Docosapentaenoic Acid
Introduction
Section titled “Introduction”Docosapentaenoic acid (DPA) is a polyunsaturated fatty acid (PUFA) that plays a role in human metabolism and health. It exists in both omega-3 (n-3) and omega-6 (n-6) forms, with the n-3 form often considered an intermediate in the metabolic pathway between eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA).[1] Levels of DPA can be measured in various biological samples, such as plasma phospholipids and red blood cells.[1], [2], [3]
Biological Basis
Section titled “Biological Basis”The metabolism of DPA, particularly n-3 DPA, is influenced by several genes. Key enzymes involved in the synthesis of PUFAs are encoded by the desaturase genes FADS1 and FADS2, and the elongase gene ELOVL2.[1], [4], [5]Genetic variants, or single nucleotide polymorphisms (SNPs), within or near these genes are significantly associated with DPA levels. For example, SNPs in theELOVL2 region, such as rs12662634 , have been identified as highly associated with DPA levels.[1], [3] Other genes like GCKR (most associated SNP: rs780094 ) and AGPAT3 on chromosome 21, involved in phospholipid metabolism, also show associations with DPA levels.[1] Beyond metabolism, DPA (n-6) has been observed to interact with SNPs near the CHCHD3 gene on chromosome 7, affecting inflammatory biomarkers like ICAM.[6]This gene codes for an inner mitochondrial membrane scaffold protein essential for mitochondrial function and crista integrity, which is relevant to cardiovascular and neurodegenerative diseases.[6]
Clinical Relevance
Section titled “Clinical Relevance”DPA, particularly the n-3 form, has been linked to several important health outcomes. Studies have shown an inverse association between red blood cell DPA (n-3) and triglycerides and C-reactive protein (CRP) in healthy adults.[2]CRP is a known inflammatory biomarker and a risk factor for cardiovascular disease (CVD).[6] Higher levels of n-3 DPA have also been associated with a reduced risk of acute coronary events.[7] The genetic interactions involving DPA(N6) and SNPs near CHCHD3 suggest a potential impact on CVD.[6]Furthermore, omega-3 PUFAs generally, including DPA, are correlated with cognitive function and brain development, and their levels can be influenced by dietary intake, such as fish consumption.[6], [8], [9]
Social Importance
Section titled “Social Importance”Understanding the genetic and environmental factors that influence DPA levels holds significant social importance. By identifying genetic variants associated with DPA, researchers can move towards personalized dietary recommendations for optimal fatty acid intake, potentially modulating genetic risk for various diseases.[6]Given its links to cardiovascular health, inflammation, and cognitive function, DPA is a valuable biomarker for public health initiatives. Large-scale genomic studies, such as those conducted by the CHARGE Consortium and the Framingham Heart Study, contribute to this understanding by examining genetic associations with fatty acid levels and their impact on health outcomes.[1], [6], [10], [11], [12]This research supports the development of precision nutrition strategies aimed at disease prevention and health promotion.
