Polyunsaturated Fatty Acid

Introduction

Background

Polyunsaturated fatty acids (PUFAs) are a class of fatty acids characterized by having two or more double bonds in their hydrocarbon chain. They are crucial components of a healthy diet and play diverse roles in human physiology. PUFAs are broadly categorized into two main families: omega-3 (n-3) and omega-6 (n-6) fatty acids, distinguished by the position of the first double bond from the methyl end of the fatty acid chain. Some PUFAs, such as alpha-linolenic acid (an omega-3) and linoleic acid (an omega-6), are considered “essential” because the human body cannot synthesize them and must obtain them through diet. These essential fatty acids are then metabolized into longer-chain, more biologically active PUFAs, such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) from omega-3s, and arachidonic acid (AA) from omega-6s.

Biological Basis

At a cellular level, PUFAs are integral components of cell membranes, influencing their fluidity, permeability, and the activity of membrane-bound proteins. They are also precursors to a wide array of signaling molecules, collectively known as eicosanoids (e.g., prostaglandins, leukotrienes, thromboxanes), as well as resolvins, protectins, and maresins. These lipid mediators are potent regulators of inflammation, immune responses, blood clotting, and blood pressure. DHA, in particular, is highly concentrated in the brain and retina, where it is vital for neural development, synaptic function, and visual acuity. Genetic variations, particularly in genes likeFADS1 and FADS2 (Fatty Acid Desaturase 1 and 2), can influence the efficiency with which individuals convert essential PUFAs into their longer-chain derivatives, impacting their circulating levels and potentially their health outcomes.

Clinical Relevance

The balance and intake of different PUFAs have significant clinical implications. Omega-3 fatty acids, especially EPA and DHA, are widely recognized for their anti-inflammatory properties and their role in cardiovascular health, including reducing triglyceride levels, lowering blood pressure, and preventing arrhythmias. They are also studied for their potential benefits in neurological and psychiatric conditions, such as depression, anxiety, and cognitive decline, as well as in autoimmune diseases and certain cancers. Omega-6 fatty acids, while essential, can contribute to pro-inflammatory processes when consumed in excess relative to omega-3s. An imbalanced ratio of omega-6 to omega-3 PUFAs is thought to contribute to the development of various chronic diseases, including heart disease, type 2 diabetes, and inflammatory disorders.

Social Importance

Given their profound impact on health, PUFAs have garnered considerable social importance, influencing dietary guidelines, public health campaigns, and the food industry. Dietary recommendations often emphasize increasing the intake of omega-3 rich foods like fatty fish, flaxseeds, and walnuts, while moderating omega-6 intake from processed foods and certain vegetable oils. The market for PUFA supplements, particularly fish oil and algal oil, has grown substantially. Awareness of PUFAs has also led to the development of fortified foods, such as eggs, milk, and bread enriched with omega-3s. Understanding individual genetic predispositions related to PUFA metabolism can further personalize dietary advice, contributing to a more precise approach to nutrition and preventive healthcare.

Limitations

Methodological and Statistical Constraints

Research into the genetic underpinnings of polyunsaturated fatty acid (PUFA) metabolism and its health effects often faces inherent methodological and statistical challenges. Many studies, particularly initial discovery efforts, may be limited by relatively small sample sizes, which can reduce statistical power and lead to an overestimation of effect sizes for identified genetic variants. Such “effect-size inflation” can occur when only statistically significant findings from underpowered studies are reported, potentially exaggerating the perceived impact of individual genetic loci.

Furthermore, the replication of genetic associations across independent cohorts is crucial for establishing robust findings, yet replication gaps are not uncommon in this field. Failure to consistently reproduce associations can stem from initial false positives, subtle differences in study designs, or population-specific genetic architectures. This necessitates larger, well-powered studies and meta-analyses to validate initial discoveries and provide a more accurate picture of genetic contributions to PUFA traits.

Generalizability and Phenotypic Complexity

A significant limitation in understanding the genetics of polyunsaturated fatty acids is the challenge of generalizability across diverse populations. Genetic associations identified in cohorts of specific ancestral backgrounds may not hold true or have the same magnitude of effect in other populations due to differences in genetic variation, linkage disequilibrium patterns, and environmental exposures. This “cohort bias” can limit the broader applicability of findings and underscore the need for inclusive research that spans a wide range of global ancestries.

