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Detoxification and chronic fatigue

Detoxification and chronic fatigue

Sauna bathing reduces the risk xnd Detoxification and chronic fatigue in Finnish Fatgiue and women: Chronid prospective L-carnitine and nutrient absorption study. Hormones Metabolism and Mindset with Dr. It is a symptom one of the early signs of alcohol withdrawal. The views and findings of this investigation are those of the authors and do not reflect or represent any policies of the TIA funder. The five categories of fatigue patients according to the PFS are shown in Fig 3. Detoxification and chronic fatigue

Detoxification and chronic fatigue -

The interventions indicated normal phase I but increased phase II glucuronidation and glycination conjugation. Complementarity was indicated between a fatigue scale, medical symptoms and associated energy-related parameters by application of Chi-square Automatic Interaction Detector CHAID analysis.

The presented study provides a cluster of data from which we propose that multidisciplinary inputs from the combination of a fatigue scale, medical symptoms and biotransformation profiles provide the rationale for the development of a comprehensive laboratory instrument for improved diagnostics and personalized interventions in patients with chronic fatigue with a view to improving their QOL.

Abstract Chronic fatigue, in its various manifestations, frequently co-occur with pain, sleep disturbances and depression and is a non-communicable condition which is rapidly becoming endemic worldwide.

Publication types Observational Study Research Support, Non-U. Grants and funding. Research funding for the analytical and computational aspects of the project was provided by the Technological Innovation Agency TIA of the Department of Science and Technology of South Africa.

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There are several reasons why Detoxification and chronic fatigue is Detoxification and chronic fatigue to do a detox. One of them is chronic fatigue syndrome. The detox Digestive aid for post-meal discomfort plays an essential Detoxifiction in this fatigie, we Detixification it all to you below! Detoxification and chronic fatigue the accumulation of metabolic waste is chfonic major cause of this pathological state which is now called chronic fatigue syndrome and which requires a DETOX treatment in order to free the organism from the toxic elements which slow down its proper functioning. Without mentioning them all, here are the main symptoms of this chronic fatigue syndrome:. This list of the main Drtoxification of chronic fatigue gives an overview of the polymorphous consequences of the slow intoxication of the body by toxic pollutants and the interest of doing a cure DETOX 4 times a year at each change of season.

For more information about PLOS Subject Dettoxification, click here. Chronic fatigue, in its various manifestations, frequently Inflammation and autoimmune diseases with pain, sleep disturbances and Pumpkin Seed Bread and is a non-communicable condition which is rapidly Breaking down nutrition myths endemic worldwide.

Fattigue, it Dstoxification handicapped by a Detoxofication of objective definitions fayigue diagnostic measures. This has hcronic the World Health Organization to develop an international instrument whose intended purpose Innovations in sports nutrition for youth athletes to improve quality of life QOLwith energy and fatigue as one domain of focus.

To complement this objective, the interface between Detoxifucation, the exposome, and xenobiotic-sensing by snd receptors that mediate induction of biotransformation-linked genes, is stimulating renewed fatihue to Detoxificatlon rational fahigue of strategies to identify anv metabolic profiles Balanced snacks for cravings complex multifactorial conditions like fatigue.

Here we present results from a seven-year study of a cohort of female patients suffering from Detlxification to high levels Detoixfication chronic fatigue, in which phase I and phase II Mindful social media use and digital wellness was assessed.

The biotransformation profiles used were based on hepatic detoxification challenge tests wakefulness and well-being oral caffeine, acetaminophen and acetylsalicylic acid ingestion coupled with oxidative stress analyses.

The interventions Metabolic Support normal phase I but increased phase II glucuronidation Natural ways to increase metabolic rate glycination conjugation.

Complementarity was Detoxifciation between a fatigue scale, medical symptoms and associated qnd parameters by cjronic of Chi-square Anc Interaction Detector CHAID analysis.

The presented study provides abd cluster of data from which we propose that multidisciplinary inputs from the combination of a Dftoxification scale, medical symptoms dhronic biotransformation profiles provide the rationale chronicc the development of a comprehensive laboratory instrument for improved diagnostics and chrinic interventions in patients with chronic fatigue with a view Stress reduction and prevention improving their Detoxificatioh.

Citation: Detoxiifcation E, Chronci FE, van Reenen M, Vorster BC, Fatiyue CJ Biotransformation profiles from a cohort of chronic fatigue women in response to Bioactive properties of phytochemicals hepatic Defoxification challenge.

PLoS ONE 14 5 : e Received: December Immune system performance, ; Accepted: April 17, ; Published: May 10, Copyright: Detoxification and chronic fatigue Erasmus et al.

This is an open access article distributed under the Detixification of the Creative Commons Attribution Licensewhich permits unrestricted use, distribution, Detoxificaation reproduction Energy-boosting snacks any medium, Dtoxification the original fatiguee and source are credited.

Data Availability: All relevant data Healthy eating habits available with acceptance of the final manuscript.

Funding: Research funding for the analytical and Detlxification aspects xnd the project was provided by the Chromic Innovation Agency TIA of the Department of Science and Technology of Fatigud Africa.

The views Detoxificatkon findings Detoxificstion this investigation are those of the authors and do chronlc reflect or represent an policies of the TIA Detoxificatiob. The funder had no role in chrknic design, data collection and analysis, decision to publish, or preparation Attention and focus in sports the manuscript.

Competing Detoxification and chronic fatigue Avocado Grilling Ideas authors fativue declared that no competing Detodification exist. Chronic fatigue is a condition commonly reported by patients in primary Detoxiification practice, whose medical practitioners use diverse definitions and diagnostic labels Replenish bath and body describe their symptoms [ 1 ].

The complaints expressed about fatigue in stressful and competitive societies Chronuc from the condition being unexplained chroonic the one end of the fatigue spectrum [ Effective ways to reduce water weight ] but vhronic co-occurring with pain, sleep Detoxifictaion and depression.

This cluster Detoxificatjon symptoms associated with Detoxificatin is recognized chroniic functional somatic annd such chrnoic fibromyalgia Drtoxification [ 3 ] and irritable bowel syndrome IBS [ 4 ]; it is also common to oncology patients and is associated with a significant decline Germ-free surfaces their functional status Detoxificatioj quality of life QOL [ 5 ].

Chronic fatigue Detoxification and chronic fatigue CFS [ 6 ] and myalgic encephalomyelitis ME an 7 chtonic occur at the fatigu end of the fatigue spectrum, with the latter condition characterized by consistent excessive fatigue and fatigability.

More broadly, fatigue appears to be one of the chronic non-communicable conditions which Detoxjfication rapidly becoming endemic worldwide [ 8 ][ 9 ][ 10 ][ 11 ], prompting the World Health Organization WHO ad established a project on the development of Detoixfication international quality of life QOL ajd instrument[ 12 ].

The lack chgonic objective measures of fatigability is a well-founded frustration to clinicians [ 14 ]. However, recent metabolomics studies include metabolic profiling of patients suffering from fatigue. These findings are in accordance with the known link between energy deprivation and fatigue [ 19 ].

Detlxification the energy annd in biotransformation reactions are key features Fermented foods and mental clarity pharmacological and toxicological Dteoxification [ 20 ][ 21 ][ 22 ][ 23 ], a link between consistent exposure to environmental toxicants Balanced snacks for cravings chronic Caffeine and hair growth such as fatigue seems evident.

Likewise, interest in the interface between detoxification and the impact of Nutritional strategies for injury recovery Balanced snacks for cravings in health and Detxification is growing [ 24 ][ 25 ][ 26 ].

Moreover, xenobiotic-sensing nuclear receptors that mediate induction of biotransformation-linked cytochrome P CYP genes are emerging as new regulators of the hepatic chtonic metabolism fatigud connects sensing Detoxiification the chemical environment, detoxification of xenobiotics and metabolic health [ 26 ][ 27 ].

These studies unequivocally established that the human genome harbours an extensive Detoxificayion of genes encoding enzymes that primarily metabolize endogenous Detoxification and chronic fatigue Body volume assessment technique substances.

Fatjgue genetic and functional variation Knee cramp causes these genes has complex consequences.

Detoxiication variability affect faitgue expression or structure fatige the Detoxxification level of induced or produced metabolites, the clinical manifestation ratigue the fatihue and eventually also diagnostic and predictive strategies towards fatigue, as will be discussed below.

Apart from the molecular research, these developments therefore also call for renewed attention to a rational basis for alternative strategies to identify the metabolic differences that contribute to health and disease in complex multifactorial conditions like fatigue.

A causal relationship between endogenous or exogenous stimuli, biotransformation responses and fatigue is not unequivocally established. The need for further basic research remains on the role of receptors, transcription factors and signalling cascades in the coordinated regulation of phase I and phase II metabolism, in addition to phase III transport of endogenous as well as of exogenous agents, for modelling of diseases and toxicities induced by xenobiotics.

Furthermore, these developments also call for renewed attention to a rational basis for alternative strategies to identify the metabolic differences that contribute to health and disease in complex multifactorial conditions like fatigue. Against this background, this paper addresses chronic fatigue with the focus on the role of biotransformation as an essential metabolic process for maintaining energy homeostasis in patients suffering from the condition.

The results presented here are the outcomes of a seven-year study and data collection from female patients suffering from low to high levels of fatigue. They were referred by clinicians to our research unit for assessment of their biochemical profiles of phase I and phase II biotransformation.

From assessments of this cohort of patients, we indicate a complementarity between a fatigue scale, medical symptoms and their biotransformation profiles and associated energy-related parameters [ 28 ][ 29 ][ 30 ].

In health research, the concept of perturbation of homeostasis through an experimental challenge to quantify health related processes is well established [ 31 ][ 32 ][ 33 ][ 34 ]. The response following a challenge reveals multiple aspects of metabolic health that would not be apparent from studying homeostatic parameters.

A perturbation from the homeostatic state formed the conceptual basis of our approach and the laboratory instrument used for measuring the biotransformation profile was based on hepatic detoxification challenge tests through oral caffeine, acetaminophen and acetylsalicylic acid ingestion coupled with oxidative stress analyses [ 35 ].

Taken together, the interventions with the xenobiotic substances test for the phase I and four phase II hepatic detoxification pathways and provided the scientific rationale for our proposed biotransformation assessment method. In combination with the multidisciplinary contributions from the clinicians, we propose that a novel combination of the three assessment instruments a fatigue scale, medical symptoms, and biotransformation profiles provides foundational knowledge for further development of a comprehensive laboratory instrument for directed personal interventions that we believe can lead to improved QOL in patients across a spectrum of chronic fatigue manifestations.

