Temple Illuminatus2024-03-28T15:50:58ZMARGARIDA MARIA MADRUGAhttps://templeilluminatus.ning.com/profile/MARGARIDAMARIAMADRUGAhttps://storage.ning.com/topology/rest/1.0/file/get/12220410273?profile=RESIZE_48X48&width=48&height=48&crop=1%3A1https://templeilluminatus.ning.com/forum/topic/listForContributor?groupUrl=supporters-and-individuals-of-special-needs&user=224pjsuu7sjuh&feed=yes&xn_auth=noADHD in the News 2023-04-13tag:templeilluminatus.ning.com,2023-04-18:6363372:Topic:36333382023-04-18T16:39:09.349ZMARGARIDA MARIA MADRUGAhttps://templeilluminatus.ning.com/profile/MARGARIDAMARIAMADRUGA
<div class="grid-item grid-item-100 adhd-header"><div class="cell-item cell-peach"><div class="header-content aligncenter"><h2><span class="title-underline">ADHD in the News 2023-04-13</span></h2>
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<div class="grid-item grid-item-100"><div class="cell-item cell-gray"><div class="text-content aligncenter"><div class="fl-post-content clearfix"><h4>What’s Driving the Demand for ADHD Drugs Like Adderall</h4>
<div>For at least the last six months, Adderall—the stimulant…</div>
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<div class="grid-item grid-item-100 adhd-header"><div class="cell-item cell-peach"><div class="header-content aligncenter"><h2><span class="title-underline">ADHD in the News 2023-04-13</span></h2>
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<div class="grid-item grid-item-100"><div class="cell-item cell-gray"><div class="text-content aligncenter"><div class="fl-post-content clearfix"><h4>What’s Driving the Demand for ADHD Drugs Like Adderall</h4>
<div>For at least the last six months, Adderall—the stimulant medication commonly used to treat attention-deficit/hyperactivity disorder (ADHD)—has been in short supply in the U.S. That seems to be in part because demand is growing as more people are diagnosed with ADHD, a condition that can make it difficult to focus, remember details, control impulses, or sit still.</div>
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<div class="news-link"><a href="https://time.com/6271049/adhd-diagnoses-rising/" target="_blank" rel="noopener">View Article: TIME, April 12, 2023</a></div>
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<h4>The Adderall shortage is still hitting Kansas City. Here’s what people with ADHD can expect</h4>
<div>The FDA announced an Adderall shortage in October. Since then, Kansas City residents with ADHD have scrambled for alternatives as the shortage drags on with no clear end in sight. Raising five children — four of whom have ADHD — while dealing with the neurodevelopmental disorder herself, Jeremy Didier is acutely aware of how chaotic things can become without proper medication.</div>
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<div class="news-link"><a href="https://www.kcur.org/health/2023-04-13/adderr" target="_blank" rel="noopener">View Article: KCUR | NPR, April 13, 2023</a></div>
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<h4>The Adderall Shortage Is Taking a Toll on These People</h4>
<div>Patients with attention-deficit hyperactivity disorder and other conditions treated with Adderall and similar stimulant medications are struggling to fill their prescriptions. As of the week of April 10, six pharmaceutical companies that manufacture Adderall and its generics reported to the Food and Drug Administration that at least some immediate-release formulations were unavailable or in shortage.</div>
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<div class="news-link"><a href="https://www.wsj.com/articles/adderall-shortage-update-patients-pauses-8e3fffb6?" target="_blank" rel="noopener">View Article: The Wall Street Journal, April 13, 2023</a></div>
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<h4>Effort Underway to Develop First U.S. Guidelines for ADHD in Adults</h4>
<div>The number of diagnosed cases of attention-deficit/hyperactivity disorder (ADHD) have increased significantly among adults in the United States within the past decade, which could be due to many factors, including overdiagnosis. A recent <em>JAMA</em> study found that diagnoses of ADHD in adults are growing four times faster than in children. Other research tells another story: that clinicians misdiagnose or miss ADHD in adults and that fewer than 20% of individuals with ADHD are diagnosed and treated by clinicians.</div>
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<div class="news-link"><a href="https://www.columbiapsychiatry.org/news/effort-underway-develop-first-u-s-guidelines-adhd-adults" target="_blank" rel="noopener">View Article: Columbia University Department of Psychiatry News, April 12, 2023</a></div>
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<h4>Choice Between Treatment Modality Remains Weak for Pediatric ADHD and Sleep Disorders</h4>
<div>Sleep interventions could increase sleep quality and quantity among children with attention-deficit/hyperactivity disorder (ADHD). Still, evidence remains limited for other sleep-related outcomes such as quality of life (QoL), sleep onset latency (SOL), sleep efficiency, and ADHD symptoms. Researchers from the School of Health and Welfare in the Department of Health and Care at Halmstad University, Sweden, published their findings in<span> </span><em>Sleep Medicine</em>.</div>
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<div class="news-link"><a href="https://www.hmpgloballearningnetwork.com/site/pcn/choice-between-treatment-modality-remains-weak-pediatric-adhd-and-sleep-disorders" target="_blank" rel="noopener">View Article: Psych Congress Network, April 6, 2023</a></div>
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<h4>How to Assess ADHD Symptoms in Children — Zachary Blumkin, PsyD, says there’s no single test that can confirm or rule out a diagnosis</h4>
<div>When evaluating individuals for attention-deficit/hyperactivity disorder (ADHD), it is typical to use multiple stages of assessment prior to a formal diagnosis. This typically involves a comprehensive evaluation of information gathered from a number of sources, including parents/carers, family members, teachers, or partners and colleagues, depending on the age of the individual.</div>
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<div class="news-link"><a href="https://www.medpagetoday.com/video-coverage/adhd-video-insights/103938" target="_blank" rel="noopener">View Article: MedPage Today, April 10, 2023</a></div>
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<h4>Housing quality may affect kids with ADHD</h4>
<div>Attention deficit/hyperactivity disorder (ADHD) is the most frequently diagnosed behavioral and neurodevelopmental disorder in childhood. Children with ADHD experience difficulty with one or more of its core symptoms—inattention, impulsivity and hyperactivity.</div>
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<div class="news-link"><a href="https://medicalxpress.com/news/2023-04-housing-quality-affect-kids-adhd.html" target="_blank" rel="noopener">View Article: Medical Xpress, April 12, 2023</a></div>
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<h4>Vitamin and mineral supplements may help reduce aggressive behaviors in children and youth</h4>
<div>A systematic review published in the journal<span> </span><em>Aggression and Violent Behavior</em><span> </span>describes the effectiveness of nutritional supplements in reducing excessive aggression in children and adolescents.</div>
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<div class="news-link"><a href="https://www.news-medical.net/news/20230411/Vitamin-and-mineral-supplements-may-help-reduce-aggressive-behaviors-in-children-and-youth.aspx" target="_blank" rel="noopener">View Article: News-Medical.net, April 11, 2023</a></div>
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<h4>Better Cardiorespiratory Fitness in ADHD Positively Related With Mental Health Status</h4>
<div>KEY POINT: There is a link between CRF levels and mental health in patients with ADHD.</div>
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<div class="news-link"><a href="https://chadd.org/weekly-editions/adhd-in-the-news-2023-04-13/KEY%20POINT:%20There%20is%20a%20link%20between%20CRF%20levels%20and%20mental%20health%20in%20patients%20with%20ADHD." target="_blank" rel="noopener">View Article: Psychiatry Advisor, April 12, 2023</a></div>
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<div class="news-link">FOR MORE INFORMATION PLEASE GO TO:</div>
<div class="news-link"><a href="https://chadd.org/weekly-editions/adhd-in-the-news-2023-04-13/">https://chadd.org/weekly-editions/adhd-in-the-news-2023-04-13/</a></div>
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</div> Neuroimaging genetics approaches to identify new biomarkers for the early diagnosis of autism spectrum disordertag:templeilluminatus.ning.com,2023-04-18:6363372:Topic:36338162023-04-18T16:36:07.546ZMARGARIDA MARIA MADRUGAhttps://templeilluminatus.ning.com/profile/MARGARIDAMARIAMADRUGA
<div class="c-article-section" id="Abs1-section"><h2 class="c-article-section__title js-section-title js-c-reading-companion-sections-item" id="Abs1">Abstract</h2>
<div class="c-article-section__content" id="Abs1-content"><p>Autism-spectrum disorders (ASDs) are developmental disabilities that manifest in early childhood and are characterized by qualitative abnormalities in social behaviors, communication skills, and restrictive or repetitive behaviors. To explore the neurobiological mechanisms…</p>
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<div class="c-article-section" id="Abs1-section"><h2 class="c-article-section__title js-section-title js-c-reading-companion-sections-item" id="Abs1">Abstract</h2>
<div class="c-article-section__content" id="Abs1-content"><p>Autism-spectrum disorders (ASDs) are developmental disabilities that manifest in early childhood and are characterized by qualitative abnormalities in social behaviors, communication skills, and restrictive or repetitive behaviors. To explore the neurobiological mechanisms in ASD, extensive research has been done to identify potential diagnostic biomarkers through a neuroimaging genetics approach. Neuroimaging genetics helps to identify ASD-risk genes that contribute to structural and functional variations in brain circuitry and validate biological changes by elucidating the mechanisms and pathways that confer genetic risk. Integrating artificial intelligence models with neuroimaging data lays the groundwork for accurate diagnosis and facilitates the identification of early diagnostic biomarkers for ASD. This review discusses the significance of neuroimaging genetics approaches to gaining a better understanding of the perturbed neurochemical system and molecular pathways in ASD and how these approaches can detect structural, functional, and metabolic changes and lead to the discovery of novel biomarkers for the early diagnosis of ASD.</p>
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<div class="c-article-section" id="Sec1-section"><h2 class="c-article-section__title js-section-title js-c-reading-companion-sections-item" id="Sec1">Introduction</h2>
<div class="c-article-section__content" id="Sec1-content"><p>Autism spectrum disorder (ASD) is a neurodevelopmental disability that manifests in early childhood and is characterized by deficits in social skills, behaviors, and communication. According to the World Health Organization, approximately 1 in 160 children worldwide [<a title="Autism spectrum disorders. https://www.who.int/news-room/fact-sheets/detail/autism-spectrum-disorders#:~:text=Epidemiology,figures%20that%20are%20substantially%20higher. , 2021." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR1" id="ref-link-section-d16158194e390" name="ref-link-section-d16158194e390">1</a>] and about 1 in 44 children in the United States have ASD [<a title="Data & Statistics on Autism Spectrum Disorder. https://www.cdc.gov/ncbddd/autism/data.html , 2021." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR2" id="ref-link-section-d16158194e393" name="ref-link-section-d16158194e393">2</a>], which can occur in all racial and ethnic groups, and is four times more prevalent in boys than in girls [<a title="Autism Spectrum Disorder (ASD). https://www.nimh.nih.gov/health/statistics/autism-spectrum-disorder-asd , 2022." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR3" id="ref-link-section-d16158194e396" name="ref-link-section-d16158194e396">3</a>]. Individuals with ASD can have co-occurring conditions, such as attention deficit hyperactivity disorder (ADHD), bipolar disorder, depression, intellectual disability, language and developmental delays, speech disorder, and gastrointestinal symptoms [<a title="Casanova MF, Frye RE, Gillberg C, Casanova EL. Editorial: comorbidity and autism spectrum disorder. Front Psychiatry. 2020;11:617395." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR4" id="ref-link-section-d16158194e399" name="ref-link-section-d16158194e399">4</a>]. Although the cause of ASD is ambiguous, genetic and non-genetic factors most likely contribute to its development [<a title="Pugsley K, Scherer SW, Bellgrove MA, Hawi Z. Environmental exposures associated with elevated risk for autism spectrum disorder may augment the burden of deleterious de novo mutations among probands. Mol Psychiatry. 2022;27:710–30." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR5" id="ref-link-section-d16158194e402" name="ref-link-section-d16158194e402">5</a>].</p>
<p>ASD is associated with several genetic syndromes, a high incidence of chromosomal rearrangements, and the presence of common and rare variants [<a title="Grove J, Ripke S, Als TD, Mattheisen M, Walters RK, Won H, et al. Identification of common genetic risk variants for autism spectrum disorder. Nat Genet. 2019;51:431–44." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR6" id="ref-link-section-d16158194e408" name="ref-link-section-d16158194e408">6</a>]. Methodologic advances have revealed that common, heritable polygenic risk accounts for ~50% of ASD cases; major-affect mutations account for 15%; and rare de novo copy number variations (CNVs) and single-nucleotide variants (SNVs) that alter the structural genome account for ~5% [<a title="Eyring KW, Geschwind DH. Three decades of ASD genetics: building a foundation for neurobiological understanding and treatment. Hum Mol Genet. 2021;30:R236–44." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR7" id="ref-link-section-d16158194e411" name="ref-link-section-d16158194e411">7</a>]. No theory posits a clear unifying mechanism of ASD at the molecular or cellular level, because it remains unclear whether ASD is many disorders converging on a few molecular pathways or a few disorders with complex, diverse mechanisms [<a title="Geschwind DH. Autism: many genes, common pathways? Cell. 2008;135:391–5." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR8" id="ref-link-section-d16158194e414" name="ref-link-section-d16158194e414">8</a>].</p>
<p>The cellular and molecular bases of autism can be attributed to increased local connectivity in brain regions, neuronal migration deficits, excitatory/inhibitory imbalance, and synaptic dysregulation [<a title="Gao R, Penzes P. Common mechanisms of excitatory and inhibitory imbalance in schizophrenia and autism spectrum disorders. Curr Mol Med. 2015;15:146–67." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR9" id="ref-link-section-d16158194e420" name="ref-link-section-d16158194e420">9</a>,<a title="Pan Y-H, Wu N, Yuan X-B. Toward a better understanding of neuronal migration deficits in autism spectrum disorders. Front Cell Dev Biol. 2019;7:205–5." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR10" id="ref-link-section-d16158194e420_1" name="ref-link-section-d16158194e420_1">10</a>,<a title="Zhang H. Synaptic dysregulation in autism spectrum disorders. J Neurosci Res. 2020;98:2111–4." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR11" id="ref-link-section-d16158194e420_2" name="ref-link-section-d16158194e420_2">11</a>,<a title="Dajani DR, Uddin LQ. Local brain connectivity across development in autism spectrum disorder: a cross-sectional investigation. Autism Res. 2016;9:43–54." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR12" id="ref-link-section-d16158194e423" name="ref-link-section-d16158194e423">12</a>]. Many studies have highlighted the genetic heterogeneity underlying ASD and indicated that several ASD-associated gene or protein products interact with neuronal, synaptic, and other neurodevelopmental pathways [<a title="Kumar S, Reynolds K, Ji Y, Gu R, Rai S, Zhou CJ. Impaired neurodevelopmental pathways in autism spectrum disorder: a review of signaling mechanisms and crosstalk. J Neurodevelop Disord. 2019;11:10." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR13" id="ref-link-section-d16158194e426" name="ref-link-section-d16158194e426">13</a>,<span> </span><a title="Lin Y-C, Frei JA, Kilander MBC, Shen W, Blatt GJ. A subset of autism-associated genes regulate the structural stability of neurons. Front Cell Neurosci. 2016;10:263." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR14" id="ref-link-section-d16158194e429" name="ref-link-section-d16158194e429">14</a>]. Neurologic disorders, such as ASD, cause microdamage to the brain, and detection of the resulting structural and functional changes requires the use of high-resolution, noninvasive imaging techniques, such as magnetic resonance imaging (MRI). Furthermore, neuroimaging studies have provided evidence of altered cortical and subcortical structures, impaired white matter (WM) connectivity, and atypical connectivity in the frontal and temporal brain regions involved in various cognitive functions [<a title="Hashem S, Nisar S, Bhat AA, Yadav SK, Azeem MW, Bagga P, et al. Genetics of structural and functional brain changes in autism spectrum disorder. Transl Psychiatry. 2020;10:229–9." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR15" id="ref-link-section-d16158194e432" name="ref-link-section-d16158194e432">15</a>].</p>
<p>Because genes directly affect brain development and function, genetic polymorphisms or aberrations might be strongly associated with the functioning of the compromised neural systems and behavioral outcomes [<a title="Bigos KL, Hariri AR. Neuroimaging: technologies at the interface of genes, brain, and behavior. Neuroimaging Clin N. Am. 2007;17:459–viii." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR16" id="ref-link-section-d16158194e438" name="ref-link-section-d16158194e438">16</a>]. Neuroimaging can be used to investigate the effect of genetic variations on brain structure, function, and connectivity; this approach is known as “neuroimaging genetics” [<a title="Klein M, van Donkelaar M, Verhoef E, Franke B. Imaging genetics in neurodevelopmental psychopathology. Am J Med Genet B Neuropsychiatr Genet. 2017;174:485–537." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR17" id="ref-link-section-d16158194e441" name="ref-link-section-d16158194e441">17</a>]. Neuroimaging genetics can delineate the molecular mechanisms induced by genetic variants (common and rare) linked to neurodevelopmental disorders (NDDs). Neuroimaging genetics enables us to investigate gene-specific effects on different functional brain systems, which will contribute to future diagnosis of various NDDs, including ASD.</p>
<p>In this review, we will explore various neuroimaging techniques that can be used to assess the impact of genetic factors on brain structure, function, and metabolism. In addition, we will discuss the neuroimaging genetics approach can be used to identify novel biomarkers for the early diagnosis of ASD.</p>
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<div class="c-article-section" id="Sec2-section"><h2 class="c-article-section__title js-section-title js-c-reading-companion-sections-item" id="Sec2">Brain changes associated with genetic changes in ASD</h2>
<div class="c-article-section__content" id="Sec2-content"><h3 class="c-article__sub-heading" id="Sec3">Structural and functional changes</h3>
