Abdominal Symptom
Abdominal symptoms refer to a broad category of sensations and discomforts experienced in the abdomen, the area of the body between the chest and the pelvis. These symptoms can include pain, cramping, bloating, nausea, vomiting, indigestion, and changes in bowel habits. They are common and can vary widely in severity and duration, ranging from temporary, mild annoyances to indicators of serious underlying health conditions.
The biological basis of abdominal symptoms is complex and often involves intricate interactions between the digestive system, nervous system, immune responses, and environmental factors. Genetic predispositions can play a significant role in an individual’s susceptibility to various conditions that manifest with abdominal symptoms. Genome-wide association studies (GWAS) are frequently employed to identify genetic variants, such as single nucleotide polymorphisms (SNPs), that are associated with specific traits and diseases[1]. For instance, genetic variants have been implicated in conditions like abdominal aortic aneurysm[2]. These studies typically involve analyzing a large number of SNPs across many individuals to identify those that occur more frequently in people experiencing particular symptoms or conditions [3].
From a clinical perspective, abdominal symptoms are vital diagnostic indicators that guide healthcare professionals in identifying and treating a wide range of diseases, including gastrointestinal disorders, inflammatory conditions, and various other systemic illnesses. Identifying genetic factors associated with abdominal symptoms can contribute to personalized medicine by aiding in risk assessment, early detection, and the development of targeted therapies. For example, genetic variants have been studied in relation to lower urinary tract symptoms (LUTS), which can sometimes present with abdominal discomfort [3]. Understanding these genetic links can provide valuable insights into an individual’s inherited susceptibility and the underlying causes of their symptoms.
The social importance of understanding abdominal symptoms is substantial, as they can significantly impact an individual’s quality of life, leading to discomfort, reduced productivity, and psychological distress. Conditions associated with chronic or severe abdominal symptoms can place a considerable burden on public health. Research into the genetic underpinnings of these symptoms contributes to a deeper understanding of human health and disease, potentially leading to improved diagnostic tools, more effective treatment options, and preventive strategies. Large-scale genetic analyses, often combining data from numerous studies and participants, are crucial for uncovering these complex associations[1].
Limitations
Section titled “Limitations”Methodological and Statistical Constraints
Section titled “Methodological and Statistical Constraints”Genetic studies often rely on the aggregation of data from multiple cohorts through meta-analysis or mega-analysis to achieve sufficient statistical power [1]. While this approach enhances the ability to detect genetic associations, it can introduce heterogeneity due to variations in study designs, population characteristics, and phenotyping methods across different cohorts [4]. Rigorous quality control steps, such as filtering single nucleotide polymorphisms (SNPs) based on imputation accuracy or minor allele frequency, and adjusting for covariates like principal components of genetic ancestry, are crucial to mitigate these issues[4]. However, despite these efforts, residual biases or uncontrolled confounders from combining diverse datasets may still influence the reported effect sizes and lead to challenges in replication across studies.
Furthermore, the statistical models employed, such as those treating true genetic effects as random effects, are dependent on underlying assumptions that, if violated, could impact the accuracy of effect estimations [1]. The declaration of genome-wide significance typically relies on stringent p-value thresholds (e.g., P<5.0×10−8), which helps minimize false positives but may also overlook true associations with smaller effect sizes [4]. While multi-trait analyses can boost statistical power [1], the interpretation of results still requires careful consideration of potential statistical artifacts and the need for independent validation.
Genetic Architecture and Generalizability
Section titled “Genetic Architecture and Generalizability”Genome-wide association studies frequently identify SNPs that are intergenic or intronic, meaning they are located in non-coding regions of the genome [3]. These identified SNPs often act as “tagging variants,” indicating linkage to a causal variant nearby rather than being the causal variant themselves [5]. This characteristic means that the precise functional mechanism by which these genetic variants contribute to abdominal symptoms is not immediately clear, necessitating further functional genomic research. Additionally, while some studies investigate variants with lower minor allele frequencies (e.g., between 1% and 5%) [6], the focus of many GWAS is on common variants, potentially missing the contributions of rarer genetic variations to the trait.