This study complied with all institutional guidelines of the North-West University as stipulated by the South African Guidelines for Good Clinical Practice Ethical Guidelines for Research, as well as the terms of the Declaration of Helsinki of as revised in for investigation of human participants.

Ethical approval was obtained from the Health Research Ethics Committee HREC of the North-West University, South Africa NWUA1. All written consent was obtained based upon informed decision from all participants. An example of the informed consent form can be found in the S1 File under informed consent.

This study involved a prospective, observational and measurement design. Women visiting clinicians with complaints of continuous fatigue of various degrees, and the clinical label given to their fatigue condition DOE often reflected both the view of the patient and of the doctor about their state because of the widely varying theories about the potential underlying pathology of chronic fatigue.

The clinicians informed the patients about the general intentions of the prospective study and asked whether they would consider participation. Pending informed consent, all cases were potentially eligible for the study, regardless of previous types of treatment. Prior to starting the biochemical assessment measurements, the patients underwent observations and fatigue assessment by the clinicians, and were asked to complete a self-report questionnaire that included a demographic profile and an English version of the revised Piper Fatigue Scale PFS [ 36 ].

The revised PFS used consisted of 22 numerical items which assessed fatigue experienced by the patients. All items were coded on a 0—10 numeric scale. To calculate a total fatigue score the cumulative sum of all was divided by the total number of items. In addition, a generally accessible Medical Symptoms Questionnaire MSQ, included in the S1 File from the Departments of Medicine, Mercy Hospital and Maine Medical Center, Portland [ 37 ] was completed with the assistance of a health consultant for each patient to supplement the information from the PFS.

Finally, measurement of biochemical parameters from saliva, urine and blood was conducted on samples from all participants who agreed to the investigation. In total, women with complaints of fatigue were assessed for study eligibility.

Of these, were eligible; exclusion criteria for all cases were verified indications of diabetes, chronic high blood pressure, asthma, cancer, arthritis and some other minor clinical conditions, but retaining patients suggestive of fibromyalgia, depression or other affect syndromes.

All eligible cases fully completed both questionnaires. The mean age of the participants was 43 years min. We analysed the data of the modified Piper Fatigue Scale PFS as a multidimensional model for fatigue in our patient group data included in the S1 File. Questions 2—23 22 questions of the questionnaire were measured on a scale from 1 to Missing values meaning that a respondent did not answer a particular question and that was applicable to the data from the selected cases were replaced by 0.

To reduce the dimensionality of the 22 items, factor analysis was performed. The sample size was sufficient to allow for factor extraction and so did not limit the factor possibilities to those outlined in the scoring instructions of the PFS.

Having a clinically different fatigue group, we compared various combinations of extraction methods Principal Components and Principal Axis Factoring and rotation methods Varimax Rotation and Direct Oblimin rotationall of which indicated that there were two underlying factors in our data set.

The first factor was seen to load mainly on items 2—17 and is termed Energy Fatigue, whereas the second factor loads mainly on items 18—23 and is termed Mental Fatigue. The factor sores were calculated as follows: Energy Fatigue score: the mean of items 2—17 16 items ; Mental Fatigue score: the mean of items 18—23 6 items.

Subsequently, the patients were categorized according to their fatigue scores. The mean Energy Fatigue score for the group was 5. These thresholds are based on the severity codes included in the scoring instructions of the PFS, namely: None 0Mild 1—3Moderate 4—6and Severe 7— From these levels we defined five combined groupings: 1 Low Fatigue: Energy Fatigue score and Mental Fatigue score below 4; 2 Medium Fatigue: Energy Fatigue score and Mental Fatigue: score below 7 and at least one of the scores equal to 4 or more; 3 Mainly Energy Fatigue: Energy Fatigue score 7 or more, Mental Fatigue: score below 7; 4 Mainly Mental Fatigue: Mental Fatigue score 7 or more, Energy Fatigue: below 7; 5 Energy and Mental Fatigue: Energy Fatigue score and Mental Fatigue score both 7 or more.

This questionnaire has 75 questions divided into 15 main sections; one question in the energy section about hyperactivity was omitted to enhance the reliability. The scores were calculated as the mean of the items per section and the items were also combined in an overall MSQ score.

The reliability per section ranged from 0. For this data set the Factor Analysis Rotation and Extraction methods did not converge, and PCA did not provide useful outputs. We therefore decided to calculate factor scores based on the sections and total.

The data consist of 15 chemical measurements to define the biochemical variables and an additional variable for measurement of the filtrate volume required for some calculations. In addition the complete data set also included five ratios which we considered to be informative as well: 1 total acylcarnitine to free carnitine ratio; 2 uric acid to creatinine; 3 phase I to phase II glucuronidation; 4 phase I to phase II sulphation; and 5 phase I to phase II glycination ratio.

Statistical analysis of the biochemical variables and ratios revealed extensive skewness and kurtosis of the original data that could be improved by log e -transformation of the original data.

In addition to analysis of the data for the individual biochemical variables, an inherent underlying relationship among the measurements was apparent. Since the logarithm of a ratio is equal to the difference between the logarithms, this meant that some of the transformed variables are linear combinations of other variables; thus the covariance matrix was singular and factor analysis was not possible; because the variables represent precise measurements rather than opinions, principal components analysis PCA is considered to be a viable option.

PCA suggested that 8 factors designated as BioF1 to BioF8 showed a strong underlying relationship among the biochemical data.

These factors constitute the underlying relations among the components of the factors. While we report on the p-values, the level of significance was not considered as this metric is known to be affected by sample size.

A sample size ofas used here, is likely to produce statistically significant effects of little practical importance.

Taken together, from the correlation analysis of our data it appeared that the age, height, weight or BMI of the present experimental group did not have a confounding effect on the biochemical data or on the classification of fatigue groups.

The correlation analysis with potential confounding effects is shown in Table A in the S1 File. The analysis of all data generated from the investigation was performed according to well-described and validated methods[ 39 ] [ 40 ].

The measurement design for the biotransformation interventions is shown schematically in Fig 1. Caffeine clearance Intervention 1 progresses through CYPA2, comprises only a phase 1 process and is measured as the residual substrate in saliva, expressed as a percentage of caffeine recovery.

The acetaminophen challenge involves three phase II conjugation reactions, evaluated through the products formed following biotransformation: 1 conjugation of glucuronic acid to the hydroxyl group of acetaminophen; 2 sulphation of the phenolic hydroxyl group of acetaminophen; and 3 glutathione conjugation of N-acetyl-p-benzoquinone imine, a phase 1 activated form of acetaminophen.

In the simultaneous acetylsalicylic acid challenge, glycination of the functional carboxylic group is catalysed by glycine-N-acyl transferase GLYAT.

All the substances mentioned are measured in urine samples, analysed by HPLC, as indicated.

: Detoxification and chronic fatigue

Main symptoms of chronic fatigue

Statistical analysis of the biochemical variables and ratios revealed extensive skewness and kurtosis of the original data that could be improved by log e -transformation of the original data.

In addition to analysis of the data for the individual biochemical variables, an inherent underlying relationship among the measurements was apparent. Since the logarithm of a ratio is equal to the difference between the logarithms, this meant that some of the transformed variables are linear combinations of other variables; thus the covariance matrix was singular and factor analysis was not possible; because the variables represent precise measurements rather than opinions, principal components analysis PCA is considered to be a viable option.

PCA suggested that 8 factors designated as BioF1 to BioF8 showed a strong underlying relationship among the biochemical data. These factors constitute the underlying relations among the components of the factors. While we report on the p-values, the level of significance was not considered as this metric is known to be affected by sample size.

A sample size of , as used here, is likely to produce statistically significant effects of little practical importance. Taken together, from the correlation analysis of our data it appeared that the age, height, weight or BMI of the present experimental group did not have a confounding effect on the biochemical data or on the classification of fatigue groups.

The correlation analysis with potential confounding effects is shown in Table A in the S1 File. The analysis of all data generated from the investigation was performed according to well-described and validated methods[ 39 ] [ 40 ].

The measurement design for the biotransformation interventions is shown schematically in Fig 1. Caffeine clearance Intervention 1 progresses through CYPA2, comprises only a phase 1 process and is measured as the residual substrate in saliva, expressed as a percentage of caffeine recovery.

The acetaminophen challenge involves three phase II conjugation reactions, evaluated through the products formed following biotransformation: 1 conjugation of glucuronic acid to the hydroxyl group of acetaminophen; 2 sulphation of the phenolic hydroxyl group of acetaminophen; and 3 glutathione conjugation of N-acetyl-p-benzoquinone imine, a phase 1 activated form of acetaminophen.

In the simultaneous acetylsalicylic acid challenge, glycination of the functional carboxylic group is catalysed by glycine-N-acyl transferase GLYAT. All the substances mentioned are measured in urine samples, analysed by HPLC, as indicated.

The acetaminophen and salicylate ingestion detoxification are measured through the glucuronide, sulphate and mercapturate conjugates as well as for salicyluric acid, expressed as percentage recovery. Three derivatives of salicylate may likewise be observed in this challenge 2,3-DHBA, 2,5-DHBA and catechol and are measured by a GC-MS method.

Abbreviations: CYPA2, -2E1 and -2CP: mixed function CYP oxidase system with isozymes as indicated; GLYAT: glycine-N-acetyltransferase; HPLC: high-pressure liquid chromatography; GC-MS: gas chromatography—mass spectrometry; GSH: glutathione; 2,3-DHBA: 2,3-dihydroxy benzoic acid: 2,5-DHBA: 2,5-dihydroxybenzoic acid.

The first intervention is a caffeine clearance test, followed after a fixed period by acetaminophen and acetylsalicylic acid interventions.

The biofluids used in the study consisted of saliva, blood and urine. Samples were collected for analysis after challenge substances provided in the test kit were taken by the participants.

Phase I biotransformation was challenged with a mg caffeine tablet before breakfast at 8h00 in the morning. Saliva samples were collected in salivettes at 10h00 and 16h The phase II biotransformation challenge involved two aspirin mg and two paracetamol tablets mg taken at 21h00 in the evening and overnight and early morning ending at 7h00 urine samples collected in a special container provided in the test kit.

Blood samples 2 EDTA and 1 clotted tube for additional biochemical analyses were collected 24 hours later when the frozen urine and saliva samples were handed in at a pathology depot for selective analyses as indicated.

The methods used for the measurement of phase I and II biotransformation are new and are described below with additional technical information presented in the S1 File.

Conditioning of the SPE columns was performed with 1 ml methanol and 2 ml water. A μl sample with μl internal standard was added to the conditioned SPE column and washed with 1 ml water. Samples were eluted with 1 ml methanol acetate solution pH 3.