Methodological and Statistical Constraints
Section titled “Methodological and Statistical Constraints”The interpretability of findings regarding docosapentaenoic acid levels is subject to several methodological and statistical limitations. Many studies, particularly those involving family-based cohorts like Framingham, faced reduced effective sample sizes due to shared genetic backgrounds, which consequently limited the statistical power to identify associated genetic variants.[3] While conservative significance levels were employed to protect against false positives, this approach inherently decreased the ability to detect true associations, especially for variants with smaller effect sizes.[3] Additionally, some research on gene-fatty acid interactions utilized preliminary significance thresholds rather than the more stringent genome-wide association study (GWAS) significance level, potentially impacting the robustness and replicability of these specific findings.[8]Furthermore, the scope of genetic variation investigated has largely been confined to common variants, leaving the potential contributions of rare genetic variations to docosapentaenoic acid levels largely unexplored.[3] The inherent biological reality of high inter-correlation among various red blood cell fatty acids also complicates analysis, suggesting a need for more sophisticated models that explicitly account for this complex correlation structure, rather than analyzing single fatty acids in isolation.[3] The cross-sectional nature of some studies further limits the generalizability and predictive power of the results, as they capture a snapshot rather than longitudinal changes or causal relationships.[8]
Generalizability and Phenotype Heterogeneity
Section titled “Generalizability and Phenotype Heterogeneity”The generalizability of genetic associations with docosapentaenoic acid levels is limited by population ancestry differences. While some gene associations, such as those involvingFADS1/2, demonstrated consistency across diverse ancestries including European, African, Chinese, and Hispanic populations, other key associations, like those with ELOVL2, were less consistent.[1] This inconsistency can be attributed to substantial variation in allele frequencies across ancestries, as well as inadequate statistical power in non-European cohorts due to smaller sample sizes, which restricts the direct applicability of findings to a global population.[1]A critical limitation across multiple studies is the frequent lack of comprehensive dietary intake data. Docosapentaenoic acid levels are significantly influenced by diet, and the absence of detailed dietary information, especially regarding essential fatty acids, means that environmental factors heavily impacting fatty acid metabolism are not fully accounted for.[3] This omission can diminish the ability to accurately detect and quantify genetic influences, potentially leading to an overestimation of heritability when dietary contributions are not considered.[3]Moreover, different studies measured docosapentaenoic acid in various biological matrices, such as total plasma, plasma phospholipids, or red blood cells, each reflecting distinct aspects of fatty acid metabolism and recent dietary intake, which can introduce heterogeneity and challenges in comparing and interpreting results across studies.[1]
Incomplete Understanding of Genetic Architecture and Environmental Interactions
Section titled “Incomplete Understanding of Genetic Architecture and Environmental Interactions”Despite significant discoveries, a substantial portion of the genetic variance in docosapentaenoic acid levels remains unexplained, highlighting the challenge of “missing heritability.” The identified common variants typically account for only a small percentage of the observed variance in fatty acid levels, ranging from 0.4% to 8.6% for different fatty acids.[1] This suggests that much of the genetic influence might stem from rare variants, complex gene-gene interactions, epigenetic modifications, or gene-environment interactions that are not fully captured by current genome-wide association studies.
The intricate interplay between genetic predispositions and environmental factors, particularly dietary intake, represents a complex area that is not yet fully elucidated. While some studies have begun to explore gene-diet interactions, a comprehensive understanding of how an individual’s genetic background modulates their optimal dietary fatty acid intake remains a significant knowledge gap.[6]This incomplete understanding limits the development of precise, personalized nutritional recommendations for managing docosapentaenoic acid levels and related health outcomes. Furthermore, some identified genetic loci associated with docosapentaenoic acid are located in genes (e.g.,PDXDC1, GCKR, AGPAT3, CHCHD3) with previously uncharacterized roles in fatty acid metabolism or cardiovascular health, underscoring the ongoing need for functional studies to fully understand their biological mechanisms and clinical relevance.[1], [6]
Variants
Section titled “Variants”Genetic variations play a crucial role in determining an individual’s docosapentaenoic acid (DPA) levels, primarily by influencing the efficiency of fatty acid metabolism pathways. Key genes involved in the synthesis of long-chain polyunsaturated fatty acids (PUFAs) include the fatty acid desaturase (FADS) gene cluster and the elongase (ELOVL) genes. The FADS1, FADS2, and FADS3 genes, located on chromosome 11, encode enzymes that introduce double bonds into fatty acid chains, a critical step in converting essential fatty acids into longer, more unsaturated forms like DPA. For instance, FADS1 is responsible for delta-5 desaturation, while FADS2 performs delta-6 desaturation, both vital for n-3 and n-6 PUFA synthesis.[3] Variants within this cluster, such as rs174547 , have been significantly associated with DPA levels, with the C/T allele of rs174547 showing an association with DPA in large meta-analyses.[1] The G allele of rs174548 (a variant in FADS1 often in linkage disequilibrium with rs174547 ) is associated with lower long-chain n-3 PUFA levels, including DPA.[1] Additionally, the FADS2 variant rs1535 has been shown to interact with plasma alpha-linolenic acid (ALA) levels in influencing eicosapentaenoic acid (EPA) levels, demonstrating the complex interplay between genetics and dietary fatty acids.[1] Other variants in this region, including rs174567 , rs4246215 (involving FADS2 and FEN1), and rs174448 (between FADS2 and FADS3), further underscore the cluster’s broad influence on fatty acid profiles.