Moreover, the precise measurement and definition of PUFA-related phenotypes present their own complexities. PUFA levels in various tissues (e.g., plasma, red blood cells, adipose tissue) can fluctuate based on recent dietary intake, making it challenging to capture stable, long-term genetic influences. The choice of specific PUFA species, ratios, or composite indices can also vary between studies, contributing to heterogeneity in results and complicating the synthesis of knowledge regarding the genetic determinants of these complex traits.

Environmental Interactions and Unexplained Variation

The interplay between genetic predispositions and environmental factors, particularly diet and lifestyle, is a critical and complex area of limitation for PUFA research. Dietary intake of specific fatty acids, overall nutrient status, physical activity, and other lifestyle choices profoundly influence circulating PUFA levels and their subsequent biological effects. Unaccounted or inadequately controlled environmental confounders and intricate gene-environment interactions can obscure or modify the true genetic signals, making it difficult to isolate the independent contribution of genetic variants.

Despite the identification of numerous genetic loci associated with PUFA metabolism, a substantial portion of the heritability for these traits often remains unexplained, a phenomenon known as “missing heritability.” This suggests that many genetic influences, including rare variants, structural variants, and complex epistatic interactions, have yet to be discovered. Furthermore, the full spectrum of biological pathways and regulatory mechanisms through which genetic variants influence PUFA synthesis, transport, and utilization is still being elucidated, representing ongoing knowledge gaps that limit a comprehensive understanding.

Variants

Genetic variations play a crucial role in shaping an individual’s lipid metabolism, fatty acid profiles, and overall metabolic health, with specific implications for polyunsaturated fatty acid (PUFA) levels and their associated health outcomes. Several genes and their variants have been identified as key modulators in these complex pathways.

Variants within genes like APOE, LIPC, TM6SF2, TRIB1 (also listed as TRIB1AL), and GCKRare central to lipid transport, metabolism, and glucose homeostasis.APOE, encoding apolipoprotein E, is a major component of very-low-density lipoproteins (VLDL) and chylomicrons, critical for the transport of fats and cholesterol in the blood. Variants such asrs7412 , rs429358 , and rs440446 are well-known for influencing cholesterol and triglyceride levels, which in turn can impact the distribution and utilization of PUFAs within the body.^[1] The LIPCgene encodes hepatic lipase, an enzyme that hydrolyzes triglycerides and phospholipids in lipoproteins, affecting high-density lipoprotein (HDL) and low-density lipoprotein (LDL) metabolism. Variants likers2070895 , rs1077835 , and rs633695 are associated with altered lipid profiles, indirectly influencing circulating PUFA levels. ^[2] Similarly, TM6SF2 variants (rs58542926 , rs187429064 , rs144821371 ) are strongly linked to hepatic fat accumulation and non-alcoholic fatty liver disease (NAFLD), conditions that can disrupt overall lipid handling, including PUFA metabolism.TRIB1 (rs28601761 , rs112875651 , rs2954021 ) and GCKR (rs1260326 , rs141428740 , rs780094 ) also influence triglyceride levels and glucose metabolism, respectively, thereby contributing to the complex interplay that determines PUFA status and related cardiovascular risks.^[3]

The FADS1 and FADS2genes are directly responsible for the synthesis of long-chain PUFAs, such as arachidonic acid (ARA), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA), from their shorter-chain precursors. These genes encode fatty acid desaturase enzymes that introduce double bonds into fatty acyl chains, a critical step in the endogenous production of these essential fatty acids.^[4] Common variants, including rs174564 and rs146063874 , are known to alter the efficiency of these desaturase enzymes, leading to significant inter-individual differences in circulating levels of various PUFAs. Individuals carrying certain alleles may have a reduced capacity to synthesize these beneficial fatty acids, potentially affecting their inflammatory responses, cardiovascular health, and neurodevelopment.^[5] This genetic predisposition highlights the importance of dietary intake of pre-formed long-chain PUFAs for some individuals.