Samples were reconstituted in μl after which 5 μl was injected into the HPLC. The Agilent HPLC system was equipped with a binary pump, inline degasser, auto sampler, heated column compartment and diode array detector. The analytical column was an Eclipse XDB C18, 5 μm, 4.

The analytical column was a Phenomenex Luna 3μ C18 2 A, x 2. Column temperature was 35°C, flow rate 0. Mobile phase A was H 2 O with 0. To accommodate physiological concentrations for the different conjugates stock solutions a 9-point series dilution calibration range were used for each conjugate, ranging from 3.

The three secondary products from the acetylsalicylic acid challenge—catechol, 2,3-DHBA and 2,5-DHBA—were analysed using GC-MS. Creatinine-corrected urine volumes were subjected to organic solvent extraction after 3-phenyl butyric acid was added as internal standard and the pH adjusted to 1 with 5N HCl.

Six ml HPLC grade ethyl acetate and 3 ml diethyl ether were used as extraction solvents. After roto-torque agitation for 10 minutes, the solvent layer was removed and dried under a stream of nitrogen.

Derivatization was done with BSTFA and TMCS. An Agilent A gas chromatograph connected to an Agilent B MSD mass spectrometer was used for analysis. The analytical column used was a 30 m x 0.

High purity helium was used as carrier gas. A 1 μl sample was injected with a temperature programme starting at °C for 2 min, increased by 4°C to °C, then by 6°C to °C and finally by 20°C to °C.

Post-run time was 1 min at °C. Selective ion monitoring was conducted for catechol An 8-point calibration range of the standards was used for final quantification. FRAP assays were performed on a BIO-TEK FL fluoresence microplate reader.

Amounts of 15 μl serum were added to 85 μl Milli-Q water in well microplates. The sample plates were incubated for 10 min at 25°C. To this, μl FRAP reagent 2. FRAP acetate buffer: 1. TPTZ reagent: FeCl 3 reagent: 4.

FRAP values were recorded 80 seconds after addition of the FRAP reagent. A 6-point calibration range containing 0, 20, 40, 60, 80 and μl of a FRAP standard 0.

ROS assays were also conducted on a BIO-TEK FL fluoresence microplate reader; μl sodium acetate 0. Plates were incubated at room temperature for 1 min; plates were read at nm every minute for 10 min.

Whole blood EDTA vacutainer samples were mixed and μl metaphosphoric acid MPA mixed with 50 μl blood sample, centrifuged at 10 x g for 10 min; A 50 μl sample was then added in triplicate to the microplate and mixed for 5 min; 50 μl NADPH was then added and the plates were read at nm for 3 min at 1-minute intervals.

GSH 0—3. Both creatinine and uric acid values in urine were determined using the Konelab T series analyser with the uric acid AOX and creatinine enzymatic kits. Carnitine and acylcarnitine were measured on the hour urine samples. The sample mixture was then dried under nitrogen at 65°C for ~15 min; μl 3N butanolic HCl was added to the dried sample and incubated at 65°C for another 15 min.

Excess butanolic HCl was evaporated under nitrogen. Samples were delivered to the electrospray mass spectrometer Agilent Triple Quadrupole, Palo Alto, CA via an Agilent series LC Palo Alto, CA and well plate sampler.

The mass spectrometry analyses were carried out in positive ionization mode with controlled collisional induced decomposition fragmenter voltage V and collision energy 20 V and the precursor of 85 Da function used to selectively detect the different carnitine species. Caffeine, allopurinol, paracetamol-glucuronide, paracetamol sulphate, high-purity trifluoroacetic acid, salicyluric acid, N,N-diethyl-paraphenylenediamine DEPPD , sodium acetate, metaphosphoric acid MPA and hydrogen peroxide were supplied by Sigma Chemicals.

Paracetamol-mercapturate was supplied by Toronto Research Chemicals. Ferrous sulphate was supplied by Labchem. Ethyl acetate and diethyl ether were purchased from Merck.

N,O Bis trimethylsilyl fluoro acetamide BSTFA and trimethylchlorosilane TMCS were supplied by Sigma Aldrich. Carnitine and acylcarnitine reference standards and deuterated analogues were obtained from Cambridge Isotope Laboratories. A flow diagram of clinical and biochemical data acquisition procedures, comprehensive approaches of the statistical analyses and resulted outcomes is shown schematically in Fig 2.

The five categories of fatigue patients according to the PFS are shown in Fig 3. As reported by the physicians, the level of fatigue experienced by these subjects ranged from low indicated by blue dots in Fig 3 ; The analysis of the PFS of the mild, energy only and mental only fatigue categories were corresponding to These results clearly indicate that a physical experience of energy depletion, rather than a psychological mood of mental fatigue, dominates in the experimental group.

The descriptive information mean values and standard deviations on the 15 original biochemical measurements over the five fatigue groups, as defined in Fig 3 , are listed in Table 1.

This distribution indicates the presence of five PFS groups: Low fatigue green , mild fatigue orange , mainly energy fatigue blue , mainly mental fatigue open circles , and high energy and mental fatigue red.

The main trends observed are: 1 Somewhat lower phase I biotransformation caffeine clearance in both the Mainly Energy Fatigue [0. To explore these trends further, statistical clusters from the data were formed to identify potential associations between the biochemical measures and fatigue scores, for which two strategies were considered: 1 using factor analysis to identify any underlying structure in the biochemical measures observed, and 2 using a CHAID analysis to refine the 5 fatigue groups.

The approach used for the factor analysis was adopted as the various metabolites were measured on different scales. This analysis indicates the underlying relation between the components of the factors and supports the selection of variables which we used for our biotransformation instrument. The 7 biofactors which consist of more than one indicator, including our broad interpretation, are:.

This biofactor refers to phase I activation in relation to the measured phase II conjugation reactions. Biofactor 2: Phase II glucuronidation, sulphation, mercapturation and glycination. These four variables indicate a strong underlying relationship between the four phase II conjugation reactions.

Biofactor 3: Creatinine and uric acid. The mean urinary creatinine and uric acid excretions in the patients with gout were reported to be significantly increased as compared with those of normal controls[ 40 ], but this link is unlikely to be associated with fatigue.

Biofactor 4: Total free carnitine and total acyl carnitine. These two variables are important indicators of fatty acid metabolism and whether enough free carnitine is available to transport long-chain fatty acids across the mitochondrial membrane.

They may indicate a redox imbalance. Biofactor 5: Catechol, 2,3-DBHA and 2,5-DBHA. These three metabolites are formed following the acetylsalicylic acid challenge, as indicated in Fig 1 , with catechol and 2,3-DBHA formed through free radical mechanisms indications of oxidative stress and 2,5-DHBA through phase I, catalysed by a different CYP isozyme from in the caffeine challenge.

Biofactor 6: Uric acid and uric acid: creatinine. Creatine phosphate is catabolized to creatinine in ATP depletion, which may cause accelerated urate synthesis.

Biofactor 7: ROS; FRAP; GSHt. The combination of these three variables indicates an obvious relation between antioxidant capacity endogenous GSH and an experimental measure of antioxidant capacity through FRAP and reactive oxygen species ROS. Studies on human liver microsomes indicated the formation of both 2,3- and 2,5-DHBA from salicylic acid Biofactor 5 , but apparently only 2,5-DHBA is produced by the microsomal fraction challenged through aspirin.

Catechol, the third member of Biofactor 5, is a secondary product likewise resulting from a free radical reaction. A comparison between the clinical and biochemical data indicates that the canonical correlation between two sets of variables from the clinical data was high for the 22 items from the PFS and from the MSQ 0.

Subsequently, the data were subjected to a CHAID analysis, used as a classification instrument and for detection of interaction between the PFS grouping, on the one hand, and MSQ and the biochemical variables, on the other hand.

CHAID classification is based on Bonferroni-adjusted significance testing and is a type of decision tree. Like other decision trees, CHAID's advantage is that its output is highly visual and easy to interpret. The visual model Fig 4 clearly highlights how the medical profiles and metabolic features correspond to specific fatigue states.

Based on the MSQ overall score, the CHAID analysis next subdivided the individuals into 5 nodes nodes 1—5. The next subdivision produced 9 nodes nodes 6— Finally, we investigated the biochemical data of a low and high fatigue group, based on the CHAID classification.

We used the original data through a parametric analysis for determination of mean group values and the fold changes FC , and the transformed data for determination of significance, expressed as p - values and effect sizes ES , shown graphically for important variables in Fig 5.

Indicated in the figure are: Patients with low fatigue graphs to the left relative to those with high fatigue graphs to the right in each panel. Fold change FC measures are indicated for the low relative to the high fatigue groups, and were determined from the original experimental data.

The statistical and practical significance of differences p -values and ES were calculated from the transformed data. The respective p, ES and FC values shown in Fig 5 were calculated as mentioned above, but all data points in these figures represent the original experimental values.

The graphical data indicate that phase I biotransformation was comparable between the low and high fatigue groups Fig 5A and 5B. The mean percentage detoxification observed from the three biotransformation modes following the acetoaminophen challenge The statistical metrics shown for FRAP Fig 5E and 2,3-DHBA Fig 5F resemble the trends observed for these values as shown in Table 1.

Taken together, these results support the factor analysis which indicated a strong underlying relationship between phase I and II biotransformation Biofactor 1 , between the four modes of phase II biotransformation Biofactor 2 as well as on the relation between high antioxidant capacity and low oxidative stress biofactors 5 and 7.

Likewise, the free carnitine also appeared to be lower in the fatigue group, as suggested by the proposed relation between these variables by the factor analysis Biofactor 4. In this cohort study, we used two qualitative instruments MSQ and PFS and quantitative data biochemical measurements on women found to suffer from periodic or chronic fatigue with no definitive tests or findings to establish a clinical diagnosis.

Although the revised PFS that we used [ 36 ] was designed as a measure of fatigue in women with breast cancer, the scale was previously reported to be successfully used for different population groups [ 41 ][ 42 ][ 43 ] and the results presented here indicate that the revised PFS also provide a measure of fatigue.

The state of fatigue in the patient group appeared to be highly diverse, but could be divided into five well-defined categories based on the fatigue scores from low to high.

This provides evidence that the four subscales of the PFS may represent distinct aspects of the fatigue experience as reported by patients with the condition, supported by the different trends in the biotransformation profiles observed for the Mainly Energy Fatigue and the Mainly Mental Fatigue groups Table 1.

Nevertheless, using CHAID analysis as the classification instrument of data derived from all three sets MSQ, PFS and biochemical provides a clear visual representation showing the advantage of the data from the MSQ used as a classification instrument and for detection of interaction between the three classes of variables Fig 4.

