Tiredness

Tiredness, often described as fatigue or low energy, is a common human experience characterized by a lack of physical or mental energy. It can manifest as a general feeling of weariness, reduced capacity for activity, or a need for rest. While transient tiredness is a normal response to exertion or insufficient sleep, persistent tiredness can significantly impact an individual’s quality of life and is often associated with poorer physical and mental health.^[1]

Biological Basis

The experience of tiredness is complex, involving interactions between various physiological systems, including the nervous, endocrine, and immune systems. Research indicates a significant genetic component to an individual’s predisposition to tiredness. Twin studies have estimated the heritability of tiredness to range between 6% and 50%.^[1]Recent genome-wide association studies (GWAS) have further explored these genetic contributions. For instance, a large-scale GWAS involving over 108,000 individuals from the UK Biobank found that common single-nucleotide polymorphisms (SNPs) collectively explain approximately 8.4% of the variance in self-reported tiredness.^[1]This study identified specific genetic loci associated with tiredness, including a genome-wide significant SNP (Affymetrix id 1:64178756C_T) on chromosome 1 and suggestive peaks near genes like _SLC44A5 and PAFAH1B1.^[1] Gene-based analyses have also implicated genes such as DRD2, PRRC2C, C3orf84, ANO10, and ASXL3in tiredness.^[1]These findings highlight the polygenic nature of tiredness, where many variants with small effects contribute to its overall expression.

Clinical Relevance

Tiredness is a prominent symptom across a wide spectrum of medical and psychological conditions, making its accurate assessment and understanding crucial in clinical settings. Studies reveal that individuals reporting higher levels of tiredness tend to exhibit lower grip strength, reduced lung function, poorer self-rated health, and lower verbal-numerical reasoning abilities.^[1]They also tend to have higher body mass index (BMI) and neuroticism scores.^[1]Genetic analyses have further demonstrated significant correlations between tiredness and numerous health-related traits. These include metabolic indicators like BMI, C-reactive protein, HDL cholesterol, HbA1c, triglycerides, type 2 diabetes, and waist-hip ratio. Physical health measures such as forced expiratory volume, grip strength, and self-rated health also show genetic links. Furthermore, tiredness shares genetic architecture with mental health conditions like attention deficit hyperactivity disorder, bipolar disorder, major depressive disorder, neuroticism, and schizophrenia.^[1]Genes implicated in tiredness have diverse functions; for example, theCRY/TYW3locus is associated with resistin levels, which play a role in insulin resistance, inflammation, and risk of type 2 diabetes and cardiovascular disease, whileSLC44A5 is involved in lipid metabolism, and PAFAH1B1 is critical for brain development.^[1] Understanding these genetic and phenotypic associations can help clinicians identify individuals at risk and develop targeted interventions.

Social Importance

Beyond its clinical implications, tiredness has considerable social importance due to its widespread impact on daily functioning, productivity, and overall public health. Chronic or severe tiredness can impair cognitive function, reduce work or academic performance, and limit participation in social activities, leading to decreased quality of life. In a broader societal context, widespread tiredness can contribute to reduced economic productivity, increased healthcare burdens, and a higher risk of accidents. Research into the genetic and environmental factors influencing tiredness not only advances our understanding of human biology but also provides avenues for developing strategies to mitigate its negative effects, promoting better public health and well-being.

Phenotypic and Heterogeneity

A significant limitation of studies on tiredness lies in its subjective nature, as it is typically measured through self-report questionnaires rather than objective physiological markers. While an objective measure of fatigue remains an “unattainable holy grail,” the reliance on single-item or double-item self-report questions, despite their widespread use and historical precedent, may introduce variability and limit the precision of genetic association findings.^[1]The “fatigue” or “tiredness” phenotype itself is highly heterogeneous, conceptualized as a final common endpoint for diverse psychological and biological processes, making it challenging to identify a singular genetic contribution.^[1] This heterogeneity implies that the genetic links identified may represent a complex interplay of various inherent factors rather than a single direct genetic cause, necessitating replication with more robust, multi-item validated measures of fatigue to confirm findings.^[1]