Beyond direct lipid processing, other genes contribute to pathways that interact with PUFA metabolism or related health traits. ALDH1A2 (Aldehyde Dehydrogenase 1 Family Member A2), with variants like rs261290 , rs2043085 , and rs1532085 , plays a role in retinol metabolism, converting retinal to retinoic acid, a crucial signaling molecule. This pathway can interact with lipid metabolism and oxidative stress responses, which are closely linked to PUFA health effects. ^[6] Genes like DOCK7 (rs1168128 , rs2934744 , rs79439217 ), TMEM258 (rs102275 , rs102274 , rs740006 ), and ZPR1 (rs964184 , rs139636218 , rs148784079 ) have diverse cellular functions, including roles in neuronal development, membrane trafficking, and cell proliferation. Emerging research suggests these genes may also have indirect links to lipid droplet formation, fatty acid transport, or broader metabolic regulation, thereby impacting the cellular handling and metabolic fate of PUFAs and contributing to various metabolic and neurological traits. ^[7] These genetic variations collectively illustrate the intricate network influencing an individual’s response to and utilization of polyunsaturated fatty acids.

Key Variants

RS ID	Gene	Related Traits
rs7412 rs429358 rs440446	APOE	low density lipoprotein cholesterol measurement clinical and behavioural ideal cardiovascular health total cholesterol measurement reticulocyte count lipid measurement
rs174564 rs146063874	FADS2, FADS1	triglyceride measurement level of phosphatidylcholine serum metabolite level cholesteryl ester 18:3 measurement lysophosphatidylcholine measurement
rs2070895 rs1077835 rs633695	ALDH1A2, LIPC	high density lipoprotein cholesterol measurement total cholesterol measurement level of phosphatidylcholine level of phosphatidylethanolamine triglyceride measurement, depressive symptom measurement
rs261290 rs2043085 rs1532085	ALDH1A2	level of phosphatidylethanolamine level of phosphatidylcholine high density lipoprotein cholesterol measurement triglyceride measurement, high density lipoprotein cholesterol measurement VLDL particle size
rs1168128 rs2934744 rs79439217	DOCK7	blood protein amount level of phosphatidylinositol phospholipids:total lipids ratio polyunsaturated fatty acid measurement omega-6 polyunsaturated fatty acid measurement
rs102275 rs102274 rs740006	TMEM258	coronary artery calcification Crohn’s disease fatty acid amount high density lipoprotein cholesterol measurement, metabolic syndrome phospholipid amount
rs964184 rs139636218 rs148784079	ZPR1	very long-chain saturated fatty acid measurement coronary artery calcification vitamin K measurement total cholesterol measurement triglyceride measurement
rs58542926 rs187429064 rs144821371	TM6SF2	triglyceride measurement total cholesterol measurement serum alanine aminotransferase amount serum albumin amount alkaline phosphatase measurement
rs28601761 rs112875651 rs2954021	TRIB1AL	mean corpuscular hemoglobin concentration glomerular filtration rate coronary artery disease alkaline phosphatase measurement YKL40 measurement
rs1260326 rs141428740 rs780094	GCKR	urate measurement total blood protein measurement serum albumin amount coronary artery calcification lipid measurement

Biological Background

Molecular Structure and Metabolic Pathways

Polyunsaturated fatty acids (PUFAs) are a class of fatty acids characterized by having two or more double bonds in their carbon chain. They are broadly categorized into omega-3 and omega-6 series, based on the position of the first double bond from the methyl end of the fatty acid chain. Essential PUFAs, such as alpha-linolenic acid (ALA, an omega-3) and linoleic acid (LA, an omega-6), cannot be synthesized by the human body and must be obtained through diet. These essential fatty acids serve as precursors for longer-chain, more biologically active PUFAs, including eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) from the omega-3 series, and arachidonic acid (AA) from the omega-6 series.

The biosynthesis of these longer-chain PUFAs involves a series of desaturation and elongation reactions primarily occurring in the endoplasmic reticulum of cells. Key enzymes in these pathways include fatty acid desaturases, such as FADS1 and FADS2, which introduce double bonds, and fatty acid elongases (ELOVL family genes), which extend the carbon chain length. The balance and efficiency of these enzymatic conversions are crucial for maintaining appropriate levels of different PUFAs, which in turn influences various cellular functions and overall physiological health.

Cellular Functions and Signaling Roles

PUFAs are integral components of cell membranes, particularly phospholipids, where they contribute to membrane fluidity, flexibility, and overall integrity, which are essential for proper cell signaling and transport processes. Beyond their structural roles, PUFAs and their metabolites act as potent signaling molecules. Arachidonic acid, EPA, and DHA are precursors to a diverse array of lipid mediators, collectively known as eicosanoids (prostaglandins, leukotrienes, thromboxanes) and specialized pro-resolving mediators (SPMs) like resolvins, protectins, and maresins. These biomolecules play critical roles in regulating inflammation, immune responses, blood clotting, and vascular tone.

