The Importance of Sleep in Overcoming Childhood Obesity and Reshaping Epigenetics.

The development of childhood obesity is a complex process influenced by a combination of genetic predisposition and environmental factors, such as sleep, diet, physical activity, and socioeconomic status. Long-term solutions for decreasing the risk of childhood obesity remain elusive, despite significant advancements in promoting health and well-being in school and at home. Challenges persist in areas such as adherence to interventions, addressing underlying social determinants, and individual differences in response to treatment. Over the last decade, there has been significant progress in epigenetics, along with increased curiosity in gaining insights into how sleep and lifestyle decisions impact an individual's health. Epigenetic modifications affect the expression of genes without causing changes to the fundamental DNA sequence. In recent years, numerous research studies have explored the correlation between sleep and the epigenome, giving a better understanding of DNA methylation, histone modification, and non-coding RNAs. Although significant findings have been made about the influence of sleep on epigenetics, a notable gap exists in the literature concerning sleep-related genes specifically associated with childhood obesity. Consequently, it is crucial to delve deeper into this area to enhance our understanding. Therefore, this review primarily focuses on the connection between sleep patterns and epigenetic modifications in genes related to childhood obesity. Exploring the interplay between sleep, epigenetics, and childhood obesity can potentially contribute to improved overall health outcomes. This comprehensive review encompasses studies focusing on sleep-related genes linked to obesity.

Omega-3 Supplementation and Its Effects on Osteoarthritis.

Osteoarthritis (OA) is a degenerative joint disease characterized by the destruction of the articular cartilage, resulting in a pro-inflammatory response. The progression of OA is multifactorial and is influenced by the underlying cause of inflammation, which includes but is not limited to trauma, metabolism, biology, comorbidities, and biomechanics. Although articular cartilage is the main tissue affected in osteoarthritis, the chronic inflammatory environment negatively influences the surrounding synovium, ligaments, and subchondral bone, further limiting their functional abilities and enhancing symptoms of OA. Treatment for osteoarthritis remains inconsistent due to the inability to determine the underlying mechanism of disease onset, severity of symptoms, and complicating comorbidities. In recent years, diet and nutritional supplements have gained interest regarding slowing the disease process, prevention, and treatment of OA. This is due to their anti-inflammatory properties, which result in a positive influence on pain, joint mobility, and cartilage formation. More specifically, omega-3 polyunsaturated fatty acids (PUFA) have demonstrated an influential role in the progression of OA, resulting in the reduction of cartilage destruction, inhibition of pro-inflammatory cytokine cascades, and production of oxylipins that promote anti-inflammatory pathways. The present review is focused on the assessment of evidence explaining the inflammatory processes of osteoarthritis and the influence of omega-3 supplementation to modulate the progression of osteoarthritis.

Moderate-Intensity Exercise Enhances Mitochondrial Biogenesis Markers in the Skeletal Muscle of a Mouse Model Affected by Diet-Induced Obesity.

Skeletal muscle is composed of bundles of muscle fibers with distinctive characteristics. Oxidative muscle fiber types contain higher mitochondrial content, relying primarily on oxidative phosphorylation for ATP generation. Notably, as a result of obesity, or following prolonged exposure to a high-fat diet, skeletal muscle undergoes a shift in fiber type toward a glycolytic type. Mitochondria are highly dynamic organelles, constantly undergoing mitochondrial biogenesis and dynamic processes. Our study aims to explore the impact of obesity on skeletal muscle mitochondrial biogenesis and dynamics and also ascertain whether the skeletal muscle fiber type shift occurs from the aberrant mitochondrial machinery. Furthermore, we investigated the impact of exercise in preserving the oxidative muscle fiber types despite obesity. Mice were subjected to a normal standard chow and water or high-fat diet with sugar water (HFS) with or without exercise training. After 12 weeks of treatment, the HFS diet resulted in a noteworthy reduction in the markers of mitochondrial content, which was recovered by exercise training. Furthermore, higher mitochondrial biogenesis markers were observed in the exercised group with a subsequent increase in the mitochondrial fission marker. In conclusion, these findings imply a beneficial impact of moderate-intensity exercise on the preservation of oxidative capacity in the muscle of obese mouse models.

Targeting Molecular Mechanisms of Obesity- and Type 2 Diabetes Mellitus-Induced Skeletal Muscle Atrophy with Nerve Growth Factor.