The generalizability of findings can be limited by the ancestry composition of the study populations. While some research endeavors explicitly include diverse populations, such as African-Americans and European-Americans [7], or utilize principal components to adjust for population stratification [4], the specific demographic details of cohorts contributing to abdominal symptom genetics are not universally described. Datasets from large consumer genetic companies, while providing vast numbers of participants, may exhibit biases towards individuals of European descent[8]. This lack of comprehensive representation across ancestries means that findings may not be directly transferable or fully applicable to all global populations, highlighting a need for broader inclusion in future genetic investigations.
Phenotypic Heterogeneity and Unaccounted Factors
Section titled “Phenotypic Heterogeneity and Unaccounted Factors”A significant limitation in genetic studies of complex traits like abdominal symptoms lies in the precise definition and measurement of the phenotype itself. The research does not detail the specific criteria or methods used to define or quantify “abdominal_symptom,” which could lead to variability in how the trait is ascertained across different studies. Such phenotypic heterogeneity can obscure true genetic associations or lead to inconsistent findings, thereby complicating the interpretation and synthesis of results.
Furthermore, a substantial portion of the heritability for many complex traits remains unexplained by identified common genetic variants, a phenomenon known as “missing heritability” [9]. This gap suggests that factors beyond common SNPs, such as rare variants, structural variations, epigenetic modifications, or complex gene-gene and gene-environment interactions, contribute significantly to the genetic architecture of abdominal symptoms but are not fully captured by current GWAS methodologies. The influence of environmental factors and their interplay with genetic predispositions on abdominal symptoms are also areas that require more comprehensive investigation, as these unmeasured confounders can modulate the phenotypic expression of genetic risk.
Variants
Section titled “Variants”Genetic variations can influence a wide array of biological processes, impacting health and disease susceptibility, including the manifestation of abdominal symptoms. Two notable variants,rs74795203 and rs6916345 , are associated with genes involved in crucial cellular functions, selenoprotein synthesis, and ribosomal activity, respectively. rs74795203 is linked to the SEPHS1gene, which encodes Selenophosphate Synthetase 1, an enzyme essential for converting inorganic selenium into selenophosphate. Selenophosphate is the universal selenium donor required for the synthesis of all 25 human selenoproteins, which play vital roles in antioxidant defense, immune response, and thyroid hormone metabolism. A variant likers74795203 could potentially alter the efficiency of SEPHS1 enzyme activity or gene expression, leading to dysregulation of selenoprotein levels. Such disruptions can contribute to oxidative stress and inflammation, potentially affecting gastrointestinal health and manifesting as various abdominal symptoms.
The variant rs6916345 is located in a genomic region associated with RNU6-793P and RPL6P17, both of which are pseudogenes. RNU6-793P is a pseudogene of RNU6, a small nuclear RNA (snRNA) that is a critical component of the spliceosome, the molecular machine responsible for removing introns from pre-mRNA. While pseudogenes are often considered non-functional copies of genes, some can play regulatory roles, for instance, by acting as decoys for microRNAs or producing non-coding RNAs that influence the expression of their functional parent genes or other genes. Similarly, RPL6P17 is a pseudogene of RPL6, which codes for a ribosomal protein integral to the large ribosomal subunit, crucial for protein synthesis. Variations like rs6916345 , even within pseudogene regions, can impact gene regulation, potentially altering the expression of functional genes involved in RNA processing or protein production.
The broad influence of these genes on fundamental cellular processes underscores their potential relevance to abdominal health. Dysregulation of selenoprotein synthesis, as potentially influenced by SEPHS1 and rs74795203 , can impair the gut’s antioxidant capacity and immune function, leading to inflammation or compromised barrier integrity that contributes to abdominal discomfort. Similarly, alterations in RNA processing or protein synthesis, which could be subtly affected by variants likers6916345 near pseudogenes such as RNU6-793P and RPL6P17, can disrupt cellular homeostasis within the gastrointestinal tract. Such disruptions might manifest as a range of abdominal symptoms, from digestive issues to more severe conditions like abdominal aortic aneurysms [4], or general somatic complaints that frequently include abdominal discomfort [10]. Understanding these genetic underpinnings helps clarify the complex interplay between genetic predisposition and the manifestation of abdominal symptoms.
Key Variants
Section titled “Key Variants”| RS ID | Gene | Related Traits |
|---|---|---|
| rs74795203 | SEPHS1 | abdominal symptom |
| rs6916345 | RNU6-793P - RPL6P17 | abdominal symptom |
Causes
Section titled “Causes”Abdominal symptoms arise from a complex interplay of genetic predispositions, environmental exposures, and physiological factors. Understanding these causal pathways requires examining how inherited traits, lifestyle, and co-occurring conditions collectively influence the abdominal region.
