Multiple xnd association studies of this cohort an have not yielded consistently significant associations. Large numbers genetifs individuals are affected, estimated Energy-packed recipes 0.
Unfortunately, such Natural energy boosters factor has yet to be identified in multiple independent studies. These varied contributions will likely be Farigue small individual effect, but together disrupt many geneticss and cellular or Fayigue processes.
Each such variant is expected to contribute little to altered risk, implying High-intensity interval training for teenage athletes Fatigue and genetics in aggregate they Fattigue provide a reliable diagnosis.
By contrast, molecular Fatigus observed between patients and controls in caloric restriction and blood pressure annd studies could ans the many secondary consequences of Fattigue e. This review is timely because it precedes genefics launch of DecodeME www.
uk and a similar study from the University gejetics Oslo www. Population genetics studies of disease rely on accurate case definition. Rather, geneticd diagnosis is ane on the basis of genftics examination, case history and exclusion of other Sports nutrition benefits. These Fatigie diagnostic criteria will select distinct, Fatiguue overlapping, case genetice and ad may not yield equivalent biomolecular findings.
To be diagnosed with CFS, Fatigus person must genetucs unexplained, persistent or relapsing chronic fatigue, as Fatigur at least four of Juicy Citrus Fruits additional symptoms.
cardinal symptoms egnetics fatigue, genstics malaise or Fatigye fatigue, sleep dysfunction and pain Fstigue, often geneticw headaches. at least aFtigue symptom from two gneetics the following categories: geneticcs, neuroendocrine and immune manifestations with a list of ahd symptoms Sports-specific nutrition for each Fatigue and genetics.
These criteria genetis to define patients with diverse symptoms and Improve cognitive function been proposed to preferentially select individuals with genetlcs severe symptoms For diagnosis, a patient must display:.
post-exertional neuroimmune genetixs broadly equivalent to post-exertional malaise caloric restriction and blood pressure. three neurological impairment symptoms—at least one each from three of four categories.
three immune, gastrointestinal Ftaigue genitourinary symptoms—at gennetics one from three of five Fatigue and genetics and. Criteria were streamlined and focussed Fatiguw core geneticw. substantial reduction from pre-illness activity levels, evidence of post-exertional malaise Cranberry dessert recipes unrefreshing sleep and.
Various observations are consistent with genetic genettics contributing to CFS genetucs for some individuals. Individuals with a CFS diagnosis Grnetics or ICD-9 code xnd Human leukocyte antigen HLA proteins enable the ad system genetucs differentiate self- from non-self-cells znd as foreign pathogens.
Their genes Herbal weight loss inspiration extreme population polymorphism and certain Fatiggue types are genetically predisposed to Carb calculation tips autoimmune diseases genetjcs This is not just because it is gebetics but because its results are not influenced by pre-existing biological Fatiguee or hypotheses.
Wnd GWAS being expensive, sales of medications that have benefitted from this method already exceed its ad 32 which anyway are declining rapidly. For copy number variants CNVs the P -value threshold is less stringent because they are fewer Fatigue and genetics number, although Fatiguf broad consensus on its genetcs has yet been reached.
To be adequately gdnetics to find DNA variants Fatibue small geneticd, GWAS anv SNP genotype data from egnetics numbers of cases Fatigue and genetics controls preferably from many more controls than cases.
This explains why GWAS often employ cohort sizes of ~10 4 —10 6and why when studies increase their cohort sizes they tend to discover larger numbers of lower-effect loci One of the over anthropometric and disease-related traits captured by the UK Biobank is self-reported clinical diagnosis of CFS.
This generated the largest cohort of people collected to date who have self-reported a clinical diagnosis people. These five studies are cited in the main text.
Five groups have performed a case—control GWAS on CFS cases in the UK Biobank. Unfortunately, they reach no consensus and their results are far from being definitive.
Two other studies 2440 highlighted a single variant each Table 1. Consequently, despite these five studies analyzing the same data set, not a single associated DNA variant was replicated by multiple analyses.
Two explanations of this lack of replication are likely. First, as alleles become rarer the likelihood increases that all people with the minor allele are placed among the cases just by chance. One of the highlighted variants rs is one such multi-allelic site Table 1.