Generalizability and Cohort Specificity

The generalizability of genetic findings for tiredness is constrained by the demographic characteristics of the study populations. For instance, the analyses are often restricted to individuals of white British ancestry, which limits the applicability of the results to individuals from diverse ethnic backgrounds due to insufficient power to generalize across different populations.^[1] Furthermore, studies frequently involve middle- and older-aged adults, raising questions about whether the identified genetic determinants are consistent across the entire adult lifespan, particularly in younger populations.^[1] While some research suggests relative stability in self-reported fatigue levels across adult age groups, the underlying genetic architecture may differ, requiring further investigation in varied age cohorts to establish broader relevance.^[1]

Genetic Architecture and Statistical Power

Despite large sample sizes, the proportion of variance in tiredness explained by common single nucleotide polymorphisms (SNPs) remains relatively small, as indicated by SNP-based heritability estimates.^[1] The polygenic profile score analyses, while identifying significant genetic correlations with various health traits, also explained only a small amount of variance, suggesting that many causal genetic variants may not be directly genotyped or accurately tagged by the SNPs included in current arrays.^[1]This limitation points to remaining “missing heritability” and implies that the identified genetic loci represent only a fraction of the total genetic contribution to tiredness. Additionally, while large studies provide robust tests for shared genetic etiology, previous smaller GWAS of fatigue have shown inconsistencies or lacked sufficient power to detect statistically significant associations, highlighting the ongoing need for replication and larger studies to consolidate findings and identify novel genetic contributions.^[1]

Environmental Confounders and Knowledge Gaps

Tiredness is profoundly influenced by a complex interplay of environmental factors and gene-environment interactions that are not fully captured in genetic association studies. External factors, such as poor sleep, can significantly contribute to tiredness, yet current GWAS primarily focus on inherent genetic factors, thus potentially underestimating the impact of modifiable environmental influences.^[1]Moreover, tiredness often serves as a co-morbid condition across a multitude of diseases, making it challenging to disentangle genetic predispositions to illness from their actual presence and their subsequent contribution to tiredness.^[1]While studies can analyze genetic predisposition to illness, the precise mechanisms through which these predispositions manifest as tiredness, and how they interact with environmental stressors or other biological pathways (e.g., allostatic load), remain areas requiring further empirical and theoretical investigation.^[1]

Variants

Self-reported tiredness, a common experience often referred to as fatigue, is a complex trait influenced by both genetic and environmental factors. Studies have indicated that the heritability of tiredness can range significantly, suggesting a notable genetic component.^[1]Genetic research has identified specific variants and genes that contribute to an individual’s predisposition to feeling tired or having low energy, often linking these to broader physiological and neurological processes. These findings highlight the intricate interplay between various bodily systems and the subjective experience of tiredness.

One such genetic variant, rs142592148 , is an intronic single-nucleotide polymorphism (SNP) located within theSLC44A5 gene on chromosome 1.^[1] SLC44A5 encodes a solute carrier protein, which are integral membrane proteins that transport various molecules across biological membranes. This gene plays an important role in the metabolism of lipids and lipoproteins.^[1] The presence of rs142592148 was identified within a “suggestive peak” associated with tiredness, suggesting its involvement in the genetic architecture of this trait.^[1] Intronic SNPs like rs142592148 do not directly alter the protein sequence but can influence gene expression, splicing, or stability, thereby affecting the quantity or function of the SLC44A5 protein.

The SLC44A5 gene, along with nearby genes CRYZ and TYW3, has been implicated in metabolic health, with associations to insulin resistance, inflammation, and an increased risk of type 2 diabetes and cardiovascular disease.^[1]These connections suggest that the genetic predisposition to tiredness may overlap with metabolic irregularities, potentially reflecting aspects of “metabolic syndrome” or “allostatic load”.^[1]Alterations in lipid and lipoprotein metabolism can impact cellular energy production and overall physiological balance, which are critical factors influencing perceived energy levels and contributing to tiredness.