Omega-3 and omega-6 derived mediators often exert opposing or modulatory effects, with omega-3 derived SPMs generally promoting the resolution of inflammation, while some omega-6 derived eicosanoids are pro-inflammatory. PUFAs can also directly interact with nuclear receptors, such as peroxisome proliferator-activated receptors (PPARs), influencing gene expression related to lipid metabolism, glucose homeostasis, and inflammatory pathways. This intricate network of interactions highlights the broad impact of PUFAs on cellular physiology, from modulating gene transcription to fine-tuning receptor activity and intercellular communication.

Genetic and Epigenetic Regulation

Genetic factors significantly influence an individual’s PUFA status and metabolism. Polymorphisms within genes encoding key enzymes in PUFA biosynthesis, such as the FADS1 and FADS2 gene cluster, are well-studied. For instance, common genetic variations can alter the activity of these desaturases, affecting the conversion efficiency of essential PUFAs into their longer-chain derivatives like EPA, DHA, and AA. These genetic differences can lead to variations in circulating PUFA levels among individuals, impacting their susceptibility to related health conditions.

Beyond direct gene sequence variations, the expression of genes involved in PUFA metabolism is also subject to complex regulatory networks. Transcription factors, including PPARs, bind to specific DNA regulatory elements to modulate the transcription of FADS and ELOVLgenes. Furthermore, epigenetic mechanisms, such as DNA methylation and histone modifications, can influence the accessibility of these genes for transcription, thereby fine-tuning their expression patterns in response to dietary intake or environmental cues. These genetic and epigenetic controls collectively contribute to the inter-individual variability in PUFA metabolism and physiological responses.

Tissue-Specific Effects and Systemic Homeostasis

PUFAs exert diverse and often tissue-specific effects throughout the body, playing crucial roles in maintaining systemic homeostasis. In the brain, DHA is particularly abundant in neuronal membranes, essential for neurodevelopment, synaptic function, and cognitive processes. Its deficiency can impair neural signaling and development. In the cardiovascular system, omega-3 PUFAs contribute to heart health by reducing inflammation, improving endothelial function, lowering triglyceride levels, and modulating blood pressure, thereby influencing the risk of cardiovascular diseases.

The liver is a central organ for lipid metabolism, where PUFAs influence hepatic lipid synthesis, fatty acid oxidation, and glucose homeostasis. In adipose tissue, PUFAs can affect adipocyte differentiation, insulin sensitivity, and the secretion of adipokines. Furthermore, PUFAs are critical for retinal health, with DHA being a major structural component of photoreceptor membranes. The balanced interplay of PUFAs across these various tissues is essential for the coordinated regulation of metabolic, inflammatory, and neurological processes, underpinning overall health and developmental trajectories, particularly during early life stages.

Pathophysiological Implications

Disruptions in PUFA metabolism or an imbalance in omega-3 to omega-6 ratios are implicated in the pathophysiology of numerous diseases. Chronic low-grade inflammation, often driven by an imbalance favoring pro-inflammatory omega-6 derivatives, is a hallmark of many non-communicable diseases, including cardiovascular disease, type 2 diabetes, and certain autoimmune disorders. Insufficient levels of omega-3 PUFAs, particularly EPA and DHA, can impair the body’s ability to resolve inflammation and may contribute to the progression of these conditions.

In neurological and psychiatric disorders, such as depression, anxiety, and neurodegenerative diseases like Alzheimer’s, alterations in brain PUFA composition and metabolism are frequently observed, suggesting a role in disease mechanisms and progression. Homeostatic disruptions, such as insulin resistance and dyslipidemia, can also be influenced by PUFA status, affecting metabolic health. The body often exhibits compensatory responses to dietary changes or genetic predispositions, attempting to restore PUFA balance, but prolonged imbalances can overwhelm these mechanisms, leading to chronic disease states.

Pathways and Mechanisms

Polyunsaturated fatty acids (PUFAs) are integral to numerous biological processes, serving as essential structural components of cell membranes and as precursors for a wide array of signaling molecules. Their diverse roles are mediated through complex metabolic and signaling pathways that are tightly regulated at multiple levels, from gene expression to protein modification, influencing cellular function and overall physiological homeostasis.