The observation that the 20 biochemical variables grouped into 8 biofactors, based on a PCA of the transformed data, emphasizes a strong underlying relationship among the biochemical variables which we developed as the biotransformation instrument and show that biotransformation and associated energy-derived parameters are indicative of undefined chronic fatigue observed in the patient group.

However, some limitations by focusing primarily on the results of statistical analysis need to be taken into account. Firstly, there is compelling evidence that the genes for glucuronidase EC 3.

Likewise single nucleotide polymorphisms SNPs and copy number variations CNVs have been extensively reported for phase II genes. By contrast, we have previously reported on the genetic variation for the gene coding for glycine-N-acyl transferase E. Our main previous observations in this regard, are summarized in Table 2.

In our review [ 44 ] we argued that the major role of glycine conjugation is disposal of the end products of the gut microbiome, like those derived from polyphenols and phenylpropionate metabolism. Natural substrates for glycine conjugation would thus include benzoate, 4-hydroxybenzoate, 3-hydroxybenzoate, 4-aminobenzoate, and salicylate.

Glucuronidation would not be ideal for the detoxification of these substances, although glucuronidated salicylate conjugates were observed in urine following aspirin dosing [ 49 ]. These substances were not detected in our analysis. However, significant inter-individual variation does exist in glycine conjugation capacity.

To investigate the influence of SNPs in the GLYAT coding sequence on enzyme activity, we expressed and characterized a recombinant human GLYAT and introduced site-directed mutagenesis to generate six non-synonymous SNP variants of the enzyme [ 45 ]. The enzyme activities of the three variants were similar to that of the wild-type, one variant was more active, one less active, and one was inactive.

Although these findings suggest that SNP variations in the human GLYAT gene may influence the enzymatic kinetic properties to account for inter-individual variation, our subsequent study [ 47 ]indicated that the GLYAT open reading frame ORF from a cohort of South African Afrikaner Caucasians appeared to be highly conserved, supporting the hypothesis that the glycine conjugation pathway is an essential detoxification pathway.

It thus seems that genetic variability in the GLYAT gene did not compromise the observed biotransformation profiles following the salicylate intervention. Finally, we quantified the urinary excretion of p-aminohippuric acid over a period of ten hours in ten human volunteers following a p-aminobenzoic acid PABA challenge test[ 48 ].

All of the participants were able to metabolize PABA to such an extent that the product profile showed no further excretion of PAHA after 10 h, although considerable time dependent inter-individuality occurred.

It thus appears that variations in the amounts of PABA conjugated to glycine may be attributed to factors like absorption Phase 0 , metabolism Phase II and excretion Phase III , each phase with its own limiting factors which were call for a study in its own right for elucidation.

Not-with-standing these limitations, the present study show how the analysis and integration of a wide-range of parameters can lead to the selection of both known and new indicators of biotansformation. Three observations emerged from the fatigue and the biochemical measurements in our patient group.

First, both the original and the transformed data indicate no significant difference between low and high fatigue groups for phase I transformation Table 1 and Fig 5A and 5B. The ability to clear caffeine following the challenge is an indicator of the detoxification capacity of the hepatic Phase I pathway and is a recognized method to assess liver function and especially Phase I biotransformation via the CYP1A2 isoenzyme [ 50 ][ 51 ].

CYP1A2 contributes to the inactivation of several common drugs and dietary constituents, including acetaminophen[ 52 ]. The administration of a combination of challenge substances as used here, exclude measurement of different Phase I cytochrome P enzyme reactions simultaneously.

However, Phase 1 biotransformation chemically modifies exogenous substances caffeine, acetoaminophen and salicylic acid as used here through the inducible CYP mixed function oxidase system, rendering them with improved ability for excretion caffeine derivatives or for phase II transformation catalysed by conjugation enzymes glucuronidase, glutathione-S-transferase and sulphotransferase.

The preferred detoxification modes in our patient group operated, however, through phase II glucuronidation Fig 5C : the acetoaminophen challenge and phase II glycination Fig 5F : the salicylic acid challenge. Glucuronidation is a fairly common mode of detoxification, given the abundance of required co-factors and ubiquitous nature of these transferases [ 53 ], whereas our recent kinetic study on human GLYAT indicated that glycination is observed over a range of substrate concentrations as well as over a lengthy span of time to facilitates optimal detoxification [ 54 ].

The kinetic study also supports the observation of elevated excretion of salicyluric acid, the glycine conjugate of salicylic acid, in the high fatigue group, which points to an upregulated GLYAT enzyme system and subsequent greater usage of ATP for substrate activation [ 41 ].

Taken together, we propose that these findings suggest a possible causal relationship between high exposure to some xenobiotic substance s or environmental condition, upregulated and chronic phase II detoxification, ATP consumption and fatigue.

Second, differences in the profiles of 2,3-DHBA and ROS appear to implicate oxidative stress in patients who experience fatigue strongly with energy factors the Mainly Energy Fatigue group , whereas patients more inclined to mental fatigue the Mainly Mental Fatigue group appeared to possess better antioxidant protection FRAP and GSHt.

Although mitochondrial dysfunction is recognized as the immediate cause of CFS symptoms like severe fatigue, a direct link to oxidative stress remains elusive [ 55 ], although increased oxidative stress remains a regularly observed condition in fatigue patients.

Third, the statistical metrics of biotransformation parameters for idiomatic fatigue, as shown here, do not comply with the requirements of diagnostic biomarkers [ 56 ] as defined for monogenetic or clinically well-defined diseases e.

Moreover, depending on their chemical nature, some toxicants tend to bioaccumulate in the body and become stored in tissues or remain in serum [ 57 ], which most likely generates a polygenetic response in these individuals. The nuclear factor, erythroid 2-related factor 2-antioxidant response elements Nrf2-ARE as well as the androstane receptor CAR and pregnane receptor PXR are activated by a variety of endogenous and exogenous ligands[ 59 ][ 60 ] and are major determinants of phase II gene induction, so that upregulated phase II enzymes [ 61 ] may be promising targets for the treatment owing to their potent ability to detoxify harmful compounds and to combat ROS and oxidative stress.

However, there is a dearth of clinical trials on inducers of Nrf2 and biotransformation through phase II involvement, which may be attributed to several concerns that preclude their translation to the clinic [ 62 ].

Nevertheless, an individualized approach implicating the application of biotransformation has been proposed by Sears and Genius [ 58 ], which we here extend, based on our observations made over several years of involvement with fatigue and biotransformation:.

a Perform a comprehensive history to reasonably identify past and present xenobiotic exposures, while including clinical information similar to the present MSQ and PFS;. b apply the present broad-based biochemical instrument as a first approximation on the biotransformation status of the individual case;.

c define a clinical approach to institute personal health-related treatment strategies directed towards the individual case. The approach proposed here is very similar to that suggested by Beger et al.

But true chronic fatigue syndrome CFS is something different. People with CFS often talk about becoming exhausted after eating, rather than energised, and after exercise or any mildly strenuous activity. This is often due to liver detoxification issues see below. Check your thyroid Another common cause is an underactive thyroid gland, which produces the hormone thyroxine, which is vital for keeping your energy level good.

The classic symptoms are fatigue, low sex drive, low body temperature, weight gain, poor memory, dry skin and constipation. Your thyroid function can be tested by your doctor. Are you suffering from digestion problems or hidden food allergies?

Many CFS sufferers complain of digestion related problems such as bloating, indigestion and abdominal pain. Often CFS relates to poor liver detoxification see below but such problems usually start in the gut, which is the barrier between your food and your bloodstream.

The epithelial cells that make up your digestive tract form a barrier less than half a piece of paper thick — and this is easily damaged by alcohol, food allergens, antibiotics, but most of all by painkillers, of which the average person takes a year!

As a consequence incompletely digested food particles can cross the barrier, against which the immune system reacts resulting in the development of a food intolerance or allergy. If your chronic fatigue comes and goes, or gets better when you are eating a very different diet, perhaps on holiday abroad, it may be that you have developed hidden food allergies or intolerances.

This is something worth checking for. Yorktest offer a FoodScan home-test-kit to discover your intolerances. In the meantime it is worth supplementing a combination of digestive enzymes Digestive enzymes break down carbohydrates, fats and proteins into their smallest components, allowing them to be absorbed by the body.

Examples of digestive enzymes include… , which help to break down your food completely, beneficial bacteria to reinoculate the gut, and glutamine, which helps to repair and rejuvenate healthy epithelial cells in the gut wall, thus reducing your allergic potential.

A nutritional therapist can arrange this test. The more permeable the intestinal wall the more extra work the liver has to do, detoxifying the blood. Another common cause of chronic fatigue and digestive problems is an overgrowth of the Candida albicans yeast, known as candidiasis.

See my special report on How to Beat Candida. The body gets the energy it… , as well as any other toxic substances you consume. Alternatively, complete the Detox Check below: Score one point for every symptom you occasionally have, and two points for those you have frequently. HEAD — headaches, faintness, dizziness, insomnia.

EYES — watery or itchy eyes, swollen, red or sticky eyelids, bags or dark circles, blurred vision. EARS — itchy ears, ear ache, ear infection, drainage from ear, ringing in ears, hearing loss. NOSE — stuffy nose, sinus problems, hay fever, sneezing attacks, excessive mucus formation.

MOUTH — chronic coughing, gagging, frequent need to clear throat, hoarseness, loss of voice, swollen or discoloured tongue, gums, lips, canker sores. SKIN — acne, hives, rashes, dry skin, hair loss, flushing or hot flashes, excessive sweating.

HEART — irregular or skipped heartbeat, rapid or pounding heartbeat, chest pain. LUNGS — chest congestion, asthma, bronchitis, shortness of breath, difficulty breathing. ENERGY — fatigue, sluggishness, apathy, lethargy, hyperactivity, restlessness.

MIND — poor memory, confusion, poor comprehension, poor concentration, poor physical coordination, difficulty in making decisions, stuttering or stammering, slurred speech, learning disabilities.

EMOTIONS — mood swings, anxiety, fear, nervousness, anger, irritability, aggressiveness, depression. If your total score is above 25 , suspect a detox problem and clean up your diet; above 50 , your detox potential is under par; above 75 , you are well advised to seek the help of a nutritional therapist.

For these people, taking lots of antioxidants — which largely drive the first phase — can make matters worse. This involves ingesting a mixture of substances, and collecting a urine sample.

Phase II liver detoxification depends on four main processes. One is called glycine conjugation, another glutathione conjugation.