Genetic Predisposition and Heritability of Abdominal Conditions
Section titled “Genetic Predisposition and Heritability of Abdominal Conditions”Genetic factors significantly contribute to an individual’s susceptibility to conditions that manifest as abdominal symptoms. Genome-wide association studies (GWAS) have identified specific inherited variants linked to such conditions. For instance, a sequence variant within the DAB2IP gene has been found to confer susceptibility to abdominal aortic aneurysm (AAA)[2], a serious condition affecting the abdominal vasculature. This highlights a direct genetic basis for the structural integrity of abdominal blood vessels, where specific gene alterations can increase the risk of developing weaknesses that lead to symptoms.
Beyond single gene variants, a polygenic risk model often contributes, where the cumulative effect of multiple genetic loci influences disease development. For example, genetic variants near the GATA3 gene are implicated in the inherited susceptibility and etiology of benign prostatic hyperplasia (BPH) and lower urinary tract symptoms (LUTS)[3], which can present with abdominal or pelvic discomfort. Research further indicates shared genetic risk factors among various types of aneurysms, including those occurring in the abdomen [4], underscoring a broader genetic predisposition to vascular vulnerabilities in the abdominal area.
Environmental and Lifestyle Influences on Abdominal Health
Section titled “Environmental and Lifestyle Influences on Abdominal Health”Environmental factors and lifestyle choices can profoundly influence abdominal health, often modulating the expression of genetic predispositions. While specific direct links between particular environmental exposures and the onset of general abdominal symptoms are complex and multifaceted, research has explored the genetic underpinnings of various lifestyle factors. For instance, genome-wide association studies have identified risk loci for nicotine dependence[11], illustrating how genetic susceptibility can interact with environmental exposures to shape health behaviors that, in turn, may impact overall bodily systems.
The intricate interplay between genetic predispositions and environmental factors can further shape an individual’s susceptibility to health issues. While the specific mechanisms linking environmental exposures to abdominal symptoms are complex, research in gene-environment interaction aims to elucidate how genetic variants might modify an individual’s response to lifestyle factors, diet, or other external influences. This dynamic interaction can ultimately impact the development and progression of various conditions, including those that manifest with abdominal discomfort, by altering physiological pathways or inflammatory responses.[12]
Developmental Factors, Epigenetics, and Comorbidities
Section titled “Developmental Factors, Epigenetics, and Comorbidities”The presence of other health conditions, or comorbidities, can significantly contribute to the development or exacerbation of abdominal symptoms. For instance, abdominal aortic aneurysm (AAA) is a distinct condition of the abdominal region where genetic factors, such as variants within the DAB2IP gene, confer susceptibility[2]. Similarly, benign prostatic hyperplasia (BPH) and associated lower urinary tract symptoms (LUTS) can cause discomfort and pain perceived in the lower abdomen or pelvic area[3], highlighting how conditions in adjacent organ systems can manifest as abdominal issues.
While detailed information on specific developmental and epigenetic factors directly linked to abdominal symptoms is not extensively provided, early life influences and epigenetic modifications, such as DNA methylation or histone modifications, are recognized as crucial regulators of gene expression and long-term health outcomes. Additionally, medication effects can sometimes contribute to or alleviate various symptoms, including those in the abdominal region. Although specific medications causing abdominal symptoms are not detailed, research has explored the genetic basis of drug efficacy for various treatments[13], indicating a complex interplay between genetics, therapeutics, and patient response.
Biological Background
Section titled “Biological Background”Abdominal symptoms can arise from a complex interplay of genetic factors, molecular pathways, and pathophysiological processes affecting various organs within the abdominal cavity. Understanding the biological underpinnings often involves examining specific conditions that manifest with such symptoms, such as abdominal aortic aneurysm (AAA) and benign prostatic hyperplasia (BPH), which can lead to lower urinary tract symptoms (LUTS).
Genetic Predisposition and Regulatory Mechanisms
Section titled “Genetic Predisposition and Regulatory Mechanisms”Genetic variants contribute significantly to the inherited susceptibility of conditions that cause abdominal symptoms. For instance, a specific sequence variant within the DAB2IPgene has been identified as conferring susceptibility to abdominal aortic aneurysm (AAA)[2]. Similarly, a variant in the low-density lipoprotein receptor-related protein 1 (LRP1) gene is also associated with AAA [14]. These genes likely play critical roles in the molecular pathways that govern vascular integrity and repair, where variations can disrupt normal function and increase risk.
