’re stuck in traffic at the end of a long day, or eagerly anticipating the release of a new book, film or album, there are times when we need to be patient. Learning to suppress the impulse for instant gratification is often vital for future success, but how patience is regulated in the brain remains poorly understood. Now, in a study on mice conducted by the Neural Computation Unit at the Okinawa Institute of Science and Technology Graduate University (OIST), the authors, Dr. Katsuhiko Miyazaki and Dr. Kayoko Miyazaki, pinpoint specific areas of the brain that individually promote patience through the action of serotonin. Their findings were published 27thNovember in Science Advances. Serotonin is one of the most famous neuromodulators of behavior, helping to regulate mood, sleep-wake cycles and appetite. Our research shows that release of this chemical messenger also plays a crucial role in promoting patience, increasing the time that mice are willing to wait for a food reward.” Dr. Katsuhiko Miyazaki, Author Their most recent work draws heavily on previous research, where the unit used a powerful technique called optogenetics – using light to stimulate specific neurons in the brain – to establish a causal link between serotonin and patience. The scientists bred genetically engineered mice which had serotonin-releasing neurons that expressed a light-sensitive protein. This meant that the researchers could stimulate these neurons to release serotonin at precise times by shining light, using an optical fiber implanted in the brain. The researchers found that stimulating these neurons while the mice were waiting for food increased their waiting time, with the maximum effect seen when the probability of receiving a reward was high but when the timing of the reward was uncertain. “In other words, for the serotonin to promote patience, the mice had to be confident that a reward would come but uncertain about when it would arrive,” said Dr. Miyazaki. In the previous study, the scientists focused on an area of the brain called the dorsal raphe nucleus – the central hub of serotonin-releasing neurons. Neurons from the dorsal raphe nucleus reach out into other areas of the forebrain and in their most recent study, the scientists explored specifically which of these other brain areas contributed to regulating patience. The team focused on three brain areas that had been shown to increase impulsive behaviors when they were damaged – a deep brain structure called the nucleus accumbens, and two parts of the frontal lobe called the orbitofrontal cortex and the medial prefrontal cortex. “Impulse behaviors are intrinsically linked to patience – the more impulsive an individual is, the less patient – so these brain areas were prime candidates,” explained Dr. Miyazaki. Good things come to those who wait (or not…) In the study, the scientists implanted optical fibers into the dorsal raphe nucleus and also one of either the nucleus accumbens, the orbitofrontal cortex, or the medial prefrontal cortex. The researchers trained mice to perform a waiting task where the mice held with their nose inside a hole, called a “nose poke”, until a food pellet was delivered. The scientists rewarded the mice in 75% of trials. In some test conditions, the timing of the reward was fixed at six or ten seconds after the mice started the nose poke and in other test conditions, the timing of the reward varied. In the remaining 25% of trials, called the omission trials, the scientists did not provide a food reward to the mice. They measured how long the mice continued performing the nose poke during omission trials – in other words, how patient they were – when serotonin-releasing neurons were and were not stimulated. When the researchers stimulated serotonin-releasing neural fibers that reached into the nucleus accumbens, they found no increase in waiting time, suggesting that serotonin in this area of the brain has no role in regulating patience. But when the scientists stimulated serotonin release in the orbitofrontal cortex and the medial prefrontal cortex while the mice were holding the nose poke, they found the mice waited longer, with a few crucial differences. In the orbitofrontal cortex, release of serotonin promoted patience as effectively as serotonin activation in the dorsal raphe nucleus; both when reward timing was fixed and when reward timing was uncertain, with stronger effects in the latter. But in the medial prefrontal cortex, the scientists only saw an increase in patience when the timing of the reward was varied, with no effect observed when the timing was fixed. “The differences seen in how each area of the brain responded to serotonin suggests that each brain area contributes to the overall waiting behavior of the mice in separate ways,” said Dr. Miyazaki. Modeling patience To investigate this further, the scientists constructed a computational model to explain the waiting behavior of the mice. The model assumes that the mice have an internal model of the timing of reward delivery and keep estimating the probability that a reward will be delivered. They can therefore judge over time whether they are in a reward or non-reward trial and decide whether or not to keep waiting. The model also assumes that the orbitofrontal cortex and the medial prefrontal cortex use different internal models of reward timing, with the latter being more sensitive to variations in timing, to calculate reward probabilities individually. The researchers found that the model best fitted the experimental data of waiting time by increasing the expected reward probability from 75% to 94% under serotonin stimulation. Put more simply, serotonin increased the mice’s belief that they were in a reward trial, and so they waited longer. Importantly, the model showed that stimulation of the dorsal raphe nucleus increased the probability from 75% to 94% in both the orbital frontal cortex and the medial prefrontal cortex, whereas stimulation of the brain areas separately only increased the probability in that particular area. “This confirmed the idea that these two brain areas are calculating the probability of a reward independently from each other, and that these independent calculations are then combined to ultimately determine how long the mice will wait,” explained Dr. Miyazaki. “This sort of complementary system allows animals to behave more flexibly to changing environments.” Ultimately, increasing our knowledge of how different areas of the brain are more or less affected by serotonin could have vital implications in future development of drugs. For example, selective serotonin reuptake inhibitors (SSRIs) are drugs that boost levels of serotonin in the brain and are used to treat depression. “This is an area we are keen to explore in the future, by using depression models of mice,” said Dr. Miyazaki. “We may find under certain genetic or environmental conditions that some of these identified brain areas have altered functions. By pinning down these regions, this could open avenues to provide more targeted treatments that act on specific areas of the brain, rather than the whole brain.” To read the original article click here.

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