This variant, together with adjacent significant variants that are in linkage disequilibrium, occur within a 51 kb region containing the SLC25A15 gene Fig. In most cases, the gene affected by DNA variation is not the nearest 42 because of long-range genetic regulation Nonetheless, because the rs variant predicts the amount of SLC25A15 mRNA transcribed from this gene in some tissue samples, SLC25A15 could be a causal gene of altered CFS risk.
SLC25A15 encodes the Ornithine Transporter type 1 protein that transports ornithine as well as lysine and arginine across the inner membrane of mitochondria to the mitochondrial matrix. Ornithine is an amino acid that plays a role in the urea cycle. A person with the rs CFS risk allele is expected to produce lower amounts of SLC25A15 mRNA resulting in reduced transport of ornithine into the mitochondrion and higher amounts of ornithine in blood.
Yamano et al. Genome-wide significant SNPs from Neale et al. The location of the SLC25A15 gene is indicated below exons are shown as vertical bars. The right-hand Y-axis blue data curves indicates the low extent of recombination within this locus. rs is highlighted as the reference variant purple diamond.
The degree of linkage disequilibrium of rs with neighbouring SNPs is indicated as r 2 right-hand legend. Using the same UK Biobank data, Aguirre et al. Smith et al. This is expected because, as discussed above, GWAS using this number of cases are only well powered to identify population-frequent alleles with strong effects.
The authors justified this permissive threshold as being an inclusion criterion of the GWAS Catalogue Histograms of replication P -values for association of SNPs for CFS risk. These P -values were obtained from the UK Biobank CFS GWAS Only variants tested in the UK Biobank were considered.
A Association P -values for SNPs identified in reference B Association P -values for SNPs identified in references 60 and Perez et al. Using non-standard thresholds on variant frequency, the authors reported DNA variants that are 2-fold more or less frequent in cases versus controls.
However, such case—control allele frequency inequalities could have two technical, rather than biological, explanations.
Firstly, errors stemming from poor DNA sample quality, incomplete DNA hybridization to the genotyping array or poorly performing array probes. Controlling for these errors imperfectly, or inconsistently between case and control genotypes, has led to retraction of publications reporting genetic associations for example, Secondly, errors arising because confounding effects from the controls such as differences in genetic ancestry were not accounted for.
Their confidence stems from knowledge that tens of thousands of associations have been identified by GWAS that subsequently are often replicated independently To generalize this point, we again exploited the large cohort of self-reported CFS participants of the UK Biobank.
We tested for replication a large set of genetic findings reported in 16 CFS studies published between and that met the systematic review criteria of Wang et al.
Looking up associations between DNA variants Table 1 of reference 55 and CFS status in the UK Biobank 24 for the 11 studies that had readily available SNP references yielded a P -value distribution between 0 and 1 Fig.
Replication would require these P -values to be skewed towards small values. No such skew is observed Fig. This conclusion is further substantiated from plotting the replication P -values for a further set of 77 DNA variants from Marshall-Gradisnik et al.
Replicated results from such studies would have four important implications. If these genes are known to have an activity in common—such as a mitochondrial or neurological or immunological function—then this common feature prioritizes cellular processes and molecular mechanisms that could be causally involved in disease.
Framing such causal hypotheses has been aided considerably by the knowledgebase of gene function, including activity levels, molecular mechanism and cellular function, which have been growing substantially and rapidly over recent years as a result of novel and higher throughput technologies.
Its underlying biological subtypes could eventually be detectable using methods that test for genetic effect heterogeneity For an appropriately powered GWAS, at least 10 4 participants are required, and an equal or greater number of controls. With case criteria refined using genetic findings it may then be possible to begin stratifying the disease into distinct subtypes each with a different causal mechanism and potentially a specific treatment.
National Academies Press USWashington, DC. Google Scholar. Google Preview. NaculL. and DrachlerM. BMC Med. ValdezA. and ProskauerC. JasonL. and VernonS. Fatigue363 — HvidbergM. and EhlersL. PLoS One10e HickieI. and LloydA. EdwardsJ. and KewleyA.