Beyond vascular issues, genetic factors also influence conditions affecting other abdominal organs. For example, a genetic variant near the GATA3 gene is implicated in the inherited susceptibility and etiology of benign prostatic hyperplasia (BPH) and lower urinary tract symptoms (LUTS) [3]. GATA3 encodes a transcription factor crucial for the development and differentiation of various tissues, including the prostate, suggesting that altered gene expression or function due to these variants can predispose individuals to abnormal prostate growth and related symptoms.
Cellular Pathways and Biomolecular Functions
Section titled “Cellular Pathways and Biomolecular Functions”At the cellular level, the proteins encoded by genes such as DAB2IP and LRP1 are integral to maintaining vascular health and integrity. DAB2IP (DAB2-interacting protein) is involved in various signaling pathways, including those regulating cell proliferation, apoptosis, and cellular migration, processes critical for the structural maintenance and repair of arterial walls. LRP1, a large cell surface receptor, plays a key role in lipid metabolism, extracellular matrix remodeling, and cell signaling, all of which are essential for arterial wall homeostasis and preventing degenerative changes [14]. Disruptions in these functions can lead to weakening and dilation of the aorta, characteristic of AAA.
In the context of prostatic health, the GATA3 gene product, a GATA-binding transcription factor, acts as a master regulator influencing the expression of numerous downstream genes [3]. Its role in the regulation of cellular differentiation and growth pathways within the prostate gland is paramount. Aberrant GATA3 activity or expression due to genetic variants can lead to dysregulated cell proliferation and survival in prostate tissue, contributing to the development of benign prostatic hyperplasia, a condition characterized by excessive growth of the prostate gland.
Pathophysiological Processes and Homeostatic Disruptions
Section titled “Pathophysiological Processes and Homeostatic Disruptions”Abdominal symptoms often arise from pathophysiological processes that disrupt normal organ function and homeostasis. Abdominal aortic aneurysm (AAA), for instance, involves a progressive weakening and dilation of the abdominal aorta, often driven by chronic inflammation, enzymatic degradation of the arterial wall, and impaired repair mechanisms. This degenerative process is strongly linked to subclinical atherosclerosis, where the accumulation of plaque in arterial territories contributes to arterial stiffness and damage, predisposing individuals to aneurysm formation[15]. The inability of the arterial wall to maintain its structural integrity under normal hemodynamic stress represents a significant homeostatic disruption.
Another common source of abdominal symptoms, particularly lower urinary tract symptoms, is benign prostatic hyperplasia (BPH). BPH is a non-malignant enlargement of the prostate gland, a developmental process that typically occurs with aging. This enlargement compresses the urethra, leading to symptoms such as urinary frequency, urgency, and difficulty voiding. The underlying mechanisms involve complex interactions of hormones, growth factors, and stromal-epithelial cell interactions within the prostate, where genetic predispositions, such as those involvingGATA3, can influence the abnormal proliferation of prostatic cells and the disruption of normal tissue architecture [3].
Organ-Specific Manifestations and Systemic Impacts
Section titled “Organ-Specific Manifestations and Systemic Impacts”The manifestation of abdominal symptoms is highly dependent on the specific organs affected and their interactions within the abdominal cavity. In the case of AAA, the primary organ involved is the abdominal aorta, a major blood vessel. The progressive dilation of this vessel can lead to localized pressure on surrounding tissues and nerves, potentially causing pain or discomfort. More critically, the weakened arterial wall is at risk of rupture, a life-threatening systemic consequence, highlighting the profound impact of localized tissue pathology on overall physiological stability[2], [14].
For BPH, the prostate gland, located inferior to the bladder, undergoes hyperplasia. While the prostate itself is the site of the primary pathology, the symptoms (LUTS) are a direct consequence of its interaction with the urinary tract [3]. The enlarged gland obstructs urine flow from the bladder, leading to symptoms that affect the quality of life and, if severe, can cause bladder dysfunction, urinary tract infections, or even kidney damage. These examples illustrate how specific tissue changes within an abdominal organ can elicit a range of localized and systemic symptoms, impacting the overall abdominal region and beyond.
