Abstract:The prevalence of psychiatry disorders such as anxiety and depression has steadily increased in recent years in the United States. This increased risk for anxiety and depression is associated with excess weight gain, which is often due to over-consumption of western diets that are typically high in fat, as well as with binge eating disorders, which often overlap with overweight and obesity outcomes. This finding suggests that diet, particularly diets high in fat, may have important consequences on the neurocir… Show more
“…We and others have reported that exposure to high‐energy diets or “western diet formulas,” such as a cafeteria diet, favors aberrant behaviors in offspring, including depression‐like (de la Garza et al, 2019; Trujillo‐Villarreal et al, 2021), addiction‐like (Camacho et al, 2017; Cruz‐Carrillo et al, 2020), asocial‐like behaviors (Maldonado‐Ruiz et al, 2022), cognitive impairments (Lépinay et al, 2015; Létondor et al, 2016; Manduca et al, 2017) and ADHD (Buss et al, 2012; Chen et al, 2014; Godfrey et al, 2017; Sanchez et al, 2018). These evidences propose that excessive consumption of a high‐energy diet might have significant effects on mental health in children's, adolescents and adults (Baker et al, 2017; Coker et al, 2021; Lof et al, 2022; Melo et al, 2019; Muscaritoli, 2021; Ortiz‐Valladares et al, 2021). As a result of the multifactorial pathogenesis in mental disorders causal links between dietary suppliers on mental health have been hard to establish, in part, based on food formulas provide natural energy substrates for brain energy metabolism.…”
Section: Diet Modulates Ceramides Metabolism and Susceptibility To Ps...mentioning
confidence: 99%
“…cognitive impairments(Lépinay et al, 2015;Létondor et al, 2016;Manduca et al, 2017) and ADHD(Buss et al, 2012;Chen et al, 2014;Godfrey et al, 2017;Sanchez et al, 2018). These evidences propose that excessive consumption of a high-energy diet might have significant effects on mental health in children's, adolescents and adults(Baker et al, 2017;Coker et al, 2021;Lof et al, 2022;Melo …”
Psychiatric disorders affect 970 million people worldwide, representing a significant source of disability. Although the underlying neurobiological traits for these disorders are not fully understood, a complex interplay between psychological, environmental, and biological factors contributes to their outcomes. Recent advances in lipidomic analysis and artificial intelligence algorithms have improved the identification of selective lipid species modulating the susceptibility to mental disorders. Sphingolipids (SLs) and ceramides‐related SLs are among the most abundant lipids species in the brain that support major key pathways during neurodevelopment and brain plasticity. High levels of ceramides in plasma and brain contribute to psychiatric illness susceptibility in humans and animal models. However, the neuropathological mechanism regarding the involvement of ceramides in these disorders remain inconclusive. The brain is highly susceptible to nutritional insults, which could lead to functional impairment and influence the development and progression of psychiatric disorders. While the brain relies on glucose metabolism to support its physiological needs, a selective nutrient formula appears to have greater effects on brain health than others. For instance, consumption of high‐energy diets is associated with brain anatomical, physiological, and metabolic changes, including ceramides metabolism. Herein, we will address the contribution of ceramides metabolism as a modulator of major psychiatric disorders such as depression, anxiety, bipolar disorder, schizophrenia, and attention deficit‐hyperactivity disorder. We will also describe molecular and cellular targets of ceramides metabolism assisting the maintenance and progression of psychiatric disorders and their modulation by dietary formulas as non‐pharmacologic treatments.
