Overweight Body Mass Index Status
Overweight body mass index (BMI) status refers to a health classification based on an individual’s weight in relation to their height. BMI is calculated as weight in kilograms divided by the square of height in meters (kg/m^2) [1]. An individual is classified as overweight if their BMI is 25 kg/m^2 or higher [1]. This condition is a significant public health concern, with a global increase in its prevalence [1].
Biological Basis
Section titled “Biological Basis”Research indicates that genetic factors play a crucial role in an individual’s susceptibility to becoming overweight or obese in response to environmental influences [1]. Twin and adoption studies have provided evidence for this genetic component [1]. Specific genetic variants have been identified that are associated with BMI. For example, a common variant in the FTOgene has been linked to BMI and an increased predisposition to both childhood and adult overweight and obesity[1]. Furthermore, large-scale association studies involving hundreds of thousands of individuals have revealed numerous genetic loci associated with BMI [2]. Many of these BMI-increasing genetic variants show consistent effects on the risk of being overweight, increasing the odds by 1.013 to 1.138-fold per allele [2].
Clinical Relevance
Section titled “Clinical Relevance”Overweight BMI status is a major contributor to morbidity and mortality worldwide[1]. It is strongly associated with an increased risk of developing several serious health conditions, including type 2 diabetes mellitus, heart disease, metabolic syndrome, hypertension, stroke, and certain forms of cancer[1]. Therefore, understanding and addressing overweight status is critical for preventing these health complications.
Social Importance
Section titled “Social Importance”The rising prevalence of overweight individuals globally is largely attributed to changes in lifestyle [1]. This trend presents a substantial challenge to public health systems and has broad social implications, affecting healthcare costs, productivity, and overall quality of life. Efforts to understand the interplay between genetic predispositions and environmental factors are essential for developing effective strategies to manage and prevent overweight status within populations.
Limitations
Section titled “Limitations”Methodological and Statistical Considerations
Section titled “Methodological and Statistical Considerations”Genetic association studies for body mass index (BMI) often leverage large sample sizes, such as cohorts involving hundreds of thousands of individuals, which enhance statistical power to detect common genetic variants [2]. However, even with extensive meta-analyses that combine data across diverse populations, the interpretation of effect sizes can be complex. While efforts are made to ensure consistency, such as evaluating heterogeneity between adolescent and adult data [3], subtle cohort biases or varying study designs across multiple contributing centers could still influence overall findings and their precise magnitude [2]. Furthermore, findings from initial genome-wide association scans often require robust replication across independent cohorts to confirm their validity and prevent potential inflation of effect estimates.
The process of combining results from various studies, including those using different marker sets or analytical methods, necessitates careful statistical approaches like inverse-variance meta-analysis [4]. While these methods are designed to provide more stable estimates, they depend on the quality and comparability of the individual study data. The observed associations, while statistically significant, may represent small individual effect sizes, and the full spectrum of genetic influences on BMI likely involves many more variants, some with even smaller effects, that are harder to detect even with current sample sizes. This highlights the ongoing need for larger, more ethnically diverse cohorts and refined analytical techniques to fully capture the genetic architecture of BMI.
Phenotypic Definition and Generalizability
Section titled “Phenotypic Definition and Generalizability”A primary limitation in the study of overweight status is the reliance on Body Mass Index (BMI) as a primary phenotype. BMI, calculated as weight divided by height squared, serves as a convenient clinical surrogate for adiposity, but it does not differentiate between fat mass and lean body mass [1]. This means individuals with high muscle mass might be classified as overweight or obese by BMI, even if their body fat percentage is healthy [4]. Future research could benefit from incorporating more precise measures of body composition to refine genetic associations and provide a more nuanced understanding of underlying biological mechanisms.