<p>Several gene polymorphisms have been linked to structural and functional changes in the brains of individuals with ASD. For example, Homeobox (<i>HOX</i>) genes that play an important role in defining cell identity and positioning during embryonic development are also associated with autism [<a title="Duverger O, Morasso MI. Role of homeobox genes in the patterning, specification, and differentiation of ectodermal appendages in mammals. J Cell Physiol. 2008;216:337–46." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR18" id="ref-link-section-d16158194e463" name="ref-link-section-d16158194e463">18</a>]. An earlier study has shown aberrant hindbrain development and craniofacial defects in<span> </span><i>HOXA1/HOXB1</i>-mutant mice as a result of rhombomere misspecification within the hindbrain [<a title="Rossel M, Capecchi MR. Mice mutant for both Hoxa1 and Hoxb1 show extensive remodeling of the hindbrain and defects in craniofacial development. Development. 1999;126:5027–40." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR19" id="ref-link-section-d16158194e469" name="ref-link-section-d16158194e469">19</a>]. Other studies have shown the association of<span> </span><i>HOXA1 A218G</i><span> </span>polymorphism with increased head circumference in autistic individuals [<a title="Conciatori M, Stodgell CJ, Hyman SL, O’Bara M, Militerni R, Bravaccio C, et al. Association between the HOXA1 A218G polymorphism and increased head circumference in patients with autism. Biol Psychiatry. 2004;55:413–9." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR20" id="ref-link-section-d16158194e476" name="ref-link-section-d16158194e476">20</a>,<span> </span><a title="Muscarella LA, Guarnieri V, Sacco R, Militerni R, Bravaccio C, Trillo S, et al. HOXA1 gene variants influence head growth rates in humans. Am J Med Genet B Neuropsychiatr Genet. 2007;144b:388–90." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR21" id="ref-link-section-d16158194e479" name="ref-link-section-d16158194e479">21</a>]. On the other hand,<span> </span><i>HOXB1</i><span> </span>alleles have been found to affect stereotypic behaviors and influence head growth rates, but to a much lesser extent than<span> </span><i>HOXA1 A218G</i><span> </span>in autistic individuals [<a title="Muscarella LA, Guarnieri V, Sacco R, Curatolo P, Manzi B, Alessandrelli R, et al. Candidate gene study of HOXB1 in autism spectrum disorder. Mol Autism. 2010;1:9." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR22" id="ref-link-section-d16158194e488" name="ref-link-section-d16158194e488">22</a>]. Current research suggests that approximately 25% of individuals with constitutional<span> </span><i>PTEN</i><span> </span>mutations might meet the criteria for ASD [<a title="Cummings K, Watkins A, Jones C, Dias R, Welham A. Behavioural and psychological features of PTEN mutations: a systematic review of the literature and meta-analysis of the prevalence of autism spectrum disorder characteristics. J Neurodevelop Disord. 2022;14:1." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR23" id="ref-link-section-d16158194e495" name="ref-link-section-d16158194e495">23</a>]. Autistic individuals with germline<span> </span><i>PTEN</i><span> </span>mutations D252G (exon 7), H93R (exon 4), and F241S (exon 7) were found to have increased head circumferences than other autistic subjects [<a title="Butler MG, Dasouki MJ, Zhou XP, Talebizadeh Z, Brown M, Takahashi TN, et al. Subset of individuals with autism spectrum disorders and extreme macrocephaly associated with germline PTEN tumour suppressor gene mutations. J Med Genet. 2005;42:318–21." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR24" id="ref-link-section-d16158194e501" name="ref-link-section-d16158194e501">24</a>]. In another study, the de novo missense<span> </span><i>PTEN</i><span> </span>mutation D326N (exon 8) was identified in an autistic patient with developmental delay, mental retardation, and extreme macrocephaly; the patient also showed prenatal and postnatal overgrowth [<a title="Buxbaum JD, Cai G, Chaste P, Nygren G, Goldsmith J, Reichert J, et al. Mutation screening of the PTEN gene in patients with autism spectrum disorders and macrocephaly. Am J Med Genet B Neuropsychiatr Genet. 2007;144b:484–91." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR25" id="ref-link-section-d16158194e507" name="ref-link-section-d16158194e507">25</a>].</p>
<p>A recent systematic review summarized brain structural MRI (sMRI) findings in monogenic disorders that are strongly associated with ASD [<a title="Frewer V, Gilchrist CP, Collins SE, Williams K, Seal ML, Leventer RJ, et al. A systematic review of brain MRI findings in monogenic disorders strongly associated with autism spectrum disorder. J Child Psychol Psychiatry. 2021;62:1339–52." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR26" id="ref-link-section-d16158194e513" name="ref-link-section-d16158194e513">26</a>]. The review included mutations in<span> </span><i>PTEN</i>,<span> </span><i>SHANK3</i>,<span> </span><i>SYNGAP1</i>,<span> </span><i>CHD8</i>,<span> </span><i>ARID1B</i>,<span> </span><i>ADNP</i>,<span> </span><i>POGZ</i>,<span> </span><i>MED13L</i>,<span> </span><i>SLC6A1</i>, and<span> </span><i>ANKDR11</i>, which are associated with different brain abnormalities, most prominently in the WM, GM, and ventricular regions [<a title="Frewer V, Gilchrist CP, Collins SE, Williams K, Seal ML, Leventer RJ, et al. A systematic review of brain MRI findings in monogenic disorders strongly associated with autism spectrum disorder. J Child Psychol Psychiatry. 2021;62:1339–52." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR26" id="ref-link-section-d16158194e548" name="ref-link-section-d16158194e548">26</a>]. Studies have also reported the association of contactin-associated protein 2 (<i>CNTNAP2</i>) polymorphisms with WM and GM abnormalities [<a title="Tan GCY, Doke TF, Ashburner J, Wood NW, Frackowiak RSJ. Normal variation in fronto-occipital circuitry and cerebellar structure with an autism-associated polymorphism of CNTNAP2. Neuroimage. 2010;53:1030–42." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR27" id="ref-link-section-d16158194e554" name="ref-link-section-d16158194e554">27</a>].<span> </span><i>CNTNAP2</i><span> </span>is a master gene that causes speech-language delay and is central to the manifestation of autism [<a title="Agarwala S, Ramachandra NB. Role of CNTNAP2 in autism manifestation outlines the regulation of signaling between neurons at the synapse. Egypt J Med Hum Genet. 2021;22:22." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR28" id="ref-link-section-d16158194e560" name="ref-link-section-d16158194e560">28</a>]. A recent MRI study involving 118 individuals with ASD and 122 typically developing (TD) controls showed the association of a<span> </span><i>CNTNAP2</i><span> </span>variant (rs2538991) with WM volume of the right anterior cingulate gyrus in ASD individuals [<a title="Chien Y-L, Chen Y-C, Gau SS-F. Altered cingulate structures and the associations with social awareness deficits and CNTNAP2 gene in autism spectrum disorder. NeuroImage: Clin. 2021;31:102729." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR29" id="ref-link-section-d16158194e567" name="ref-link-section-d16158194e567">29</a>].</p>
<p>MET receptor tyrosine kinase and its ligand, hepatocyte growth factor help mediate neurodevelopmental events that are associated with brain structural pattern and circuitry and has a pleiotropic role in multiple organs’ ontogenesis [<a title="Peng Y, Huentelman M, Smith C, Qiu S. MET receptor tyrosine kinase as an autism genetic risk factor. Int Rev Neurobiol. 2013;113:135–65." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR30" id="ref-link-section-d16158194e573" name="ref-link-section-d16158194e573">30</a>]. Functional polymorphism in<span> </span><i>MET</i><span> </span>gene has been associated with increased risk for autism [<a title="Campbell DB, Sutcliffe JS, Ebert PJ, Militerni R, Bravaccio C, Trillo S, et al. A genetic variant that disrupts MET transcription is associated with autism. Proc Natl Acad Sci USA. 2006;103:16834–9." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR31" id="ref-link-section-d16158194e579" name="ref-link-section-d16158194e579">31</a>]. A study involving 75 individuals with ASD and 87 TD controls showed an ASD-risk variant in the<span> </span><i>met receptor tyrosine kinase</i><span> </span>gene to be associated with altered WM connectivity in individuals with ASD, relative to TD controls [<a title="Rudie JD, Hernandez LM, Brown JA, Beck-Pancer D, Colich NL, Gorrindo P, et al. Autism-associated promoter variant in MET impacts functional and structural brain networks. Neuron. 2012;75:904–15." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR32" id="ref-link-section-d16158194e585" name="ref-link-section-d16158194e585">32</a>].</p>
<p>Mutations associated with the chromodomain helicase DNA-binding protein 8 (<i>CHD8</i>) gene are also implicated in autism. CHD8 is a transcriptional regulator that is involved in the remodeling of chromatin structure and is crucial for dendrite development and neuronal migration [<a title="Xu Q, Liu Y-Y, Wang X, Tan G-H, Li H-P, Hulbert SW, et al. Autism-associated CHD8 deficiency impairs axon development and migration of cortical neurons. Mol Autism. 2018;9:65." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR33" id="ref-link-section-d16158194e594" name="ref-link-section-d16158194e594">33</a>]. A case report study, using whole-exome sequencing (WES), identified a de novo mutation of the<span> </span><i>CHD8</i><span> </span>gene in a clinical ASD phenotype including intellectual disability (ID), macrocephaly, and craniofacial abnormalities observed in a boy with developmental delay [<a title="Alotaibi M, Ramzan K. A de novo variant of CHD8 in a patient with autism spectrum disorder. Discoveries (Craiova). 2020;8:e107–7." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR34" id="ref-link-section-d16158194e600" name="ref-link-section-d16158194e600">34</a>].</p>
<p>In a study comparing mouse models of autism to wild-type (WT) controls,<span> </span><i>NLGN3-</i><span> </span>and<span> </span><i>MECP2-</i>mutant mice showed increased cerebellar volumes, and<span> </span><i>ITGB3-</i>mutant mice showed reduced cerebellar volume [<a title="Steadman PE, Ellegood J, Szulc KU, Turnbull DH, Joyner AL, Henkelman RM, et al. Genetic effects on cerebellar structure across mouse models of autism using a magnetic resonance imaging atlas. Autism Res: Off J Int Soc Autism Res. 2014;7:124–37." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR35" id="ref-link-section-d16158194e616" name="ref-link-section-d16158194e616">35</a>]. Functional analysis of cortical neurons in<span> </span><i>MECP2</i>-mutant mice showed abnormal growth of dendrites and axons, suggesting that<span> </span><i>MECP2</i><span> </span>mutations impair neuronal development which might lead to ASD [<a title="Wen Z, Cheng T-L, Li G-Z, Sun S-B, Yu S-Y, Zhang Y, et al. Identification of autism-related MECP2 mutations by whole-exome sequencing and functional validation. Mol Autism. 2017;8:43." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR36" id="ref-link-section-d16158194e626" name="ref-link-section-d16158194e626">36</a>]. Mutations associated with the SH3 and multiple ankyrin repeat domains 3 (SHANK3), a synaptic scaffolding protein required for synaptic functioning, have been implicated in ASD, with knockout (KO) mice having reduced total brain volume, hippocampus, and thalami, and enlarged basal ganglia [<a title="Schoen M, Asoglu H, Bauer HF, Müller HP, Abaei A, Sauer AK, et al. Shank3 transgenic and prenatal zinc-deficient autism mouse models show convergent and individual alterations of brain structures in MRI. Front Neural Circuits. 2019;13:6." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR37" id="ref-link-section-d16158194e629" name="ref-link-section-d16158194e629">37</a>]. Loss of<span> </span><i>SHANK3</i><span> </span>has been associated with altered prefrontal functional connectivity in mice, suggesting that this deletion impairs social and communication behaviors and contributes to ASD pathogenesis [<a title="Pagani M, Bertero A, Liska A, Galbusera A, Sabbioni M, Barsotti N, et al. Deletion of autism risk gene Shank3 disrupts prefrontal connectivity. J Neurosci. 2019;39:5299." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR38" id="ref-link-section-d16158194e635" name="ref-link-section-d16158194e635">38</a>].</p>
<p>Neurexins are presynaptic cell-adhesion proteins that are involved in synapse formation. Single-cell RNA sequencing analysis on induced pluripotent stem cells-derived neural stem cells revealed that, compared to neurons of a healthy patient, those of an autistic patient carrying the biallelic neurexin 1-alpha (<i>NRXN1-α</i>) deletion had impaired maturation of action potentials and decreased calcium signaling [<a title="Lam M, Moslem M, Bryois J, Pronk RJ, Uhlin E, Ellström ID, et al. Single cell analysis of autism patient with bi-allelic NRXN1-alpha deletion reveals skewed fate choice in neural progenitors and impaired neuronal functionality. Exp Cell Res. 2019;383:111469." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR39" id="ref-link-section-d16158194e644" name="ref-link-section-d16158194e644">39</a>]. Additionally, diffusion MRI analyses of the brain tissues of<span> </span><i>NRXN2-α–</i>KO mice showed altered microstructures in the social brain regions and impaired structural connectivity between the amygdala and orbitofrontal cortex regions, suggesting a role of<span> </span><i>NRXN2</i><span> </span>in altering social behaviors [<a title="Pervolaraki E, Tyson AL, Pibiri F, Poulter SL, Reichelt AC, Rodgers RJ, et al. The within-subject application of diffusion tensor MRI and CLARITY reveals brain structural changes in Nrxn2 deletion mice. Mol Autism. 2019;10:8." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR40" id="ref-link-section-d16158194e653" name="ref-link-section-d16158194e653">40</a>].</p>
<p>In another study, homozygous<span> </span><i>CNTNAP2</i><sup><i>–/–</i></sup><span> </span>mice exhibited reduced long-range and local functional connectivity in the prefrontal and midline brain regions, suggesting that homozygous loss-of-function mutations in<span> </span><i>CNTNAP2</i><span> </span>predispose individuals to NDDs, such as autism [<a title="Liska A, Bertero A, Gomolka R, Sabbioni M, Galbusera A, Barsotti N, et al. Homozygous loss of autism-risk gene CNTNAP2 results in reduced local and long-range prefrontal functional connectivity. Cereb Cortex. 2018;28:1141–53." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR41" id="ref-link-section-d16158194e668" name="ref-link-section-d16158194e668">41</a>]. Another study using a forebrain organoid model generated from induced pluripotent stem cells of patients with syndromic ASD carrying the homozygous<span> </span><i>CNTNAP2</i><span> </span>c.3709DelG mutation showed that the mutation causes cortical overgrowth in the organoids that was rescued by repairing the pathogenic mutation via CRISPR–Cas9, thus confirming the causative effect of homozygous<span> </span><i>CNTNAP2</i><span> </span>mutation in ASD [<a title="de Jong JO, Llapashtica C, Genestine M, Strauss K, Provenzano F, Sun Y, et al. Cortical overgrowth in a preclinical forebrain organoid model of CNTNAP2-associated autism spectrum disorder. Nat Commun. 2021;12:4087." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR42" id="ref-link-section-d16158194e678" name="ref-link-section-d16158194e678">42</a>].</p>
<p>CD38, a transmembrane protein plays an important role in controlling social behaviors due to its role in regulating oxytocin secretion processes [<a title="Jin D, Liu H-X, Hirai H, Torashima T, Nagai T, Lopatina O, et al. CD38 is critical for social behaviour by regulating oxytocin secretion. Nature. 2007;446:41–5." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR43" id="ref-link-section-d16158194e684" name="ref-link-section-d16158194e684">43</a>]. Two single-nucleotide polymorphisms (SNPs) in the<span> </span><i>CD38</i><span> </span>gene (rs3796863 and rs1800561) have been detected in individuals with ASD [<a title="Higashida H, Yokoyama S, Huang JJ, Liu L, Ma WJ, Akther S, et al. Social memory, amnesia, and autism: brain oxytocin secretion is regulated by NAD+ metabolites and single nucleotide polymorphisms of CD38. Neurochem Int. 2012;61:828–38." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR44" id="ref-link-section-d16158194e690" name="ref-link-section-d16158194e690">44</a>]. Plasma levels of oxytocin were lower in individuals with ASD carrying the R140W allele than in those lacking the allele [<a title="Higashida H, Yokoyama S, Huang JJ, Liu L, Ma WJ, Akther S, et al. Social memory, amnesia, and autism: brain oxytocin secretion is regulated by NAD+ metabolites and single nucleotide polymorphisms of CD38. Neurochem Int. 2012;61:828–38." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR44" id="ref-link-section-d16158194e693" name="ref-link-section-d16158194e693">44</a>]. Treating a proband carrying the R140W allele with intranasal oxytocin improved social, communication, and emotional behaviors [<a title="Higashida H, Yokoyama S, Huang JJ, Liu L, Ma WJ, Akther S, et al. Social memory, amnesia, and autism: brain oxytocin secretion is regulated by NAD+ metabolites and single nucleotide polymorphisms of CD38. Neurochem Int. 2012;61:828–38." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR44" id="ref-link-section-d16158194e696" name="ref-link-section-d16158194e696">44</a>].</p>
<p>Along with CD38, oxytocin receptor (<i>OXTR</i>) genes influence social behavior, and<span> </span><i>OXTR</i><span> </span>mutations are a risk factor for ASD [<a title="LoParo D, Waldman ID. The oxytocin receptor gene (OXTR) is associated with autism spectrum disorder: a meta-analysis. Mol Psychiatry. 2015;20:640–6." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR45" id="ref-link-section-d16158194e708" name="ref-link-section-d16158194e708">45</a>]. Genotyping for SNPs and fMRI analysis of 38 adolescents with high-functioning autism (HFA) and 33 TD controls [<a title="Uzefovsky F, Bethlehem RAI, Shamay-Tsoory S, Ruigrok A, Holt R, Spencer M, et al. The oxytocin receptor gene predicts brain activity during an emotion recognition task in autism. Mol Autism. 2019;10:12." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR46" id="ref-link-section-d16158194e711" name="ref-link-section-d16158194e711">46</a>] showed<span> </span><i>OXTR</i><span> </span>SNPs association with brain activation within the right supramarginal gyrus and inferior parietal lobule during an emotion-recognition task in autistic individuals [<a title="Uzefovsky F, Bethlehem RAI, Shamay-Tsoory S, Ruigrok A, Holt R, Spencer M, et al. The oxytocin receptor gene predicts brain activity during an emotion recognition task in autism. Mol Autism. 2019;10:12." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR46" id="ref-link-section-d16158194e718" name="ref-link-section-d16158194e718">46</a>]. Another study involving 209 probands with ASD investigated the influence of two polymorphisms (rs1042778, rs53576) in<span> </span><i>OXTR</i><span> </span>on ASD-related clinical symptoms including panic and aggressive behaviors [<a title="de Oliveira Pereira Ribeiro L, Vargas-Pinilla P, Kappel DB, Longo D, Ranzan J, Becker MM, et al. Evidence for association between OXTR gene and ASD clinical phenotypes. J Mol Neurosci. 2018;65:213–21." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR47" id="ref-link-section-d16158194e724" name="ref-link-section-d16158194e724">47</a>]. The presence of<span> </span><i>OXTR</i><span> </span>rs1042778 T allele was associated with panic and aggressive behaviors in individuals with ASD, suggesting the importance of<span> </span><i>OXTR</i><span> </span>in ASD diagnosis and clinical phenotypes [<a title="de Oliveira Pereira Ribeiro L, Vargas-Pinilla P, Kappel DB, Longo D, Ranzan J, Becker MM, et al. Evidence for association between OXTR gene and ASD clinical phenotypes. J Mol Neurosci. 2018;65:213–21." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR47" id="ref-link-section-d16158194e733" name="ref-link-section-d16158194e733">47</a>]. The disparity in the prevalence of ASD among males and females gives rise to a sex bias, a concept that is poorly understood in the neurobiology of autism. In relation to this, an imaging-genetics study consisting of 50 females with HFA and 52 females as TD controls and 37 males with HFA and 34 males as TD controls between the ages of 8 and 17 assessed the impact of ASD-associated<span> </span><i>OXTR</i><span> </span>variants on reward network functional connectivity in both male and female subjects with ASD [<a title="Hernandez LM, Lawrence KE, Padgaonkar NT, Inada M, Hoekstra JN, Lowe JK, et al. Imaging-genetics of sex differences in ASD: distinct effects of OXTR variants on brain connectivity. Transl Psychiatry. 2020;10:82." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR48" id="ref-link-section-d16158194e740" name="ref-link-section-d16158194e740">48</a>]. Females carrying more ASD-associated<span> </span><i>OXTR</i><span> </span>variants showed increased connectivity between reward-related brain regions (nucleus accumbens) and the prefrontal cortex region, compared to males with ASD [<a title="Hernandez LM, Lawrence KE, Padgaonkar NT, Inada M, Hoekstra JN, Lowe JK, et al. Imaging-genetics of sex differences in ASD: distinct effects of OXTR variants on brain connectivity. Transl Psychiatry. 2020;10:82." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR48" id="ref-link-section-d16158194e746" name="ref-link-section-d16158194e746">48</a>].</p>