Another significant variant is rs7219015 , an intronic SNP found within the PAFAH1B1 gene on chromosome 17.^[1] PAFAH1B1encodes a subunit of platelet-activating factor acetylhydrolase 1b, an enzyme crucial for normal brain development and spermatogenesis.^[1] Mutations in PAFAH1B1 are known to cause lissencephaly, a severe neurological disorder characterized by abnormal brain development and intellectual disability.^[1] The identification of rs7219015 in a suggestive peak associated with tiredness underscores the link between brain function and the experience of low energy.^[1] The role of PAFAH1B1in brain development is highly relevant to understanding tiredness, as it suggests a genetic overlap between fatigue and cognitive traits. The brain’s proper functioning, including neuronal migration and synaptic plasticity, is essential for maintaining alertness, concentration, and overall cognitive performance. Disruptions in these processes, even subtle ones influenced by intronic variants likers7219015 , could manifest as increased tiredness or reduced mental energy. This aligns with findings of significant enrichment for variants associated with tiredness in the central nervous system, further supporting the neurological basis of this complex trait.^[1]

Key Variants

RS ID	Gene	Related Traits
rs142592148	SLC44A5	tiredness
rs7219015	PAFAH1B1	tiredness cortical thickness brain attribute major depressive disorder insomnia

Defining the Trait and its Operational Assessment

Tiredness, in research contexts, is often operationally defined through self-reported questionnaires that capture an individual’s subjective experience of the sensation.^[1] For instance, studies have precisely defined the trait by asking participants, “Over the past two weeks, how often have you felt tired or had little energy?”.^[1] This approach yields a four-category variable, ranging from “Not at all” to “Nearly every day,” which reflects the frequency and, implicitly, the severity of the experience.^[1]While referred to as ‘tiredness,’ it inherently encompasses both the feeling of tiredness and a lack of energy, acknowledging the often intertwined nature of these sensations.^[1] This self-assessment method, often drawn from standardized instruments like the Patient Health Questionnaire, allows for consistent data collection in large population studies.^[1] The broader concept of “negative affectivity” has also been explored as having a central role in health complaints, including stress and distress, suggesting a psychological dimension to such self-reported states.^[2]

Classification and Conceptual Frameworks

Tiredness is often classified dimensionally based on its reported frequency, rather than as a strict categorical diagnosis, allowing for gradients of severity from occasional to nearly constant.^[1]While not a formal disease classification, the trait shows significant genetic correlations with various established physical and mental health conditions, including major depressive disorder, bipolar disorder, schizophrenia, type 2 diabetes, and obesity.^[1]This suggests that while subjectively reported, tiredness is embedded within complex nosological systems related to broader health. A key conceptual framework for understanding the underlying mechanisms of chronic tiredness, or fatigue, is “allostatic load”.^[1]Allostatic load represents the cumulative physiological ‘wear and tear’ resulting from a prolonged response to stressors, with its first-order factors encompassing cardiovascular, immune, metabolic, anthropometric, and neuroendocrine markers.^[3]The observed genetic overlap between tiredness and several metabolic and anthropometric markers lends coherence to the allostatic load concept at a genetic level.^[1]

Criteria and Associated Biomarkers

The primary criterion for tiredness in population-based studies is typically a direct, self-reported assessment of its frequency and impact.^[1]Beyond subjective reports, research criteria extend to identifying objective physiological markers, or biomarkers, that are genetically correlated with the trait. Significant genetic correlations have been identified between tiredness and several metabolic, anthropometric, and physical health biomarkers.^[1]These include body mass index (BMI), C-reactive protein, high-density lipoprotein (HDL) cholesterol, forced expiratory volume, grip strength, HbA1c, triglycerides, and waist-hip ratio.^[1]Such biomarkers provide objective insights into the biological underpinnings of tiredness, with many of them being indicators of allostatic load, reflecting cumulative physiological dysregulation.^[1]The identification of such biological correlates helps establish thresholds and cut-off values for classifying individuals at higher risk for persistent tiredness or related health issues, contributing to both clinical and research evaluations.^[1]