Skeletal muscle plays a critical role in metabolic diseases, such as obesity and type 2 diabetes mellitus (T2DM). Muscle atrophy, characterized by a decrease in muscle mass and function, occurs due to an imbalance between the rates of muscle protein synthesis and degradation. This study aimed to investigate the molecular mechanisms that lead to muscle atrophy in obese and T2DM mouse models. Additionally, the effect of nerve growth factor (NGF) on the protein synthesis and degradation pathways was examined. Male mice were divided into three groups: a control group that was fed a standard chow diet, and two experimental groups that were fed a Western diet. After 8 weeks, the diabetic group was injected with streptozotocin to induce T2DM. Each group was then further divided into NGF-treated or non-treated control group. In the gastrocnemius muscles of the Western diet group, increased expressions of myostatin, autophagy markers, and ubiquitin ligases were observed. Skeletal muscle tissue morphology indicated signs of muscle atrophy in both obese and diabetic mice. The NGF-treated group showed a prominent decrease in the protein levels of myostatin and autophagy markers. Furthermore, the NGF-treated group showed an increased Cyclin D1 level. Western diet-induced obesity and T2DM may be linked to muscle atrophy through upregulation of myostatin and subsequent increase in the ubiquitin and autophagy systems. Moreover, NGF treatment may improve muscle protein synthesis and cell cycling.

Influence of Race and High Laminar Shear Stress on TNFR1 Signaling in Endothelial Cells.

Tumor necrosis factor (TNF) binding to endothelial TNF receptor-I (TNFR-I) facilitates monocyte recruitment and chronic inflammation, leading to the development of atherosclerosis. In vitro data show a heightened inflammatory response and atherogenic potential in endothelial cells (ECs) from African American (AA) donors. High laminar shear stress (HSS) can mitigate some aspects of racial differences in endothelial function at the cellular level. We examined possible racial differences in TNF-induced monocyte adhesion and TNFR1 signaling complex expression/activity, along with the effects of HSS. Tohoku Hospital Pediatrics-1 (THP-1) monocytes were used in a co-culture system with human umbilical vein ECs (HUVECs) from Caucasian American (CA) and AA donors to examine racial differences in monocyte adhesion. An in vitro exercise mimetic model was applied to investigate the potential modulatory effect of HSS. THP-1 adherence to ECs and TNF-induced nuclear factor kappa B (NF-κB) DNA binding were elevated in AA ECs compared to CA ECs, but not significantly. We report no significant racial differences in the expression of the TNFR-I signaling complex. Application of HSS significantly increased the expression and shedding of TNFR-I and the expression of TRAF3, and decreased the expression of TRAF5 in both groups. Our data does not support TNF-induced NF-κB activation as a potential mediator of racial disparity in this model. Other pathways and associated factors activated by the TNFR1 signaling complex are recommended targets for future research.

Association of the DNA Methylation of Obesity-Related Genes with the Dietary Nutrient Intake in Children.

The occurrence of obesity stems from both genetic and external influences. Despite thorough research and attempts to address it through various means such as dietary changes, physical activity, education, and medications, a lasting solution to this widespread problem remains elusive. Nutrients play a crucial role in various cellular processes, including the regulation of gene expression. One of the mechanisms by which nutrients can affect gene expression is through DNA methylation. This modification can alter the accessibility of DNA to transcription factors and other regulatory proteins, thereby influencing gene expression. Nutrients such as folate and vitamin B12 are involved in the one-carbon metabolism pathway, which provides the methyl groups necessary for DNA methylation. Studies have shown that the inadequate intake of these nutrients can lead to alterations in DNA methylation patterns. For this study, we aim to understand the differences in the association of the dietary intake between normal weight and overweight/obese children and between European American and African American children with the DNA methylation of the three genes NRF1, FTO, and LEPR. The research discovered a significant association between the nutritional intake of 6-10-years-old children, particularly the methyl donors present in their diet, and the methylation of the NRF1, FTO, and LEPR genes. Additionally, the study emphasizes the significance of considering health inequalities, particularly family income and maternal education, when investigating the epigenetic impact of methyl donors in diet and gene methylation.

Novel Differentially Methylated Regions Identified by Genome-Wide DNA Methylation Analyses Contribute to Racial Disparities in Childhood Obesity.