Another critical gene for DPA and other long-chain n-3 PUFAs is ELOVL2(Elongation Of Very Long Chain Fatty Acids 2), which encodes an enzyme responsible for elongating fatty acids, including the conversion of DPA to docosahexaenoic acid (DHA). Genetic variations inELOVL2 are strongly associated with plasma phospholipid levels of DPA, EPA, and DHA.[1] For example, the rs3734398 variant in ELOVL2 is particularly influential; its C allele is associated with higher DPA levels and lower DHA levels in individuals of Hispanic ancestry, while it is associated with EPA, DPA, and DHA in European and African ancestries.[1] Other variants in this region, such as rs8523 in ELOVL2 and rs1321535 in ELOVL2-AS1 (an antisense RNA that regulates ELOVL2 expression), contribute to the genetic regulation of fatty acid elongation and, consequently, DPA concentrations. These associations highlight how genetic differences in elongation capacity can impact the availability of various n-3 PUFAs, influencing overall metabolic health.
Beyond the core FADS and ELOVL pathways, other genetic loci also contribute to DPA levels. Variants in genes like TMEM258 and MYRF have been implicated in fatty acid metabolism. Specifically, the rs174535 variant, located within or near TMEM258 and MYRF, is associated with DPA levels.[1] While the precise mechanisms by which TMEM258 (a transmembrane protein) or MYRF (Myelin Regulatory Factor) influence DPA are still under investigation, their genetic variations, including rs102275 and rs102274 in TMEM258, suggest broader regulatory roles in lipid homeostasis. Furthermore, variants like rs4713103 in SYCP2L (Synaptonemal Complex Protein 2 Like) and rs174468 in the FADS3 - RAB3IL1 region (RAB3B Interacting Protein 1 Like) also represent regions of interest, indicating that a complex network of genes, not just those directly involved in desaturation and elongation, influences circulating DPA levels. These diverse genetic influences collectively shape an individual’s capacity to process and maintain optimal levels of DPA, which is an important intermediate n-3 fatty acid linked to various health outcomes.
Docosapentaenoic Acid: Definition and Nomenclature
Section titled “Docosapentaenoic Acid: Definition and Nomenclature”Docosapentaenoic acid (DPA) is a long-chain polyunsaturated fatty acid (PUFA).[1] It exists in two primary forms: omega-3 DPA (DPA n-3) and omega-6 DPA (DPA n-6).[3]The “n-3” and “n-6” designations refer to the position of the first double bond from the methyl end of the fatty acid chain, which critically influences their metabolic pathways and biological functions. DPA n-3 is recognized as one of the main omega-3 PUFA species, alongside alpha-linolenic acid (ALA), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA).[8] These distinctions are crucial for understanding their dietary sources, metabolic interconversions, and varied roles in human health.
The precise terminology of DPA reflects its molecular structure and its classification within the broader family of fatty acids. DPA n-3, often derived from fish oil, has been studied for its association with cardiovascular health.[7] In genetic studies, DPA levels are often expressed as a percentage of total fatty acids in plasma phospholipids, with observed mean levels varying across cohorts, for instance, from 0.83% to 0.98%.[1] These operational definitions allow for standardized quantification and comparison of DPA levels in research and clinical settings, acknowledging the different biological matrices where it can be measured.
Classification and Biological Context
Section titled “Classification and Biological Context”Docosapentaenoic acid is classified based on its omega family, which dictates its metabolic origin and potential physiological roles. DPA n-3 is an intermediate product in the metabolic pathway that converts ALA to EPA and DHA, with enzymes like delta-6 desaturase playing a key role in its synthesis.[5] Genetic variations within gene clusters such as FADS1/FADS2 are known to influence the composition of n-3 PUFAs, including DPA, in biological tissues.[1] This genetic influence highlights the interplay between dietary intake and endogenous fatty acid metabolism in determining an individual’s DPA status.