Biological Background

Tiredness, a pervasive and often debilitating symptom, is a complex biological phenomenon influenced by a confluence of genetic, molecular, and physiological factors. It represents a final common endpoint for a variety of psychological and biological processes, making its underlying mechanisms inherently multifactorial and heterogeneous.^[1]Understanding the biological underpinnings of tiredness involves dissecting its genetic architecture, metabolic and hormonal pathways, neural and systemic regulatory networks, and its intricate connections to various pathophysiological states.

Genetic Architecture of Tiredness

Genetic factors play a significant role in an individual’s propensity for tiredness, with studies indicating that common genetic variations explain a notable portion of its phenotypic expression. The heritability of fatigue has been estimated to range from 6% to 50%, with common single nucleotide polymorphisms (SNPs) accounting for approximately 8.4% of the variation in self-reported tiredness.^[1]Genome-wide association studies (GWAS) have identified specific genes and genomic regions associated with tiredness, includingDRD2, PRRC2C, C3orf84, ANO10, and ASXL3. Notably, variants within C3orf84suggest a convergence point where the genetic architecture of tiredness overlaps with other traits, indicating shared genetic influences.^[1] Further investigation has revealed enrichment for variants in evolutionarily conserved regions and within the central nervous system, suggesting that critical regulatory loci contribute to the trait.^[1]Beyond individual genes, there is substantial shared genetic etiology between tiredness and a multitude of physical and mental health traits. Genetic correlations have been observed with metabolic indicators such as body mass index (BMI), C-reactive protein, HbA1c, obesity, triglycerides, and waist-hip ratio, as well as with cardiovascular markers like high-density lipoprotein (HDL) cholesterol and type 2 diabetes.^[1]Furthermore, tiredness shows significant genetic overlap with measures of physical function like grip strength and forced expiratory volume, and cognitive/psychological traits including neuroticism, major depressive disorder, bipolar disorder, and schizophrenia.^[1]These extensive genetic interconnections highlight that tiredness is not an isolated symptom but is deeply embedded within the polygenic architecture governing overall health and disease susceptibility.

Metabolic and Hormonal Regulation

Metabolic processes and hormonal signaling are critically involved in the manifestation of tiredness, often reflecting the body’s energy status and inflammatory state. TheCRY/TYW3locus, for instance, has been linked to circulating resistin levels, a hormone that plays a role in insulin resistance, inflammation, and the risk of type 2 diabetes and cardiovascular disease.^[1] Another gene, SLC44A5, encoding a solute carrier protein, is important for the metabolism of lipids and lipoproteins, further underscoring the connection between tiredness and metabolic function.^[1]These genetic associations are consistent with the broader identification of regions linked to both tiredness and metabolic irregularities, often conceptualized within the framework of “metabolic syndrome” and “allostatic load”.^[1]The allostatic load model posits that chronic or repeated stress leads to physiological wear and tear on the body, affecting multiple systems including metabolic and endocrine functions. An individual’s genetic predisposition can influence their physiological stress response, potentially leading to an over-compensatory reaction that contributes to tiredness.^[1]Disruptions in metabolic homeostasis, such as those indicated by elevated HbA1c (a marker for long-term blood glucose control) or triglycerides, show significant genetic correlation with tiredness, suggesting that imbalances in energy metabolism and glucose regulation directly impact perceived energy levels.^[1] Hormonal axes like the Hypothalamic-pituitary-adrenal (HPA) axis are also implicated in regulating stress responses and energy balance, and while research findings are sometimes inconclusive due to methodological challenges, their involvement in the biological pathways leading to fatigue is widely acknowledged.^[1]