Furthermore, the generalizability of genetic findings for BMI can be constrained by the ancestry and demographic characteristics of the study populations. While studies have included individuals from various European locations [2] and involved replication in populations like Chinese individuals [4], or specific isolated founder populations [5], genetic architectures can vary across different ancestral groups. Allele frequencies, linkage disequilibrium patterns, and gene-environment interactions may differ substantially, meaning that variants identified in one population may have different effects or even be absent in others. This underscores the need for comprehensive studies across a wider array of global populations to ensure broad applicability of findings.
Environmental and Genetic Complexity
Section titled “Environmental and Genetic Complexity”The genetic predisposition to overweight status is profoundly influenced by complex interactions with environmental factors. The global rise in obesity prevalence is largely attributed to shifts in lifestyle, emphasizing the powerful role of diet, physical activity, and other environmental exposures[1]. Genetic studies, while identifying specific loci associated with BMI, often do not fully account for these intricate gene-environment interactions, which determine how an individual’s genetic makeup translates into a phenotype in a given environment [1]. Understanding these complex interplay remains a significant knowledge gap, as the identified genetic variants alone only explain a fraction of the total heritability of BMI.
The phenomenon often referred to as “missing heritability” suggests that many genetic factors contributing to BMI remain undiscovered. This could be due to a multitude of reasons, including the presence of rare variants with stronger effects not captured by common variant GWAS, complex epistatic interactions between genes, or the limitations of current statistical models to fully capture the polygenic nature of the trait. Consequently, despite the identification of numerous genetic loci, a substantial portion of the genetic variance underlying overweight BMI status is yet to be elucidated, indicating that current knowledge provides only a partial picture of the genetic landscape.
Variants
Section titled “Variants”The genetic architecture underlying body mass index (BMI) and the predisposition to overweight status is complex, involving numerous genetic variants across the human genome. These variants often exert subtle effects that collectively contribute to an individual’s susceptibility. Understanding their roles offers insights into the biological pathways influencing energy balance, metabolism, and appetite regulation.
The FTO(Fat Mass and Obesity-associated) gene is a highly significant genetic contributor to variations in BMI and the predisposition to childhood and adult obesity. Variants within the first intron ofFTO, such as rs8043757 , are consistently associated with increased BMI across diverse populations.
Key Variants
Section titled “Key Variants”| RS ID | Gene | Related Traits |
|---|---|---|
| rs8043757 | FTO | leptin measurement obesity body mass index overweight body mass index status snoring measurement |
| rs7818910 | ABRA - HMGB1P46 | overweight body mass index status |
| rs1554116 | KCNK13 | overweight body mass index status restless legs syndrome |
| rs12101726 | LINC01579, LINC01581 | overweight body mass index status overall survival, pancreatic carcinoma |
| rs1475010 | LINC02306 | overweight body mass index status |
| rs1161397 | DEFB112 - TFAP2D | overweight body mass index status |
| rs7863750 | MFSD14B | overweight body mass index status |
| rs7500401 | LINC02152 - TMEM114 | overweight body mass index status |
Classification, Definition, and Terminology
Section titled “Classification, Definition, and Terminology”Definition and Standardized Measurement of Body Mass Index
Section titled “Definition and Standardized Measurement of Body Mass Index”Overweight body mass index status is primarily defined and measured through the Body Mass Index (BMI), a widely adopted metric for assessing adiposity. BMI is precisely calculated as an individual’s weight in kilograms divided by the square of their height in meters (kg/m²)[1]. This operational definition allows for a standardized approach to evaluating body fatness across diverse populations, serving as a critical surrogate measure in clinical settings and research studies [1]. While BMI is a foundational tool, its values are often subject to adjustments for covariates such as age, sex, smoking status, and menopausal status in various analytical models to account for potential confounding factors [6]. Furthermore, for statistical analyses, BMI values may be natural log-transformed to achieve a more normal distribution, satisfying model assumptions in research contexts [7].