The different DPA forms exhibit distinct biological activities and clinical associations. For example, DPA n-3 has been found to be inversely associated with inflammatory biomarkers such as C-reactive protein (CRP) and with triglyceride levels in healthy adults, suggesting a beneficial role in cardiovascular health.[2] In contrast, DPA n-6, while present, is also studied for its interactions with specific genetic variants, such as rs17424324 and rs17424227 near the CHCHD3gene, which may influence cardiovascular disease risk.[6] These classifications underscore the importance of differentiating between DPA n-3 and DPA n-6 when evaluating their impact on health outcomes.
Diagnostic Criteria and Approaches
Section titled “Diagnostic Criteria and Approaches”The assessment of docosapentaenoic acid levels relies on precise approaches, which are critical for both clinical diagnostics and research. Fatty acid composition is commonly analyzed in biological samples such as red blood cells (RBCs) or plasma phospholipids.[13] A standard method involves gas chromatography, where fatty acids are typically extracted and transesterified to fatty acid methyl esters (FAMEs) before analysis.[3] This technique predominantly quantifies fatty acids from glycerophospholipids in RBCs, providing a reliable reflection of long-term fatty acid status.[3] In genetic association studies, DPA levels serve as quantitative traits, with statistical analyses often employing linear regression models to assess associations between genetic variants and fatty acid concentrations.[1] These analyses typically adjust for confounding factors such as age, sex, and population genetic substructure to ensure robust findings.[1]While specific diagnostic cut-off values for DPA are not universally established for disease classification, its levels are recognized as biomarkers that can indicate dietary intake and influence risk for conditions like acute coronary events.[13] The interpretation of DPA levels often considers its correlation with other n-3 PUFAs like EPA and DHA, and the influence of genetic loci such as ELOVL2, GCKR, and AGPAT3 on its plasma concentrations.[1]
Biological Background
Section titled “Biological Background”Docosapentaenoic acid (DPA) is a polyunsaturated fatty acid (PUFA) that exists in both n-3 (omega-3) and n-6 (omega-6) forms, playing diverse roles in human physiology. Its levels in the body, often assessed in red blood cell glycerophospholipids or plasma phospholipids, are influenced by a complex interplay of dietary intake, genetic predisposition, and metabolic processes.[1], [3], [14]DPA’s significance stems from its involvement in cellular membrane structure, signaling pathways, and its associations with various health outcomes, including cardiovascular and cognitive health.
Docosapentaenoic Acid: Sources and Metabolism
Section titled “Docosapentaenoic Acid: Sources and Metabolism”Docosapentaenoic acid, particularly the n-3 variant, is a long-chain polyunsaturated fatty acid that can be obtained directly from the diet or synthesized endogenously from its precursor, alpha-linolenic acid (ALA), an essential dietary fatty acid.[3]The metabolic pathway for converting ALA into longer-chain omega-3 fatty acids, including DPA and ultimately docosahexaenoic acid (DHA), involves a series of desaturation and elongation steps.[15] Key enzymes in this metabolic cascade are the delta-5 and delta-6 desaturases, encoded by genes within the FADS1-FADS2 gene cluster, which introduce double bonds into fatty acid chains.[4], [5], [16] Following desaturation, fatty acid chains are elongated by enzymes such as those encoded by the ELOVL2 gene, which is critical for extending DPA into DHA.[1] The efficiency of these conversions, particularly the conversion of DPA-n3 to tetracosahexaenoic acid (TPA) via ELOVL2, can be a rate-limiting factor in determining the overall DPA-n3 content in cellular membranes.[3]
Genetic Regulation of Docosapentaenoic Acid Levels
Section titled “Genetic Regulation of Docosapentaenoic Acid Levels”Individual docosapentaenoic acid (DPA) levels are significantly influenced by genetic variations, as revealed by genome-wide association studies (GWAS).[1], [3] The FADS1-FADS2gene cluster on chromosome 11 is a primary genetic locus associated with DPA concentrations, with specific single nucleotide polymorphisms (SNPs) in this region influencing the activity of delta-5 and delta-6 desaturases, which are crucial for polyunsaturated fatty acid synthesis.[1] These genetic variants can explain a substantial portion of the variability in DPA levels, directly impacting the body’s capacity to synthesize these fatty acids.