Neural and Systemic Regulation

Tiredness involves intricate regulatory networks spanning cellular signaling, neural pathways, and systemic physiological interactions. Genes likeDRD2, which encodes the dopamine D2 receptor, suggest a role for neurotransmission in the central nervous system in regulating energy and mood.^[1] Dopamine signaling is crucial for motivation, reward, and motor control, and dysregulation can manifest as low energy and fatigue. Furthermore, the gene PAFAH1B1, found within a suggestive peak on chromosome 17, is vital for brain development and is associated with neurological disorders like lissencephaly.^[1]Its link to tiredness highlights the importance of proper neural structure and function in maintaining wakefulness and energy.^[1]The central nervous system shows significant enrichment for variants associated with tiredness, emphasizing its role as a primary site for processing and experiencing this sensation.^[1]Beyond the brain, tiredness is influenced by a vast array of systemic interactions, as it acts as a “material and formal cause” that integrates various bodily and psychosocial processes.^[1]This involves complex feedback loops between different organ systems, where signals related to inflammation, metabolic stress, and cellular dysfunction converge to produce the subjective experience of tiredness. These systemic consequences are evident in the genetic links between tiredness and overall self-rated health, as well as specific measures of organ function like forced expiratory volume, indicating that optimal functioning across multiple physiological systems is crucial for preventing tiredness.^[1]

Pathophysiological Connections and Allostatic Load

Tiredness frequently serves as a common co-morbid condition across a broad spectrum of diseases, reflecting its deep connections to various pathophysiological processes and homeostatic disruptions. It is not merely a symptom but can be a manifestation of underlying disease mechanisms or compensatory responses to physiological stress.^[1]The significant genetic correlations between tiredness and conditions like type 2 diabetes, coronary artery disease, and major depressive disorder underscore how genetic predispositions to these illnesses also contribute to the experience of tiredness.^[1]For example, the genetic association between tiredness and type 2 diabetes remains significant even when individuals already diagnosed with the condition are excluded, suggesting an inherent genetic vulnerability to both that is independent of overt disease.^[1]The concept of allostatic load provides a unifying framework for understanding how cumulative physiological stress from various sources contributes to tiredness and illness proneness.^[1]Genetic overlap between tiredness and markers of allostatic load—including metabolic (e.g., HbA1c, triglycerides, BMI) and anthropometric (e.g., waist-hip ratio) indicators—suggests a shared biological propensity for an over-compensatory physiological stress response.^[1]This implies that individuals with certain genetic profiles may be more susceptible to the physiological dysregulation that results from chronic stressors, manifesting as persistent tiredness. The links extend to inflammatory markers like C-reactive protein, highlighting how systemic inflammation, often a component of disease, can contribute to the sensation of fatigue.^[1]Consequently, tiredness can be viewed as an integrative signal reflecting disruptions in homeostasis across multiple organ systems and a heightened allostatic burden.

Clinical Relevance

The assessment of self-reported tiredness holds significant clinical relevance, extending beyond a mere subjective complaint to act as an indicator of underlying physiological and psychological states. Genetic studies highlight that individual differences in tiredness are partly heritable and share genetic architecture with numerous physical and mental health conditions, underscoring its potential utility in diagnostic, prognostic, and personalized medicine contexts.^[1]Understanding the genetic underpinnings of tiredness allows for a more nuanced interpretation of this common symptom in clinical practice.

Associations with Complex Health Conditions

Self-reported tiredness demonstrates significant genetic correlations and associations with a wide array of physical and mental health conditions, suggesting it is often an intertwined component of complex disease phenotypes . These findings are mirrored by a London-based study of 15,283 general practice patients aged 18–45 years, which found 36.7% reported substantial fatigue, and 18.3% experienced this for six months or more, with 1% also meeting CFS criteria.^[4]Such epidemiological data underscore the widespread impact of tiredness on public health.