Classification and Categorization of Body Mass Index Status
Section titled “Classification and Categorization of Body Mass Index Status”The classification of overweight body mass index status relies on specific thresholds established by major health organizations. Individuals with a BMI equal to or greater than 25 kg/m² are categorized as overweight[1]. This categorical classification helps to identify individuals at increased health risk, forming a key part of disease classifications and nosological systems. Expanding on this, a BMI of 30 kg/m² or greater is used to define obesity, which represents a more severe gradation of adiposity[1]. These standardized cut-off values are essential for clinical diagnosis, public health surveillance, and for understanding the global prevalence of these conditions, with studies indicating that in 2003–2004, 66% of the U.S. population had a BMI ≥ 25 kg/m², and 32% were obese [8].
Complementary Adiposity Measures and Clinical Context
Section titled “Complementary Adiposity Measures and Clinical Context”While BMI is a primary indicator, a comprehensive assessment of adiposity often necessitates the integration of other diagnostic and measurement criteria. For a more accurate judgment of adiposity, BMI measurements should be considered in conjunction with other metrics like waist circumference and body fat percentage [9]. Waist circumference, which can be measured at the level of the umbilicus, provides insight into central adiposity, a significant factor in metabolic health [6]. Advanced imaging techniques, such as computed tomography, further allow for the precise measurement of subcutaneous fat, visceral fat, and sagittal diameter, offering detailed insights into fat distribution and volume [6]. These complementary measures are crucial because higher BMI, weight, and waist circumference are independently associated with an increased risk of chronic conditions such as type 2 diabetes, cardiovascular disease, hypertension, and certain cancers, underscoring the clinical significance of these various adiposity assessments[1].
Causes
Section titled “Causes”The development of an overweight body mass index is a multifaceted process influenced by a complex interplay of genetic, environmental, developmental, and lifestyle factors. Understanding these contributing elements is crucial for comprehending the global prevalence and individual susceptibility to overweight status.
Genetic Predisposition and Inheritance
Section titled “Genetic Predisposition and Inheritance”Genetic factors play a significant role in influencing an individual’s susceptibility to developing an overweight body mass index, as demonstrated by twin and adoption studies . Understanding the biological underpinnings involves exploring genetic predispositions, intricate metabolic regulation, the role of adipose tissue, and the subsequent pathophysiological consequences across organ systems.
Genetic Predisposition to Body Mass Index Status
Section titled “Genetic Predisposition to Body Mass Index Status”Genetic factors play a substantial role in determining an individual’s susceptibility to overweight and obesity. Studies, including those involving twins and adoptees, have consistently shown that genetic inheritance significantly influences how individuals within a population respond to environmental factors that contribute to weight gain. Genome-wide association studies (GWAS) have been instrumental in identifying numerous specific genetic loci associated with BMI, underscoring the polygenic nature of this trait, where many genes each contribute a small effect[1].
A prominent genetic discovery is a common variant within the FTO gene, which is robustly associated with BMI and an increased risk for both childhood and adult obesity. Research suggests that FTO primarily influences BMI by affecting energy intake, rather than energy expenditure, implying its involvement in appetite regulation. Another gene, MC4R, also contains variants linked to body size and is known to be involved in crucial hypothalamic signaling pathways that control energy balance. Furthermore, the TRHR gene has been identified for its association with lean body mass, a key component of overall body weight contributing to BMI[1].
Regulation of Energy Balance and Metabolic Pathways
Section titled “Regulation of Energy Balance and Metabolic Pathways”The maintenance of a healthy body weight relies on intricate molecular and cellular pathways that tightly regulate energy balance. Central to this regulation are specific neuronal functions, particularly those within the hypothalamus, which act as the body’s control center for appetite and satiety. Key biomolecules, such as the receptors influenced by MC4R gene variants, are integral to these hypothalamic signaling pathways, modulating an individual’s hunger and thus their caloric intake. Disruptions in these complex regulatory networks can lead to an imbalance between the energy consumed and the energy expended, promoting the accumulation of excess body fat [9].