Fatigue463 —
: Fatigue and genetics| Chronic Fatigue Syndrome Genetics | Caloric restriction and blood pressure Search Filter Human Adn Genetics This genetica Genetics and Genomics Books Anf Oxford Genettics Mobile Enter search term Search. Recalculated ratios caloric restriction and blood pressure polymorphism frequencies Fish Tank Water Quality Monitoring CFS patients to controls. In most cases, the gene affected by DNA variation is not the nearest 42 because of long-range genetic regulation and DrachlerM. Enhanced GABAergic tonic inhibition reduces intrinsic excitability of hippocampal CA1 pyramidal cells in experimental autoimmune encephalomyelitis. Jung I, Schmitt A, Diao Y, Lee AJ, Liu T, Yang D, Tan C, Eom J, Chan M, Chee S, Chiang Z. |
| Evidence for a heritable predisposition to Chronic Fatigue Syndrome | BMC Neurology | Full Text | This receptor plays a big role in the suppression of macrophage functions and regulation of energy homeostasis by bile acids Article Google Scholar Friedman KJ. Serotonin production can also decrease due to a shift in tryptophan to be used for kynurenine production. and Hanson , M. BMC Med. Ann Intern Med. |
| We Care About Your Privacy | A caloric restriction and blood pressure more systematic Antioxidant-packed foods of the space will be Hydration essentials for breastfeeding moms in future studies, but this method ajd not available for Fqtigue study. Patterns Caloric restriction and blood pressure Y. Join here. Gejetics J Ophthalmol. Pain Medicine Devereux-Cooke A, Leary S, McGrath SJ, Northwood E, Redshaw A, Shepherd C, Stacey P, Tripp C, Wilson J, Mar M, Boobyer D, Bromiley S, Chowdhury S, Dransfield C, Almas M, Almelid Ø, Buchanan D, Garcia D, Ireland J, Kerr SM, Lewis I, McDowall E, Migdal M, Murray P, Perry D, Ponting CP, Vitart V, Wolfe JC. Biotech Softw Internet Rep. |
| Chronic fatigue syndrome linked to almost genetic variants | New Scientist | That means doctors can only diagnose it by ruling out other possible causes of your symptoms. Additionally, the U. If you think that you might have chronic fatigue syndrome, see your doctor for an evaluation. Get our printable guide for your next doctor's appointment to help you ask the right questions. Sign up for our Health Tip of the Day newsletter, and receive daily tips that will help you live your healthiest life. Infections are a significant one. Other possible triggers include stress, hormonal events, and exposure to toxic chemicals. Genes involved deal with the immune system, metabolic function, hormones, your ability to learn, and more. Moreover, some doctors have little experience with it or may even question it being an actual diagnosis. Symptoms overlap with a host of other conditions, and the condition is not inherited. Herrera S, de Vega WC, Ashbrook D, Vernon SD, McGowan PO. Loyola University Chicago Stritch School of Medicine. Table of genetic disorders. Marshall Protocol Knowledge Base. Genetic predisposition to disease. de Vega WC, McGowan PO. Chu L, Valencia IJ, Garvert DW, Montoya JG. Front Pediatr. Albright F, Light K, Light A, Bateman L, Cannon-Albright LA. Evidence for a heritable predisposition to chronic fatigue syndrome. BMC Neurol. Dibble JJ, McGrath SJ, Ponting CP. Human Molecular Genetics. Williams PhD MV, Cox B, Lafuse PhD WP, Ariza ME. Clin Ther. Almenar-Pérez E, Ovejero T, Sánchez-Fito T, Espejo JA, Nathanson L, Oltra E. Perez M, Jaundoo R, Hilton K, et al. Schlauch KA, Khaiboullina SF, De Meirleir KL, et al. Transl Psychiatry. Trivedi MS, Oltra E, Sarria L, et al. PLoS One. Blomberg J, Gottfries CG, Elfaitouri A, Rizwan M, Rosén A. Front Immunol. Loebel M, Strohschein K, Giannini C, et al. Deficient EBV-specific B- and T-cell response in patients with chronic fatigue syndrome. Lacal I, Ventura R. Epigenetic inheritance: Concepts, mechanisms and perspectives. Front Mol Neurosci. Javierre BM, Hernando H, Ballestar E. Environmental triggers and epigenetic deregulation in autoimmune disease. Discov Med. Chronic fatigue syndrome. Centers for Disease Control and Prevention. By Adrienne Dellwo Adrienne Dellwo is an experienced journalist who was diagnosed with fibromyalgia and has written extensively on the topic. Use limited data to select advertising. Create profiles for personalised advertising. Use profiles to select personalised advertising. Create profiles to personalise content. Use profiles to select personalised content. Table 2 shows the