Metabolic Fates and Energy Dynamics

Polyunsaturated fatty acids are actively integrated into diverse metabolic pathways, influencing both structural integrity and energy homeostasis. Following dietary intake or de novo synthesis (for some non-essential PUFAs), these fatty acids can be esterified into triglycerides for energy storage or incorporated into phospholipids, which are fundamental components of cellular membranes. The elongation and desaturation of shorter-chain fatty acids into longer-chain PUFAs, such as arachidonic acid (ARA), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA), are precisely controlled by enzymes like fatty acid desaturases (FADS1, FADS2) and elongases (ELOVL5, ELOVL2). These enzymatic steps are critical for maintaining the specific PUFA composition of tissues, which in turn affects membrane fluidity, receptor function, and overall cellular signaling. ^[8]

Catabolism of PUFAs occurs primarily through beta-oxidation in mitochondria and peroxisomes, yielding acetyl-CoA for entry into the citric acid cycle and subsequent ATP production. The complex double bond structure of PUFAs necessitates additional enzymatic steps, such as those involving enoyl-CoA isomerase and 2,4-dienoyl-CoA reductase, to facilitate complete degradation. Metabolic regulation of PUFA flux is tightly controlled, responding to cellular energy demands and nutrient availability, often involving allosteric control of key enzymes and transcriptional regulation of genes encoding enzymes involved in both synthesis and degradation. This intricate balance ensures that PUFAs are appropriately utilized for energy, structural support, or as precursors for signaling molecules, preventing their accumulation to potentially toxic levels or depletion below essential thresholds.^[9]

Signaling Transduction and Gene Regulation

Polyunsaturated fatty acids act as potent signaling molecules, directly and indirectly influencing cellular processes through receptor activation and intricate intracellular cascades. Derivatives of PUFAs, known as eicosanoids (prostaglandins, leukotrienes, thromboxanes) and docosanoids (resolvins, protectins, maresins), activate specific G protein-coupled receptors (GPCRs) on the cell surface, initiating diverse signaling pathways that modulate inflammation, immunity, and vascular tone. Beyond their roles as precursors, PUFAs themselves, particularly DHA and EPA, can directly bind to and activate nuclear receptors such as peroxisome proliferator-activated receptors (PPARs), notably PPARα and PPARγ. This activation leads to the recruitment of coactivators and subsequent binding to specific DNA response elements, thereby regulating the transcription of numerous genes involved in lipid metabolism, glucose homeostasis, and inflammatory responses.^[10]

The transcriptional regulation mediated by PUFAs extends to other transcription factors, including sterol regulatory element-binding proteins (SREBPs) and carbohydrate response element-binding protein (ChREBP), often leading to a suppression of lipogenic gene expression. This intricate network involves feedback loops where the products of PUFA metabolism can modulate the activity of enzymes or transcription factors involved in their own synthesis or degradation, ensuring precise homeostatic control. Furthermore, PUFAs can influence protein modification through effects on kinase and phosphatase activities, altering phosphorylation states of key signaling proteins, and can also impact post-translational regulation by modulating protein stability or localization, thereby fine-tuning cellular responses to metabolic and environmental cues. ^[11]

Cellular Integration and Network Interactions

The biological effects of polyunsaturated fatty acids are manifested through extensive pathway crosstalk and complex network interactions, demonstrating systems-level integration across various physiological domains. PUFA-mediated signaling pathways do not operate in isolation but interact profoundly with pathways governing glucose metabolism, insulin sensitivity, and immune responses. For instance,PPARαactivation by PUFAs can influence the insulin signaling cascade by upregulating genes involved in fatty acid oxidation, thereby reducing intracellular lipid accumulation and improving insulin sensitivity in peripheral tissues. This crosstalk is crucial for maintaining metabolic health and preventing conditions associated with metabolic syndrome.^[12]

Hierarchical regulation ensures that PUFA availability and metabolism are integrated into the broader physiological context, with systemic hormones and nutrient sensors providing overarching control. For example, hormones like insulin and glucagon modulate the activity of desaturase and elongase enzymes, thereby affecting the synthesis of specific PUFAs. The emergent properties arising from these complex interactions include the finely tuned inflammatory resolution processes mediated by specialized pro-resolving mediators (SPMs) derived from EPA and DHA, which actively dampen inflammation rather than passively allowing it to subside. These sophisticated regulatory networks highlight how PUFAs contribute to overall cellular resilience and adaptive responses to stress and disease.^[13]