Another key genetic determinant is the ELOVL2 gene region, where SNPs such as rs12662634 and rs8523 are strongly associated with DPA-n3 levels.[1], [3] The ELOVL2 gene codes for an elongase enzyme that plays a vital role in extending fatty acid chains, thus directly affecting the production of DPA and its subsequent conversion to other longer-chain polyunsaturated fatty acids.[1], [3] These genetic insights highlight how an individual’s inherited genetic makeup can modulate the metabolism and circulating levels of DPA.
Furthermore, other genes such as GCKR(glucokinase regulatory protein) on chromosome 2 andAGPAT3(1-acylglycerol-3-phosphate O-acyltransferase 3) on chromosome 21 have also been linked to DPA levels.[1] These associations suggest that DPA concentrations are influenced by a broader network of genes involved in lipid and phospholipid metabolism, underscoring the complex genetic architecture underlying fatty acid homeostasis. The interaction between DPA(N6) and SNPs like rs17424324 and rs17424227 near the CHCHD3 gene on chromosome 7 has also been identified as a predictor for inflammatory biomarkers, further demonstrating the intricate gene-fatty acid interactions that impact health.[6]
Cellular and Molecular Functions of Docosapentaenoic Acid
Section titled “Cellular and Molecular Functions of Docosapentaenoic Acid”Docosapentaenoic acid, particularly the omega-3 form, is a critical component of cellular membranes, where it is primarily incorporated into glycerophospholipids, such as those found in red blood cells.[3] Its presence contributes to the fluidity, integrity, and overall function of these membranes, which are essential for cellular processes like signal transduction, receptor binding, and ion channel activity. Beyond its structural role, DPA and other omega-3 fatty acids serve as precursors for the synthesis of various signaling molecules, influencing diverse cellular pathways that regulate inflammation, immunity, and cell growth.
DPA’s influence extends to critical cellular organelles, including mitochondria. Genetic interactions involving DPA(N6) and single nucleotide polymorphisms (SNPs) near theCHCHD3 gene on chromosome 7 have been observed, with implications for cellular health.[6] The CHCHD3 gene encodes an inner mitochondrial membrane scaffold protein that is vital for maintaining the structural integrity of mitochondrial cristae, which are essential for efficient energy production through oxidative phosphorylation.[6]Disruptions in crista structure are implicated in various cardiovascular and neurodegenerative diseases, suggesting that DPA, through its interaction with proteins likeCHCHD3, may play a role in modulating mitochondrial function and cellular resilience.[6]In the brain, DPA and its related omega-3 fatty acids contribute to neuroplasticity and maintain membrane homeostasis, which are fundamental for optimal cognitive function.[17] These fatty acids modulate neurotransmission and are crucial for brain development and the maintenance of cognitive abilities throughout life.[18], [19] The integration of DPA into neural cell membranes underscores its importance in supporting complex brain functions and protecting against neurological insults.[20], [21]
Docosapentaenoic Acid and Systemic Health: Pathophysiological Implications
Section titled “Docosapentaenoic Acid and Systemic Health: Pathophysiological Implications”Docosapentaenoic acid, particularly the n-3 variant, is increasingly recognized for its significant contributions to systemic health and its association with the prevention and progression of various diseases. DPA-n3 has been shown to be inversely associated with levels of triglycerides and C-reactive protein (CRP), both of which are established inflammatory biomarkers and independent risk factors for cardiovascular disease.[2], [6]This suggests a crucial role for DPA in modulating inflammatory responses and contributing to the maintenance of cardiovascular health, potentially by influencing lipid metabolism and reducing systemic inflammation.
Beyond cardiovascular health, DPA and other omega-3 polyunsaturated fatty acids (PUFAs) are linked to improved neurological function and protection against cognitive decline.[6] Studies indicate that omega-3 supplementation can enhance cognition, modulate brain activation, and offer protection against learning impairment in models of neurodegenerative diseases.[17], [20], [21] The interaction between DPA(N6) and genetic variants near the CHCHD3gene, which codes for a protein essential for mitochondrial crista integrity, further implicates DPA in the pathophysiology of cardiovascular and neurodegenerative diseases by affecting mitochondrial function.[6]Furthermore, DPA, along with docosahexaenoic acid (DHA), derived from fish oil, is associated with a reduced risk of acute coronary events and influences various other disease phenotypes, including overall mortality, serum lipid levels, and brain size.[6], [7], [22]These broad systemic effects underscore DPA’s crucial role in maintaining homeostasis and its potential as a biomarker for assessing and managing disease risk.