Further research in the United States has also highlighted the pervasive nature of tiredness across different demographic segments. A study on the US workforce reported a 2-week prevalence of fatigue at 37.9%.^[5] indicating its common occurrence in working adults. Another investigation focusing on community-dwelling adults aged 51 years and over identified a 6-month prevalence rate of 27.5%.^[6] While large-scale studies often focus on specific age ranges, evidence suggests that levels of self-reported fatigue remain fairly stable across the adult life course.^[1]Moreover, analyses stratified by age and sex indicate that the proportion of variance in tiredness explained by common genetic factors is comparable between females (8.4%) and males (8.2%) within large cohorts, suggesting consistent underlying biological influences.^[1]

Large-Scale Cohort Studies and Associated Health Traits

Large-scale cohort studies, such as the UK Biobank, are instrumental in elucidating the population-level determinants of complex traits like tiredness. The UK Biobank is a substantial resource, recruiting over 502,000 community-dwelling individuals aged 37 to 73 years across the United Kingdom between 2006 and 2010.^[1]This cohort underwent extensive baseline assessments, including physical and mental health measures, cognitive testing, and personality self-reports. For genetic analyses of tiredness, data from over 108,000 participants with available genome-wide genotyping and responses to a self-reported tiredness question were utilized.^[1] enabling robust investigations into its genetic and phenotypic landscape.

Within these expansive cohorts, numerous epidemiological associations between self-reported tiredness and various health-related traits have been identified. Phenotypic correlations demonstrated that individuals reporting higher levels of tiredness tended to exhibit lower grip strength, reduced forced expiratory volume in 1 second, poorer self-rated health, and lower verbal-numerical reasoning abilities.^[1]Conversely, increased tiredness was significantly correlated with a higher Body Mass Index (BMI) and elevated neuroticism scores.^[1]Furthermore, polygenic profile score analyses revealed independent contributions to tiredness from a broad spectrum of traits, including BMI, high-density lipoprotein (HDL) cholesterol, triglycerides, waist-hip ratio, childhood cognitive ability, major depressive disorder, neuroticism, and schizophrenia.^[1]highlighting the multi-systemic nature of tiredness.

Cross-Population Generalizability and Methodological Considerations

The generalizability of findings from large population studies is a critical consideration, particularly when examining genetic contributions to traits like tiredness. The UK Biobank cohort, while extensive, primarily comprises individuals of white British ancestry.^[1]This demographic characteristic limits the direct extrapolation of genetic insights to populations with different ancestral backgrounds, as the genetic architecture and environmental factors influencing tiredness may vary across diverse ethnic groups.^[1]Therefore, future research is essential to explore population-specific effects and ancestry differences, ensuring a comprehensive understanding of tiredness across the global population.

Methodological choices in measuring tiredness also bear significant implications for population-level interpretations. The reliance on self-reported measures, such as the single-item question “Over the past two weeks, how often have you felt tired or had little energy?” employed in the UK Biobank, is a common approach in epidemiological studies.^[1] This is largely due to the inherently subjective nature of fatigue, which has been described as an “unattainable holy grail” for objective.^[1]While self-reports capture individuals’ subjective experiences and are valuable for assessing population burden, their interpretation can be influenced by individual perceptions and cultural contexts. Nevertheless, the consistent use of self-reported measures across numerous studies has provided crucial data on the prevalence and correlates of tiredness in various populations.^[4]

Frequently Asked Questions About Tiredness

These questions address the most important and specific aspects of tiredness based on current genetic research.

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1. Why am I always tired when my sibling has so much energy?

Even within families, people inherit different combinations of genetic variants. Research shows tiredness has a genetic component, with heritability estimated to range between 6% and 50%. This means your unique genetic makeup, involving many small-effect genes, can make you more prone to feeling tired than your sibling.

2. Does my tiredness get worse because I’m getting older?

While tiredness can be influenced by many factors that change with age, such as health conditions, genetic studies suggest self-reported fatigue levels can be relatively stable across adult age groups. However, the exact underlying genetic influences might differ across age cohorts, requiring further investigation.