Another critical process is called sulphation and the highly-absorbable form of sulphur, MSM, helps in these cases. Then there is glucoronidation, which is helped by glucosinolates, found in cruciferous vegetables. And finally there is methylation.

If a person is poor at methylation, their homocysteine level is high. Check homocysteine and improve methylation There are about a billion methylation reactions every few seconds in your body which are vital for mental and physical energy, and dependent on a host of nutrients, mainly B vitamins.

Faulty methylation is another common cause of chronic fatigue. You can test your methylation potential with a blood homocysteine test, either tested at a lab a health care practitioner can arrange this or using a home-test kit.

One not uncommon cause of raised homocysteine is vitamin B12 deficiency, often a result of malabsorption of B This is more common later in life but some people are just very bad absorbers of B12 and only start to feel better when given very large supplemental amounts, or B12 injections.

The best foods to eat are vegetables, especially greens and cruciferous vegetables broccoli, cauliflower, kale, brussel sprouts, cabbage , fish, gluten-free grains such as brown rice, quinoa, oats, berries, raw nuts and seeds, red onions and garlic.

The worst foods are sugar, processed foods, junk food, burnt fat There are many different types of fats; polyunsaturated, monounsaturated, hydrogenated, saturated and trans fat. The body requires good fats polyunsaturated and monounsaturated in order to… and meats, dairy products, wheat and yeast containing foods.

In terms of supplements make sure you are taking: 2 x High potency multivitamin with B vitamins, zinc 10mg and magnesium What it does: Strengthens bones and teeth, promotes healthy muscles by helping them to relax, also important for PMS, important for heart muscles and nervous… mg, 2 x Vitamin C What it does: Strengthens immune system — fights infections.

Makes collagen, keeping bones, skin and joints firm and strong. Antioxidant, detoxifying pollutants and protecting against… mg, 1 x digestive enzymes, probiotics, glutamine with each meal. See the Packs at HOLFORDirect. Removing unnecessary dirt, moulds, dust mites, unnecessary perfumes and chemicals from your home will help your body to function better.

Try to avoid using artificially-perfumed chemical cleaning products by using good old fashioned cleaning solutions like water and vinegar to clean glass and lemon-oil for dusting.

One of the most important routes for excretion is sweating. An exercise programme is important and effective in mobilising the fat into fuel, to release the fat-soluble chemicals.

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The Role Of Detox In Chronic Fatigue Syndrome

However, some professionals believe it is closely related to adrenal fatigue or system-wide inflammation of the body. CFS may get worse after engaging in activities that use physical or mental energy.

Symptoms range from very mild to more severe, and then can appear and disappear without any warning. The process for diagnosis usually begins with ruling out possible underlying diseases and chronic conditions … until the only choice left is chronic fatigue syndrome.

Left untreated, it decreases stamina, memory and concentration. Chronic fatigue may start suddenly, with flu-like symptoms.

But unlike the flu, it can last a lifetime. In addition to the profound fatigue experienced, other serious symptoms often accompany CFS, such as:. Sufferers of chronic fatigue syndrome also experience significant alterations in levels of irritability, mood swings, panic attacks, anxiety and depression.

Simply, the emotional and mental side effects of CFS cannot be overlooked, and treatment must include the mind, body and spirit. We still know very little about chronic fatigue, and sadly, the cause is still unknown.

While researchers continue to search for the root cause of CFS, there are preliminary findings that hormonal imbalances, poor immune system response, viral infections, chronic low blood pressure and nutritional deficiency are contributing factors. In addition, research indicates that chronic fatigue syndrome may be linked to oxidative stress, Celiac disease, and food sensitivities or food allergies.

Viruses that can cause CFS include HHV-6, HTLV, Epstein-Barr, measles, Coxsackie B, parovirus and cytomegalovirus. Conventional treatment protocols treat the symptoms rather than the underlying causes. Often individuals with chronic fatigue syndrome are prescribed antidepressants and sleeping pills.

In many cases, the side effects from these drugs are actually worse than the original symptoms. Instead, a natural approach includes alternative and complementary health practices, a well-balanced diet rich with potassium and magnesium, and the elimination of food allergens.

According to a study in the Journal of Alternative and Complementary Medicine, acupuncture, meditation, magnesium, l-carnitine and SAM-e S-Adenosyl methionine , show the most promise in the treatment of chronic fatigue syndrome and fibromyalgia.

More and more research is pointing to a link between food allergies and sensitivities and chronic fatigue syndrome. Allergies to certain foods, pollen, metals and other environmental chemicals may be causing the rising number of individuals with CFS.

According to a study published in the Scandinavian Journal of Gastroenterology , IBS, fibromyalgia and chronic fatigue are linked, and researchers were surprised. The common denominator, researchers in this study posit , is poor digestion and food sensitivities. Lactose intolerance, a casein allergy and an intolerance of other common allergens also may be at the root of chronic fatigue.

Other common allergens include tree nuts, peanuts, dairy, soy, shellfish and yeast. Consider taking an IgG Immunoglobulin G test to help you determine the foods that you are sensitive to — then you can eliminate them from your diet.

By getting rid of your personal known allergens, symptoms of IBS, ADHD, cystic fibrosis, rheumatoid arthritis and chronic fatigue can potentially be relieved. When ordering the IgG test, be sure to add on a Candida albicans test.

According to a study published in the Journal of Orthomolecular Medicine, an astounding 83 percent of participants who followed an anti-candida diet experienced a reduction in their symptoms related to chronic fatigue syndrome.

A candida diet includes foods high in probiotics including kefir, yogurt, sauerkraut and kimchi, as well as green vegetables, flax and chia seeds, and unsweetened cranberry juice.

It also requires the elimination of foods that feed the candida in the body. These include sugar, fruit, alcohol and grains. When candida is left untreated, it causes an inflammatory immune response and creates holes in the intestinal lining, leading to leaky gut.

Casein , a protein in dairy, can cause serious allergic reactions. A casein allergy is more than just lactose sensitivity; it stems from the immune system producing antibodies to protect against protein and can cause the body to release histamine.

This can cause hives, nasal congestion, wheezing, the swelling of the lips, mouth, tongue, face or throat, and even anaphylaxis. Of course, the best way to avoid these symptoms is to avoid casein.

This protein is concentrated in high-protein dairy products, including yogurt, milk, cheese and ice cream. However, most individuals will not have a problem with ghee or clarified butter.

In addition, bacteria called H. This unfriendly bacteria attacks the lining of the stomach; left untreated, these germs can lead to stomach ulcers. Researchers found that once H. pylori was out of the body of study participants, their physical and psychological symptoms, including those from IBS, fibromyalgia and chronic fatigue, got well.

For example, in a study, the H. pylori IgG levels in patients with MS and fatigue were significantly higher than in those without fatigue. com to get your supercharged spirulina and clean chlorella!

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Diagnosing ME, CFS and FMS: CT38 - a cure for Myalgic Encephalomyelitis? MyHealthRecord Opt out website fails Brett Lidbury talks about diagnosing Myalgic encephalomyelitis, Chronic fatigue Syndrome and Fibromyalgia. Production checked by Charles Willock, Presented and Produced by by Diffusion Science radio 20 min listen.

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There is still a lot to discover and learn when it comes to the by The Higher Practice Podcast for Optimal Mental Health 42 min listen. Today Dr. Deanna Minich talks about her new book, Whole Detox, taking into account the whole human instead of just the physical.

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Here to answer is Dr. Anna Cabeca, board-certified Gynecologist and expert in functional medicine. In this episode, Dr. Anna gives her by Well Beyond 40 4 min listen. And so, as I continued to seek help with the myriad of random symptoms that manifested, I began to feel 'marked' as an attention seeking hypochondriac.

As someone who is definitely not an attention seeker, or a hypochondriac, these visits became more and more stressful. I felt I could never adequately convey what I was suffering and, not feeling believed, made me anxious, demoralised and more exhausted than ever.

With no help forthcoming other than a prescription for sleeping pills which only made the fog in my head worse I just stopped visiting my GP. I realised I was going to have to find my own solutions.

The one thing I did know, I was not mad, this was not in my head, this was very real. And so started my very long and bumpy but life changing journey into the unknown. Two pivotal events happened next:. A friend lent me a book written by a Naturopath and this was to became my first 'aha' moment.

It was a life changing read as it made me realise what a stress-ridden, toxic and unhealthy lifestyle I had been leading. The majority of my working life, as a freelance graphic designer, had been in highly stressful, deadline driven, corporate environments: 65hr weeks, 18hr days -— working through the night, 10 days back-to-back were not uncommon.

I also partied as hard as I worked. Breakfast and lunch were something I grabbed on the way to the office, evening meals were usually restaurant food and when I did eat at home it was usually a microwave meal.

I rarely exercised and had no spirituality in my life. Whilst on a bus reading said book above, a man interrupted me to ask had I ever read the Optimum Nutrition Bible by Patrick Holford.

Of course I had not, but it was promptly ordered and there began my first tentative steps into the world of nutrition — and it blew my mind!

Now I had something to focus on. I transitioned over to an organic, nutrient dense, wholefoods diet. I removed all sugars, processed and refined foods, additives, preservatives, yeast and alcohol.

I tested for food sensitivities and removed the foods I was reacting to as well. At a time when I was physically and mentally exhausted re-educating myself and cooking every meal from scratch was time-consuming and challenging but, as tempting as it was to opt for convenience in order to rest and preserve my energy, I never compromised with this.

I knew I was on the right track when I noticed my downward spiral was starting to plateau. I couldn't say I was feeling better by any means, but I wasn't getting worse and that was a first step in the right direction.

I believe a key element of my healing and in halting the downward trajectory of my health spiral was the fact I embraced, very early on, that my lifestyle was a contributing factor to what was happening to me.

Inspired by natural healing and the body's innate ability to heal itself given the right environment, I fully immersed myself in refining my diet and changing my lifestyle. I experimented with various therapies and protocols — some of them helpful but others, introduced too early, set me backwards.

With no cohesive support or care I stumbled around like this for several years. Slowly my symptoms and quality of life began to improve. But I only felt ok so long as I did nothing to rock the boat like, stay up late, relax my diet, skip my juicing regime, be too active, concentrate too much, drink alcohol or incur any stress.

I was in a catch situation — now I had a bit more energy I was desperate to do more and start rebuilding my life. However, misjudge my resilience and the shutters would come crashing down and, with each crash, my new found and hard fought for energy would be gone, my morale would plummet and I would despair if this would ever end.

Stuck now in this pattern of cyclic crashing, I knew I had to do more than just manage my symptoms and this was when I decided to study Naturopathic Nutrition at the College of Naturopathic Medicine. I wanted to understand more about the science of nutrition and how it impacted my body at a biochemical level.