The magnitude of the childhood obesity epidemic and its effects on public health has accelerated the pursuit of practical preventative measures. Epigenetics is one subject that holds a lot of promise, despite being relatively new. The study of potentially heritable variations in gene expression that do not require modifications to the underlying DNA sequence is known as epigenetics. Here, we used Illumina MethylationEPIC BeadChip Array to identify differentially methylated regions in DNA isolated from saliva between normal weight (NW) and overweight/obese (OW/OB) children and between European American (EA) and African American (AA) children. A total of 3133 target IDs (associated with 2313 genes) were differentially methylated (p < 0.05) between NW and OW/OB children. In OW/OB children, 792 target IDs were hypermethylated and 2341 were hypomethylated compared to NW. Similarly, in the racial groups EA and AA, a total of 1239 target IDs corresponding to 739 genes were significantly differentially methylated in which 643 target IDs were hypermethylated and 596 were hypomethylated in the AA compared to EA participants. Along with this, the study identified novel genes that could contribute to the epigenetic regulation of childhood obesity.

The Role of Dietary Antioxidants and Their Potential Mechanisms in Alzheimer's Disease Treatment.

Alzheimer's disease (AD) is a progressive neurodegenerative disorder associated with cognitive decline and characterized by amyloid-ß plaques and neurofibrillary tau tangles. Although AD's exact pathophysiology remains unclear, oxidative stress is known to play a role in the neurodegenerative process. Since no curative treatment exists, antioxidants represent a potential treatment for AD due to their ability to modulate oxidative stress. Therefore, this review aims to examine the impact of antioxidant supplementation and its potential mechanisms on cognitive function. The review primarily discusses research articles published between 2012 and 2022 reporting the results of clinical trials involving antioxidant supplementation on cognitive function in individuals with AD. Antioxidant supplementation included probiotics, selenium, melatonin, resveratrol, rosmarinic acid, carotenoids, curcumin, vitamin E, and coenzyme Q. While the studies included in this review did not provide much evidence for the beneficial role of antioxidant supplements on cognitive function in AD, the results varied from antioxidant to antioxidant and among trials examining the same antioxidant. Furthermore, many of the studies' findings face several limitations, including short trial durations, small sample sizes, and a lack of diversity among study participants. As a result, more research is required to examine the impact of antioxidant supplementation on cognitive function in AD.

The Effects of Momordica charantia on Type 2 Diabetes Mellitus and Alzheimer's Disease.

T2DM is a complex metabolic disorder characterized by hyperglycemia and glucose intolerance. It is recognized as one of the most common metabolic disorders and its prevalence continues to raise major concerns in healthcare globally. Alzheimer's disease (AD) is a gradual neurodegenerative brain disorder characterized by the chronic loss of cognitive and behavioral function. Recent research suggests a link between the two diseases. Considering the shared characteristics of both diseases, common therapeutic and preventive agents are effective. Certain bioactive compounds such as polyphenols, vitamins, and minerals found in vegetables and fruits can have antioxidant and anti-inflammatory effects that allow for preventative or potential treatment options for T2DM and AD. Recently, it has been estimated that up to one-third of patients with diabetes use some form of complementary and alternative medicine. Increasing evidence from cell or animal models suggests that bioactive compounds may have a direct effect on reducing hyperglycemia, amplifying insulin secretion, and blocking the formation of amyloid plaques. One plant that has received substantial recognition for its numerous bioactive properties is Momordica charantia (M. charantia), otherwise known as bitter melon, bitter gourd, karela, and balsam pear. M. charantia is utilized for its glucose-lowering effects and is often used as a treatment for diabetes and related metabolic conditions amongst the indigenous populations of Asia, South America, India, and East Africa. Several pre-clinical studies have documented the beneficial effects of M. charantia through various postulated mechanisms. Throughout this review, the underlying molecular mechanisms of the bioactive components of M. charantia will be highlighted. More studies will be necessary to establish the clinical efficacy of the bioactive compounds within M. charantia to effectively determine its pertinence in the treatment of metabolic disorders and neurodegenerative diseases, such as T2DM and AD.

Prevalence and Mechanisms of Skeletal Muscle Atrophy in Metabolic Conditions.