The FTO gene, whose common variants are strongly linked to higher BMI, is believed to impact energy intake, further highlighting the critical role of appetite control in body weight regulation. While the exact cellular and molecular mechanisms of FTO are still being elucidated, its effect on energy consumption suggests its involvement in metabolic processes that govern nutrient sensing and storage. These interconnected pathways are designed to maintain energy homeostasis, but when compromised by genetic predispositions or environmental factors, they can result in a chronic positive energy balance, leading to overweight and obesity[1].
Adipose Tissue Biology and Systemic Interactions
Section titled “Adipose Tissue Biology and Systemic Interactions”BMI status reflects an individual’s overall body composition, which includes both lean body mass and fat body mass, with overweight status specifically characterized by excess adiposity. Adipose tissue, commonly known as body fat, is not merely a passive storage site for excess energy but an active endocrine organ that communicates extensively with other tissues and organs throughout the body. The abnormal expansion and dysfunction of adipose tissue, particularly in overweight individuals, can initiate widespread homeostatic disruptions, negatively affecting metabolic processes in organs such as the liver, skeletal muscle, and pancreas[6].
These systemic tissue interactions are fundamental to understanding the broader physiological consequences of being overweight. For instance, studies show correlations among various adiposity traits, indicating that increased fat mass is part of a more extensive set of physiological changes rather than an isolated phenomenon. The dysregulation stemming from altered adipose tissue function can contribute to a state of chronic low-grade inflammation and insulin resistance. These cellular and tissue-level changes collectively predispose individuals to a cascade of metabolic disorders, illustrating how adipose tissue biology profoundly influences overall organ-level function and systemic health[6].
Pathophysiological Consequences and Disease Risk
Section titled “Pathophysiological Consequences and Disease Risk”Overweight and obesity are significant contributors to a wide range of pathophysiological processes that substantially increase morbidity and mortality. The chronic metabolic stress and widespread homeostatic disruptions associated with excess body weight elevate the risk for numerous chronic diseases. These include, but are not limited to, type 2 diabetes mellitus, various forms of heart disease, hypertension, stroke, metabolic syndrome, and certain types of cancer, demonstrating the broad systemic impact of overweight status[1].
The underlying mechanisms involve a complex series of events, often commencing with cellular dysfunction and progressing to organ-level damage. For example, the chronic inflammation and insulin resistance frequently observed in individuals with excess adiposity can lead to impaired pancreatic beta-cell function in type 2 diabetes or the development of atherosclerosis, which underlies cardiovascular diseases. While the body may initially activate compensatory responses to these disruptions, prolonged overweight status ultimately overwhelms these protective mechanisms, leading to the manifestation of overt disease and underscoring the critical importance of maintaining a healthy BMI for long-term health[1].
Clinical Relevance
Section titled “Clinical Relevance”Overweight body mass index (BMI) status, defined clinically as a BMI ≥ 25 kg/m2, holds significant clinical relevance due to its profound associations with a wide spectrum of health complications and its utility in risk stratification and patient management [1]. The increasing global prevalence of overweight and obesity underscores the importance of understanding its implications for patient care and public health[1].
Risk Assessment and Disease Associations
Section titled “Risk Assessment and Disease Associations”Overweight status is strongly linked to a range of serious health conditions, serving as a critical indicator for increased disease risk. These comorbidities include, but are not limited to, type 2 diabetes mellitus, various forms of heart disease, metabolic syndrome, hypertension, stroke, and certain cancers[1]. Research indicates that the rising prevalence of excess weight contributes significantly to the global burden of these associated diseases [1]. Furthermore, specific associations extend to cardiovascular remodeling, such as left ventricular hypertrophy (LVH), where BMI is a contributing factor to changes in cardiac mass [10]. The presence of excess adiposity, particularly visceral fat measured by advanced imaging techniques like computed tomography, further highlights the complex interplay between body composition and heightened health risks[6].