Metabolic Regulation and Genetic Influences on Docosapentaenoic Acid Synthesis
Section titled “Metabolic Regulation and Genetic Influences on Docosapentaenoic Acid Synthesis”The synthesis and metabolism of docosapentaenoic acid (DPA) are intricately regulated by a network of enzymes, with genetic variations significantly influencing its levels. Key among these are genes within theFADS (Fatty Acid Desaturase) cluster, specifically FADS1 and FADS2, which encode delta-5 and delta-6 desaturases essential for the desaturation steps in polyunsaturated fatty acid (PUFA) biosynthesis. Single nucleotide polymorphisms (SNPs) in this cluster are associated with the activity of these desaturases, thereby impacting the ratios of various fatty acids in serum . Since CRP is a known inflammatory biomarker and a risk factor for cardiovascular disease (CVD), these findings suggest that DPA n-3 could serve as a valuable indicator for assessing and monitoring cardiovascular risk and inflammation.[6] Furthermore, DPA n-3 levels have been shown to increase in a dose-dependent manner following n-3 fatty acid supplementation, highlighting a potential for dietary intervention.[2]Beyond its association with inflammatory markers, DPA (n-3) has demonstrated prognostic value for cardiovascular outcomes. Research suggests that fish oil-derived fatty acids, including DPA, are linked to a reduced risk of acute coronary events and may act as a negative risk factor for myocardial infarction.[7]This evidence positions DPA as a relevant biomarker for predicting disease progression and long-term implications in cardiovascular health. Additionally, genetic interactions, such as those between docosapentaenoic acid (n-6) and single nucleotide polymorphisms (SNPs) near theCHCHD3 gene, have been explored for their potential impact on CVD, given that CHCHD3is essential for mitochondrial function, and its disruption is implicated in cardiovascular diseases.[6]
Docosapentaenoic Acid and Cognitive Function
Section titled “Docosapentaenoic Acid and Cognitive Function”Docosapentaenoic acid (DPA), as one of the key omega-3 polyunsaturated fatty acid (PUFA) species, holds relevance for neurological and cognitive function. Research has linked general omega-3 fatty acid levels to cognitive function and brain size, suggesting DPA’s broader involvement in brain health.[6], [8]While related omega-3s like docosahexaenoic acid (DHA) have been more extensively studied for their protective effects against learning impairment in Alzheimer’s models, beneficial impacts on cognition, neuroplasticity, and neurotransmission.[23], [24] DPA’s specific contributions to these outcomes are an active area of investigation.
Ongoing prospective cohort studies are examining the association between blood omega-3 fatty acids, including DPA, and incident dementia or cognitive decline.[8] These investigations aim to determine if DPA levels could serve as a diagnostic utility or risk assessment tool for cognitive impairments, potentially overlapping with conditions such as depression, where omega-3 PUFAs have shown efficacy . The use of standardized cognitive assessments, such as the Trail Making Test, in these studies helps to characterize the relationship between omega-3 PUFAs and various aspects of cognitive performance, offering insights into potential monitoring strategies and long-term implications for brain health.[8]
Genetic Influences and Personalized Approaches to Docosapentaenoic Acid Levels
Section titled “Genetic Influences and Personalized Approaches to Docosapentaenoic Acid Levels”The of docosapentaenoic acid (DPA) is particularly relevant in the context of personalized medicine due to significant genetic influences on its levels and biological effects. Genome-wide association studies (GWAS) have identified several genetic loci strongly associated with circulating DPA concentrations. These include specific SNPs on chromosome 6, variants within theGCKR gene on chromosome 2, and a possible association with AGPAT3 on chromosome 21, a gene involved in phospholipid metabolism.[1] Crucially, the ELOVL2 region on chromosome 11 has reached genome-wide significance for its strong association with DPA-n3 levels, indicating a major genetic determinant.