<p>Genetic variants of arginine vasopressin receptor 1 A (<i>AVPR1A</i>) gene have also been linked with autism [<a title="Meyer-Lindenberg A, Kolachana B, Gold B, Olsh A, Nicodemus KK, Mattay V, et al. Genetic variants in AVPR1A linked to autism predict amygdala activation and personality traits in healthy humans. Mol Psychiatry. 2009;14:968–75." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR49" id="ref-link-section-d16158194e755" name="ref-link-section-d16158194e755">49</a>]. In a study involving 121 healthy volunteers, a functional imaging task was performed to assess the association between<span> </span><i>AVPR1A</i><span> </span>genetic variants and amygdala activation [<a title="Meyer-Lindenberg A, Kolachana B, Gold B, Olsh A, Nicodemus KK, Mattay V, et al. Genetic variants in AVPR1A linked to autism predict amygdala activation and personality traits in healthy humans. Mol Psychiatry. 2009;14:968–75." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR49" id="ref-link-section-d16158194e761" name="ref-link-section-d16158194e761">49</a>]. Carriers of the<span> </span><i>AVPR1A</i><span> </span>ASD-risk alleles (RS1 and RS3) had differential activation of the amygdala [<a title="Meyer-Lindenberg A, Kolachana B, Gold B, Olsh A, Nicodemus KK, Mattay V, et al. Genetic variants in AVPR1A linked to autism predict amygdala activation and personality traits in healthy humans. Mol Psychiatry. 2009;14:968–75." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR49" id="ref-link-section-d16158194e768" name="ref-link-section-d16158194e768">49</a>]. In another study involving 1104 healthy subjects, MRI, genotyping, and learning and memory assessment were performed to assess the effect of<span> </span><i>AVPR1A</i><span> </span>RS3-RS1 haplotypes on verbal learning and memory: individuals carrying the short alleles of RS3-RS1 haplotypes displayed poor verbal memory performance than those carrying the long alleles [<a title="Zhang Y, Zhu D, Zhang P, Li W, Qin W, Liu F, et al. Neural mechanisms of AVPR1A RS3-RS1 haplotypes that impact verbal learning and memory. Neuroimage. 2020;222:117283." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR50" id="ref-link-section-d16158194e774" name="ref-link-section-d16158194e774">50</a>]. A study consisting of 212 ASD probands and their biological parents conducted a family-based association test to assess the effect of polymorphisms in the<span> </span><i>AVPR1A</i><span> </span>promoter region on social behavior [<a title="Yang SY, Kim SA, Hur GM, Park M, Park J-E, Yoo HJ. Replicative genetic association study between functional polymorphisms in AVPR1A and social behavior scales of autism spectrum disorder in the Korean population. Mol Autism. 2017;8:44." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR51" id="ref-link-section-d16158194e780" name="ref-link-section-d16158194e780">51</a>]. The study found two<span> </span><i>AVPR1A</i><span> </span>SNPs (rs7294536 and rs10877969) to be over-transmitted as a risk allele in Korean families with ASD; suggesting their involvement in dysregulating social behavior and contributing to the pathophysiology of ASD [<a title="Yang SY, Kim SA, Hur GM, Park M, Park J-E, Yoo HJ. Replicative genetic association study between functional polymorphisms in AVPR1A and social behavior scales of autism spectrum disorder in the Korean population. Mol Autism. 2017;8:44." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR51" id="ref-link-section-d16158194e787" name="ref-link-section-d16158194e787">51</a>].</p>
<p>Mutations associated with the reelin (<i>RELN</i>) gene, which encodes a large glycoprotein RELN that guides neuronal migration and positioning during embryonic development [<a title="Bosch C, Muhaisen A, Pujadas L, Soriano E, Martínez A. Reelin exerts structural, biochemical and transcriptional regulation over presynaptic and postsynaptic elements in the adult hippocampus. Front Cell Neurosci. 2016;10:138–8." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR52" id="ref-link-section-d16158194e797" name="ref-link-section-d16158194e797">52</a>], have been implicated in ASD pathology [<a title="Fatemi SH. The role of Reelin in pathology of autism. Mol Psychiatry. 2002;7:919–20." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR53" id="ref-link-section-d16158194e800" name="ref-link-section-d16158194e800">53</a>,<span> </span><a title="Lammert DB, Howell BW. RELN mutations in autism spectrum disorder. Front Cell Neurosci. 2016;10:84." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR54" id="ref-link-section-d16158194e803" name="ref-link-section-d16158194e803">54</a>]. A de novo RELN R2290C mutation identified in an ASD proband in a conserved arginine-amino acid-arginine domain were found to impair RELN protein secretion and these effects were recapitulated in a heterozygous<span> </span><i>RELN</i><span> </span>mouse mutant model [<a title="Lammert DB, Middleton FA, Pan J, Olson EC, Howell BW. The de novo autism spectrum disorder RELN R2290C mutation reduces Reelin secretion and increases protein disulfide isomerase expression. J Neurochem. 2017;142:89–102." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR55" id="ref-link-section-d16158194e810" name="ref-link-section-d16158194e810">55</a>]. Analysis of<span> </span><i>RELN</i><span> </span>R2290C heterozygous neurospheres revealed an upregulation in Protein Disulfide Isomerase A1, a chaperone protein responsible for the formation of disulfide bonds [<a title="Lammert DB, Middleton FA, Pan J, Olson EC, Howell BW. The de novo autism spectrum disorder RELN R2290C mutation reduces Reelin secretion and increases protein disulfide isomerase expression. J Neurochem. 2017;142:89–102." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR55" id="ref-link-section-d16158194e816" name="ref-link-section-d16158194e816">55</a>]. In contrast, a study comparing plasma RELN levels between 40 ASD and 19 healthy children found higher RELN levels in children with ASD than in healthy controls [<a title="Cuchillo-Ibáñez I, Andreo-Lillo P, Pastor-Ferrándiz L, Carratalá-Marco F, Sáez-Valero J. Elevated plasma reelin levels in children with autism. Front Psychiatry. 2020;11:242." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR56" id="ref-link-section-d16158194e819" name="ref-link-section-d16158194e819">56</a>].</p>
<p>The gene T-brain 1 (<i>TBR1</i>) encodes the transcription factor TBR1, which mediates gene transcription and cortical neurogenesis and is crucial for normal neurodevelopment. Several preclinical and clinical studies have shown<span> </span><i>TBR1</i><span> </span>to be implicated in ASD [<a title="Huang T-N, Yen T-L, Qiu LR, Chuang H-C, Lerch JP, Hsueh Y-P. Haploinsufficiency of autism causative gene Tbr1 impairs olfactory discrimination and neuronal activation of the olfactory system in mice. Mol Autism. 2019;10:5." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR57" id="ref-link-section-d16158194e831" name="ref-link-section-d16158194e831">57</a>,<a title="Huang TN, Chuang HC, Chou WH, Chen CY, Wang HF, Chou SJ, et al. Tbr1 haploinsufficiency impairs amygdalar axonal projections and results in cognitive abnormality. Nat Neurosci. 2014;17:240–7." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR58" id="ref-link-section-d16158194e831_1" name="ref-link-section-d16158194e831_1">58</a>,<a title="Sapey-Triomphe L-A, Reversat J, Lesca G, Chatron N, Bussa M, Mazoyer S, et al. A de novo frameshift pathogenic variant in TBR1 identified in autism without intellectual disability. Hum Genomics. 2020;14:32–32." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR59" id="ref-link-section-d16158194e831_2" name="ref-link-section-d16158194e831_2">59</a>,<a title="Yook C, Kim K, Kim D, Kang H, Kim S-G, Kim E, et al. A TBR1-K228E mutation induces Tbr1 upregulation, altered cortical distribution of interneurons, increased inhibitory synaptic transmission, and autistic-like behavioral deficits in mice. Front Mol Neurosci. 2019;12:241." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR60" id="ref-link-section-d16158194e831_3" name="ref-link-section-d16158194e831_3">60</a>,<a title="Deriziotis P, O’Roak BJ, Graham SA, Estruch SB, Dimitropoulou D, Bernier RA, et al. De novo TBR1 mutations in sporadic autism disrupt protein functions. Nat Commun. 2014;5:4954–4." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR61" id="ref-link-section-d16158194e834" name="ref-link-section-d16158194e834">61</a>].<span> </span><i>TBR1</i><span> </span>haploinsufficiency results in defective axonal projections of amygdala neurons and impairs social interaction, memory, cognitive flexibility [<a title="Huang TN, Chuang HC, Chou WH, Chen CY, Wang HF, Chou SJ, et al. Tbr1 haploinsufficiency impairs amygdalar axonal projections and results in cognitive abnormality. Nat Neurosci. 2014;17:240–7." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR58" id="ref-link-section-d16158194e841" name="ref-link-section-d16158194e841">58</a>], and neuronal activation of the olfactory system in mice models [<a title="Huang T-N, Yen T-L, Qiu LR, Chuang H-C, Lerch JP, Hsueh Y-P. Haploinsufficiency of autism causative gene Tbr1 impairs olfactory discrimination and neuronal activation of the olfactory system in mice. Mol Autism. 2019;10:5." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR57" id="ref-link-section-d16158194e844" name="ref-link-section-d16158194e844">57</a>]. Additionally, mice carrying the heterozygous<span> </span><i>TBR1 K228E</i><span> </span>mutation showed altered cortical development, increased levels of TBR1, inhibitory synaptic transmission, and ASD-like behavioral phenotypes [<a title="Yook C, Kim K, Kim D, Kang H, Kim S-G, Kim E, et al. A TBR1-K228E mutation induces Tbr1 upregulation, altered cortical distribution of interneurons, increased inhibitory synaptic transmission, and autistic-like behavioral deficits in mice. Front Mol Neurosci. 2019;12:241." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR60" id="ref-link-section-d16158194e850" name="ref-link-section-d16158194e850">60</a>]. De novo and missense<span> </span><i>TBR1</i><span> </span>mutations also disrupt TBR1 functions, such as subcellular localization and transcriptional repression, in individuals with sporadic ASD [<a title="Deriziotis P, O’Roak BJ, Graham SA, Estruch SB, Dimitropoulou D, Bernier RA, et al. De novo TBR1 mutations in sporadic autism disrupt protein functions. Nat Commun. 2014;5:4954–4." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR61" id="ref-link-section-d16158194e856" name="ref-link-section-d16158194e856">61</a>]. Moreover, TBR1 interacts with FOXP2, which is associated with speech and language disorders and the TBR1–FOXP2 interaction was shown to be abolished in patients with sporadic ASD [<a title="Deriziotis P, O’Roak BJ, Graham SA, Estruch SB, Dimitropoulou D, Bernier RA, et al. De novo TBR1 mutations in sporadic autism disrupt protein functions. Nat Commun. 2014;5:4954–4." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR61" id="ref-link-section-d16158194e860" name="ref-link-section-d16158194e860">61</a>].</p>
<p>Ankyrin 2 (<i>ANK2</i>), an important gene that encodes for ankyrin B (ankB) protein is involved in membrane stabilization and localization of ion channels and transporters.<span> </span><i>ANK2</i><span> </span>mutation in mice has been found to increase axon branching and ectopic connectivity and impairs social and communication behaviors [<a title="Yang R, Walder-Christensen Kathryn K, Kim N, Wu D, Lorenzo Damaris N, Badea A, et al. ANK2 autism mutation targeting giant ankyrin-B promotes axon branching and ectopic connectivity. Proc Natl Acad Sci. 2019;116:15262–71." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR62" id="ref-link-section-d16158194e872" name="ref-link-section-d16158194e872">62</a>].<span> </span><i>ANK2</i><span> </span>is highly expressed during early neurodevelopmental stages and is an important regulator of neurogenesis [<a title="Kawano S, Baba M, Fukushima H, Miura D, Hashimoto H, Nakazawa T. Autism-associated ANK2 regulates embryonic neurodevelopment. Biochem Biophys Res Commun. 2022;605:45–50." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR63" id="ref-link-section-d16158194e878" name="ref-link-section-d16158194e878">63</a>]. Loss of<span> </span><i>ANK2</i><span> </span>impaired differentiation of neural stem cells to neurons and altered the expression of genes involved in neural development, suggesting<span> </span><i>ANK2</i><span> </span>haploinsufficiency as a risk factor for ASD [<a title="Kawano S, Baba M, Fukushima H, Miura D, Hashimoto H, Nakazawa T. Autism-associated ANK2 regulates embryonic neurodevelopment. Biochem Biophys Res Commun. 2022;605:45–50." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR63" id="ref-link-section-d16158194e888" name="ref-link-section-d16158194e888">63</a>].</p>
<p>Mice carrying the<span> </span><i>NLGN3 R351C</i><span> </span>mutation showed delayed synapse elimination in the cerebellum suggesting NLGN3 involvement in synapse refinement of the cerebellar circuitry that might be associated with ASD pathogenesis [<a title="Lai ESK, Nakayama H, Miyazaki T, Nakazawa T, Tabuchi K, Hashimoto K, et al. An autism-associated neuroligin-3 mutation affects developmental synapse elimination in the cerebellum. Front Neural Circuits. 2021;15:676891." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR64" id="ref-link-section-d16158194e897" name="ref-link-section-d16158194e897">64</a>]. Additionally,<span> </span><i>NLGN3 R451C</i>–mutant mice displayed more aggressive and repetitive behaviors than WT controls [<a title="Burrows EL, Laskaris L, Koyama L, Churilov L, Bornstein JC, Hill-Yardin EL, et al. A neuroligin-3 mutation implicated in autism causes abnormal aggression and increases repetitive behavior in mice. Mol Autism. 2015;6:62." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR65" id="ref-link-section-d16158194e903" name="ref-link-section-d16158194e903">65</a>]. Another study observed that<span> </span><i>NLGN3</i>-knockin mice exhibited reduced GM and WM volumes and reduced social and anxiety-related behaviors compared to WT controls [<a title="Kumar M, Duda JT, Hwang W-T, Kenworthy C, Ittyerah R, Pickup S, et al. High resolution magnetic resonance imaging for characterization of the neuroligin-3 knock-in mouse model associated with autism spectrum disorder. PLOS ONE. 2014;9:e109872." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR66" id="ref-link-section-d16158194e910" name="ref-link-section-d16158194e910">66</a>].</p>
<p>These studies provide evidence that monogenic risk factors for autism share common involvement of the prefrontal cortex, cerebellum, amygdala, and hippocampus. In addition, most of the genetic mutations responsible for structural and functional brain changes converge on biological pathways that are involved in corticogenesis, synaptogenesis, chromatin modification, and transcriptional and translational processes, all of which contribute to social and behavioral impairments, the core deficits associated with ASD.</p>
<h3 class="c-article__sub-heading" id="Sec4">Metabolic changes</h3>
<p>Proper regulation of cellular metabolism is essential for maintaining cellular function, which is crucial for the central nervous system (CNS), specifically for the brain, where energy consumption and metabolic changes are dynamic [<a title="Watts ME, Pocock R, Claudianos C. Brain energy and oxygen metabolism: emerging role in normal function and disease. Front Mol Neurosci. 2018;11:216." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR67" id="ref-link-section-d16158194e924" name="ref-link-section-d16158194e924">67</a>], and metabolic changes in neurons are critical for neuroplasticity and cognitive functions [<a title="Watts ME, Pocock R, Claudianos C. Brain energy and oxygen metabolism: emerging role in normal function and disease. Front Mol Neurosci. 2018;11:216." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR67" id="ref-link-section-d16158194e927" name="ref-link-section-d16158194e927">67</a>]. The heterogeneous and multifaceted pathological nature of ASD clearly explains why the genes affecting brain metabolism have been under-investigated. Nevertheless, to refine the search for metabolic biomarkers in ASD, the effect of candidate genes involved in ASD must be explored in metabolic pathways specifically affecting brain energy metabolism and neuron-astrocyte interactions to provide insight into which metabolic pathways are disrupted in ASD and how to target those pathways via neuroimaging genetics.</p>
<p>Autism is a multifactorial disease, with many candidate genes in its etiology. However, only a few of those genes such as such as<span> </span><i>DISC1</i>,<span> </span><i>SHANK3</i>,<span> </span><i>ITGB3</i>,<span> </span><i>SLC6A4</i>,<span> </span><i>RELN</i>,<span> </span><i>RPL10</i>, and<span> </span><i>AVPR1α</i><span> </span>are found to be associated with brain metabolism [<a title="Lopes Cardoso I, Almeida S. Genes involved in the development of autism. Int Arch Commun Disord. 2019;2:011." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR68" id="ref-link-section-d16158194e955" name="ref-link-section-d16158194e955">68</a>]. Moreover, several metabolic pathways are found to be altered in the prefrontal cortex of ASD individuals [<a title="Kurochkin I, Khrameeva E, Tkachev A, Stepanova V, Vanyushkina A, Stekolshchikova E, et al. Metabolome signature of autism in the human prefrontal cortex. Commun Biol. 2019;2:234." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR69" id="ref-link-section-d16158194e958" name="ref-link-section-d16158194e958">69</a>]. These metabolic pathways include glutathione metabolism, galactose metabolism, purine and pyruvate metabolism, starch and sucrose metabolism, arginine and proline metabolism, cysteine and methionine metabolism, propanoate metabolism, nicotinate, and nicotinamide metabolism, and the tricarboxylic acid (TCA) cycle [<a title="Kurochkin I, Khrameeva E, Tkachev A, Stepanova V, Vanyushkina A, Stekolshchikova E, et al. Metabolome signature of autism in the human prefrontal cortex. Commun Biol. 2019;2:234." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR69" id="ref-link-section-d16158194e961" name="ref-link-section-d16158194e961">69</a>].</p>
<p>The RNA-binding fox 1 (<i>RBFOX1</i>) gene is associated with various neuropsychiatric disorders (e.g., ASD, ADHD, epilepsy, intellectual disability, and schizophrenia) [<a title="Elia J, Glessner JT, Wang K, Takahashi N, Shtir CJ, Hadley D, et al. Genome-wide copy number variation study associates metabotropic glutamate receptor gene networks with attention deficit hyperactivity disorder. Nat Genet. 2011;44:78–84." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR70" id="ref-link-section-d16158194e970" name="ref-link-section-d16158194e970">70</a>,<a title="Lal D, Pernhorst K, Klein KM, Reif P, Tozzi R, Toliat MR, et al. Extending the phenotypic spectrum of RBFOX1 deletions: Sporadic focal epilepsy. Epilepsia. 2015;56:e129–133." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR71" id="ref-link-section-d16158194e970_1" name="ref-link-section-d16158194e970_1">71</a>,<a title="Griswold AJ, Dueker ND, Van Booven D, Rantus JA, Jaworski JM, Slifer SH, et al. Targeted massively parallel sequencing of autism spectrum disorder-associated genes in a case control cohort reveals rare loss-of-function risk variants. Mol Autism. 2015;6:43." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR72" id="ref-link-section-d16158194e970_2" name="ref-link-section-d16158194e970_2">72</a>,<a title="Xu B, Roos JL, Levy S, van Rensburg EJ, Gogos JA, Karayiorgou M. Strong association of de novo copy number mutations with sporadic schizophrenia. Nat Genet. 2008;40:880–5." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR73" id="ref-link-section-d16158194e973" name="ref-link-section-d16158194e973">73</a>]. A study has also highlighted the role of cytoplasmic RBFOX1 in regulating the expression of genes involved in synaptic transmission and autism [<a title="Lee JA, Damianov A, Lin CH, Fontes M, Parikshak NN, Anderson ES, et al. Cytoplasmic Rbfox1 regulates the expression of synaptic and autism-related genes. Neuron. 2016;89:113–28." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR74" id="ref-link-section-d16158194e976" name="ref-link-section-d16158194e976">74</a>]. No association of<span> </span><i>RBFOX1</i><span> </span>with brain metabolism in ASD has been found, but its role in Alzheimer’s disease suggests its exploration in ASD.</p>