Prognostic Implications and Long-term Outcomes
Section titled “Prognostic Implications and Long-term Outcomes”Overweight and obesity are recognized as major contributors to morbidity and mortality, emphasizing their critical prognostic value in clinical practice[1]. Extensive studies have consistently shown a substantial disease burden associated with excess weight, impacting overall health and increasing the risk of premature mortality[11]. The long-term implications of overweight status also extend to significant societal and economic costs, primarily driven by the direct healthcare expenditures linked to managing obesity-associated conditions[11]. Genetic factors play a role in influencing an individual’s likelihood of developing obesity, with common variants in genes like FTO predisposing to both childhood and adult obesity[1]. The identification of numerous genetic loci associated with BMI, some showing consistent effects on the risk of extreme and early-onset obesity, provides valuable insights into predicting disease progression and long-term health trajectories, especially in individuals with a genetic predisposition[2].
Clinical Utility and Personalized Approaches
Section titled “Clinical Utility and Personalized Approaches”Body Mass Index (BMI) is a foundational clinical tool, calculated as weight divided by height squared, used to classify individuals as overweight (BMI ≥ 25 kg/m2) or obese (BMI ≥ 30 kg/m2) [1]. This classification is essential for initial diagnostic utility and comprehensive risk assessment, enabling healthcare providers to identify individuals at elevated risk for related comorbidities. Beyond BMI, other adiposity traits, such as waist circumference and the distribution of subcutaneous and visceral fat, offer additional insights for refined risk stratification [6]. Integrating an understanding of genetic influences on BMI, including variants in genes like FTO or MC4R, can contribute to personalized medicine strategies [1]. Such genetic information, when combined with lifestyle assessments, can guide tailored prevention strategies, inform treatment selection, and suggest specific monitoring approaches to mitigate the development or progression of overweight-related health complications.
Ethical and Social Considerations for Overweight Body Mass Index Status
Section titled “Ethical and Social Considerations for Overweight Body Mass Index Status”Understanding the genetic underpinnings of overweight body mass index (BMI) status, as revealed by numerous genome-wide association studies, brings forth a range of complex ethical and social considerations. While research has identified genetic variants associated with BMI and acknowledged the role of genetics in influencing an individual’s susceptibility to obesity in specific environments[2], the interpretation and application of this knowledge require careful thought to ensure equitable and responsible practices.
Ethical Implications of Genetic Insights into BMI
Section titled “Ethical Implications of Genetic Insights into BMI”The identification of genetic variants associated with body mass index, such as those revealing new loci or variants in genes like FTO [2], raises important ethical considerations regarding genetic testing. If such genetic information becomes widely available, individuals might face decisions about whether to undergo testing for susceptibility to overweight or obesity. This necessitates robust frameworks for informed consent, ensuring individuals fully understand the implications, limitations, and potential psychosocial impacts of receiving such genetic results.
Concerns about privacy and potential genetic discrimination are paramount. Knowledge of an individual’s genetic predisposition to overweight status could, for example, lead to discrimination in employment or insurance, despite legal protections in some regions. Furthermore, the availability of such genetic insights could introduce complex reproductive choices, as prospective parents might consider genetic information related to BMI susceptibility in family planning, raising debates about eugenics and the societal valuation of certain traits.
Societal Impacts and Challenges to Health Equity
Section titled “Societal Impacts and Challenges to Health Equity”Understanding the genetic components of overweight BMI status has profound social implications, particularly concerning the pervasive stigma often associated with higher body weight. While genetic factors are recognized as playing a role in influencing an individual’s likelihood of developing obesity in response to their environment[1], an overemphasis on genetics could inadvertently exacerbate blame or reinforce the idea that overweight individuals cannot control their weight, potentially increasing social prejudice and mental health burdens. This intersects with health disparities, as socioeconomic factors and access to nutritious food and safe environments for physical activity significantly influence BMI, creating a complex interplay where genetic predispositions may interact with environmental disadvantages.