[1], [3] Understanding these genetic factors is essential for risk stratification and developing personalized prevention and treatment strategies. An individual’s unique genetic background can significantly influence their response to dietary or supplemental omega-3 interventions, suggesting that optimal dietary fatty acid intake may vary by individual.[6], [8]This genetic insight can help identify individuals at higher risk for certain conditions or those most likely to benefit from specific interventions, such as increasing DPA intake through diet or supplementation. Such personalized approaches can refine treatment selection and monitoring strategies, leading to more targeted and effective patient care for conditions influenced by DPA levels, including cardiovascular and cognitive health.[8]
Key Variants
Section titled “Key Variants”| RS ID | Gene | Related Traits |
|---|---|---|
| rs174547 rs174567 | FADS1, FADS2 | metabolite high density lipoprotein cholesterol triglyceride comprehensive strength index, muscle heart rate |
| rs102275 rs102274 | TMEM258 | coronary artery calcification Crohn’s disease fatty acid amount high density lipoprotein cholesterol , metabolic syndrome phospholipid amount |
| rs1535 | FADS2 | inflammatory bowel disease high density lipoprotein cholesterol , metabolic syndrome response to statin level of phosphatidylcholine level of phosphatidylethanolamine |
| rs174535 | TMEM258, MYRF | ankylosing spondylitis, psoriasis, ulcerative colitis, Crohn’s disease, sclerosing cholangitis fatty acid amount, oleic acid triacylglycerol 56:7 cholesteryl ester 18:3 docosapentaenoic acid |
| rs4246215 | FEN1, FADS2 | fatty acid amount, linoleic acid inflammatory bowel disease alpha-linolenic acid eicosapentaenoic acid docosapentaenoic acid |
| rs174448 | FADS2 - FADS3 | alpha-linolenic acid docosapentaenoic acid eicosapentaenoic acid cis/trans-18:2 fatty acid , trans fatty acid serum metabolite level |
| rs3734398 rs8523 | ELOVL2 | docosapentaenoic acid level of phosphatidylcholine docosapentaenoate n3 DPA; 22:5n3 |
| rs1321535 | ELOVL2-AS1 | eicosapentaenoic acid docosapentaenoic acid |
| rs4713103 | SYCP2L | docosahexaenoic acid docosapentaenoic acid |
| rs174468 | FADS3 - RAB3IL1 | eicosapentaenoic acid alpha-linolenic acid docosapentaenoic acid |
Frequently Asked Questions About Docosapentaenoic Acid
Section titled “Frequently Asked Questions About Docosapentaenoic Acid”These questions address the most important and specific aspects of docosapentaenoic acid based on current genetic research.
1. Why are my DPA levels different from my friend’s, even if we eat similarly?
Section titled “1. Why are my DPA levels different from my friend’s, even if we eat similarly?”Your DPA levels can be quite personal, even if your diets are alike. This is largely due to your unique genetic makeup. Variations in genes like FADS1, FADS2, and ELOVL2, which are crucial for processing fatty acids, significantly influence how your body synthesizes and maintains DPA levels. So, what’s optimal for one person might not be for another.
2. Can eating more fish really improve my DPA levels?
Section titled “2. Can eating more fish really improve my DPA levels?”Yes, absolutely! Your dietary intake, especially regular consumption of fish, is known to influence your omega-3 fatty acid levels, including DPA. While your genes play a role in how efficiently you process these fats, increasing your intake of omega-3 rich foods can help boost your DPA levels.
3. Can knowing my DPA levels help my heart health?
Section titled “3. Can knowing my DPA levels help my heart health?”Yes, measuring your DPA levels can offer valuable insights into your cardiovascular health. Higher levels of n-3 DPA are associated with a reduced risk of acute coronary events and are inversely linked to inflammatory markers like C-reactive protein (CRP) and triglycerides, which are known risk factors for heart disease.
4. Is it true some people naturally have better DPA levels?
Section titled “4. Is it true some people naturally have better DPA levels?”Yes, it is true. Your genetics play a significant role in determining your baseline DPA levels. Specific genetic variants, such as those near the ELOVL2 gene (like rs12662634 ), are highly associated with how much DPA your body naturally produces or maintains, leading to individual differences.