“…We and others have reported that exposure to high‐energy diets or “western diet formulas,” such as a cafeteria diet, favors aberrant behaviors in offspring, including depression‐like (de la Garza et al, 2019; Trujillo‐Villarreal et al, 2021), addiction‐like (Camacho et al, 2017; Cruz‐Carrillo et al, 2020), asocial‐like behaviors (Maldonado‐Ruiz et al, 2022), cognitive impairments (Lépinay et al, 2015; Létondor et al, 2016; Manduca et al, 2017) and ADHD (Buss et al, 2012; Chen et al, 2014; Godfrey et al, 2017; Sanchez et al, 2018). These evidences propose that excessive consumption of a high‐energy diet might have significant effects on mental health in children's, adolescents and adults (Baker et al, 2017; Coker et al, 2021; Lof et al, 2022; Melo et al, 2019; Muscaritoli, 2021; Ortiz‐Valladares et al, 2021). As a result of the multifactorial pathogenesis in mental disorders causal links between dietary suppliers on mental health have been hard to establish, in part, based on food formulas provide natural energy substrates for brain energy metabolism.…”
Section: Diet Modulates Ceramides Metabolism and Susceptibility To Ps...mentioning
confidence: 99%
“…cognitive impairments(Lépinay et al, 2015;Létondor et al, 2016;Manduca et al, 2017) and ADHD(Buss et al, 2012;Chen et al, 2014;Godfrey et al, 2017;Sanchez et al, 2018). These evidences propose that excessive consumption of a high-energy diet might have significant effects on mental health in children's, adolescents and adults(Baker et al, 2017;Coker et al, 2021;Lof et al, 2022;Melo …”
Psychiatric disorders affect 970 million people worldwide, representing a significant source of disability. Although the underlying neurobiological traits for these disorders are not fully understood, a complex interplay between psychological, environmental, and biological factors contributes to their outcomes. Recent advances in lipidomic analysis and artificial intelligence algorithms have improved the identification of selective lipid species modulating the susceptibility to mental disorders. Sphingolipids (SLs) and ceramides‐related SLs are among the most abundant lipids species in the brain that support major key pathways during neurodevelopment and brain plasticity. High levels of ceramides in plasma and brain contribute to psychiatric illness susceptibility in humans and animal models. However, the neuropathological mechanism regarding the involvement of ceramides in these disorders remain inconclusive. The brain is highly susceptible to nutritional insults, which could lead to functional impairment and influence the development and progression of psychiatric disorders. While the brain relies on glucose metabolism to support its physiological needs, a selective nutrient formula appears to have greater effects on brain health than others. For instance, consumption of high‐energy diets is associated with brain anatomical, physiological, and metabolic changes, including ceramides metabolism. Herein, we will address the contribution of ceramides metabolism as a modulator of major psychiatric disorders such as depression, anxiety, bipolar disorder, schizophrenia, and attention deficit‐hyperactivity disorder. We will also describe molecular and cellular targets of ceramides metabolism assisting the maintenance and progression of psychiatric disorders and their modulation by dietary formulas as non‐pharmacologic treatments.
“…The contradictory findings seem to be due the exposure length of alcohol (acute or chronic), mode of electrophysiologic recording, and the subregion of the CeA. Additionally, diet composition may play an important role in regulating alcohol modulation of CeA neurotransmission ( Coker et al, 2020 ; Mahajan et al, 2021 ).…”
Alcohol use disorder is a highly significant medical condition characterized by an impaired ability to stop or control alcohol use, compulsive alcohol seeking behavior, and withdrawal symptoms in the absence of alcohol. Understanding how alcohol modulates neurocircuitry critical for long term and binge-like alcohol use, such as the central amygdala (CeA), may lead to the development of novel therapeutic strategies to treat alcohol use disorder. In clinical studies, reduction in the volume of the amygdala has been linked with susceptibility to relapse to alcohol use. Preclinical studies have shown the involvement of the CeA in the effects of alcohol use, with lesions of the amygdala showing a reduction in alcohol drinking, and manipulations of cells in the CeA altering alcohol drinking. A great deal of work has shown that acute alcohol, as well as chronic alcohol exposure via intake or dependence models, alters glutamatergic and GABAergic transmission in the CeA. The CeA, however, contains heterogeneous cell populations and distinct subregional differences in neurocircuit architecture which may influence the mechanism by which alcohol modulates CeA function overall. The current review aimed to parse out the differences in alcohol effects on the medial and lateral subregions of the CeA, and what role neuroinflammatory cells and markers, the endocannabinoid system, and the most commonly studied neuropeptide systems play in mediating these effects. A better understanding of alcohol effects on CeA subregional cell type and neurocircuit function may lead to development of more selective pharmacological interventions for alcohol use disorder.
“…However, the involvement of metabolising enzymes, that are primarily expressed in the liver, does not address why many people choose to drink alcohol and why alcohol use may develop into an addiction. It is widely understood that the decision to drink alcohol is modulated by regions of the brain, that include the hypothalamus and that addiction involves regions that include the nucleus accumbens [8 , 9] . Aside from the afore mentioned metabolic genes, the majority of genetic risk seems to be spread amongst a large number of variants each with small effects, a known common feature of the genetics of complex diseases [10] .…”
Section: The Problem At Handmentioning
confidence: 99%
“…Based on these observations it is likely that the greatest burden of AUD causing SNPs do not lie within the coding regions of genes but within the unknown, and enigmatic, non-coding genome. Consequently, the main aim of the current review will not be to explore the known genetics or neuroscience of AUD in any depth, a subject which has been well reviewed in a number of other publications [8 , 9] , but to briefly and critically appraise what we know about the information sources contained in the “non-coding” genome that are important in health, what techniques are currently used to understand the role of the non-coding genome in alcohol intake and what we need to do in the future to better understand its biology. Fig.…”
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