Addressing overweight BMI status from an equity and justice perspective requires careful consideration of resource allocation and access to care. Vulnerable populations, often disproportionately affected by health disparities, may lack access to comprehensive healthcare, genetic counseling, or personalized interventions that could arise from genetic insights. Cultural considerations also play a vital role, as perceptions of body size, health, and diet vary widely across different communities. A global health perspective is essential to ensure that advances in genetic understanding contribute to equitable health outcomes worldwide, rather than widening existing gaps in health and wellness.
Policy, Regulation, and Research Ethics
Section titled “Policy, Regulation, and Research Ethics”The increasing understanding of genetic associations with BMI necessitates the development and enforcement of clear policy and regulatory frameworks. This includes comprehensive genetic testing regulations to ensure the accuracy, clinical utility, and ethical delivery of any tests related to BMI susceptibility. Strong data protection measures are crucial to safeguard sensitive genetic information, preventing misuse and ensuring individual control over personal health data in an era of large-scale genomic studies [2].
Research ethics must continue to evolve to guide studies involving genetic data related to complex traits like BMI, ensuring participant protection, transparency, and the responsible dissemination of findings. Furthermore, clinical guidelines need to be established for integrating genetic information into healthcare practices for individuals with overweight BMI status. These guidelines should balance the potential benefits of personalized medicine with the risks of overmedicalization, psychological distress, and the perpetuation of health inequities, ensuring that genetic insights are used to support holistic, patient-centered care.
Frequently Asked Questions About Overweight Body Mass Index Status
Section titled “Frequently Asked Questions About Overweight Body Mass Index Status”These questions address the most important and specific aspects of overweight body mass index status based on current genetic research.
1. Why can’t I lose weight even when my friend eats more than me?
Section titled “1. Why can’t I lose weight even when my friend eats more than me?”Your genetics play a significant role in how your body processes food and stores energy. For example, variants in genes like FTO can make some people more prone to weight gain and influence appetite, even with similar food intake compared to others. This means your body might respond differently to the same diet and exercise routine.
2. Can I overcome my family’s history of being overweight?
Section titled “2. Can I overcome my family’s history of being overweight?”Yes, you absolutely can. While genetics contribute significantly to your susceptibility to being overweight, accounting for a substantial portion of BMI heritability, lifestyle choices are powerful. Healthy diet and regular physical activity are crucial environmental factors that interact with your genes, allowing you to influence your weight trajectory despite a family predisposition.
3. If I’m very muscular, is my “overweight” BMI still a health risk?
Section titled “3. If I’m very muscular, is my “overweight” BMI still a health risk?”Not necessarily. BMI is a convenient measure but doesn’t differentiate between fat mass and lean muscle mass. If you have a high amount of muscle, your BMI might classify you as overweight even if your body fat percentage is healthy. More precise body composition measurements would offer a clearer picture of your actual health risks.
4. Does my ethnicity affect my risk of being overweight?
Section titled “4. Does my ethnicity affect my risk of being overweight?”Yes, it can. Genetic architectures and allele frequencies for weight-related genes can vary across different ancestral groups. This means that genetic variants associated with BMI in one population might have different effects or even be absent in others, influencing your individual risk based on your background.
5. Why does my sibling stay thin while I gain weight easily?
Section titled “5. Why does my sibling stay thin while I gain weight easily?”Even within families, individuals inherit different combinations of genetic variants that influence weight. For example, you might have certain genetic predispositions, like a variant in the FTO gene, that make you more susceptible to weight gain than your sibling, even with similar environmental exposures and lifestyles.
6. Does stress or lack of sleep affect my weight gain?
Section titled “6. Does stress or lack of sleep affect my weight gain?”Yes, lifestyle factors like chronic stress and insufficient sleep are significant environmental influences on weight. While genetics predispose you, these environmental stressors can impact your hormones and metabolism, interacting with your genetic makeup to potentially contribute to weight gain or make weight loss more challenging.