<p>Mitochondrial dysfunction is one of the most common metabolic abnormalities in ASD [<a title="Frye RE. Mitochondrial dysfunction in autism spectrum disorder: unique abnormalities and targeted treatments. Semin Pediatr Neurol. 2020;35:100829." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR75" id="ref-link-section-d16158194e985" name="ref-link-section-d16158194e985">75</a>], and lactate and pyruvate are important biomarkers for mitochondrial energy metabolism [<a title="Boenzi S, Diodato D. Biomarkers for mitochondrial energy metabolism diseases. Essays Biochem. 2018;62:443–54." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR76" id="ref-link-section-d16158194e988" name="ref-link-section-d16158194e988">76</a>]. Many studies have shown that lactate dehydrogenase A (<i>LDHA</i>) and B (<i>LDHB</i>) are involved in ASD pathophysiology [<a title="Khemakhem AM, Frye RE, El-Ansary A, Al-Ayadhi L, Bacha AB. Novel biomarkers of metabolic dysfunction is autism spectrum disorder: potential for biological diagnostic markers. Metab Brain Dis. 2017;32:1983–97." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR77" id="ref-link-section-d16158194e997" name="ref-link-section-d16158194e997">77</a>,<a title="Correia C, Coutinho AM, Diogo L, Grazina M, Marques C, Miguel T, et al. Brief report: High frequency of biochemical markers for mitochondrial dysfunction in autism: no association with the mitochondrial aspartate/glutamate carrier SLC25A12 gene. J Autism Dev Disord. 2006;36:1137–40." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR78" id="ref-link-section-d16158194e997_1" name="ref-link-section-d16158194e997_1">78</a>,<a title="Ramirez-Celis A, Edmiston E, Schauer J, Vu T, Van de Water J. Peptides of neuron specific enolase as potential ASD biomarkers: from discovery to epitope mapping. Brain Behav Immun. 2020;84:200–8." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR79" id="ref-link-section-d16158194e997_2" name="ref-link-section-d16158194e997_2">79</a>,<a title="Ramirez-Celis A, Becker M, Nuño M, Schauer J, Aghaeepour N, Van de Water J. Risk assessment analysis for maternal autoantibody-related autism (MAR-ASD): a subtype of autism. Mol Psychiatry. 2021;26:1551–60." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR80" id="ref-link-section-d16158194e997_3" name="ref-link-section-d16158194e997_3">80</a>,<a title="Braunschweig D, Krakowiak P, Duncanson P, Boyce R, Hansen RL, Ashwood P, et al. Autism-specific maternal autoantibodies recognize critical proteins in developing brain. Transl Psychiatry. 2013;3:e277–7." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR81" id="ref-link-section-d16158194e1001" name="ref-link-section-d16158194e1001">81</a>].</p>
<p>Glucose fuels neuronal oxidative metabolism by providing ATP and the precursors required for neurotransmitter synthesis; glucose is also transported across the blood–brain barrier and into neurons by facilitative glucose transporters [<a title="Mergenthaler P, Lindauer U, Dienel GA, Meisel A. Sugar for the brain: the role of glucose in physiological and pathological brain function. Trends Neurosci. 2013;36:587–97." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR82" id="ref-link-section-d16158194e1008" name="ref-link-section-d16158194e1008">82</a>]. Glucose transporter-1 (GLUT-1) is predominantly found in the endothelial cells of the blood–brain barrier; GLUT-3 is the main transporter expressed in neurons [<a title="Vannucci SJ. Developmental expression of GLUT1 and GLUT3 glucose transporters in rat brain. J Neurochem. 1994;62:240–6." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR83" id="ref-link-section-d16158194e1011" name="ref-link-section-d16158194e1011">83</a>]. Increased mRNA levels of GLUT-1, GLUT-3, and three key enzymes in glucose metabolism (hexokinase 1, pyruvate kinase, and pyruvate dehydrogenase) have been observed in the contralateral brain area of a mouse model of traumatic brain injury (TBI) [<a title="Zhou J, Burns MP, Huynh L, Villapol S, Taub DD, Saavedra JM, et al. Temporal changes in cortical and hippocampal expression of genes important for brain glucose metabolism following controlled cortical impact injury in mice. Front Endocrinol. 2017;8:231." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR84" id="ref-link-section-d16158194e1014" name="ref-link-section-d16158194e1014">84</a>]. Additionally, increased expression of lactate transporter in astrocytes and reduced expression of neuronal MCT-2 has been observed in the ipsilateral cortex and hippocampus of the TBI mouse model, suggesting that sustained impairment of glucose metabolism after TBI is neuron-specific [<a title="Zhou J, Burns MP, Huynh L, Villapol S, Taub DD, Saavedra JM, et al. Temporal changes in cortical and hippocampal expression of genes important for brain glucose metabolism following controlled cortical impact injury in mice. Front Endocrinol. 2017;8:231." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR84" id="ref-link-section-d16158194e1017" name="ref-link-section-d16158194e1017">84</a>]. Neuronal<span> </span><i>GLUT-3</i>-deficient heterozygous mice demonstrated ASD-like features, and this phenotype was associated with increased GLUT-1 and MCT-2 concentrations suggesting that the neuronal glucose deficiency was compensated for enhanced uptake of lactate by the brain [<a title="Zhao Y, Fung C, Shin D, Shin BC, Thamotharan S, Sankar R, et al. Neuronal glucose transporter isoform 3 deficient mice demonstrate features of autism spectrum disorders. Mol Psychiatry. 2010;15:286–99." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR85" id="ref-link-section-d16158194e1024" name="ref-link-section-d16158194e1024">85</a>]. Despite this metabolic compensation, neuronal function was altered in<span> </span><i>GLUT-3</i>–heterozygous mice, as observed by increased electroencephalographic seizure activity, neurobehavioral abnormalities (i.e., abnormal spatial learning and working memory), and deficits in social behavior, all features observed in ASD [<a title="Zhao Y, Fung C, Shin D, Shin BC, Thamotharan S, Sankar R, et al. Neuronal glucose transporter isoform 3 deficient mice demonstrate features of autism spectrum disorders. Mol Psychiatry. 2010;15:286–99." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR85" id="ref-link-section-d16158194e1030" name="ref-link-section-d16158194e1030">85</a>,<span> </span><a title="Liu M, Chen Y, Sun M, Du Y, Bai Y, Lei G, et al. Auts2 regulated autism-like behavior, glucose metabolism and oxidative stress in mice. Exp Neurol. 2022;361:114298." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR86" id="ref-link-section-d16158194e1033" name="ref-link-section-d16158194e1033">86</a>]</p>
<p>In the adult CNS, cholesterol is derived through de novo synthesis by astrocytes [<a title="Orth M, Bellosta S. Cholesterol: its regulation and role in central nervous system disorders. Cholesterol. 2012;2012:292598." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR87" id="ref-link-section-d16158194e1039" name="ref-link-section-d16158194e1039">87</a>]. A major constituent of cholesterol catabolism is the neuronal enzyme cytochrome P450 family 46 subfamily A member 1 (<i>CYP46A1</i>), which protects neurons and helps convert cholesterol to 24-hydroxycholesterol (24 HC), enabling it to cross the blood-brain barrier [<a title="Pikuleva IA, Cartier N. Cholesterol hydroxylating cytochrome P450 46A1: from mechanisms of action to clinical applications. Front Aging Neurosci. 2021;13:696778." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR88" id="ref-link-section-d16158194e1045" name="ref-link-section-d16158194e1045">88</a>]. An indirect association of CYP46A1 has been shown in autistic children with high plasma levels of 24 HC [<a title="Grayaa S, Zerbinati C, Messedi M, HadjKacem I, Chtourou M, Ben Touhemi D, et al. Plasma oxysterol profiling in children reveals 24-hydroxycholesterol as a potential marker for Autism Spectrum Disorders. Biochimie. 2018;153:80–5." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR89" id="ref-link-section-d16158194e1048" name="ref-link-section-d16158194e1048">89</a>]. Moreover, 24 HC plasma levels have been inversely correlated with age in autistic individuals [<a title="Grayaa S, Zerbinati C, Messedi M, HadjKacem I, Chtourou M, Ben Touhemi D, et al. Plasma oxysterol profiling in children reveals 24-hydroxycholesterol as a potential marker for Autism Spectrum Disorders. Biochimie. 2018;153:80–5." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR89" id="ref-link-section-d16158194e1051" name="ref-link-section-d16158194e1051">89</a>].</p>
<p>The disrupted in Schizophrenia 1 (<i>DISC1</i>) gene is involved in neurodevelopmental processes, such as neuronal proliferation, differentiation, and migration [<a title="Bradshaw NJ, Porteous DJ. DISC1-binding proteins in neural development, signalling and schizophrenia. Neuropharmacology. 2012;62:1230–41." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR90" id="ref-link-section-d16158194e1060" name="ref-link-section-d16158194e1060">90</a>]. Prenatal disruption of<span> </span><i>DISC1</i><span> </span>in fetal neural progenitor cells of the dominant-negative<span> </span><i>DISC1</i><span> </span>(DN-DISC1) adult mice has been found to cause significant anxiety and depression-like behavioral changes [<a title="Deng D, Jian C, Lei L, Zhou Y, McSweeney C, Dong F, et al. A prenatal interruption of DISC1 function in the brain exhibits a lasting impact on adult behaviors, brain metabolism, and interneuron development. Oncotarget. 2017;8:84798–817." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR91" id="ref-link-section-d16158194e1069" name="ref-link-section-d16158194e1069">91</a>], elevated levels of GABA, and increased cell density of parvalbumin<sup>+</sup><span> </span>interneurons in the cingulate cortex, motor cortex, and the retrosplenial granular cortex [<a title="Deng D, Jian C, Lei L, Zhou Y, McSweeney C, Dong F, et al. A prenatal interruption of DISC1 function in the brain exhibits a lasting impact on adult behaviors, brain metabolism, and interneuron development. Oncotarget. 2017;8:84798–817." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR91" id="ref-link-section-d16158194e1075" name="ref-link-section-d16158194e1075">91</a>]. Alternatively, somatostatin<sup>+</sup><span> </span>and neuropeptide-Y<sup>+</sup><span> </span>interneurons were found to be decreased in other brain regions, suggesting that disrupting DISC1 function affects the localization of interneuron subtypes [<a title="Deng D, Jian C, Lei L, Zhou Y, McSweeney C, Dong F, et al. A prenatal interruption of DISC1 function in the brain exhibits a lasting impact on adult behaviors, brain metabolism, and interneuron development. Oncotarget. 2017;8:84798–817." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR91" id="ref-link-section-d16158194e1082" name="ref-link-section-d16158194e1082">91</a>]. Moreover, DN-DISC1 was found to interact with Dlx2 and negatively regulate Dlx2-mediated Wnt-signaling pathway activation [<a title="Deng D, Jian C, Lei L, Zhou Y, McSweeney C, Dong F, et al. A prenatal interruption of DISC1 function in the brain exhibits a lasting impact on adult behaviors, brain metabolism, and interneuron development. Oncotarget. 2017;8:84798–817." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR91" id="ref-link-section-d16158194e1085" name="ref-link-section-d16158194e1085">91</a>]. Knocking down<span> </span><i>DISC1</i><span> </span>and the expression of DN-DISC1 was found to decrease GLUT-4 mRNA and protein levels and reduce glucose uptake by primary astrocytes, which was associated with reduced oxidative phosphorylation, glycolysis, and lactate production in vitro and in vivo [<a title="Jouroukhin Y, Kageyama Y, Misheneva V, Shevelkin A, Andrabi S, Prandovszky E, et al. DISC1 regulates lactate metabolism in astrocytes: implications for psychiatric disorders. Transl Psychiatry. 2018;8:76–6." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR92" id="ref-link-section-d16158194e1092" name="ref-link-section-d16158194e1092">92</a>]. Moreover, treatment with lactate rescued the behavioral abnormalities in DN-DISC1 mice [<a title="Jouroukhin Y, Kageyama Y, Misheneva V, Shevelkin A, Andrabi S, Prandovszky E, et al. DISC1 regulates lactate metabolism in astrocytes: implications for psychiatric disorders. Transl Psychiatry. 2018;8:76–6." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR92" id="ref-link-section-d16158194e1095" name="ref-link-section-d16158194e1095">92</a>]. Thus, altered<span> </span><i>DISC1</i><span> </span>function in astrocytes contributes to metabolic abnormalities that might cause cognitive and behavioral deficits in various neuropsychiatric disorders [<a title="Jouroukhin Y, Kageyama Y, Misheneva V, Shevelkin A, Andrabi S, Prandovszky E, et al. DISC1 regulates lactate metabolism in astrocytes: implications for psychiatric disorders. Transl Psychiatry. 2018;8:76–6." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR92" id="ref-link-section-d16158194e1101" name="ref-link-section-d16158194e1101">92</a>]. In a recent study, deletion of<span> </span><i>AUTS2</i><span> </span>was found to impair social interactions, reduce uptake of brain glucose, and inhibit the pentose phosphate pathway in a conditional knockout mouse model with<span> </span><i>AUTS2</i><span> </span>deletion (<i>AUTS2</i>-cKO) [<a title="Liu M, Chen Y, Sun M, Du Y, Bai Y, Lei G, et al. Auts2 regulated autism-like behavior, glucose metabolism and oxidative stress in mice. Exp Neurol. 2022;361:114298." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR86" id="ref-link-section-d16158194e1114" name="ref-link-section-d16158194e1114">86</a>].</p>
<p>Obesity is a common risk factor associated with NDDs, such as ADHD and ASD [<a title="Wentz E, Björk A, Dahlgren J. Neurodevelopmental disorders are highly over-represented in children with obesity: a cross-sectional study. Obes (Silver Spring). 2017;25:178–84." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR93" id="ref-link-section-d16158194e1120" name="ref-link-section-d16158194e1120">93</a>,<span> </span><a title="Köse S, Yılmaz Kafalı H, Erkan İdris ZG, Şentürk Pilan B, Özbaran B, Erermiş S. The prevalence and risk factors for overweight/obesity among Turkish children with neurodevelopmental disorders. Res Develop Disab. 2021;114:103992" href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR94" id="ref-link-section-d16158194e1123" name="ref-link-section-d16158194e1123">94</a>]. The adolescent medial prefrontal cortex region is found to be vulnerable to high-fat diets (HFDs) via<span> </span><i>RELN</i><span> </span>deficiency [<a title="Labouesse MA, Lassalle O, Richetto J, Iafrati J, Weber-Stadlbauer U, Notter T, et al. Hypervulnerability of the adolescent prefrontal cortex to nutritional stress via reelin deficiency. Mol Psychiatry. 2017;22:961–71." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR95" id="ref-link-section-d16158194e1129" name="ref-link-section-d16158194e1129">95</a>].<span> </span><i>RELN</i><span> </span>acts through ApoER2 and very-low-density lipoprotein receptor (VLDLR) and plays an important role in cholesterol and fatty acid metabolism [<a title="Lane-Donovan C, Herz J. The ApoE receptors Vldlr and Apoer2 in central nervous system function and disease: thematic review series: ApoE and lipid homeostasis in Alzheimer’s Disease. J Lipid Res. 2017;58:1036–43." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR96" id="ref-link-section-d16158194e1136" name="ref-link-section-d16158194e1136">96</a>]. Hypothalamic levels of RELN protein and APoER2 and VLDLR mRNA were found to be altered in mice fed with HFD [<a title="Roberts BL, Bennett BJ, Bennett CM, Carroll JM, Dalbøge LS, Hall C, et al. Reelin is modulated by diet-induced obesity and has direct actions on arcuate proopiomelanocortin neurons. Mol Metab. 2019;26:18–29." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR97" id="ref-link-section-d16158194e1139" name="ref-link-section-d16158194e1139">97</a>]. Moreover, the recombinant central fragment of RELN affects membrane potential and action potential firing by altering pre- and postsynaptic inputs on the arcuate nucleus satiety-promoting proopiomelanocortin (ARH-POMC) neurons in a POMC-EGFP mouse model, thus suggesting the role of RELN in mediating energy homeostasis by acting on ARH-POMC neurons [<a title="Roberts BL, Bennett BJ, Bennett CM, Carroll JM, Dalbøge LS, Hall C, et al. Reelin is modulated by diet-induced obesity and has direct actions on arcuate proopiomelanocortin neurons. Mol Metab. 2019;26:18–29." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR97" id="ref-link-section-d16158194e1142" name="ref-link-section-d16158194e1142">97</a>].</p>
<p>The role of SHANK3 in synaptic function and development and its recognition as an important candidate gene in ASD has been well established [<a title="Uchino S, Waga C. SHANK3 as an autism spectrum disorder-associated gene. Brain Dev. 2013;35:106–10." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR98" id="ref-link-section-d16158194e1148" name="ref-link-section-d16158194e1148">98</a>], but that in cerebral metabolism has not been well studied. Increased rates of cerebral synthesis have been reported in several brain regions of the<span> </span><i>SHANK3-</i>KO mice, thus indicating high protein turnover [<a title="Torossian A, Saré RM, Loutaev I, Smith CB. Increased rates of cerebral protein synthesis in Shank3 knockout mice: Implications for a link between synaptic protein deficit and dysregulated protein synthesis in autism spectrum disorder/intellectual disability. Neurobiol Dis. 2021;148:105213." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR99" id="ref-link-section-d16158194e1154" name="ref-link-section-d16158194e1154">99</a>]. Moreover, increased pERK in hippocampal tissues, and reduced pERK/ERK and pmTOR/mTOR ratios in synaptosomal-enriched frontal cortex lysates suggested a loss of protein-synthesis regulation via these pathways [<a title="Torossian A, Saré RM, Loutaev I, Smith CB. Increased rates of cerebral protein synthesis in Shank3 knockout mice: Implications for a link between synaptic protein deficit and dysregulated protein synthesis in autism spectrum disorder/intellectual disability. Neurobiol Dis. 2021;148:105213." href="https://www.nature.com/articles/s41380-023-02060-9#ref-CR99" id="ref-link-section-d16158194e1157" name="ref-link-section-d16158194e1157">99</a>].</p>
<p>The heterogeneous and multifaceted pathological nature of ASDs clearly explains why the genes affecting brain metabolism are under-investigated. To refine the search for metabolic biomarkers in ASD, the effect of candidate genes involved in ASD must be explored in different metabolic pathways specifically affecting brain energy metabolism and neuron-astrocyte interactions. Identification of these metabolic alterations in the brain can provide an insight into the metabolic pathways disrupted in ASD and help target those pathways using the “neuroimaging genetics” approach.</p>
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<div class="c-article-section" id="Sec5-section"><h2 class="c-article-section__title js-section-title js-c-reading-companion-sections-item" id="Sec5">Role of imaging in detecting brain changes</h2>
<div class="c-article-section__content" id="Sec5-content"><p>Neuroimaging is vital to understanding the structure and functioning of the brain. In the field of ASD, most neuroimaging genetics studies are focused on structural and functional brain assessments. In this review article, we emphasize the imaging techniques used for monitoring changes in brain metabolism and neurotransmitter levels in individuals with ASD.</p>
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<p>FOR MORE INFORMATION PLEASE GO TO LINK:</p>
<p><a href="https://www.nature.com/articles/s41380-023-02060-9">https://www.nature.com/articles/s41380-023-02060-9</a></p>
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</div> Health care extension project enables community-based physicians to diagnose autism in young childrentag:templeilluminatus.ning.com,2023-04-18:6363372:Topic:36336282023-04-18T16:31:17.061ZMARGARIDA MARIA MADRUGAhttps://templeilluminatus.ning.com/profile/MARGARIDAMARIAMADRUGA
<h1 class="text-extra-large line-low my-2">Health care extension project enables community-based physicians to diagnose autism in young children</h1>
<p class="article-byline text-low">by<span> </span><a class="article-byline__link" href="http://www.missouri.edu/" rel="noopener" target="_blank">University of Missouri</a></p>
<div class="mt-4 article-main"><div class="article-gallery lightGallery"><div><img alt="autism" height="529" src="https://scx1.b-cdn.net/csz/news/800a/2023/autism.jpg" title="Credit: Pixabay/CC0 Public Domain" width="800"></img> Credit: Pixabay/CC0 Public Domain