3. Can exercising more help my constant tiredness, even if I’m genetically prone?

Absolutely, lifestyle factors like exercise are crucial, even if you have a genetic predisposition to tiredness. While common genetic variants explain about 8.4% of the variance in self-reported tiredness, environmental factors like poor sleep and lack of physical activity significantly contribute. Regular exercise can improve energy levels and overall health.

4. Does my tiredness mean I’m more likely to get other health problems?

Yes, research shows strong genetic connections between tiredness and various health conditions. For example, individuals reporting more tiredness often have higher BMI and are genetically linked to metabolic issues like type 2 diabetes, higher triglycerides, and lower HDL cholesterol. Understanding these links can help identify potential risks.

5. Is my tiredness linked to how I feel emotionally?

There’s a significant genetic overlap between tiredness and mental health. Studies show genetic correlations with traits like neuroticism, major depressive disorder, bipolar disorder, and even attention deficit hyperactivity disorder. This means that some of the same genetic factors contributing to your emotional well-being can also influence how tired you feel.

6. Does my family background affect how tired I feel?

Your family background, particularly your ancestry, can influence your genetic predisposition to tiredness. Current genetic studies have often focused on specific populations, like those of white British ancestry, meaning the genetic factors identified might not fully apply or be as powerful in other ethnic groups. More diverse research is needed to understand these differences better.

7. Can I overcome my “tiredness genes” with good habits?

While genetics contribute significantly to your predisposition to tiredness, they are not the sole determinant. Common genetic variants collectively explain only a small portion of the total variance in tiredness, suggesting “missing heritability.” This implies that good habits, like sufficient sleep, healthy diet, and regular exercise, play a substantial role and can significantly mitigate genetic tendencies.

8. Why is it so hard for doctors to measure how tired I am objectively?

Measuring tiredness objectively is challenging because it’s a very subjective experience, often described as an “unattainable holy grail” for scientists. It’s usually assessed through self-report questionnaires, as there isn’t a single physiological marker that accurately captures its complex nature. Tiredness is also a “final common endpoint” for many different biological and psychological processes, making it very heterogeneous.

9. Does my constant tiredness mean I’ll struggle more at work?

Unfortunately, chronic tiredness can indeed impact your work performance. It’s known to impair cognitive function, including verbal-numerical reasoning abilities, and can significantly reduce your overall productivity and capacity for activity. This can lead to difficulties in concentration and reduced efficiency in daily tasks.

10. Could my tiredness be linked to my cholesterol levels?

Yes, surprisingly, there are genetic connections between tiredness and lipid metabolism. Studies have found genetic correlations with markers like HDL cholesterol and triglycerides. Genes implicated in tiredness, such asSLC44A5, are involved in lipid metabolism, and the CRY/TYW3locus is associated with resistin levels, which play a role in insulin resistance and cardiovascular disease risk.

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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

[1] Deary V, et al. “Genetic contributions to self-reported tiredness.”Molecular Psychiatry, vol. 23, no. 3, 2018, pp. 609-620.

[2] Watson, D., and J.W. Pennebaker. “Health complaints, stress, and distress: exploring the central role of negative affectivity.” Psychol Rev, vol. 96, 1989, pp. 234–254.

[3] Booth, T., J.M. Starr, and I. Deary. “Modeling multisystem biological risk in later life: allostatic load in the Lothian birth cohort study 1936.”Am J Hum Biol, vol. 25, 2013.

[4] Pawlikowska, T., et al. “Population based study of fatigue and psychological distress.” BMJ, vol. 308, 1994, pp. 763–766.

[5] Ricci, J. A., et al. “Fatigue in the US workforce: prevalence and implications for lost productive work time.” Journal of Occupational and Environmental Medicine, vol. 49, 2007.

[6] Meng, H., et al. “Prevalence and predictors of fatigue among middle-aged and older adults: evidence from the Health and Retirement study.” Journal of the American Geriatrics Society, vol. 58, 2010, p. 2033.