5. Do my DPA levels affect my brain function?
Section titled “5. Do my DPA levels affect my brain function?”Yes, they do. DPA, as part of the omega-3 polyunsaturated fatty acid family, is correlated with cognitive function and brain development. Maintaining healthy levels of these fatty acids is important for overall brain health, though more research is always ongoing.
6. Why do my DPA levels matter for inflammation?
Section titled “6. Why do my DPA levels matter for inflammation?”DPA levels are closely linked to your body’s inflammatory responses. Specifically, higher n-3 DPA is inversely associated with C-reactive protein (CRP), a key inflammatory biomarker. Additionally, n-6 DPA has been observed to interact with genetic variants near theCHCHD3 gene, influencing other inflammatory markers like ICAM.
7. If heart disease runs in my family, is DPA testing useful for me?
Section titled “7. If heart disease runs in my family, is DPA testing useful for me?”It can be very useful. Given DPA’s strong links to cardiovascular health and inflammation, understanding your DPA levels can help you and your doctor make personalized dietary and lifestyle choices. This approach, known as precision nutrition, aims to modulate genetic risks for conditions like heart disease.
8. Could a DNA test help me choose the best diet for DPA?
Section titled “8. Could a DNA test help me choose the best diet for DPA?”Potentially, yes. By identifying genetic variants associated with your DPA metabolism, a DNA test could provide insights into how your body processes fats. This information could then guide personalized dietary recommendations, helping you optimize your intake for better DPA levels and overall health.
9. Why might my DPA levels be different from my sibling’s?
Section titled “9. Why might my DPA levels be different from my sibling’s?”Even though you share many genes with your sibling, you still inherit a unique combination of genetic variants from your parents. Small differences in genes like FADS1, FADS2, or ELOVL2 can lead to noticeable variations in how your bodies synthesize and regulate DPA, resulting in different levels.
10. Can certain genes make my body better at using DPA?
Section titled “10. Can certain genes make my body better at using DPA?”Yes, absolutely. Genes like FADS1, FADS2, and ELOVL2 encode enzymes essential for synthesizing polyunsaturated fatty acids like DPA. Variations in these genes can make some individuals naturally more efficient at converting precursor fatty acids into DPA, contributing to higher levels in their body.
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] Lemaitre, R. N., et al. “Genetic loci associated with plasma phospholipid n-3 fatty acids: a meta-analysis of genome-wide association studies from the CHARGE Consortium.” PLoS Genet, vol. 7, no. 7, 2011, p. e1002193.
[2] Skulas-Ray, A.C., et al. “Red blood cell docosapentaenoic acid (DPA n-3) is inversely associated with triglycerides and c-reactive protein (CRP) in healthy adults and dose-dependently increases following n-3 fatty acid supplementation.”Nutrients, 2015. PMID: 26247926.
[3] Tintle, N. L., et al. “A genome-wide association study of saturated, mono- and polyunsaturated red blood cell fatty acids in the Framingham Heart Offspring Study.” Prostaglandins Leukot Essent Fatty Acids, vol. 92, 2015, pp. 15-21.
[4] Bokor, S., et al. “Single nucleotide polymorphisms in the FADS gene cluster are associated with delta-5 and delta-6 desaturase activities estimated by serum fatty acid ratios.”J Lipid Res, 2010.
[5] Tang, C., et al. “Regulation of human delta-6 desaturase gene transcription: identification of a functional direct repeat-1 element.” J Lipid Res, vol. 44, 2003, pp. 686–693.
[6] Veenstra, J, et al. “Genome-Wide Interaction Study of Omega-3 PUFAs and Other Fatty Acids on Inflammatory Biomarkers of Cardiovascular Health in the Framingham Heart Study.”Nutrients, 2017. PMID: 28820441.
[7] Rissanen, T. H., et al. “Fish oil-derived fatty acids, docosahexaenoic acid and docosapentaenoic acid, and the risk of acute coronary events: the Kuopio ischaemic heart disease risk factor study.”Circulation, vol. 102, no. 22, 2000, pp. 2677–2679.
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