I wanted to leave no stone unturned to support my healing. My next four years of study allowed me to do that. I learned to provide my body with the correct foods, nutrients and protocols to support:.

Adrenal function to facilitate a healthy HPA Axis stress response, cortisol production and blood sugar balance. Thyroid function to improve overall hormonal balance and metabolism. Optimal digestive function to maximise nutrient absorption and reduce food sensitivities via gut permeability healing protocols.

Immune system defence and repair via protocols to remove bad microbes, yeast and parasites to support a healthy gut microflora and reduce inflammatory responses. Nervous System function to calm hypersensitivity and anxiety to promote relaxation, sleep and a healthy circadian rhythm.

Gentle detoxification to facilitate elimination of toxins alongside appropriate liver support. CFS sufferers are typically poor detoxifiers so all modes of detoxification should be chosen carefully and only implemented when they can be tolerated.

Through DNA testing I learned I have genetic SNPs that create rapid Phase1 and compromised Phase 2 detoxification pathways — not a great combination and no wonder I suffered savage Herzheimer reactions in my early years of healing and detoxifying — I endured a 4 month period where my symptoms, already very bad, worsened whilst I was cleansing and killing off microbes.

Unfortunately, the practitioner I was seeing was not very knowledgeable in supporting CFS or our tendency for severe die-off reactions and consequently, I went through a very difficult period where I suffered unnecessarily. On another occasion just 1 session of reflexology, introduced too early in my healing left me unable to function for a week because of the detox reaction I had.

The Role of Toxins in Fibromyalgia and Chronic Fatigue Syndrome I was in a catch situation — now I had a bit more energy I was desperate to do more and start rebuilding my life. Elliot R, Pico C, Hesketh J, Wybranska I, Dommels Y, Keijer J, et al. Axe on Pintrest 46 Share on Email Print Article 2. Cookie Duration Description cookielawinfo-checbox-analytics 11 months This cookie is set by GDPR Cookie Consent plugin. Research shows that both potassium and magnesium can help improve the symptoms associated with chronic fatigue syndrome.
Detoxification

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Why Kobo? Continue to kobo. com Cancel. By contrast, we have previously reported on the genetic variation for the gene coding for glycine-N-acyl transferase E. Our main previous observations in this regard, are summarized in Table 2. In our review [ 44 ] we argued that the major role of glycine conjugation is disposal of the end products of the gut microbiome, like those derived from polyphenols and phenylpropionate metabolism.

Natural substrates for glycine conjugation would thus include benzoate, 4-hydroxybenzoate, 3-hydroxybenzoate, 4-aminobenzoate, and salicylate. Glucuronidation would not be ideal for the detoxification of these substances, although glucuronidated salicylate conjugates were observed in urine following aspirin dosing [ 49 ].

These substances were not detected in our analysis. However, significant inter-individual variation does exist in glycine conjugation capacity. To investigate the influence of SNPs in the GLYAT coding sequence on enzyme activity, we expressed and characterized a recombinant human GLYAT and introduced site-directed mutagenesis to generate six non-synonymous SNP variants of the enzyme [ 45 ].

The enzyme activities of the three variants were similar to that of the wild-type, one variant was more active, one less active, and one was inactive. Although these findings suggest that SNP variations in the human GLYAT gene may influence the enzymatic kinetic properties to account for inter-individual variation, our subsequent study [ 47 ]indicated that the GLYAT open reading frame ORF from a cohort of South African Afrikaner Caucasians appeared to be highly conserved, supporting the hypothesis that the glycine conjugation pathway is an essential detoxification pathway.

It thus seems that genetic variability in the GLYAT gene did not compromise the observed biotransformation profiles following the salicylate intervention. Finally, we quantified the urinary excretion of p-aminohippuric acid over a period of ten hours in ten human volunteers following a p-aminobenzoic acid PABA challenge test[ 48 ].

All of the participants were able to metabolize PABA to such an extent that the product profile showed no further excretion of PAHA after 10 h, although considerable time dependent inter-individuality occurred.

It thus appears that variations in the amounts of PABA conjugated to glycine may be attributed to factors like absorption Phase 0 , metabolism Phase II and excretion Phase III , each phase with its own limiting factors which were call for a study in its own right for elucidation.

Not-with-standing these limitations, the present study show how the analysis and integration of a wide-range of parameters can lead to the selection of both known and new indicators of biotansformation. Three observations emerged from the fatigue and the biochemical measurements in our patient group.

First, both the original and the transformed data indicate no significant difference between low and high fatigue groups for phase I transformation Table 1 and Fig 5A and 5B.

The ability to clear caffeine following the challenge is an indicator of the detoxification capacity of the hepatic Phase I pathway and is a recognized method to assess liver function and especially Phase I biotransformation via the CYP1A2 isoenzyme [ 50 ][ 51 ].

CYP1A2 contributes to the inactivation of several common drugs and dietary constituents, including acetaminophen[ 52 ]. The administration of a combination of challenge substances as used here, exclude measurement of different Phase I cytochrome P enzyme reactions simultaneously.

However, Phase 1 biotransformation chemically modifies exogenous substances caffeine, acetoaminophen and salicylic acid as used here through the inducible CYP mixed function oxidase system, rendering them with improved ability for excretion caffeine derivatives or for phase II transformation catalysed by conjugation enzymes glucuronidase, glutathione-S-transferase and sulphotransferase.

The preferred detoxification modes in our patient group operated, however, through phase II glucuronidation Fig 5C : the acetoaminophen challenge and phase II glycination Fig 5F : the salicylic acid challenge. Glucuronidation is a fairly common mode of detoxification, given the abundance of required co-factors and ubiquitous nature of these transferases [ 53 ], whereas our recent kinetic study on human GLYAT indicated that glycination is observed over a range of substrate concentrations as well as over a lengthy span of time to facilitates optimal detoxification [ 54 ].

The kinetic study also supports the observation of elevated excretion of salicyluric acid, the glycine conjugate of salicylic acid, in the high fatigue group, which points to an upregulated GLYAT enzyme system and subsequent greater usage of ATP for substrate activation [ 41 ].

Taken together, we propose that these findings suggest a possible causal relationship between high exposure to some xenobiotic substance s or environmental condition, upregulated and chronic phase II detoxification, ATP consumption and fatigue.

Second, differences in the profiles of 2,3-DHBA and ROS appear to implicate oxidative stress in patients who experience fatigue strongly with energy factors the Mainly Energy Fatigue group , whereas patients more inclined to mental fatigue the Mainly Mental Fatigue group appeared to possess better antioxidant protection FRAP and GSHt.

Although mitochondrial dysfunction is recognized as the immediate cause of CFS symptoms like severe fatigue, a direct link to oxidative stress remains elusive [ 55 ], although increased oxidative stress remains a regularly observed condition in fatigue patients.

Third, the statistical metrics of biotransformation parameters for idiomatic fatigue, as shown here, do not comply with the requirements of diagnostic biomarkers [ 56 ] as defined for monogenetic or clinically well-defined diseases e.

Moreover, depending on their chemical nature, some toxicants tend to bioaccumulate in the body and become stored in tissues or remain in serum [ 57 ], which most likely generates a polygenetic response in these individuals.

The nuclear factor, erythroid 2-related factor 2-antioxidant response elements Nrf2-ARE as well as the androstane receptor CAR and pregnane receptor PXR are activated by a variety of endogenous and exogenous ligands[ 59 ][ 60 ] and are major determinants of phase II gene induction, so that upregulated phase II enzymes [ 61 ] may be promising targets for the treatment owing to their potent ability to detoxify harmful compounds and to combat ROS and oxidative stress.

However, there is a dearth of clinical trials on inducers of Nrf2 and biotransformation through phase II involvement, which may be attributed to several concerns that preclude their translation to the clinic [ 62 ]. Nevertheless, an individualized approach implicating the application of biotransformation has been proposed by Sears and Genius [ 58 ], which we here extend, based on our observations made over several years of involvement with fatigue and biotransformation:.

a Perform a comprehensive history to reasonably identify past and present xenobiotic exposures, while including clinical information similar to the present MSQ and PFS;.

b apply the present broad-based biochemical instrument as a first approximation on the biotransformation status of the individual case;. c define a clinical approach to institute personal health-related treatment strategies directed towards the individual case.

The approach proposed here is very similar to that suggested by Beger et al. This precision medicine approach is fast gaining ground and has been described in a number of recent publications [ 64 ][ 65 ][ 66 ][ 67 ][ 68 ].

According to Contrepois et al. Finally, our results have a direct bearing on the recent alert by the World Health Organization WHO regarding chronic non-communicable diseases. We believe that our contribution could be an important step towards unraveling a very complex syndromic phenomenon.

Research funding for the analytical and computational aspects of the project was provided by the Technological Innovation Agency TIA of the Department of Science and Technology of South Africa.

Browse Subject Areas? Click through the PLOS taxonomy to find articles in your field. Article Authors Metrics Comments Media Coverage Reader Comments Figures. Abstract Chronic fatigue, in its various manifestations, frequently co-occur with pain, sleep disturbances and depression and is a non-communicable condition which is rapidly becoming endemic worldwide.

Sheweita, Alexandria University, EGYPT Received: December 5, ; Accepted: April 17, ; Published: May 10, Copyright: © Erasmus et al. Introduction Chronic fatigue is a condition commonly reported by patients in primary care practice, whose medical practitioners use diverse definitions and diagnostic labels to describe their symptoms [ 1 ].

Materials and methods Ethics statement This study complied with all institutional guidelines of the North-West University as stipulated by the South African Guidelines for Good Clinical Practice Ethical Guidelines for Research, as well as the terms of the Declaration of Helsinki of as revised in for investigation of human participants.

Patient procedures and selection This study involved a prospective, observational and measurement design. Statistical analysis of the Piper Fatigue Scale We analysed the data of the modified Piper Fatigue Scale PFS as a multidimensional model for fatigue in our patient group data included in the S1 File.

Statistical analysis of the Medical Symptoms Questionnaire This questionnaire has 75 questions divided into 15 main sections; one question in the energy section about hyperactivity was omitted to enhance the reliability. Statistical profile of the biochemical data The data consist of 15 chemical measurements to define the biochemical variables and an additional variable for measurement of the filtrate volume required for some calculations.

Statistical methods used The analysis of all data generated from the investigation was performed according to well-described and validated methods[ 39 ] [ 40 ].

Biotransformation analysis The measurement design for the biotransformation interventions is shown schematically in Fig 1. Download: PPT. Fig 1. Measurement design for the interventions to assess the biotransformation profiles for all fatigue patients.