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<p>As the number of children in…</p>
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<h1 class="text-extra-large line-low my-2">Health care extension project enables community-based physicians to diagnose autism in young children</h1>
<p class="article-byline text-low">by<span> </span><a class="article-byline__link" href="http://www.missouri.edu/" target="_blank" rel="noopener">University of Missouri</a></p>
<div class="mt-4 article-main"><div class="article-gallery lightGallery"><div><img src="https://scx1.b-cdn.net/csz/news/800a/2023/autism.jpg" alt="autism" title="Credit: Pixabay/CC0 Public Domain" width="800" height="529"/>
Credit: Pixabay/CC0 Public Domain<br />
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<p>As the number of children in need of access to timely evaluation and intervention for autism spectrum disorder (ASD) continues to rise, new research is showing how barriers to diagnoses and treatment can be reduced through an innovative training program first developed at the University of Missouri.</p>
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<p>ASD can be identified and diagnosed in<span> </span><a href="https://medicalxpress.com/tags/young+children/" rel="tag" class="textTag">young children</a><span> </span>by a well-trained clinician, and early diagnosis is vital to quickly establishing access to evidence-based therapies and interventions. However, long specialty center waitlists, distance, and cost often hinder<span> </span><a href="https://medicalxpress.com/tags/early+diagnosis/" rel="tag" class="textTag">early diagnosis</a>.</p>
<p>The Extension for Community Healthcare Outcomes (ECHO) Autism STAT model shows promise at eliminating these barriers. The program leverages the existing Project ECHO model to build the capacity of primary care physicians and clinicians to evaluate and diagnose children in local communities.</p>
<p>The University of Missouri's ECHO program uses video-conferencing technology to create learning communities that promote<span> </span><a href="https://medicalxpress.com/tags/best+practices/" rel="tag" class="textTag">best practices</a><span> </span>among primary care clinicians through case-based learning and guided practice. The ECHO Autism STAT model builds on the existing ECHO Autism framework by adding more intensive training elements specifically focused on the diagnostic assessment of young children.</p>
<p>"By adding to and using the skills of community-based primary care doctors and advanced practice providers, there exists the potential to drastically increase critical access to diagnostic assessment for ASD among children in underserved areas," said lead researcher Kristin Sohl, MD, professor, Department of Child Health at the University of Missouri School of Medicine and the founder of ECHO Autism.</p>
<p>"This accelerates the process for these children to receive the essential therapies and services, while allowing<span> </span><a href="https://medicalxpress.com/tags/autism/" rel="tag" class="textTag">autism</a><span> </span>specialty centers to focus on care for those with more complex diagnostic needs."</p>
<p>Through an evaluation of participants in the program, the researchers found that the ECHO Autism STAT primary care physician diagnoses were congruent with gold-standard evaluations completed at autism specialty centers. Likert scale surveys showed families were overwhelmingly pleased with their experiences and preferred to undergo diagnostic assessments in their<span> </span><a href="https://medicalxpress.com/tags/local+communities/" rel="tag" class="textTag">local communities</a><span> </span>with local doctors.</p>
<p>"These results support the ECHO Autism STAT model as an effective means to advance the skills of community doctors and strengthen their confidence to diagnose young children with obvious signs of autism," said Alexandra James, MD, assistant professor of clinical child health University of Missouri School of Medicine.</p>
<p>"Training and supporting primary care clinicians to diagnose ASD builds capacity and expertise in underserved areas, such as<span> </span><a href="https://medicalxpress.com/tags/rural+communities/" rel="tag" class="textTag">rural communities</a>, which in turn decreases wait times at specialty centers and speeds access to care."</p>
<p>The findings are published in the<span> </span><i>Journal of Developmental & Behavioral Pediatrics</i>.</p>
<div class="article-main__more p-4"><p><strong>More information:</strong><span> </span>Kristin Sohl et al, ECHO (Extension for Community Healthcare Outcomes) Autism STAT: A Diagnostic Accuracy Study of Community-Based Primary Care Diagnosis of Autism Spectrum Disorder,<span> </span><i>Journal of Developmental & Behavioral Pediatrics</i><span> </span>(2023).<span> </span><a href="https://dx.doi.org/10.1097/DBP.0000000000001172" target="_blank" rel="noopener">DOI: 10.1097/DBP.0000000000001172</a></p>
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<p>LINK: <a href="https://medicalxpress.com/news/2023-04-health-extension-enables-community-based-physicians.html">https://medicalxpress.com/news/2023-04-health-extension-enables-community-based-physicians.html</a></p>
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</div> Schizophrenia: mental illness or spiritual gift?tag:templeilluminatus.ning.com,2021-12-01:6363372:Topic:36068032021-12-01T23:08:04.106ZMARGARIDA MARIA MADRUGAhttps://templeilluminatus.ning.com/profile/MARGARIDAMARIAMADRUGA
<p><a href="https://www.yogitimes.com/article/schizophrenia-mental-illness-or-spiritual-gift">https://www.yogitimes.com/article/schizophrenia-mental-illness-or-spiritual-gift</a></p>
<p><a href="https://www.yogitimes.com/article/schizophrenia-mental-illness-or-spiritual-gift">https://www.yogitimes.com/article/schizophrenia-mental-illness-or-spiritual-gift</a></p> Multi-Personality Disorder and Channelingtag:templeilluminatus.ning.com,2021-10-03:6363372:Topic:36026512021-10-03T16:09:13.170ZMARGARIDA MARIA MADRUGAhttps://templeilluminatus.ning.com/profile/MARGARIDAMARIAMADRUGA
<p><a href="https://jdc.jefferson.edu/cgi/viewcontent.cgi?article=1292&context=jeffjpsychiatry">https://jdc.jefferson.edu/cgi/viewcontent.cgi?article=1292&context=jeffjpsychiatry</a></p>
<p><a href="https://jdc.jefferson.edu/cgi/viewcontent.cgi?article=1292&context=jeffjpsychiatry">https://jdc.jefferson.edu/cgi/viewcontent.cgi?article=1292&context=jeffjpsychiatry</a></p> Hallucinations or Spiritual Experiencestag:templeilluminatus.ning.com,2021-08-02:6363372:Topic:35996862021-08-02T17:50:04.336ZMARGARIDA MARIA MADRUGAhttps://templeilluminatus.ning.com/profile/MARGARIDAMARIAMADRUGA
<div class="articleHeader column"><h1 class="headline t53 font-weight-bold tm40">Hallucinations or spiritual experiences?</h1>
<h3 class="subtitle t20 font-weight-bold">When is a visit by your deceased uncle a spiritual experience, and when it is a mental illness? It’s not always obvious, one psychiatrist says.</h3>
<div class="meta"><div class="bylines"><div class="byline column"><div class="content"><address class="name"><span class="firstname">Ingrid P.</span><span> …</span></address>
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<div class="articleHeader column"><h1 class="headline t53 font-weight-bold tm40">Hallucinations or spiritual experiences?</h1>
<h3 class="subtitle t20 font-weight-bold">When is a visit by your deceased uncle a spiritual experience, and when it is a mental illness? It’s not always obvious, one psychiatrist says.</h3>
<div class="meta"><div class="bylines"><div class="byline column"><div class="content"><address class="name"><span class="firstname">Ingrid P.</span><span> </span><span class="lastname">Nuse</span></address>
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<div class="byline column"><div class="content"><address class="name"><span class="firstname">based on an article by</span><span> </span><span class="lastname">Ida Kvittingen</span></address>
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<div class="dates"><span class="dateGroup datePublished">Monday 03. October 2016 - 06:20</span></div>
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<div class="bodytext large-12 small-12"><p><span>Religious revelations and psychotic hallucinations are sometimes confusingly similar.</span></p>
<p>“The two can resemble each other. It’s difficult to separate out what contributes to the disease,” says psychiatrist Hilde Hanevik, who works at Jæren District Psychiatric Centre in southern Norway. She has just finished her doctorate, for which she interviewed 29 patients with psychotic disorders.</p>
<p>People with psychotic issues may see visions or hear voices. They experience hallucinations as so real that they are unable to distinguish between fantasy and reality.</p>
<p>It’s not uncommon for these experiences to have spiritual content. They can range from visits by the dead to contact with higher powers. Or the patient may believe that he is Jesus and omnipotent.</p>
<div class="column image large-4 small-12 floatRight"><img title="Psychiatrist Hilde Hanevik. (Photo: private)" alt="Psychiatrist Hilde Hanevik. (Photo: private)" src="https://image.sciencenorway.no/1438238.jpg?imageId=1438238&width=353&height=265"/>
Psychiatrist Hilde Hanevik. (Photo: private)<br />
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<p>The participants in the study have different types of psychoses, including schizophrenia and depression. They must meet a number of criteria to receive these diagnoses, but hallucinations are a symptom of several illnesses.</p>
<h5>Crop circles and reincarnation</h5>
<div class="column adnuntius-ad widthFull display-label"><div id="adn-00000000000c6146" class="adnuntius-ad-content"><span class="ad-label">ANNONSE</span></div>
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<p>Holy wars, crop circles, reincarnation, good and evil forces, meetings with ancestors and a personal relationship with a holy figure are just some of the incidents that patients report.</p>
<p>Many people without a mental disorder claim to have similar experiences. Some see the Virgin Mary, others find angel feathers in their couch.</p>
<p>Occurrences like these extend beyond religious ranks. A 1991 survey shows that twelve per cent of the Norwegian population report having contact with dead people. American and British studies suggest that up to half of grieving individuals experience contact with the deceased.</p>
<div class="column image large-4 small-12 floatRight"><img title="Social anthropologist Mona Kiil (Photo: private)" alt="Social anthropologist Mona Kiil (Photo: private)" src="https://image.sciencenorway.no/1438271.jpg?imageId=1438271&width=353&height=265"/>
Social anthropologist Mona Kiil (Photo: private)<br />
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<p>Hanevik refers to an American study that compared the beliefs of charismatic churches and psychosis patients and concluded that the content of their thoughts was about equally unusual.</p>
<p>One of the things that separate the two groups is how preoccupied psychosis patients become with those thoughts.</p>
<p>“The thoughts take over their world,” Hanevik says.</p>
<p>Whereas believers usually share their experiences with others, the psychotic patient remains isolated,” she says.</p>
<p>“The problem with psychosis is that no one else identifies with the perception of reality you have. The sense experiences lead a psychotic person to create their own very private world,” she adds.</p>
<h5>Uncomfortable exploration</h5>
<p>But Hanevik believes that psychotic patients must be allowed to have a spiritual life, too.</p>
<p>She wants the health care system to dare to explore the distinction between faith and illness, and admits that “we may have been a little uncomfortable with this”.</p>
<p>She is the daughter of a priest and attends church, and is open to the idea that spiritual experiences can be real.</p>
<p>But since it’s impossible to ascertain whether God exists or whether relatives can continue to make visitations after they’ve died, the psychiatrist is trying another approach.</p>
<p>Hanevik is more interested in what function the experiences have for patients.</p>
<p>Can faith help them through difficult times or does it contribute to them becoming even sicker?</p>
<div class="column adnuntius-ad widthFull display-label"><div id="adn-00000000000c6147" class="adnuntius-ad-content"><span class="ad-label">ANNONSE</span></div>
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<p>Like healthy believers, several of the patients in the study say that the events are important to them.</p>
<p>“Feeling God’s presence, or the presence of whatever you feel is sacred, can give you meaning, support and confidence in life,” she says.</p>
<p>This is the experience of Betty, a participant in the study. She feels that she finally gets to rest in the arms of God after being plagued by depression and hallucinations and lying in bed sleepless.</p>
<h5>Thinks he's Jesus</h5>
<p>Not everyone in the study was religious to begin with. But it can be comforting for patients to put their hallucinations into a religious framework. It can also help them understand their mystical, confusing and sometimes frightening experiences. God can be a companion through a difficult illness.</p>
<p>The psychosis itself also appropriates religious elements.</p>
<p>Elmer believes he is closer to God than most people. He believes he is God's son, although he has never had a Bible, and doesn’t know what Jesus did.</p>
<p>"I can’t walk around and think that I’m Jesus without getting signs,” he says and tells about one of them:</p>
<p>"It began to burn something fierce. I took my hand and put it on top [of the fire] and it hurt like heck, you know, but I just kept it there until all the flames died down and then I looked at my hand afterwards – no burn marks! Try to explain that! It’s impossible to explain. "</p>
<p>Experiences like those Elmer describes can be both good and bad for patients, says Hanevik.</p>
<p>Elmer feels they’ve saved him. "If I hadn’t had this belief (of being Jesus), I would have killed myself," he says.</p>
<p>Believing that he has supernatural abilities can give Elmer a sense of control in his life. Maybe he likes the ideas of being a powerful, important person for the very reason that as a human being he feels the opposite, that he has no power or value.</p>
<p>“At the same time, that notion becomes an escape from reality and isolates him even more from other people,” says Hanevik.</p>
<h5>Dangerous convictions</h5>
<p>Several of the patients that Hanevik interviewed use faith to cope with their psychosis.</p>
<p>But belief in higher powers can also be dangerous for them. Voices and visions do not always have good intentions. Evil spirits can bring messages for a patient to harm himself or others.</p>
<p>This happened to Hans. "I can see that I’ve been drawn to dark forces... I believe so strongly that there are outside forces, and I’ve heard voices, good and evil ones, and I’ve seen some kinds of shapes. There’s a lot that’s so intense... ," he says.</p>
<p>Danny believes that Jesus is an astronaut who will pick him up if he tries to commit suicide by jumping from a bridge.</p>
<p>And although Elmer thinks it’s a lifesaver to be Jesus, Hanevik sees that it doesn’t help him integrate back into society.</p>
<p>She has treated psychotic patients over several years and found this to be an advantage when she was interviewing patients. It can be tricky business to follow the logic of a twisted view of reality.</p>
<h5>Can get even sicker</h5>
<p>One-third of schizophrenia patients will never be cured of the illness, which is one of the psychoses Hanevik has studied.</p>
<p>Some psychiatrists believe that focusing on the content of the psychosis can make patients sicker. Hanevik belongs to a tradition that believes exploring experiences can help patients sort out the ideas whirling in their heads.</p>
<p>Some studies show that patients with religious delusions are sicker than other psychotic patients. They may find it difficult to accept that they’re sick, because they’re convinced that their experiences are religious.</p>
<p>Yet Hanevik thinks it’s wrong to categorize all visions and voices as evidence of delusions,. Some experiences can be part of a healthy faith life.</p>
<p>Conversely, patients who do consider themselves religious don’t necessarily interpret their hallucinations as religious experiences.</p>
<p>If they do, they may run into problems with their faith. When vexing hallucinations are related to God, religion can turn into something negative. Then God is not longer a safe haven.</p>
<p>Ingrid had a good relationship with God before she began to feel that he was after her. The voice she heard and believed was God’s, changed from caring to uncomfortable and judgmental.</p>
<p>“This led to her losing her faith,” says Hanevik. She believes that religion can also affect people negatively. “But I don’t think any religion has a God who wants believers to make fools of themselves.</p>
<h5>Tradition or illness?</h5>
<p>Some of the patients that Hanevik talked to are afraid to talk about their faith because they fear that it will always be seen in light of their illness.</p>
<p>Social anthropologist Mona Kiil interviewed patients for her doctoral thesis who have mental disorders but are not psychotic. These individuals share the same concerns.</p>
<p>They believe in healing through rituals and that they can see the dead. And they’re afraid that psychologists will classify these experiences as signs of psychosis,” explains Kiil.</p>
<p>She thinks it’s all about what society regards as inside and outside of social boundaries.</p>
<p>“When you live in a community where this is part of the worldview, faith provides security for people. That isn’t psychosis. But faith can become a double-edged sword if it prevents them from participating in society,” says Kiil, who is doing her doctoral work at UiT - The Arctic University of Norway.</p>
<p>She encourages health care clinicians in to explore patients’ cultural backgrounds, to go into their stories and not categorize something as sick simply because they’ve never heard of it before.</p>
<p>But patients can also use religion as a drug, says Kiil. It's not necessarily healthy to numb the pain instead of dealing with the problems.</p>
<p>“People have a need to cling to something when things get difficult,” she says.</p>
<p>Hanevik agrees, but thinks that religion becomes more of a way to explain their experiences for patients with psychosis.</p>
<h5>Normal religiosity</h5>
<p>Kiil and Hanevik agree, however, that it is particularly difficult to separate religion from illness when the patient has a psychosis.</p>
<p>UiT ethnography professor Jens Ivar Nergård researched how young psychotic patients in Sweden built up their alternative reality understanding.</p>
<p>He found that a narrow interpretation of what is real in psychiatry poses a challenge for patients. Then they find support in understanding themselves in a religious space. But if you are psychotic and think you’re Jesus, you lose the possibility to be human. You take on religion to throw yourself out of the world.</p>
<p>Nergård thinks Hanevik offers an exciting contribution to the discussion of what can be considered normal religiosity and believes that healthcare professionals should think through questions like this.</p>
<p>“The boundaries between psychosis and religion may not be something they think about everyday,” he says.</p>
</div> How to raise an adult with special needstag:templeilluminatus.ning.com,2021-05-31:6363372:Topic:35959902021-05-31T23:37:46.904ZMARGARIDA MARIA MADRUGAhttps://templeilluminatus.ning.com/profile/MARGARIDAMARIAMADRUGA
<div class="post-meta"><p><span class="date updated">March 20, 2019</span><span> </span><span class="vcard author"><span class="author fn">| Posted by<span> </span><a href="https://www.especialneeds.com/blog/author/katherine-blanner/" rel="author" title="Posts by Katherine Blanner">Katherine Blanner</a></span></span></p>
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<div class="featured-thumbnail"><img alt="" class="attachment-post-thumbnail size-post-thumbnail wp-post-image" height="315" src="https://www.especialneeds.com/blog/wp-content/uploads/2019/03/raising-an-adult-with-special-needs.png" width="560"></img></div>
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<div class="featured-thumbnail"><p>There is a lot of information about…</p>
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<div class="post-meta"><p><span class="date updated">March 20, 2019</span><span> </span><span class="vcard author"><span class="author fn">| Posted by<span> </span><a href="https://www.especialneeds.com/blog/author/katherine-blanner/" title="Posts by Katherine Blanner" rel="author">Katherine Blanner</a></span></span></p>