7. Is a genetic test worth it to understand my weight problems?
Section titled “7. Is a genetic test worth it to understand my weight problems?”It depends on what you’re hoping to learn. Genetic tests can identify some variants, such as those in the FTO gene, associated with BMI. However, these identified variants only explain a fraction of the total heritability of BMI, as weight is also strongly influenced by complex gene-environment interactions.
8. Will my kids definitely be overweight if I am?
Section titled “8. Will my kids definitely be overweight if I am?”Not necessarily, but they may have an increased genetic predisposition. Research shows that genetic factors play a crucial role in the susceptibility to being overweight. However, lifestyle and environmental factors are also very powerful, and by fostering healthy habits, you can help mitigate their genetic risk.
9. Why do some diets work for others but not for me?
Section titled “9. Why do some diets work for others but not for me?”Your individual genetic makeup influences how your body responds to different diets and environmental factors. For instance, specific genetic variants can affect your metabolism, appetite regulation, or how your body processes certain nutrients, meaning a diet effective for someone else might not align with your unique genetic predispositions.
10. Am I at higher risk for health issues just because I’m “overweight”?
Section titled “10. Am I at higher risk for health issues just because I’m “overweight”?”Yes, an overweight BMI is strongly associated with an increased risk of developing several serious health conditions. This includes type 2 diabetes, heart disease, metabolic syndrome, hypertension, stroke, and certain forms of cancer. Understanding and addressing your weight status is crucial for preventing these potential health complications.
This FAQ was automatically generated based on current genetic research and may be updated as new information becomes available.
Disclaimer: This information is for educational purposes only and should not be used as a substitute for professional medical advice. Always consult with a healthcare provider for personalized medical guidance.
References
Section titled “References”[1] Frayling, T. M. et al. “A common variant in the FTO gene is associated with body mass index and predisposes to childhood and adult obesity.”Science, vol. 316, 2007, pp. 889-894.
[2] Speliotes, E. K. et al. “Association analyses of 249,796 individuals reveal 18 new loci associated with body mass index.” Nat Genet, vol. 42, 2010.
[3] Benyamin, Beben, et al. “Common variants in TMPRSS6 are associated with iron status and erythrocyte volume.” Nature Genetics, vol. 41, no. 11, 2009, pp. 1178-1180.
[4] Liu, Xian-Guang, et al. “Genome-wide association and replication studies identified TRHR as an important gene for lean body mass.” American Journal of Human Genetics, vol. 84, no. 3, 2009, pp. 418-423.
[5] Lowe, Jason K., et al. “Genome-wide association studies in an isolated founder population from the Pacific Island of Kosrae.” PLoS Genetics, vol. 5, no. 2, 2009, p. e1000365.
[6] Fox, Caroline S., et al. “Genome-wide association to body mass index and waist circumference: the Framingham Heart Study 100K project.” BMC Med Genet, vol. 8, no. S1, 2007, p. S9.
[7] Croteau-Chonka, D. C., et al. “Genome-wide association study of anthropometric traits and evidence of interactions with age and study year in Filipino women.” Obesity (Silver Spring), vol. 18, no. 12, 2010, pp. 2311-19.
[8] National Institutes of Health.“Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults—The Evidence Report.”Obesity Research, vol. 6, no. S2, 1998, pp. 51S-209S.
[9] Liu, J. Z., et al. “Genome-wide association study of height and body mass index in Australian twin families.” Twin Research and Human Genetics, vol. 13, no. 2, 2010, pp. 109-23.
[10] Arnett, Donna K., et al. “Genome-wide association study identifies single-nucleotide polymorphism in KCNB1 associated with left ventricular mass in humans: the HyperGEN Study.”BMC Med Genet, vol. 10, no. 1, 2009, p. 47.
[11] Scuteri, A, et al. “Genome-wide association scan shows genetic variants in the FTO gene are associated with obesity-related traits.”PLoS Genet, vol. 3, no. 7, Jul. 2007, p. e115. PMID: 17658951.