Skeletal muscle atrophy is prevalent in a myriad of pathological conditions, such as diabetes, denervation, long-term immobility, malnutrition, sarcopenia, obesity, Alzheimer's disease, and cachexia. This is a critically important topic that has significance in the health of the current society, particularly older adults. The most damaging effect of muscle atrophy is the decreased quality of life from functional disability, increased risk of fractures, decreased basal metabolic rate, and reduced bone mineral density. Most skeletal muscle in humans contains slow oxidative, fast oxidative, and fast glycolytic muscle fiber types. Depending on the pathological condition, either oxidative or glycolytic muscle type may be affected to a greater extent. This review article discusses the prevalence of skeletal muscle atrophy and several mechanisms, with an emphasis on high-fat, high-sugar diet patterns, obesity, and diabetes, but including other conditions such as sarcopenia, Alzheimer's disease, cancer cachexia, and heart failure.

The Effects of Food Environment on Obesity in Children: A Systematic Review.

Childhood obesity is an epidemic connected with poor eating. According to the United States Department of Agriculture's Economic Research Service (USDA-ERS), food deserts are geographical locations in which residents have restricted or nonexistent access to healthful and quality food. Restricted access to healthy food is commonly associated with poor nutrition-related health outcomes, including obesity. This review aims to highlight the relationship between residing in a food desert or a similar environment on body mass index (BMI) in school-aged children in North America, predominantly in the Midwest region of the United States and Mexico. In this study, 17 articles were included from PubMed/Medline, Google Scholar, and Crossref. Most of these studies showed no association between the food environment and increased BMI. This discrepancy emphasizes the need for further research; the lack of access to healthful foods in food deserts is an issue that deserves additional attention.

Potential Role of Oxidative Stress in the Production of Volatile Organic Compounds in Obesity.

Obesity is associated with numerous health issues such as sleep disorders, asthma, hepatic dysfunction, cancer, renal dysfunction, diabetes, cardiovascular complications, and infertility. Previous research has shown that the distribution of excess body fat, rather than excess body weight, determines obesity-related risk factors. It is widely accepted that abdominal fat is a serious risk factor for illnesses associated with obesity and the accumulation of visceral fat promotes the release of pro-oxidants, pro-inflammatory, and reactive oxygen species (ROS). The metabolic process in the human body produces several volatile organic compounds (VOCs) via urine, saliva, breath, blood, skin secretions, milk, and feces. Several studies have shown that VOCs are released by the interaction of ROS with underlying cellular components leading to increased protein oxidation, lipid peroxidation, or DNA damage. These VOCs released via oxidative stress in obese individuals may serves as a biomarker for obesity-related metabolic alterations and disease. In this review, we focus on the relationship between oxidative stress and VOCs in obesity.

The Role of Diet and Dietary Patterns in Parkinson's Disease.

Parkinson's Disease (PD) is a neurodegenerative disorder associated with diminished nutrition status and decreased quality of life. While the prevalence of PD is expected to increase, no preventative or curative therapy for PD exists at this time. Although nutrition and diet represent modifiable risk factors for reducing chronic disease risk, research on the impact of single nutrients on PD has yielded mixed results. As a result, this single-nutrient approach may be the driving force behind the inconsistency, and a holistic dietary approach may overcome this inconsistency by accounting for the interactions between nutrients. The following review aims to examine the impact of a generally healthy dietary pattern, the protein-restricted diet (PRD), the ketogenic diet (KD), the Mediterranean diet (MD), and the Mediterranean-DASH Intervention for Neurodegenerative Delay (MIND) diet on PD risk, progression, and severity. While most of the included studies support the role of diet and dietary patterns in reducing the risk of PD or alleviating PD severity, the inconsistent results and need for further evidence necessitate more research being conducted before making dietary recommendations. Research on the potential beneficial effects of dietary patterns on PD should also investigate potential risks.

Racial Disparities in Methylation of NRF1, FTO, and LEPR Gene in Childhood Obesity.

Childhood obesity has affected the health of millions of children around the world despite vigorous efforts by health experts. The obesity epidemic in the United States has disproportionately afflicted certain racial and ethnic minority groups. African American children are more likely than other children to have obesity-related risk factors such as hyperlipidemia, diabetes, cardiovascular disease, and coronavirus disease (COVID-19). For the reduction in obesity-related health inequalities to be successful, it is essential to identify the variables affecting various groups. A notable advancement in epigenetic biology has been made over the past decade. Epigenetic changes like DNA methylation impact on many genes associated with obesity. Here, we evaluated the DNA methylation levels of the genes NRF1, FTO, and LEPR from the saliva of children using real-time quantitative PCR-based multiplex MethyLight technology. ALU was used as a reference gene, and the Percent of Methylated Reference (PMR) was calculated for each sample. European American children showed a significant increase in PMR of NRF1 and FTO in overweight/obese participants compared to normal weight, but not in African American children. After adjusting for maternal education and annual family income by regression analysis, the PMR of NRF1 and FTO was significantly associated with BMI z-score only in European American children. While for the gene LEPR, African American children had higher methylation in normal weight participants as compared to overweight/obese and no methylation difference in European American children. The PMR of LEPR was significantly negative associated with the obesity measures only in African American children. These findings contribute to a race-specific link between NRF1, FTO, and LEPR gene methylation and childhood obesity.