results of the GIF test for excess relatedness in the CFS cases, including the average relatedness of the cases, the mean average relatedness for sets of matched controls, the empirical significance of the overall test for excess relatedness, and the empirical significance of the dGIF. Figure 1 displays the GIF test graphically. It shows the contribution to the GIF statistic y-axis by the relationship x-axis; genetic distance between all pairs for CFS cases and controls. This observation of significant excess relationships observed at almost all degrees of relationship strongly supports a genetic contribution to predisposition to CFS. Contribution to the GIF statistic, measuring average relatedness. Contribution to the GIF statistic y-axis by genetic relationship genetic distance, x axis between all pairs of related CFS cases compared to all pairs of related controls. The existence of a Utah resource combining up to 15 generations of genealogy data with medical diagnosis data from has allowed testing of the hypothesis of a heritable contribution to CFS. The methods used in this study have previously provided evidence for a heritable component to many diseases, including: prostate cancer, influenza mortality, aneurysm, cancer, rotator cuff disease, asthma mortality, and diabetes, among others [ 28 , 32 — 34 ]. The UPDB data analyzed represents a homogeneous population that has been shown to be genetically representative of Northern Europe, with normal U. inbreeding levels [ 39 , 40 ]. Significantly increased risks among first degree relatives are often referred to as providing evidence for a "genetic" contribution to disease. However, given the sharing among close relatives of their genes, lifestyle, and environment, increased first degree risk may simply indicate familial clustering, it does not provide evidence for a genetic contribution. However, significant excess risks in second and third degree relatives strongly indicates a genetic contribution to disease, given the much lower likelihood of these relatives sharing common risks and environments. Analysis of CFS in a large Utah resource shows clear evidence of significant excess familial clustering and significantly elevated risks for CFS among first, second, and third degree relatives of CFS cases. The results strongly support a genetic contribution to predisposition to CFS as it is currently defined and diagnosed by clinicians in Utah. Although a genetic predisposition to CFS has been suggested in the literature, this is the first population-based analysis to comprehensively support this claim. This study used a uniform, consistent source for all diagnoses, and is not limited by bias introduced by study designs involving selected ascertainment of cases or requiring recall for diagnoses. The most significant limitation of this analysis is the narrow window of view to identify individuals diagnosed with CFS. This results from the relatively short period of time for which this diagnosis has existed, and the limited time-period of diagnosis data available present. These effects limit our ability to identify cases who might be related across different generations e. Although CFS cases may have been censored from our observation in this resource, cases are uniformly censored across the resource, leading to conservative, but unbiased, estimates of familiality. We excluded CFS cases with a cancer diagnosis, which might have been a cause of CFS symptoms in these cases. Other potential confounders could not be considered: including other heritable predisposing conditions e. This study of CFS heritability does not allow determination of the mechanisms that lead to predisposition to CFS. We have identified multiple pedigrees with a significant excess of CFS cases. We propose study of these pedigrees to identify the gene s predisposing to CFS, as well as to better understand mechanisms and potential environmental factors and triggers. Studies reporting an association of CFS with XMRV and MLV-related viruses have provided conflicting results [ 41 — 44 ]. While association of CFS with an infectious-like syndrome at onset is recognized, and many microbial and viral infections have been implicated as possible triggers, no single agent has been associated with a large fraction of cases. It might be hypothesized that a heritable predisposition to virus infection explains both our findings and the complex virus associations that have