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<div class="featured-thumbnail"><img width="560" height="315" src="https://www.especialneeds.com/blog/wp-content/uploads/2019/03/raising-an-adult-with-special-needs.png" class="attachment-post-thumbnail size-post-thumbnail wp-post-image" alt=""/></div>
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<div class="featured-thumbnail"><p>There is a lot of information about school-aged individuals with special needs. From IEPs to fun toys and adaptive equipment, there’s plenty of readily available support. However, things can be tougher once your kiddo is not so little anymore.</p>
<h2>Encourage independence when they’re young</h2>
<p>Yes, we talk about how crucial independence is all the time. But in all seriousness, allowing your child to make mistakes under your supervision while they’re younger can encourage self-soothing, problem-solving skills, and independence. Allowing your child to harness their personal and practical life skills encourages them to grow as an individual.</p>
<p>The fact of the matter is that you will not always be there for them, and that doesn’t have to be a bad or scary thing. It’s important to be a warrior for your child, but it might be just as important to allow them to experience success and failure for themselves.</p>
<p>Understanding that there are aspects of your child’s life that are out of your control is an imperative step to beginning to transition your special needs kiddo into adulthood and make the experience a little bit easier for them.</p>
<p>Look at options for programs where your child can go to interact with other kids. There are day programs, respite, camps, etc. A respite program will do wonders, not just for building independence for the child, but for the family as well. While most families are concerned that their child may not do well or be upset or scared, in most cases, it is the parents who are scared… not the child. The staff at these facilities are trained to work with all individuals with special needs and have plans in place to work with all behaviors. This is their job so let them do what to do best.</p>
<p>Here’s a secret: most children with developmental and physical disabilities are much the same or normal developing kids and the fact is, they do not always want to hang out with their parents. It’s not cool! They strive or desire as much independence as possible to allow them as much freedom as possible while keeping in mind issues which prevent them from achieving this but give them as much as is safe.</p>
<h2>Plan ahead</h2>
<p>Whether we like it or not, the unfortunate side effect of living is aging. Unfortunately, the entire plot of Peter Pan is not a reality, and your kiddo is going to grow up. This can be especially difficult for individuals with special needs. Thinking ahead to their adulthood can be a great tactic to alleviating stress and subsequent confusion that comes with parenting an adult with special needs.</p>
<p>It is recommended at age 17, before they become a legal adult at 18, to seek out legal guardianship if this is needed. The process can take some time to complete and you want to have everything in place and scheduled with the courts prior to their 18<sup>th</sup><span> </span>birthday</p>
<p>Before your child turns 18 and therefore becomes a legal adult, be sure to consider seeking legal guardianship. If your child is intellectually and/or physically disabled to the point where they require your care, it may be a good idea to seek guardianship of them when they are over the age of 18. According to<span> </span><a href="https://www.parentingnh.com/September-2014/My-child-with-a-disability-is-an-adult-now-what/">Parenting New Hampshire’s</a><span> </span>blog, “To obtain guardianship, the parent or other third person must file a petition with the probate court in the county where the child resides.”</p>
<h2>Do your homework</h2>
<p>When your child is about to age out of the school system, consider having a conversation with professionals. Whether it’s your occupational therapist, special education teacher, or even pediatrician, where they think that the best place for your child would be after graduation. Depending on your state and school district the age of graduation can be 18 or 21. And in most cases, the amount of available resources for adults is far less than for children creating a bottleneck of available resources for families.</p>
<p>If you are looking at a day program for your child, you should plan to start researching and applying for the wait list at least two years in advance and apply at several different locations.</p>
<p>If looking at work opportunities through an agency or workshop, speak with the school’s transition facilitator on upcoming transition workshops they may have available or agencies that offer such programs. All of these can make the transition from high school to an adult program.</p>
<p>Of course, take all the information that is given to you with an objective eye and a grain of salt. Professionals in the special needs field in your community will probably provide the greatest insights and connections, and if they have been working with your kiddo for a long time, you may have similar insights as to what may be best for your child.</p>
<p>That being said, you know your child best. It’s best to take the guidance of professionals and your own personal experience with your kiddo into account when decision making.</p>
<p>There is no such things as too much information when it comes to making a decision, so being well educated and informed on the matters of your child’s life after school can be a great way to help them transition into adulthood. Find day programs or jobs that will be fulfilling for your loved one.</p>
<h2>Learn to transition yourself</h2>
<p>One of the things that some parents forget is that their children will not always be young. It’s tough to stop time, and as of right now it’s impossible. Your kiddo will grow older. Learning how they can be more independent and self-sufficient can make you feel unneeded. Sometimes, when your kiddo grows up, you have to transition yourself into a new phase of life. Take up gardening, do some yoga, learn how to make sushi!</p>
<p>This will much harder for the family then it will be on the child. Families that have dedicated their lives to their child sometimes find they have to give up certain things or interests for the greater good. When you find you have more time available, it will take a bit of adjustment.</p>
<h2>It takes time</h2>
<p>Transitioning a special needs adult into “adulting” is much easier said than done. Just remember to be patient and acknowledge that these things take time.</p>
<p>Always remember that you as the parent or caregiver will always be the strongest advocate for your child, so always be advocating for them. Just like the proverb ‘squeaky wheel gets the oil”, you will need to advocate and push to get what is needed. Not because people do not care but because everyone is busy.</p>
<p>Any of these transitions will require a fair amount of planning and meetings to ensure a proper transition. You will need to follow up with everyone to make sure meetings are scheduled, documents have been sent, contracts have been signed and scripts/doctor’s notes have been submitted. This includes coordinating with your support coordinator for the state, any therapists, the agencies you are pursuing just to start. Everyone is working towards the same goal for your child which is to make sure they are happy, prosperous and independent in life.</p>
<h3>Article content contributions from Scott Kouri.</h3>
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<p>LINK: <a href="https://www.especialneeds.com/blog/raise-adult-special-needs/">https://www.especialneeds.com/blog/raise-adult-special-needs/</a></p>
</div> Is Mania a Spiritual Experience?tag:templeilluminatus.ning.com,2021-05-31:6363372:Topic:35957092021-05-31T16:40:14.252ZMARGARIDA MARIA MADRUGAhttps://templeilluminatus.ning.com/profile/MARGARIDAMARIAMADRUGA
<div class="et_post_meta_wrapper"><h1 class="entry-title">Is Mania a Spiritual Experience?</h1>
<img alt="Is Mania a Spiritual Experience?" class=" lazyloaded" height="675" src="https://ibpf.org/wp-content/uploads/2016/09/bipolar-mania-and-spirituality.jpg" width="1080"></img></div>
<div class="entry-content"><p>I was eighteen years old when I first experienced acute manic psychosis. I had just arrived at the University of Georgia for my freshman fall semester when I suddenly had what seemed like a profound spiritual awakening. I felt as if I was waking up from a bad dream, as if my mind and body were merely figments of my imagination. I felt an incredible…</p>
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<div class="et_post_meta_wrapper"><h1 class="entry-title">Is Mania a Spiritual Experience?</h1>
<img alt="Is Mania a Spiritual Experience?" width="1080" height="675" class=" lazyloaded" src="https://ibpf.org/wp-content/uploads/2016/09/bipolar-mania-and-spirituality.jpg"/></div>
<div class="entry-content"><p>I was eighteen years old when I first experienced acute manic psychosis. I had just arrived at the University of Georgia for my freshman fall semester when I suddenly had what seemed like a profound spiritual awakening. I felt as if I was waking up from a bad dream, as if my mind and body were merely figments of my imagination. I felt an incredible transcendence and oneness with the universe, an experience I could only fathom to be spiritual. Back then, I didn’t know anything about bipolar disorder. </p>
<p>My first thought upon being struck with this overwhelmingly blissful state was, “This is what God feels like; I must be Jesus!” It was from there that I began my deluded descent into madness. I ran upstairs in my dormitory, assuming that my friends would be my first disciples, and tried to perform miracles to prove my divinity. When they attempted to calm me down, I punched one of them in the face, calling him the devil, and ran back downstairs. Campus police promptly met me in the dorm lobby and arrested me on the spot. </p>
<p>On my way to jail, I was no longer feeling so ecstatic. In fact, it was the most excruciating fear I had ever experienced. I began believing that the police officers were the Pharisees taking me to my crucifixion. They placed me in my own jail cell, and I began stripping off my clothes, demanding for the officers to come look at my naked body. Throughout the whole experience, I felt almost completely dissociated, as if I was watching a movie of myself with little to no control of the actor. </p>
<p>After a few days of trying to convince my parents that I was returning humanity to the Garden of Eden, they realized my condition might not be from taking psychedelic drugs as they had thought. I was escorted to my local psychiatric hospital, and once medicated, came down from my messianic mission to create heaven on earth. The only problem was, I had never been more certain of God in my life, and the clinicians just kept telling me that it was normal for grandiose delusions to take on religious and spiritual themes. I was not convinced. </p>
<p>My thoughts immediately went to the biblical stories I grew up with: how God tested Abraham’s faith when he was told to sacrifice his son, and how God communicated to Moses through a burning bush. Were these not examples of delusions and hallucinations? Even Jesus was convinced to be the Son of God. Were the holy men of the Bible bipolar? I had a lot of questions, and my questions seemed to be forcing me to choose one side or the other—either spirituality or psychiatry.</p>
<p>It took me about a decade to finally integrate both truths and find some peace around my manic episodes. I studied spirituality and psychology, and I came to the conclusion that bipolar disorder and spiritual experiences didn’t need to exist in opposition. I’ve come to some basic definition of spirituality as the transcendence of ego. In this sense, mania was indeed a spiritual experience, albeit an unmanageable one. This didn’t mean my bipolar diagnosis was bogus, and I’m not saying all psychotic episodes are spiritual. But I can now rest easy knowing that my experiences were both spiritual and bipolar. </p>
<p>If I’m honest with myself, a major sign of my mania is increased spirituality, but at the same time, a major sign of my depression is a lack of spiritual significance. Finding balance in recovery means that I am able to seek both spiritual and clinical solutions to my bipolar symptoms without fear that I am falling out of grace with God. When I was first diagnosed, I had the idea that either bipolar existed or God existed. There was no space for both. </p>
<p>My spirituality has necessarily evolved over the years. Because of my history with manic psychosis, I have to guard myself against dogmatic or superstitious beliefs. I try my best to live a life of love, and I rest assured knowing that the more kindness I spread to the world, the more aligned I am with my spiritual path. Telling my story of recovery has become part of this spiritual process. My faith means a great deal to my health, and without it, my recovery wouldn’t be as strong as it is today. I hope that by sharing my story, others going through the same difficulties might not take so long to make sense of their own experiences. </p>
<p><em>Chris Cole is the author of </em><a href="http://www.amazon.com/Body-Chris-Obsession-Addiction-Madness/dp/1941758142/" target="_blank" rel="noopener">The Body of Chris: A Memoir of Obsession, Addiction, and Madness</a><em>, and he’s a </em><a href="http://colecoaching.com/" target="_blank" rel="noopener"><em>life coach</em></a><em> for people in recovery.<br/><br/></em>Source: <a href="https://ibpf.org/is-mania-a-spiritual-experience/">https://ibpf.org/is-mania-a-spiritual-experience/</a></p>
</div> Religion, Spirituality, and Schizophrenia: A Reviewtag:templeilluminatus.ning.com,2021-05-01:6363372:Topic:35938932021-05-01T20:03:51.939ZMARGARIDA MARIA MADRUGAhttps://templeilluminatus.ning.com/profile/MARGARIDAMARIAMADRUGA
<div class="fm-sec half_rhythm no_top_margin"><h1 class="content-title">Religion, Spirituality, and Schizophrenia: A Review</h1>
<div class="half_rhythm"><div class="contrib-group fm-author"><a class="affpopup" href="https://www.ncbi.nlm.nih.gov/pubmed/?term=Grover%20S%5BAuthor%5D&cauthor=true&cauthor_uid=24860209">Sandeep Grover</a>,<span> …</span></div>
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<div class="fm-sec half_rhythm no_top_margin"><h1 class="content-title">Religion, Spirituality, and Schizophrenia: A Review</h1>
<div class="half_rhythm"><div class="contrib-group fm-author"><a href="https://www.ncbi.nlm.nih.gov/pubmed/?term=Grover%20S%5BAuthor%5D&cauthor=true&cauthor_uid=24860209" class="affpopup">Sandeep Grover</a>,<span> </span><a href="https://www.ncbi.nlm.nih.gov/pubmed/?term=Davuluri%20T%5BAuthor%5D&cauthor=true&cauthor_uid=24860209" class="affpopup">Triveni Davuluri</a>,<span> </span>and<span> </span><a href="https://www.ncbi.nlm.nih.gov/pubmed/?term=Chakrabarti%20S%5BAuthor%5D&cauthor=true&cauthor_uid=24860209" class="affpopup">Subho Chakrabarti</a></div>
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<div id="pmclinksbox" class="links-box whole_rhythm"><div class="fm-panel"><div>This article has been<span> </span><a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/citedby/">cited by</a><span> </span>other articles in PMC.</div>
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<div id="idm139903052892992" lang="en" class="tsec sec" xml:lang="en"><div class="goto jig-ncbiinpagenav-goto-container"><span><a class="tgt_dark page-toc-label jig-ncbiinpagenav-goto-heading" href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#" title="Go to other sections in this page">Go to:</a></span></div>
<h2 class="head no_bottom_margin ui-helper-clearfix" id="idm139903052892992title">Abstract</h2>
<div><p id="__p1" class="p p-first-last">Religion and spirituality exert a significant role in the lives of many individuals, including people with schizophrenia. However, the contribution of religion and spirituality to various domains (psychopathology, explanatory models, treatment seeking, treatment adherence, outcome, etc.) has not received much attention. In this article, we review the exiting data with regards to the relationship of religion, spirituality, and various domains in patients with schizophrenia. Available evidence suggests that for some patients, religion instills hope, purpose, and meaning in their lives, whereas for others, it induces spiritual despair. Patients with schizophrenia also exhibit religious delusions and hallucinations. Further, there is some evidence to suggest that religion influences the level of psychopathology. Religion and religious practices also influence social integration, risk of suicide attempts, and substance use. Religion and spirituality also serves as an effective method of coping with the illness. Religion also influences the treatment compliance and outcome in patients with schizophrenia.</p>
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<div class="sec"><strong class="kwd-title">Keywords:<span> </span></strong><span class="kwd-text"><em>Religion</em>,<span> </span><em>schizophrenia</em>,<span> </span><em>spirituality</em></span></div>
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<div id="sec1-1" class="tsec sec"><div class="goto jig-ncbiinpagenav-goto-container"><a class="tgt_dark page-toc-label jig-ncbiinpagenav-goto-heading" href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#" title="Go to other sections in this page">Go to:</a></div>
<h2 class="head no_bottom_margin ui-helper-clearfix" id="sec1-1title">INTRODUCTION</h2>
<p id="__p2" class="p p-first">Schizophrenia is often a chronic, disabling condition, associated with impairments in multiple domains of functioning. The usual treatment of schizophrenia is based on the biopsychosocial model, and involves the prescription of antipsychotic medications and psychological interventions for the patients and family intervention.[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref1" class=" bibr popnode">1</a>] This model of schizophrenia does not take into account the religious beliefs of the patient. However, religion and spirituality exert a significant role in the lives of people with schizophrenia. Keeping this in mind, the present review aims to evaluate the relationship of religion, spirituality, and schizophrenia.</p>
<p id="__p3" class="p">For this review, electronic searches were conducted using PubMed, Science Direct, and Google Scholar. The search terms used were schizophrenia, religion, religiosity, religious practices, and spirituality. These terms were used in different combinations and all the relevant articles were identified. Articles which assessed various aspects of religion in relation to schizophrenia were included. However, we did not include the articles that assessed religion and caregivers of patients with schizophrenia.</p>
<div id="sec2-1" class="sec"><h3 id="sec2-1title">Religiousness/religious practices among patients with schizophrenia</h3>
<p id="__p4" class="p p-first-last">Studies have evaluated religious practices among patients with schizophrenia. A study from Switzerland suggested that about one-third of the patients with schizophrenia are very highly involved in religious community. Another 10% of the patients in same study were involved in minority religious movements.[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref2" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271885" name="__tag_378271885">2</a>] Another study from the same country reported that one-third of the patients were highly involved in a religious community, and another one third considered that spirituality had significant role in their life and they carried out spiritual practices every day, without getting involved in a religious community.[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref3" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271877" name="__tag_378271877">3</a>] Studies from other parts of the world which have assessed the religious practices of psychiatrically ill patients suggest that these are common in Europe[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref4" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271832" name="__tag_378271832">4</a>,<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref5" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271869" name="__tag_378271869">5</a>] and North America.[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref6" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271853" name="__tag_378271853">6</a>,<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref7" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271864" name="__tag_378271864">7</a>] A study found that as high as 91% of patients reported indulging in private religious or spiritual activities and 68% reported participation in public religious services or activities.[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref8" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271846" name="__tag_378271846">8</a>] Some studies which have compared religious practices in patients with schizophrenia and in the general population suggest that religious involvement is higher among patients,[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref9" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271881" name="__tag_378271881">9</a>] whereas others suggest that religious attendance is less in patients of schizophrenia.[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref10" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271849" name="__tag_378271849">10</a>]</p>