Salivary Neurotrophins Brain-Derived Neurotrophic Factor and Nerve Growth Factor Associated with Childhood Obesity: A Multiplex Magnetic Luminescence Analysis.

Obesity is linked with higher inflammatory markers and is characterized by chronic low-grade inflammation. Neurotrophins brain-derived neurotrophic factor (BDNF) and ß-nerve growth factor (ß-NGF), in addition to their neuronal functions, act on several immune cells and have been recently designated as metabokines due to their regulatory role in energy homeostasis and food intake. The current study evaluates the salivary BDNF and ß-NGF and their association with anthropometric measurement, blood pressure, and salivary insulin in children. Anthropometric measurements and saliva samples were obtained from 76 children, aged 6-10 years. Multiplex analysis was carried out for the salivary analysis of BDNF, NGF, and insulin by human magnetic Luminex performance assay. Statistical analysis was performed to analyze the best fit diagnostic value for biomarkers and the relationship of the neurotrophic levels of BDNF and NGF with obesity measures and blood pressure. Salivary BDNF and ß-NGF showed a significantly higher concentration in obese children than normal-weight children. Both neurotrophins are positively associated with obesity anthropometric measures, blood pressure, and salivary insulin. Multinominal regression analysis reported a significant association between salivary BDNF, ß-NGF, insulin, and systolic pressure adjusted for age, gender, income, and maternal education. The salivary concentration of BDNF and NGF was higher in obese children, and it is positively associated with anthropometric measures, suggesting that neurotrophins can be used as a non-invasive predictor of obesity-related complications in children.

Effects of Genistein and Exercise Training on Brain Damage Induced by a High-Fat High-Sucrose Diet in Female C57BL/6 Mice.

In recent decades, a shift in the nutritional landscape to the Western-style diet has led to an unprecedented rise in the prevalence of obesity and neurodegenerative diseases. Consumption of a healthy diet and engaging in regular physical activity represents safe and affordable approaches known to mitigate the adverse consequences of the Western diet. We examined whether genistein treatment, exercise training, and a combination treatment (genistein and exercise training) mitigated the effects of a Western diet-induced by high-fat, high-sugar (HFHS) in brain of female mice. HFHS increased the amyloid-beta (Aß) load and phosphorylation of tau, apoptosis, and decreased brain-derived neurotrophic factor (BDNF) levels. Exercise training and genistein each afforded modest protection on Aß accumulation and apoptosis, and both increased BDNF. The greatest neuroprotective effect occurred with combination treatment. BDNF and all markers of Aß accumulation, phosphorylation of tau, and apoptosis were improved with combined treatment. In a separate series of experiments, PC12 cells were exposed to high glucose (HG) and palmitate (PA) to determine cell viability with genistein as well as in the presence of tamoxifen, an estrogen receptor antagonist, to assess a mechanism of action of genistein on cell apoptosis. Genistein prevented the neurotoxic effects of HG and PA in PC12 cells and tamoxifen blocked the beneficial effects of genistein on apoptosis. Our results indicate the beneficial effects of genistein and exercise training on HFHS-induced brain damage. The benefits of genistein may occur via estrogen receptor-mediated pathways.

Genistein: A focus on several neurodegenerative diseases.