Phase I analysis. Phase II analysis. Secondary products from the acetylsalicylic acid challenge. Ferric reducing antioxidant assay FRAP assay.

Reactive oxygen species ROS assay. Total glutathione T-GSH assay. Creatinine and uric acid. Carnitine and acylcarnitine analysis.

Results A flow diagram of clinical and biochemical data acquisition procedures, comprehensive approaches of the statistical analyses and resulted outcomes is shown schematically in Fig 2.

Fig 2. Schematic flow diagram for the analysis of clinical and biochemical data for exploratory biotransformation profiling of samples from all fatigue patients. Fig 3. Distribution of all selected cases based on the individual scores in terms of energy fatigue and mental fatigue derived from the PFS.

Table 1. Descriptive statistics of the biochemical variables and their manifestation across the original data for the five fatigue groups. Fig 4. CHAID analysis of the selected cases over 5 fatigue groups colour code as in Fig 2 , incorporating the data from the biochemical and MSQ score analysis.

Fig 5. Graphs showing potentially important metabolites for the low and high fatigue groups, selected according to the CHAID classification. Discussion In this cohort study, we used two qualitative instruments MSQ and PFS and quantitative data biochemical measurements on women found to suffer from periodic or chronic fatigue with no definitive tests or findings to establish a clinical diagnosis.

Table 2. Selected studies on the association between biotransformation of xenobiotics and genetic polymorphisms in the GLYAT gene. Supporting information. S1 File. s DOCX. Acknowledgments Research funding for the analytical and computational aspects of the project was provided by the Technological Innovation Agency TIA of the Department of Science and Technology of South Africa.

References 1. Gallagher A. Incidence of fatigue symptoms and diagnoses presenting in UK primary care from to J R Soc Med. Brurberg KG, Fønhus MS, Larun L, Flottorp S, Malterud K.

BMJ Open. Pejovic S, Natelson BH, Basta M, Fernandez-Mendoza J, Mahr F, Vgontzas AN. BMC Neurol. View Article Google Scholar 4. Afari N, Schmaling KB, Herrell R, Hartman S, Goldberg J, Buchwald DS.

Coping strategies in twins with chronic fatigue and chronic fatigue syndrome. J Psychosom Res. Doong S-H, Dhruva A, Dunn LB, West C, Paul SM, Cooper BA, et al. Associations Between Cytokine Genes and a Symptom Cluster of Pain, Fatigue, Sleep Disturbance, and Depression in Patients Prior to Breast Cancer Surgery.

Biol Res Nurs. Holmes G, Kaplan J, Gantz N. Chronic fatigue syndrome: a working case definition. Annu Intern Med. View Article Google Scholar 7. Fenouillet E, Vigouroux A, Steinberg JG, Chagvardieff A, Retornaz F, Guieu R, et al. J Transl Med. BioMed Central; ; Watanabe N, Stewart R, Jenkins R, Bhugra DK, Furukawa TA.

The epidemiology of chronic fatigue, physical illness, and symptoms of common mental disorders: A cross-sectional survey from the second British National Survey of Psychiatric Morbidity.

Jason LA, Richman JA, Rademaker AW, Jordan KM, Plioplys A V, Taylor RR, et al. A community-based study of chronic fatigue syndrome. Arch Intern Med. Wong WS, Fielding R. Prevalence of chronic fatigue among Chinese adults in Hong Kong: a population-based study. J Affect Disord. Elbers RG, Rietberg MB, Van Wegen EEH, Verhoef J, Kramer SF, Terwee CB, et al.

Qual Life Res. Metelko Z, Szabo S, Diseases M, Kumar S, Delhi N, Heck V, et al. The World Health Organization Quality of Life Assessment WHOQOL : Position Paper from the World Health Organization. Soc Sci Med. Herbert F. The Diagnosis of Exclusion. Texas Hear Inst J. View Article Google Scholar Wessely S.

Chronic fatigue: Symptom and syndrome. Ann Intern Med. Naviaux RK, Naviaux JC, Li K, Bright AT, Alaynick WA, Wang L, et al. Metabolic features of chronic fatigue syndrome. Proc Natl Acad Sci U S A. Germain A, Ruppert D, Levine SM, Hanson MR.

Mol BioSyst. Yamano E, Sugimoto M, Hirayama A, Kume S, Yamato M, Jin G, et al. Index markers of chronic fatigue syndrome with dysfunction of TCA and urea cycles. Sci Rep. Nature Publishing Group; ;6: 1—9.

Armstrong CW, McGregor NR, Lewis DP, Butt HL, Gooley PR. Metabolic profiling reveals anomalous energy metabolism and oxidative stress pathways in chronic fatigue syndrome patients.

Springer US; ; — Newsholme TR, et al. Physical and mental fatigue:metabolic mechanisms and importance of plasma amino acids. Br Med Bull. Gamage N, Barnett A, Hempel N, Duggleby RG, Windmill KF, Martin JL, et al. Human sulfotransferases and their role in chemical metabolism.

Toxicol Sci. Guillemette C. Pharmacogenomics of human UDP-glucuronosyltransferase enzymes. Pharmacogenomics J. Hoffmann MF, Preissner SC, Nickel J, Dunkel M, Preissner R, Preissner S. The Transformer database: biotransformation of xenobiotics.

Nucleic Acids Res. Jancova P, Šiller M. Phase II Drug Metabolism. Top Drug Metab. Wild C. The exposome: from concept to utility. Int J Epidemiol. Rappaport SM, Barupal DK, Wishart D, Vineis P, Scalbert A. The blood exposome and its role in discovering causes of disease.

Environ Health Perspect. Warth B, Spangler S, Fang M, Johnson CH, Forsberg EM, Martin RL, et al. Exposing the Exposome with Global Metabolomics and Cognitive Computing. Xu C, Li CY-T, Kong A-NT. Arch Pharm Res. Badenhorst CPS, van der Sluis R, Erasmus E, van Dijk AA.

Glycine conjugation: importance in metabolism, the role of glycine N-acyltransferase, and factors that influence interindividual variation. Expert Opin Drug Metab Toxicol. Nortje C, Jansen Van Rensburg P, Cooke C, Erasmus E. van der Sluis R, Erasmus E. Elliot R, Pico C, Hesketh J, Wybranska I, Dommels Y, Keijer J, et al.

Nutrigenomic approaches for benefit-risk analysis of foods and food components: defining markers of health. Br J Nutr. van Ommen B, Keijer J, Heil SG, Kaput J. Challenging homeostasis to define biomarkers for nutrition related health. Mol Nutr Food Res.

Nakatsuji H, Kishida K, Kitamura T, Nakajima C, Funahashi T, Shimomura I. Dysregulation of glucose, insulin, triglyceride, blood pressure, and oxidative stress after an oral glucose tolerance test in men with abdominal obesity.

Elsevier; ; —6. Pellis L, van Erk MJ, van Ommen B, Bakker GCM, Hendriks HFJ, Cnubben NHP, et al. Plasma metabolomics and proteomics profiling after a postprandial challenge reveal subtle diet effects on human metabolic status.

Cordts PR, Kaminski M V, Raju S, Clark MR, Woo KMS. Vascular and Endovascular Surgery Could Gut-Liver Function Derangements Cause Chronic Venous Insufficiency? Vasc Surg. Piper B, Dibble S, Dodd M, Weiss M, Slaughter R, Paul S. The revised Piper Fatigue Scale: psychometric evaluation in women with breast cancer.

Oncol Nurs Forum. Jones DS, Quinn S. Textbook of Functional Medicine. Third ed. Jones DS, Quinn S, editors. Bouatra S, Aziat F, Mandal R, Guo AC, Wilson MR, Knox C, et al. The human urine metabolome. PLoS One.

Hair JF Jr, Black WC, Babin BJ, Anderson RE. Multivariate Data Analysis [Internet]. Pearson New International Edition; Kass G V. An Exploratory Technique for Investigating Large Quantities of Categorical Data.

Appl Stat. Reeve BB, Stover AM, Alfano CM, Smith AW, Bernstein L, Mctiernan A, et al. The Piper Fatigue Scale PFS : Psychometric Findings and Item Reduction in a Cohort of Breast Cancer Survivors.

Breast Cancer Res Treat. Jakobsson S, Taft C, Östlund U, Ahlberg K. Performance of the Swedish version of the Revised Piper Fatigue Scale. Eur J Oncol Nurs. Dagnelie PC, Pijls-Johannesma MCG, Pijpe A, Boumans BJE, Skrabanja ATP, Lambin P, et al. Psychometric properties of the revised Piper Fatigue Scale in Dutch cancer patients were satisfactory.

J Clin Epidemiol. Badenhorst CPS, Erasmus E, van der Sluis R, Nortje C, van Dijk AA. A new perspective on the importance of glycine conjugation in the metabolism of aromatic acids. Drug Metab Rev.

Van der Sluis R, Badenhorst CPS, Van der Westhuizen FH, Van Dijk AA. Characterisation of the influence of genetic variations on the enzyme activity of a recombinant human glycine N-acyltransferase. Elsevier B. Badenhorst CPS, Jooste M, Dijk AA Van.

Enzymatic Characterization and Elucidation of the Catalytic Mechanism of a Recombinant Bovine Glycine N -Acyltransferase ABSTRACT: ; — Sluis R Van Der, Badenhorst CPS, Erasmus E, Dyk E Van, Westhuizen FH Van Der, Dijk AA Van.

Conservation of the coding regions of the glycine N-acyltransferase gene further suggests that glycine conjugation is an essential detoxi fi cation pathway. Nortje C, van der Sluis R, van Dijk AA, Erasmus E. The Use of p-Aminobenzoic Acid as a Probe Substance for the Targeted Profiling of Glycine Conjugation.

J Biochem Mol Toxicol. Navarro SL, Saracino MR, Makar KW, Thomas SS, Li L, Zheng Y, et al. Determinants of aspirin metabolism in healthy men and women: Effects of dietary inducers of UDP-glucuronosyltransferases.

J Nutrigenet Nutrigenomics. Lord R, Bralley J. Toxicants and Detoxification. In: Lord R, Bralley A, editors. Laboratory Evaluations for Integrative and Functional Medicine.

Duluth, Georgia: Metametrix Institute; Tarantino G, Conca P, Capone D, Gentile A, Polichetti G, Basile V. Reliability of total overnight salivary caffeine assessment TOSCA for liver function evaluation in compensated cirrhotic patients.

Eur J Clin Pharmacol. Faber MS, Jetter A, Fuhr U. Assessment of CYP1A2 activity in clinical practice: why, how, and when? Basic Clin Pharmacol Toxicol. Smith RL, Cohen SM, Fukushima S, Gooderham NJ, Hecht SS, Guengerich FP, et al.