Pathways and Mechanisms
Section titled “Pathways and Mechanisms”Genetic Basis of Abdominal Aneurysm Susceptibility
Section titled “Genetic Basis of Abdominal Aneurysm Susceptibility”A key mechanism underlying certain abdominal symptoms, specifically abdominal aortic aneurysm, involves genetic susceptibility. Genome-wide association studies (GWAS) are instrumental in identifying genetic variations, or risk loci, that contribute to disease predisposition . Such genetic markers are crucial for identifying individuals at higher risk of developing these potentially severe conditions, enabling personalized screening programs and earlier diagnostic interventions. Similarly, a genetic variant near GATA3 has been implicated in the inherited susceptibility and etiology of benign prostatic hyperplasia (BPH) and lower urinary tract symptoms (LUTS), which often involve abdominal discomfort or pain[3]. These findings support the integration of genetic information into clinical practice to stratify risk and guide targeted surveillance strategies for at-risk populations. Early identification through genetic screening could facilitate timely medical imaging or specialized evaluations, potentially leading to interventions before symptom onset or disease progression. This personalized medicine approach holds promise for improving patient outcomes by shifting from reactive treatment to proactive prevention and early management.
Prognostic Insights and Management Strategies
Section titled “Prognostic Insights and Management Strategies”The identification of genetic predispositions offers valuable prognostic insights for conditions associated with abdominal symptoms, predicting an individual’s likelihood of developing the disease. For example, understanding susceptibility variants for Abdominal Aortic Aneurysm (AAA) can inform clinicians about the long-term risk of aneurysm formation and progression, guiding surveillance frequency and intensity for optimal patient care[16]. While direct prognostication of treatment response for general abdominal symptoms is complex and multifactorial, genetic markers for specific conditions like AAA or lower urinary tract symptoms (LUTS) can inform disease trajectories. This genetic understanding allows for more informed patient counseling regarding potential disease courses and supports the development of tailored management strategies. For instance, individuals identified with a genetic susceptibility to LUTS and benign prostatic hyperplasia (BPH) via variants like GATA3 could benefit from earlier lifestyle modifications or pharmacological interventions, potentially mitigating symptom severity or disease progression[3]. Such approaches aim to optimize patient care by anticipating future health challenges and implementing preventive or early therapeutic measures.
Overlapping Phenotypes and Related Conditions
Section titled “Overlapping Phenotypes and Related Conditions”Genetic research has begun to unravel shared genetic architectures and overlapping phenotypes among conditions manifesting with abdominal symptoms, enhancing our understanding of their underlying etiologies. A notable example is the genetic variant near GATA3, which has been implicated in the inherited susceptibility to both benign prostatic hyperplasia (BPH) and lower urinary tract symptoms (LUTS), highlighting a shared genetic pathway for these related conditions [3]. This indicates that some genetic factors might predispose individuals to a constellation of symptoms or conditions within the abdominal and pelvic regions, rather than isolated disorders. Recognizing these shared genetic underpinnings can lead to a more holistic approach to patient assessment, where the presence of one condition might prompt screening for genetically related disorders. This integrated perspective can improve diagnostic efficiency and inform comprehensive management plans that address the spectrum of an individual’s genetic predispositions. Further research into these shared genetic links could uncover novel therapeutic targets that are effective across multiple related abdominal conditions.
Frequently Asked Questions About Abdominal_Symptom
Section titled “Frequently Asked Questions About Abdominal_Symptom”These questions address the most important and specific aspects of abdominal_symptom based on current genetic research.
1. My parents have gut issues; will I get them too?
Section titled “1. My parents have gut issues; will I get them too?”Yes, there’s a good chance you might. Genetic predispositions play a significant role in susceptibility to various conditions that cause abdominal symptoms. If your parents have certain genetic variants, you could inherit those, increasing your risk for similar experiences. This highlights how family history can be a clue to your own potential health challenges.
2. Why do my stomach problems seem worse than my friend’s, even if we eat the same?
Section titled “2. Why do my stomach problems seem worse than my friend’s, even if we eat the same?”It’s not just about what you eat; your genetics can make a big difference. Even with similar lifestyles, genetic variants you carry can influence how your digestive system, nervous system, and immune responses interact, leading to different levels of discomfort or different symptoms. This is part of why abdominal symptoms are so complex and vary widely among individuals.