Neurodegenerative diseases are caused by the progressive loss of function or structure of nerve cells in the central nervous system. The most common neurodegenerative diseases include Alzheimer's disease, Huntington's disease, motor neuron disease, and Parkinson's disease. Although the physical or mental symptoms of neurodegenerative disease may be relieved by various treatment combinations, there are currently no strategies to directly slow or prevent neurodegeneration. Given the demographic evidence of a rapidly growing aging population and the associated prevalence of these common neurodegenerative diseases, it is paramount to develop safe and effective ways to protect against neurodegenerative diseases. Most neurodegenerative diseases share some common etiologies such as oxidative stress, neuroinflammation, and mitochondrial dysfunction. Genistein is an isoflavone found in soy products that have been shown to exhibit antioxidant, anti-inflammation, and estrogenic properties. Increasing evidence indicates the protective potential of genistein in neurodegenerative disorders. In this review, we aim to provide an overview of the role that genistein plays in delaying the development of neurodegenerative disease. PRACTICAL APPLICATIONS: Genistein is a naturally occurring isoflavone found mainly in soybean, but also green peas, legumes, and peanuts. Genistein is found to pass through the blood-brain barrier and possess a neuroprotective effect. In this review, we discuss studies in support of these actions and the underlying biological mechanisms. Together, these data indicate that genistein may hold neuroprotective effects in either delaying the onset or relieving the symptoms of neurodegenerative disease.

Multiplexed measurements of salivary fetuin-A, insulin, and adiponectin as potential non-invasive biomarkers in childhood obesity.

BACKGROUND: Obesity increases the risk of developing insulin resistance, diabetes, and cardiovascular disease. The current study is designed to evaluate the association of salivary fetuin-A, insulin, and adiponectin with the obesity measures in children. METHODS: Seventy-six children aged 6-10 years participated in the study. Anthropometric measurements were recorded, and saliva was collected from the participants. Based on the Center for Disease Control and Prevention (CDC), the participants were classified into normal weight (NW), overweight (OW), and obese (OB). Multiplex analysis for salivary markers fetuin-A, insulin, and adiponectin was performed using Luminex performance assay. The diagnostic value of the salivary marker was identified by receiver operating characteristics (ROC) curve, the correlation between obesity measures and markers were performed by regression analysis. RESULTS: Salivary fetuin-A and insulin were significantly increased in OW and OB in comparison to NW. Adiponectin was significantly decreased in the OB compared to NW and OW groups. Fetuin-A and insulin had the highest area under the curve with the best diagnostic value of a biomarker than adiponectin. Fetuin-A and insulin showed a positive association with obesity measures and among the parameters, but adiponectin was inversely associated. CONCLUSIONS: Salivary fetuin-A, insulin, and adiponectin levels are associated with the obesity in elementary school-aged children.

Role of macronutrient intake in the epigenetics of obesity.

Obesity is caused by a combination of hereditary and environmental factors. Despite extensive study, contemporary through diet, exercise, education, surgery, and pharmacological treatments, no effective long-term solution has been found to this epidemic. Over the last decade, there has been a tremendous advancement in understanding the science of epigenetics, as well as a rise in public interest in learning more about the influence of diet and lifestyle choices on the health of an individual. Without affecting the underlying DNA sequence, epigenetic alterations impact gene expression. Previous animal studies have shown a link between the type of diet and expression or suppression of obesity genes, but there are very few human studies that demonstrate the relationship between dietary intake and obesity gene expression. This review highlights the effects of carbohydrates, lipids, and protein intake from the diet on obesity-related genes.

High Olfactory Receptor-Rich 11q11 Copy Number in Girls and African American Children.

Copy number variants (CNVs) provide numerous genetic differences between individuals, and they have been linked with multiple human diseases. Obesity is one of the highly heritable complex disorders, which is associated with copy number variance (CNV). A recent report shows that the 11q11 gene, a novel olfactory receptor, and its copy number variants are involved in the early onset of obesity. In the current study, we analyzed the 11q11 gene copy number variance (CNV) based on gender in White/European American (EA) and African American (AA) normal weight and overweight/obese children. Sixty-nine boys and fifty-eight girls between the ages of 6 and 10 years belonging to either EA or AA ethnicity were involved in this study. As per World Health Organization (WHO) guidelines, each participant's body weight and height were recorded. DNA was extracted from saliva, and the copy number variants for the 11q11 gene were measured using digital PCR. The descriptive analysis of the 11q11 copy number showed significantly more copies in girls compared to boys; similarly, AA participants had significantly increased CNV compared to EA. The normal weight (NW) and overweight/obese (OW/OB) girls were significantly less likely to belong to the low copy number variant (LCNV) group of 11q11 compared to boys; similarly, NW and OW/OB AA children were significantly less likely to belong to the LCNV group. The AA girls in LCNV had significantly higher BMI z-scores. Our findings suggest that the 11q11 copy number in children is race and gender-specific.