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<div id="sec2-2" class="sec"><h3 id="sec2-2title">Religion and psychopathology</h3>
<p id="__p5" class="p p-first">Among the various aspects of religion and spirituality, the influence of religion and spirituality on psychopathology has been one of the most explored areas of research. Broadly speaking, delusions and hallucinations of religious nature are further categorized as those with religious and supernatural themes.[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref11" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271830" name="__tag_378271830">11</a>] The religious delusions and hallucinations have a direct reference to organized religious themes (e.g., prayer, sin, possession) or religious figures (e.g., God, Jesus, devil, Prophet). The supernatural delusions and hallucinations have more general mystic references (e.g., black magic, spirits, demons, being bewitched, mythical forces, ghosts, sorcery, and voodoo).[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref11" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271897" name="__tag_378271897">11</a>] However, in the literature, delusions and hallucinations of either type are usually referred to as religious delusions.</p>
<p id="__p6">Studies conducted among inpatients of schizophrenia suggest that the prevalence of religious delusions and hallucinations varies from country to country and the prevalence rates of the same vary from 6 to 63.3%.[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref12" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271829" name="__tag_378271829">12</a>,<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref13" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271919" name="__tag_378271919">13</a>,<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref14" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271930" name="__tag_378271930">14</a>,<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref15" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271937" name="__tag_378271937">15</a>,<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref16" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271837" name="__tag_378271837">16</a>] Studies which have compared religious delusions across different countries suggest that religious delusions are more common in Germany compared to Japan.[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref13" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271882" name="__tag_378271882">13</a>]</p>
<p id="__p7">Studies which have evaluated the delusional themes of various religious/spiritual delusions report that the common themes are that of persecution (by malevolent spiritual entities), influence (being controlled by spiritual entities), and self-significance (delusions of sin/guilt or grandiose delusions).[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref17" class=" bibr popnode">17</a>,<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref18" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271900" name="__tag_378271900">18</a>] Studies also suggest that when the non-content dimensions (conviction, pervasiveness, preoccupation, action, inaction, and negative affect) of different types of delusions (persecutory, body/mind control, grandiose, thought broadcasting, religious, guilt, somatic, influence on others, jealousy, and other) are compared, findings suggest that religious delusions are held with more conviction and pervasiveness than other delusions.[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref12" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271907" name="__tag_378271907">12</a>] Data also suggest that patients with religious/spiritual delusions value religion as much as those without these types of delusions, but patients presenting delusions with religious content report receiving less support from religious communities.[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref18" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271942" name="__tag_378271942">18</a>]</p>
<p id="__p8">Studies which have evaluated the religion in the context of psychopathology suggest that Christian patients have more religious delusions, especially delusions of guilt and sin, than their counterparts belonging to other religions (Islam).[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref11" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271903" name="__tag_378271903">11</a>] Other studies have shown that compared to Christians, Buddhists have a lower frequency of religious themed delusions[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref19" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271873" name="__tag_378271873">19</a>] and that protestants experience more religious delusions than Catholics and those without religious affiliations.[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref20" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271879" name="__tag_378271879">20</a>] Another study reported higher prevalence of religious delusions of guilt in schizophrenia patients of Roman Catholic affiliations, when compared to Protestants and Muslims.[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref21" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271828" name="__tag_378271828">21</a>] Cross-cultural studies which have compared people from different ethnic backgrounds suggest that in case of paranoid delusions, Christian patients more often report persecutors to be supernatural beings, compared to Muslims and Buddhists patients.[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref21" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271852" name="__tag_378271852">21</a>] Other studies suggest that religious and supernatural themes in delusions are more common in Korean patients than Korean-Chinese patients or Chinese patients.[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref22" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271914" name="__tag_378271914">22</a>]</p>
<p id="__p9">Greenberg and Brom[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref23" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271835" name="__tag_378271835">23</a>] investigated hallucinations of patients belonging to Judaism and reported that hallucinations occurred more frequently during the night and this was linked to beliefs of the patients that they were more susceptible to evil spirits and demons at the night time. Peters<span> </span><em>et al</em>.[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref24" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271874" name="__tag_378271874">24</a>] compared patients belonging to Hinduism (Hare Krishna followers), Christianity, and New Religious Movements with those of non-religious groups and found that patients from New Religious Movements scored higher on delusional measures than the other two groups. Other studies suggest that compared to the patients from Saudi Arabia, patients from the United Kingdom more clearly hear the religious-based auditory hallucinations.[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref25" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271910" name="__tag_378271910">25</a>]</p>
<p id="__p10">With regards to the relationship between religiosity and presence of religious delusions and hallucinations, findings are contradictory with some studies suggesting higher prevalence of religious delusions and hallucinations in those with higher religiosity[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref26" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271875" name="__tag_378271875">26</a>] and others suggesting lack of relationship between the two.[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref16" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271857" name="__tag_378271857">16</a>]</p>
<p id="__p11">With regard to socio-demographic variables, reports suggest that the religious content of delusions is related to the marital status and education of schizophrenic patients.[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref16" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271865" name="__tag_378271865">16</a>] Occasional studies suggest a relationship between religious delusions and cognitive deficits.[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref27" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271847" name="__tag_378271847">27</a>]</p>
<p id="__p12">Religious delusions influence help seeking, treatment, and outcome. Evidence suggests that those with religious delusions take longer to establish service contact,[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref28" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271904" name="__tag_378271904">28</a>,<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref29" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271836" name="__tag_378271836">29</a>] receive more medications, have overall higher symptom scores, and have poorer functioning.[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref28" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271891" name="__tag_378271891">28</a>] Those with religious delusion/hallucination are more likely to receive magico-religious healing, are not satisfied with psychiatric treatment,[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref26" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271845" name="__tag_378271845">26</a>] and are more likely not to adhere to psychiatric treatment.[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref27" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271936" name="__tag_378271936">27</a>] Evidence also suggests that those with religious delusions have poor outcome[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref30" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271913" name="__tag_378271913">30</a>,<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref31" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271889" name="__tag_378271889">31</a>] and more frequently indulge in violence[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref32" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271868" name="__tag_378271868">32</a>,<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref33" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271940" name="__tag_378271940">33</a>] and self-harm.[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref34" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271843" name="__tag_378271843">34</a>,<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref35" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271863" name="__tag_378271863">35</a>,<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref36" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271883" name="__tag_378271883">36</a>] Some authors suggest that religious delusions can influence the health beliefs models and consequently lead to poor treatment compliance.[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref37" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271854" name="__tag_378271854">37</a>]</p>
<p id="__p13">In a review of 70 studies, the authors evaluated the relationship between religion, supernatural beliefs, and psychopathology.[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref11" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271844" name="__tag_378271844">11</a>] The authors reported that 30 out of the 70 studies (43%) have found a relationship between delusions and hallucinations, and religion and the supernatural beliefs. Majority of the studies (27 of 30 studies) directly described religious delusions, of which 20 studies described delusions to be of a religion-based nature and 14 considered delusions to be of supernatural nature. Thirteen studies reported on religious hallucinations, with 11 having religious content and 9 finding more supernatural content.[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref11" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271926" name="__tag_378271926">11</a>]</p>
<p id="__p14" class="p p-last">Many studies have evaluated the influence of religion on severity of psychopathology and the findings are contradictory. Some suggest that religious activities and beliefs are more in persons who experience more severe symptoms, especially psychotic and general symptoms,[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref38" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271901" name="__tag_378271901">38</a>] whereas others suggest that increased religious activity is associated with reduced level of symptoms.[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref39" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271931" name="__tag_378271931">39</a>] Data also suggest that higher religiosity is associated with absence of first-rank symptoms.[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref40" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271911" name="__tag_378271911">40</a>]</p>
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<div id="sec2-3" class="sec"><h3 id="sec2-3title">Relationship of religion and other clinical aspects in patients of schizophrenia</h3>
<p id="__p15" class="p p-first-last">Researchers have shown that religion/religiousness in patients with schizophrenia is associated with increased social integration, reduced risk of suicide attempts,[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref38" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271922" name="__tag_378271922">38</a>,<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref41" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271906" name="__tag_378271906">41</a>] reduce risk of substance use,[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref38" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271870" name="__tag_378271870">38</a>,<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref42" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271871" name="__tag_378271871">42</a>] decreased rate of smoking,[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref43" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271861" name="__tag_378271861">43</a>] better quality of life,[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref10" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271848" name="__tag_378271848">10</a>,<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref44" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271921" name="__tag_378271921">44</a>,<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref45" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271938" name="__tag_378271938">45</a>] lower level of functioning,[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref26" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271916" name="__tag_378271916">26</a>] and better prognoses.[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref46" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271834" name="__tag_378271834">46</a>] With regard to the relationship of religion and psychosocial adaptation, the findings are contradictory, with some reporting better psychosocial adaptation[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref47" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271899" name="__tag_378271899">47</a>] and others reporting poor social and psychological status in a majority of patients.[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref9" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271896" name="__tag_378271896">9</a>] Religious support and spirituality has also been found to be associated with better recovery[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref42" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271892" name="__tag_378271892">42</a>,<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref48" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271941" name="__tag_378271941">48</a>,<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref49" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271912" name="__tag_378271912">49</a>] and reduced relapse rate.[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref47" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271928" name="__tag_378271928">47</a>,<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref50" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271909" name="__tag_378271909">50</a>] However, in some patients, higher religiosity has been linked to higher risk of suicide attempt.[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref38" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271860" name="__tag_378271860">38</a>]</p>
</div>
<div id="sec2-4" class="sec"><h3 id="sec2-4title">Religion and treatment adherence in schizophrenia</h3>
<p id="__p16" class="p p-first-last">Some studies suggest that religion/religiousness in patients with schizophrenia is associated with better treatment adherence with psychiatric treatment,[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref4" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271888" name="__tag_378271888">4</a>,<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref38" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271933" name="__tag_378271933">38</a>,<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref47" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271840" name="__tag_378271840">47</a>] whereas others suggest association of religion with poor treatment adherence.[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref38" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271856" name="__tag_378271856">38</a>,<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref51" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271862" name="__tag_378271862">51</a>] Some studies suggest that higher religiosity is associated with lower preference for psychiatric treatment.</p>
</div>
<div id="sec2-5" class="sec"><h3 id="sec2-5title">Religious coping in schizophrenia</h3>
<p id="__p17" class="p p-first">Religious coping is multidimensional and refers to functionally oriented expressions of religion in times of stress. Religious coping is operationally defined as “the use of religious beliefs or behaviors to facilitate problem-solving to prevent or alleviate the negative emotional consequences of stressful life circumstances.”[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref52" class=" bibr popnode">52</a>] The concept of religious coping has been refined and categorized as helpful or positive, harmful or negative, and with mixed implications. The positive religious coping strategies include religious purification/forgiveness, religious direction/conversion, religious helping, seeking support from clergy/members, collaborative religious coping, religious focus, active religious surrender, benevolent religious reappraisal, spiritual connection, and marking religious boundaries. The negative religious coping strategies include spiritual discontent, demonic reappraisal, passive religious deferral, interpersonal religious discontent, reappraisal of God's powers, punishing God reappraisal, and pleading for direct intercession.[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref53" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271827" name="__tag_378271827">53</a>] The religious coping strategies with mixed implications include religious rituals in response to crisis, self-directing, deferring, and pleading religious coping.</p>