3. Does my ethnic background affect my risk for stomach problems?
Section titled “3. Does my ethnic background affect my risk for stomach problems?”Yes, your ancestry can play a role. Genetic findings are sometimes limited by the populations studied, with many large datasets having a bias towards individuals of European descent. This means different genetic risk factors might be more common or act differently in various ethnic groups, affecting your specific susceptibility to certain conditions. Research is ongoing to better understand these differences across diverse populations.
4. Could a DNA test tell me why I get so much indigestion?
Section titled “4. Could a DNA test tell me why I get so much indigestion?”A DNA test might offer some clues, but it’s not a complete answer yet. Genetic variants identified through studies can help with risk assessment for conditionsthat cause abdominal symptoms, like lower urinary tract symptoms or abdominal aortic aneurysm. While it can inform your inherited susceptibility, the direct genetic causes for general indigestion are still being researched and are often complex.
5. Can healthy eating overcome my family history of abdominal pain?
Section titled “5. Can healthy eating overcome my family history of abdominal pain?”While healthy eating is always beneficial, genetics can make it more challenging to completely overcome a strong family history. Your inherited genetic predispositions can significantly influence your susceptibility to conditions that cause abdominal pain. However, lifestyle choices like diet are environmental factors that interact with your genes, and they can certainly help manage or reduce the severity of symptoms, even if they don’t erase the genetic risk entirely.
6. Does stress really make my stomach hurt more, or is it just me?
Section titled “6. Does stress really make my stomach hurt more, or is it just me?”It’s not just you; stress can absolutely impact your stomach. The biological basis of abdominal symptoms involves complex interactions between your digestive system and your nervous system. While genetics influences your baseline susceptibility, environmental factors like stress can trigger or worsen symptoms by affecting these intricate biological pathways. So, your body’s response to stress can indeed manifest as increased abdominal discomfort.
7. Why do my stomach issues keep coming back, unlike others I know?
Section titled “7. Why do my stomach issues keep coming back, unlike others I know?”Your genetic makeup likely plays a role in the persistence of your symptoms. Genetic predispositions can make you more susceptible to chronic conditions that manifest with recurring abdominal symptoms. For some people, specific genetic variants might influence how their body responds to triggers or how effectively it recovers, leading to ongoing discomfort that others might not experience.
8. Why do some treatments work for others’ stomach issues but not mine?
Section titled “8. Why do some treatments work for others’ stomach issues but not mine?”Your unique genetic profile can influence how you respond to different treatments. Genetic factors associated with abdominal symptoms are being studied to contribute to personalized medicine, aiding in the development of targeted therapies. What works for someone else might not be effective for you because of differences in your inherited susceptibility and how your body processes or reacts to specific interventions.
9. Can my genes tell me if I’m at risk for serious abdominal problems later?
Section titled “9. Can my genes tell me if I’m at risk for serious abdominal problems later?”Yes, to some extent, your genes can provide insights into future risks. Genetic studies are identifying variants linked to conditions like abdominal aortic aneurysm or lower urinary tract symptoms, which can present with abdominal discomfort. Understanding these genetic links can contribute to risk assessment and early detection, potentially allowing for preventive strategies or earlier intervention for serious conditions.
10. Why do some people just seem to have ‘iron stomachs’ no matter what they eat?
Section titled “10. Why do some people just seem to have ‘iron stomachs’ no matter what they eat?”It’s likely due to their unique genetic makeup and how it interacts with their environment. Some individuals may have genetic variants that confer greater resilience or different biological responses in their digestive, nervous, or immune systems. This can make them less susceptible to discomfort even when exposed to factors that cause symptoms in others, giving them what seems like an “iron stomach.”
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
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[12] Sherva, R. “Genome-wide Association Study of Cannabis Dependence Severity, Novel Risk Variants, and Shared Genetic Risks.”JAMA Psychiatry, vol. 73, no. 5, May 2016, pp. 478-485.
[13] Li, Q. et al. “Genome-wide association study of paliperidone efficacy.” Pharmacogenet Genomics, 2016.
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[16] Jones, G. T., et al. “Meta-Analysis of Genome-Wide Association Studies for Abdominal Aortic Aneurysm Identifies Four New Disease-Specific Risk Loci.”Circ Res, vol. 119, no. 12, 2016, pp. 1291-1301. PMID: 27899403.