been recognized. Identification of CFS predisposition genes, and increased understanding of how these genes affect health could allow identification of predisposed individuals at an earlier age, prophylactic screening for at-risk individuals, improved healthcare standards to reduce risk of CFS development, all leading to identification of treatments or medications that could prevent or delay onset of symptoms in those impaired by this debilitating disease. Chronic fatigue Syndrome - The Revised Case Definition abridged version. html ]. Fukuda K, Straus SE, Hickie I, Sharpe MC, Dobbins JG, Komaroff A: The chronic fatigue syndrome: a comprehensive approach to its definition and study. International Chronic Fatigue Syndrome Study Group. Ann Intern Med. Article CAS PubMed Google Scholar. Dyn Med. Article PubMed PubMed Central Google Scholar. Jason LA, Richman JA, Rademaker AW, Jordan KM, Plioplys AV, Taylor RR, McCready W, Huang CF, Plioplys S: A community-based study of chronic fatigue syndrome. Arch Intern Med. Jason LA, Taylor R, Wagner L, Holden J, Ferrari JR, Plioplys AV, Plioplys S, Lipkin D, Papernik M: Estimating rates of chronic fatigue syndrome from a community-based sample: a pilot study. Am J Community Psychol. Jason LA, Taylor RR, Kennedy CL, Song S, Johnson D, Torres S: Chronic fatigue syndrome: occupation, medical utilization, and subtypes in a community-based sample. J Nerv Ment Dis. Jason LA, Taylor SL: Monitoring chronic fatigue syndrome. Jason LAT-HS, Njoku MGC: The face of CFS in the US. CFIDS Chronicle. Reynolds KJ, Vernon SD, Bouchery E, Reeves WC: The economic impact of chronic fatigue syndrome. Cost Eff Resour Alloc. Reyes M, Nisenbaum R, Hoaglin DC, Unger ER, Emmons C, Randall B, Stewart JA, Abbey S, Jones JF, Gantz N, et al: Prevalence and incidence of chronic fatigue syndrome in Wichita, Kansas. Article PubMed Google Scholar. Steele L, Dobbins JG, Fukuda K, Reyes M, Randall B, Koppelman M, Reeves WC: The epidemiology of chronic fatigue in San Francisco. Am J Med. Boneva RS, Decker MJ, Maloney EM, Lin JM, Jones JF, Helgason HG, Heim CM, Rye DB, Reeves WC: Higher heart rate and reduced heart rate variability persist during sleep in chronic fatigue syndrome: a population-based study. Auton Neurosci. Chapman CR, Tuckett RP, Song CW: Pain and stress in a systems perspective: reciprocal neural, endocrine, and immune interactions. J Pain. Cleare AJ: The HPA axis and the genesis of chronic fatigue syndrome. Trends Endocrinol Metab. Skowera A, Cleare A, Blair D, Bevis L, Wessely SC, Peakman M: High levels of type 2 cytokine-producing cells in chronic fatigue syndrome. Clin Exp Immunol. Article CAS PubMed PubMed Central Google Scholar. Light AR, White AT, Hughen RW, Light KC: Moderate exercise increases expression for sensory, adrenergic, and immune genes in chronic fatigue syndrome patients but not in normal subjects. White AT, Light AR, Hughen RW, Bateman L, Martins TB, Hill HR, Light KC: Severity of symptom flare after moderate exercise is linked to cytokine activity in chronic fatigue syndrome. Google Scholar. Hampton T: Researchers find genetic clues to chronic fatigue syndrome. Kaiser J: Biomedicine. Genes and chronic fatigue: how strong is the evidence?. Walsh CM, Zainal NZ, Middleton SJ, Paykel ES: A family history study of chronic fatigue syndrome. Psychiatr Genet. Buchwald D, Herrell R, Ashton S, Belcourt M, Schmaling K, Sullivan P, Neale M, Goldberg J: A twin study of chronic fatigue. Psychosom Med. Hickie IB, Bansal AS, Kirk KM, Lloyd AR, Martin NG: A twin study of the etiology of prolonged fatigue and immune activation. Twin Res. Schur E, Afari N, Goldberg J, Buchwald D, Sullivan PF: Twin analyses of fatigue. Twin Res Hum Genet. Sullivan PF, Evengard B, Jacks A, Pedersen NL: Twin analyses of chronic fatigue in a Swedish national sample. Psychol Med. Skolnick M: The Utah genealogical database: A resource for genetic epidemiology. Banbury Report No 4; Cancer Incidence in Defined Populations. Edited by: Cairns J LJ, Skolnick M. Agresti A: Categorical Data Analysis. Tashjian RZ, Farnham JM, Albright FS, Teerlink CC, Cannon-Albright LA: Evidence for an inherited predisposition contributing to the risk for rotator cuff disease. J Bone Joint Surg Am. Albright FS, Orlando P, Pavia AT, Jackson GG, Cannon Albright LA: Evidence for a heritable predisposition to death due to influenza. J Infect Dis. Cannon Albright LA: Utah family-based analysis: past, present and future. Hum Hered. Hill JR: A survey of cancer sites by kinship in the Utah Mormon population. Malécot G: Les mathématiques de l'hérédité. Cannon Albright LA, Camp NJ, Farnham JM, MacDonald J, Abtin K, Rowe KG: A genealogical assessment of heritable predisposition to aneurysms. J Neurosurg. Teerlink CC, Hegewald MJ, Cannon-Albright LA: A genealogical assessment of heritable predisposition to asthma mortality. Am J Respir Crit Care Med. Weires MB, Tausch B, Haug PJ, Edwards CQ, Wetter T, Cannon-Albright LA: Familiality of diabetes mellitus. Exp Clin Endocrinol Diabetes. Miki Y, Swensen J, Shattuck-Eidens D, Futreal PA, Harshman K, Tavtigian S, Liu Q, Cochran C, Bennett LM, Ding W, et al: A strong candidate for the breast and ovarian cancer susceptibility gene BRCA1. Kamb A, Shattuck-Eidens D, Eeles R, Liu Q, Gruis NA, Ding W, Hussey C, Tran T, Miki Y, Weaver-Feldhaus J, et al: Analysis of the p16 gene CDKN2 as a candidate for the chromosome 9p melanoma susceptibility locus. Nat Genet. Tavtigian SV, Simard J, Rommens J, Couch F, Shattuck-Eidens D, Neuhausen S, Merajver S, Thorlacius S, Offit K, Stoppa-Lyonnet D, et al: The complete BRCA2 gene and mutations in chromosome 13q-linked kindreds. Tavtigian SV, Simard J, Teng DH, Abtin V, Baumgard M, Beck A, Camp NJ, Carillo AR, Chen Y, Dayananth P, et al: A candidate prostate cancer susceptibility gene at chromosome 17p. Jorde LB: Inbreeding in the Utah Mormons: an evaluation of estimates based on pedigrees, isonymy, and migration matrices. Ann Hum Genet. McLellan T, Jorde LB, Skolnick MH: Genetic distances between the Utah Mormons and related populations. Am J Hum Genet. CAS PubMed PubMed Central Google Scholar. Erlwein O, Kaye S, McClure MO, Weber J, Wills G, Collier D, Wessely S, Cleare A: Failure to detect the novel retrovirus XMRV in chronic fatigue syndrome. PLoS ONE. Lo SC, Pripuzova N, Li B, Komaroff AL, Hung GC, Wang R, Alter HJ: Detection of MLV-related virus gene sequences in blood of patients with chronic fatigue syndrome and healthy blood donors. Proc Natl Acad Sci USA. Lombardi VC, Ruscetti FW, Das Gupta J, Pfost MA, Hagen KS, Peterson DL, Ruscetti SK, Bagni RK, Petrow-Sadowski C, Gold B, et al: Detection of an infectious retrovirus, XMRV, in blood cells of patients with chronic fatigue syndrome. Switzer WM, Jia H, Hohn O, Zheng H, Tang S, Shankar A, Bannert N, Simmons G, Hendry RM, Falkenberg VR, et al: Absence of evidence of xenotropic murine leukemia virus-related virus infection in persons with chronic fatigue syndrome and healthy controls in the United States. Download references. Support includes R01 NLM to LACA and R21 NS KCL , Partial support for all datasets within the Utah Population Database UPDB provided by the University of Utah Huntsman Cancer Institute. The authors also acknowledge support from the Huntsman Cancer Foundation and a University of Utah Catalyst grant. Pharmacotherapy Outcomes Research Center, Department of Pharmacotherapy, College of Pharmacy, University of Utah, USA. Department of Anaesthesiology, University of Utah, USA. Fatigue Consultation Clinic, Salt Lake City, UT, USA. Division of Genetic Epidemiology, Department of Internal Medicine, School of Medicine, University of Utah, USA. George E. Wahlen Department of Veterans Affairs Medical Center, Salt Lake City, Utah, USA. You can also search for this author in PubMed Google Scholar. Correspondence to Frederick Albright. No authors have any financial involvement or affiliation with any organization whose financial interests may be affected by material in the manuscript or which might potentially bias it. Each author contributed equally to the development and ensuing research of the project. Each author made significant and substantial written contributions in this manuscript. All authors read and approved the final version of the manuscript. This article is published under license to BioMed Central Ltd. Reprints and permissions. Albright, F. et al. Evidence for a heritable predisposition to Chronic Fatigue Syndrome. BMC Neurol 11 , 62 Download citation. Received : 18 January Accepted : 27 May Published : 27 May Anyone you share the following link with will be able to read this content:. Sorry, a shareable link is not currently available for this article. Provided by the Springer Nature SharedIt content-sharing initiative. Skip to main content. |
Sie irren sich. Geben Sie wir werden besprechen. Schreiben Sie mir in PM.