<p id="__p18">Few studies have evaluated the types of religious coping employed by patients with schizophrenia and their role in dealing with the stressful situation.[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref18" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271833" name="__tag_378271833">18</a>,<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref54" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271920" name="__tag_378271920">54</a>,<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref55" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271851" name="__tag_378271851">55</a>] Studies suggest that up to 80% of patients use religious coping as a means of dealing with their illness.[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref39" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271878" name="__tag_378271878">39</a>] Others have reported that in 45% of patients, spirituality and religiousness was helpful in coping with the illness.[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref18" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271943" name="__tag_378271943">18</a>] Studies which have compared different disorders suggest that patients with schizophrenia, bipolar disorder, and schizoaffective disorder use religious coping for a significantly greater number of years and perceive the same to be more helpful than those diagnosed with depressive disorders.[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref56" class=" bibr popnode">56</a>]</p>
<p id="__p19" class="p p-last">Studies also suggest that religious coping influences other parameters. Studies suggest that religious coping in patients of schizophrenia is associated positively with psychological and existential well-being, with positive religious coping being the primary predictor of psychological well-being.[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref57" class=" bibr popnode">57</a>] A study revealed that benevolent religious reappraisal was associated with better well-being, better adjustment, and lesser personal loss from mental illness, whereas punishing God reappraisal and reappraisal of God's powers were associated, with a greater correlation, with lesser well-being and adjustment and greater personal loss from mental illness.[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref58" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271839" name="__tag_378271839">58</a>] Positive religious coping has also been associated with higher quality of life in the domain of psychological health.[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref8" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271867" name="__tag_378271867">8</a>] Negative religious coping has been associated with lower quality of life[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref8" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271918" name="__tag_378271918">8</a>] and higher distress (assessed by Depression, Anxiety and Stress scale).[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref59" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271872" name="__tag_378271872">59</a>] Longitudinal studies have shown that higher salience of religion and use of positive religious coping at the baseline are predictive of lesser negative symptoms, better quality of life, and better clinical global impression.[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref49" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271880" name="__tag_378271880">49</a>] Participation in spiritual activities has been shown to be associated with better social functioning and dealing with negative symptoms.[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref60" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271876" name="__tag_378271876">60</a>]</p>
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<div id="sec2-6" class="sec"><h3 id="sec2-6title">Religion and explanatory models held by patients with schizophrenia</h3>
<p id="__p20" class="p p-first-last">Studies from different parts of the world have evaluated the explanatory models of illness held by the patients with schizophrenia and suggest that many patients have non-medical explanations for their illness.[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref61" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271925" name="__tag_378271925">61</a>,<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref62" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271939" name="__tag_378271939">62</a>,<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref63" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271929" name="__tag_378271929">63</a>,<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref64" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271859" name="__tag_378271859">64</a>,<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref65" class="bibr popnode tag_hotlink tag_tooltip" id="__tag_378271908" name="__tag_378271908">65</a>] Most of the non-medical explanations across different studies pertain to the supernatural causes. The different explanations include obsession by witches or jinns,[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref61" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271917" name="__tag_378271917">61</a>] esoteric,[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref66" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271895" name="__tag_378271895">66</a>] spiritual, and mystical factors,[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref63" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271866" name="__tag_378271866">63</a>] family trouble, inner problems of self, economic difficulties, supernatural forces,[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref64" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271855" name="__tag_378271855">64</a>] sorcery, ghosts/evil spirit, spirit intrusion, divine wrath, planetary/astrological influences, dissatisfied or evil spirits, and bad deeds of the past.[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref65" class="bibr popnode tag_hotlink tag_tooltip" id="__tag_378271850" name="__tag_378271850">65</a>] A study from India reported that about 66-70% of the patients have at least one non-biomedical explanatory model of supernatural type,[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref65" class="bibr popnode tag_hotlink tag_tooltip" id="__tag_378271842" name="__tag_378271842">65</a>] whereas studies from other parts of the world have reported presence of supernatural explanatory models in about 10% of patients.[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref64" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271905" name="__tag_378271905">64</a>] A cross-cultural study which included Arab-Islamic, Jordanian, and German patients suggests that Jordanian patients tend to believe more in esoteric factors underlying their illness, and they perceive the illness to be more threatening.[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref66" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271841" name="__tag_378271841">66</a>] Other studies suggest that Whites cited biological causes more frequently than African-Caribbeans and Bangladeshis, who cited social causes more frequently.[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref67" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271924" name="__tag_378271924">67</a>] Studies also suggest that non-medical explanatory models influence the insight[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref63" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271831" name="__tag_378271831">63</a>] and help seeking,[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref63" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271893" name="__tag_378271893">63</a>,<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref64" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271858" name="__tag_378271858">64</a>] and are associated with poor outcome.[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref62" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271934" name="__tag_378271934">62</a>]</p>
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<div id="sec2-7" class="sec"><h3 id="sec2-7title">Religion and quality of life of patients with schizophrenia</h3>
<p id="__p21" class="p p-first-last">The World Health Organization (WHO) considers spirituality, religion, and personal beliefs as an important area in the evaluation of the quality of life (QOL).[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref68" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271887" name="__tag_378271887">68</a>] The different mechanisms that have been proposed to link religiousness and spirituality to health outcome include behavioral (spirituality may be associated with a healthy lifestyle), social (religious groups provide supportive communities for their members), psychological (beliefs about God, ethics, human relationships, life and death), and physiological (religious practices elicit a relaxation response). Keeping the importance of religion and spirituality, the WHO designed a scale known as World Health Organization Quality of life-Spirituality, Religiousness, and Personal Belief scale (WHOQOL-SRPB). A study from our center suggests that spirituality and religiosity have an important influence on the overall QOL of patients with schizophrenia.[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref69" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271932" name="__tag_378271932">69</a>] The same group of authors also suggested a relationship between spirituality and religiosity domain of QOL, as assessed by WHOQOL-SRPB and the coping mechanisms used by the patients.[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref70" class="bibr popnode tag_hotlink tag_tooltip" id="__tag_378271838" name="__tag_378271838">70</a>]</p>
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<div id="sec2-8" class="sec sec-last"><h3 id="sec2-8title">Religion and help-seeking behavior</h3>
<p id="__p22" class="p p-first-last">A study from India showed that many patients seek the help of faith healers to get rid of patient's symptoms[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref71" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271902" name="__tag_378271902">71</a>] and it has also been shown that indigenous healing methods are considered complementary to the medical management of mental illness.[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref72" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271915" name="__tag_378271915">72</a>] A survey of consecutive psychiatric patients attending a hospital in Tamil Nadu, South India showed that 58% of psychotic patients saw a religious healer prior to psychiatric consultation.[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref73" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271898" name="__tag_378271898">73</a>] In fact, some of the studies suggest that seeking religious help for mental disorders is often the first step in the management of mental disorders, as a result of cultural explanations for the illness.[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref74" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271890" name="__tag_378271890">74</a>] Studies from other parts of the world suggest that patients with schizophrenia who are admitted for long duration experience spiritual distress.[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref75" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271923" name="__tag_378271923">75</a>] Studies which have specifically evaluated religiosity suggest that higher religiosity is associated with lower preference for psychiatric treatment.[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref26" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271894" name="__tag_378271894">26</a>]</p>
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</div>
<div id="sec1-2" class="tsec sec"><div class="goto jig-ncbiinpagenav-goto-container"><a class="tgt_dark page-toc-label jig-ncbiinpagenav-goto-heading" href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#" title="Go to other sections in this page">Go to:</a></div>
<h2 class="head no_bottom_margin ui-helper-clearfix" id="sec1-2title">CONCLUSIONS AND FUTURE DIRECTIONS</h2>
<p id="__p23" class="p p-first-last">Despite the close relationship of religion with various aspects of schizophrenia, this area has been mostly ignored in mental health assessment, diagnoses, and treatment.[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref6" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_378271927" name="__tag_378271927">6</a>] The limited existing data show that religion has an influence on the expression of psychopathology, treatment-seeking behavior, as well as treatment outcome. Given the importance of religion and spirituality for many patients, biopsychosocial model of schizophrenia should integrate the same, in order to achieve a whole-person approach to treatment. Findings also suggest that clinicians are rarely aware of the importance of religiosity for patients, even if spirituality needs are to be integrated into patient care.[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/#ref76" class=" bibr popnode tag_hotlink tag_tooltip" id="__tag_447818215" name="__tag_447818215">76</a>] Hence, there is an urgent need to make the clinicians aware of this need of the patients and they should evaluate the religious and spiritual issues of their patients. There is a need to further evaluate this area, especially from cross-cultural perspective. It is hoped that understanding the relationship of religion with various aspects of schizophrenia will lead to better understanding of the patients by the clinicians, better organization of services as per the needs of the patients, and better outcome of the patients.<br/><br/>Source: <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031576/</a></p>
</div> The Monarch (MK ULTRA)tag:templeilluminatus.ning.com,2021-04-04:6363372:Topic:35924852021-04-04T15:17:19.434ZMARGARIDA MARIA MADRUGAhttps://templeilluminatus.ning.com/profile/MARGARIDAMARIAMADRUGA
<p><a href="http://storage.ning.com/topology/rest/1.0/file/get/1226990141?profile=original" target="_self"><img class="align-center" src="http://storage.ning.com/topology/rest/1.0/file/get/1226990141?profile=original" width="640"></img></a></p>
<p>This is going to be hard to put into words, but I find this important to see if anyone else experiences this. I've googled multiple sites and I've gotten together as much information as best as I could about these experiences.</p>
<p>For one, I was born in Altus, Oklahoma. Both my parents were in the air force. Later on, when I moved into Virginia, this where I got my…</p>
<p><a href="http://storage.ning.com/topology/rest/1.0/file/get/1226990141?profile=original" target="_self"><img src="http://storage.ning.com/topology/rest/1.0/file/get/1226990141?profile=original" width="640" class="align-center"/></a></p>
<p>This is going to be hard to put into words, but I find this important to see if anyone else experiences this. I've googled multiple sites and I've gotten together as much information as best as I could about these experiences.</p>
<p>For one, I was born in Altus, Oklahoma. Both my parents were in the air force. Later on, when I moved into Virginia, this where I got my high school diploma. I had actually failed my senior year and I had to go to a place called Fork Union Military Academy. That's when I finally got my degree and then got a scholarship to play football at Virginia Military Institute, or simply V.M.I.</p>
<p>I had actually dropped out my second year because of severe depression. Not only that but I had two weird spiritual experiences concerning my coach and when I went to the Bahamas during spring break. Before I had even come to the realization of why these experiences happened, it didn't make sense until just a few years ago, and i dropped out of college in 2007.</p>
<p>Now, Im going to try and channel my guides at this next part.</p>
<p>For once, it made sense. The countless encounters with law enforcement. And yes, the cop said, "We knew you were coming," while smiling. I'm thinking to myself that he was actually telling the truth considering there were twenty cop cars with their lights flashing across the street from my home. Of course, I went home and told my mom and she just said it was a considence. Just like when I received a book on the Law of Attraction with no return address. I received this book months later after the VA Tech shooting. And yes, I use to live a couple doors down from this young adult who did the shooting in Centreville, Virginia.</p>
<p>With all this going on I became paranoid that I was being watched one way or another. I find that deep down, none of this made sense. A cop first beating me to the punchline and admitting he was waiting for me before I was pulled over. And now a random book on the Law of Attraction being sent to me when I was already a typical Christian Conspiracy Theorist. This whole thing me getting closer to "Christ" had happened after me lucid dreaming and seeing a "demon". Only a few years ago that I found out that the demon was actually a Satan. He was extremely talk with point wolf ears (Sirian) and green reptilian skin with no genetils (Orion) had big black teeth and black eyes like a Grey. Yes, an Draconian/Orion/Sirian hybrid.</p>
<p>Then in 2008 when I was diagnosed with schizoaffective. Yup, the. The up and downs and constant visions. The dream with the Satan I was actually drinking a bud(wiser) in the dream with a Dark African guy. After research, I figured this African guy was a Nommo initiating me into this sect of the Amphibian Sirians, hence Bud(WISER).Then I ran into what I thought was a demon but actually a Satan.</p>
<p>The constant going back to the hospitals and trying to make my mom see my point or view was going no where. There would be days when I was completely fine, then BOOM, I'd have an episode. This is what I could being "activated" when I became manic. My mindset would change and I was constantly downloading information within my crown chakra.</p>
<p>I have no other way of explaining it but in starting to understand these MK Ultra Sleepers. The ethereal realm, or your ancestors, intelligence agencies, or whatever you want to call them, activate you. It's like when Matt Damon in the first Bourne movie expresses to the woman about why he didn't understand why he kept gathering intel at a high level. That includes remembering street names, license plates, the supposed weight of an individual, and if that individual could "handle" himself. This what goes on in my head when I become "active". Not to that extent, but you get the picture.</p>
<p>There's more to this but I got a funny feeling that there will ill will towards me after dropping out of college. You can only imagine since I was the best defensive player. But my point is this, I think I finally understand monarch mind control.</p>
<p>See, it isn't literal when a sleeper checks in at this agencies like the CIA. What I'm saying is that there interdimensional beings that these agencies work with can contact you through telepathic means without meeting you face to face. You have to understand that the government is ahead at least fifty years in technology ahead of the public. I've had countless visions where I see multiple explosions, interdimensional beings fighting one another, or getting messages from either the radio or television sets. Of course, I don't explain this to anyone because of what they might think and the fact that I'm already diagnosed with an illness. But let me put it this way, someone is looking out for me because of my seeds to be a lightwarrior disguised as a darkworker. I find that the decisions I make in my head are paramount to what might happen to me in the future.</p>
<p>Now, my computer had been hacked in front of me, I've gotten profiled multiple times and I'm forever in contact with the higher intelligences on a day to day basis. This information about the stars and particularly about this subject comes straight from the head. And it's as if the Ethereal realm "appreciates" it. What I mean is that I have my own apartment and enough funds to live in my own. Like I was telling my mom, I was saying that we must be doing something right for the right things to happen. Thank God.</p>
<p>Now I know I didn't get too specific on my experiences but I wanted to write this because I feel it is needed for those that my have visions or what you would call hallucinations. Do not ever write it off as fantasy, there's a reason why your third eye is activated. And when you can have the understanding of why you have these spiritual gifts you can finally live the life you're supposed to.</p>
<p>I hope yall got something out of this</p>