PUFA Dysregulation in Health and Disease

Dysregulation of polyunsaturated fatty acid pathways is implicated in the pathogenesis and progression of numerous diseases, highlighting their critical role in maintaining physiological balance. Imbalances in the omega-6 to omega-3 PUFA ratio, often skewed towards higher omega-6 intake in Western diets, can lead to an overproduction of pro-inflammatory eicosanoids, contributing to chronic inflammatory conditions such as cardiovascular disease, autoimmune disorders, and certain cancers. Genetic variations in enzymes likeFADS1 and FADS2 can impair the synthesis of longer-chain omega-3 and omega-6 PUFAs, leading to altered lipid profiles and increased susceptibility to metabolic and inflammatory diseases. ^[14]

Compensatory mechanisms often attempt to restore PUFA homeostasis during dysregulation, such as the upregulation of FADS enzymes in response to dietary omega-3 deficiency. However, prolonged stress or genetic predisposition can overwhelm these mechanisms, leading to persistent pathway dysregulation. Understanding these mechanisms offers significant opportunities for therapeutic intervention. For instance, dietary supplementation with omega-3 PUFAs (EPA and DHA) aims to shift the balance towards anti-inflammatory mediators and activate beneficial PPARpathways. Moreover, targeting specific enzymes in PUFA metabolism or their downstream signaling receptors represents a promising strategy for developing novel therapeutics for conditions ranging from atherosclerosis and neurodegenerative disorders to inflammatory bowel disease.^[15]

Clinical Relevance

Risk Assessment and Disease Prognosis

Polyunsaturated fatty acid (PUFA) profiles, particularly the balance of omega-3 and omega-6 fatty acids, serve as important biomarkers in clinical risk assessment. For instance, a low omega-3 index is consistently associated with an elevated risk of cardiovascular events, including myocardial infarction and sudden cardiac death. Monitoring these levels can help identify individuals who may benefit from targeted preventative interventions, contributing to personalized medicine approaches for primary and secondary prevention. Beyond initial risk stratification, PUFA status holds prognostic value in predicting disease progression and long-term outcomes across various chronic conditions. Studies indicate that specific PUFA concentrations can predict the severity of inflammatory diseases, cognitive decline, and even certain psychiatric disorders. Understanding an individual’s PUFA profile can therefore inform clinicians about potential disease trajectories and help anticipate complications, guiding a more proactive management strategy.

Therapeutic Applications and Monitoring

Polyunsaturated fatty acids play a crucial role in therapeutic strategies, particularly in the management of dyslipidemia and inflammatory conditions. Omega-3 fatty acid supplementation, for example, is a recognized treatment for severe hypertriglyceridemia, significantly reducing triglyceride levels and subsequent cardiovascular risk. The selection of appropriate PUFA interventions can be tailored based on individual patient profiles, including their baseline PUFA status and specific clinical indications. Effective monitoring of PUFA levels is integral to assessing treatment response and optimizing patient care. For individuals undergoing PUFA supplementation, periodic measurement of circulating fatty acid profiles can confirm adherence and determine if therapeutic targets are being achieved. This monitoring allows for adjustments in dosage or formulation, ensuring patients derive maximal clinical benefit and mitigating potential complications associated with suboptimal or excessive intake, while also informing long-term implications of these interventions.

Associations with Comorbidities and Personalized Prevention

Imbalances in polyunsaturated fatty acid metabolism are frequently associated with a spectrum of comorbidities, highlighting their interconnectedness in complex disease phenotypes. Conditions such as metabolic syndrome, type 2 diabetes, and non-alcoholic fatty liver disease often present with altered PUFA profiles, suggesting a shared underlying pathophysiology. Understanding these associations can aid in identifying individuals at risk for developing multiple related conditions and guide comprehensive management strategies. The intricate relationship between PUFAs and various health conditions underscores the potential for personalized prevention strategies. By assessing an individual’s unique PUFA status, clinicians can develop tailored dietary and lifestyle recommendations aimed at optimizing fatty acid balance. This personalized approach can contribute to preventing the onset or progression of chronic diseases, including cardiovascular disease, certain neurological disorders, and inflammatory conditions, thereby improving long-term health outcomes and reducing the overall burden of disease.

References

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