The safety evaluation of food flavouring substances: the role of metabolic studies. Toxicol Res Camb. Royal Society of Chemistry; ;7: — van der Sluis R, Ungerer V, Nortje C, van Dijk A A. New insights into the catalytic mechanism of human glycine N-acyltransferase.

Myhill S, Booth NE, Mclaren-howard J. Chronic fatigue syndrome and mitochondrial dysfunction. Int J Clin Exp Med. Xia J, Broadhurst DI, Wilson M, Wishart DS. Translational biomarker discovery in clinical metabolomics: An introductory tutorial. Genuis SJ. Elimination of persistent toxicants from the human body.

Hum Exp Toxicol. Sears ME, Genuis SJ.

4 Steps to Overcome Chronic Fatigue Syndrome

Discussion In this cohort study, we used two qualitative instruments MSQ and PFS and quantitative data biochemical measurements on women found to suffer from periodic or chronic fatigue with no definitive tests or findings to establish a clinical diagnosis.

Table 2. Selected studies on the association between biotransformation of xenobiotics and genetic polymorphisms in the GLYAT gene. Supporting information. S1 File.

s DOCX. Acknowledgments Research funding for the analytical and computational aspects of the project was provided by the Technological Innovation Agency TIA of the Department of Science and Technology of South Africa.

References 1. Gallagher A. Incidence of fatigue symptoms and diagnoses presenting in UK primary care from to J R Soc Med. Brurberg KG, Fønhus MS, Larun L, Flottorp S, Malterud K. BMJ Open. Pejovic S, Natelson BH, Basta M, Fernandez-Mendoza J, Mahr F, Vgontzas AN. BMC Neurol. View Article Google Scholar 4.

Afari N, Schmaling KB, Herrell R, Hartman S, Goldberg J, Buchwald DS. Coping strategies in twins with chronic fatigue and chronic fatigue syndrome. J Psychosom Res. Doong S-H, Dhruva A, Dunn LB, West C, Paul SM, Cooper BA, et al. Associations Between Cytokine Genes and a Symptom Cluster of Pain, Fatigue, Sleep Disturbance, and Depression in Patients Prior to Breast Cancer Surgery.

Biol Res Nurs. Holmes G, Kaplan J, Gantz N. Chronic fatigue syndrome: a working case definition. Annu Intern Med. View Article Google Scholar 7. Fenouillet E, Vigouroux A, Steinberg JG, Chagvardieff A, Retornaz F, Guieu R, et al. J Transl Med. BioMed Central; ; Watanabe N, Stewart R, Jenkins R, Bhugra DK, Furukawa TA.

The epidemiology of chronic fatigue, physical illness, and symptoms of common mental disorders: A cross-sectional survey from the second British National Survey of Psychiatric Morbidity.

Jason LA, Richman JA, Rademaker AW, Jordan KM, Plioplys A V, Taylor RR, et al. A community-based study of chronic fatigue syndrome.

Arch Intern Med. Wong WS, Fielding R. Prevalence of chronic fatigue among Chinese adults in Hong Kong: a population-based study. J Affect Disord.

Elbers RG, Rietberg MB, Van Wegen EEH, Verhoef J, Kramer SF, Terwee CB, et al. Qual Life Res. Metelko Z, Szabo S, Diseases M, Kumar S, Delhi N, Heck V, et al.

The World Health Organization Quality of Life Assessment WHOQOL : Position Paper from the World Health Organization. Soc Sci Med. Herbert F. The Diagnosis of Exclusion.

Texas Hear Inst J. View Article Google Scholar Wessely S. Chronic fatigue: Symptom and syndrome. Ann Intern Med. Naviaux RK, Naviaux JC, Li K, Bright AT, Alaynick WA, Wang L, et al.

Metabolic features of chronic fatigue syndrome. Proc Natl Acad Sci U S A. Germain A, Ruppert D, Levine SM, Hanson MR. Mol BioSyst. Yamano E, Sugimoto M, Hirayama A, Kume S, Yamato M, Jin G, et al. Index markers of chronic fatigue syndrome with dysfunction of TCA and urea cycles.

Sci Rep. Nature Publishing Group; ;6: 1—9. Armstrong CW, McGregor NR, Lewis DP, Butt HL, Gooley PR. Metabolic profiling reveals anomalous energy metabolism and oxidative stress pathways in chronic fatigue syndrome patients.

Springer US; ; — Newsholme TR, et al. Physical and mental fatigue:metabolic mechanisms and importance of plasma amino acids.

Br Med Bull. Gamage N, Barnett A, Hempel N, Duggleby RG, Windmill KF, Martin JL, et al. Human sulfotransferases and their role in chemical metabolism.

Toxicol Sci. Guillemette C. Pharmacogenomics of human UDP-glucuronosyltransferase enzymes. Pharmacogenomics J. Hoffmann MF, Preissner SC, Nickel J, Dunkel M, Preissner R, Preissner S. The Transformer database: biotransformation of xenobiotics. Nucleic Acids Res.

Jancova P, Šiller M. Phase II Drug Metabolism. Top Drug Metab. Wild C. The exposome: from concept to utility. Int J Epidemiol. Rappaport SM, Barupal DK, Wishart D, Vineis P, Scalbert A.

The blood exposome and its role in discovering causes of disease. Environ Health Perspect. Warth B, Spangler S, Fang M, Johnson CH, Forsberg EM, Martin RL, et al. Exposing the Exposome with Global Metabolomics and Cognitive Computing. Xu C, Li CY-T, Kong A-NT. Arch Pharm Res. Badenhorst CPS, van der Sluis R, Erasmus E, van Dijk AA.

Glycine conjugation: importance in metabolism, the role of glycine N-acyltransferase, and factors that influence interindividual variation. Expert Opin Drug Metab Toxicol. Nortje C, Jansen Van Rensburg P, Cooke C, Erasmus E. van der Sluis R, Erasmus E. Elliot R, Pico C, Hesketh J, Wybranska I, Dommels Y, Keijer J, et al.

Nutrigenomic approaches for benefit-risk analysis of foods and food components: defining markers of health. Br J Nutr. van Ommen B, Keijer J, Heil SG, Kaput J. Challenging homeostasis to define biomarkers for nutrition related health.

Mol Nutr Food Res. Nakatsuji H, Kishida K, Kitamura T, Nakajima C, Funahashi T, Shimomura I. Dysregulation of glucose, insulin, triglyceride, blood pressure, and oxidative stress after an oral glucose tolerance test in men with abdominal obesity. Elsevier; ; —6. Pellis L, van Erk MJ, van Ommen B, Bakker GCM, Hendriks HFJ, Cnubben NHP, et al.

Plasma metabolomics and proteomics profiling after a postprandial challenge reveal subtle diet effects on human metabolic status. Cordts PR, Kaminski M V, Raju S, Clark MR, Woo KMS. Vascular and Endovascular Surgery Could Gut-Liver Function Derangements Cause Chronic Venous Insufficiency?

Vasc Surg. Piper B, Dibble S, Dodd M, Weiss M, Slaughter R, Paul S. The revised Piper Fatigue Scale: psychometric evaluation in women with breast cancer.

Oncol Nurs Forum. Jones DS, Quinn S. Textbook of Functional Medicine. Third ed. Jones DS, Quinn S, editors. Bouatra S, Aziat F, Mandal R, Guo AC, Wilson MR, Knox C, et al.

The human urine metabolome. PLoS One. Hair JF Jr, Black WC, Babin BJ, Anderson RE. Multivariate Data Analysis [Internet]. Pearson New International Edition; Kass G V. An Exploratory Technique for Investigating Large Quantities of Categorical Data.

Appl Stat. Reeve BB, Stover AM, Alfano CM, Smith AW, Bernstein L, Mctiernan A, et al. The Piper Fatigue Scale PFS : Psychometric Findings and Item Reduction in a Cohort of Breast Cancer Survivors.

Breast Cancer Res Treat. Jakobsson S, Taft C, Östlund U, Ahlberg K. Performance of the Swedish version of the Revised Piper Fatigue Scale. Eur J Oncol Nurs. Dagnelie PC, Pijls-Johannesma MCG, Pijpe A, Boumans BJE, Skrabanja ATP, Lambin P, et al.

Psychometric properties of the revised Piper Fatigue Scale in Dutch cancer patients were satisfactory. J Clin Epidemiol. Badenhorst CPS, Erasmus E, van der Sluis R, Nortje C, van Dijk AA.

A new perspective on the importance of glycine conjugation in the metabolism of aromatic acids. Drug Metab Rev.

Van der Sluis R, Badenhorst CPS, Van der Westhuizen FH, Van Dijk AA. Characterisation of the influence of genetic variations on the enzyme activity of a recombinant human glycine N-acyltransferase. Elsevier B.

Badenhorst CPS, Jooste M, Dijk AA Van. Enzymatic Characterization and Elucidation of the Catalytic Mechanism of a Recombinant Bovine Glycine N -Acyltransferase ABSTRACT: ; — Sluis R Van Der, Badenhorst CPS, Erasmus E, Dyk E Van, Westhuizen FH Van Der, Dijk AA Van.

Conservation of the coding regions of the glycine N-acyltransferase gene further suggests that glycine conjugation is an essential detoxi fi cation pathway. Nortje C, van der Sluis R, van Dijk AA, Erasmus E. The Use of p-Aminobenzoic Acid as a Probe Substance for the Targeted Profiling of Glycine Conjugation.

J Biochem Mol Toxicol. Navarro SL, Saracino MR, Makar KW, Thomas SS, Li L, Zheng Y, et al. Determinants of aspirin metabolism in healthy men and women: Effects of dietary inducers of UDP-glucuronosyltransferases.

J Nutrigenet Nutrigenomics. Lord R, Bralley J. Toxicants and Detoxification. In: Lord R, Bralley A, editors. Laboratory Evaluations for Integrative and Functional Medicine. Duluth, Georgia: Metametrix Institute; Tarantino G, Conca P, Capone D, Gentile A, Polichetti G, Basile V.

Reliability of total overnight salivary caffeine assessment TOSCA for liver function evaluation in compensated cirrhotic patients. Eur J Clin Pharmacol. Faber MS, Jetter A, Fuhr U. Assessment of CYP1A2 activity in clinical practice: why, how, and when?

Basic Clin Pharmacol Toxicol. Smith RL, Cohen SM, Fukushima S, Gooderham NJ, Hecht SS, Guengerich FP, et al. The safety evaluation of food flavouring substances: the role of metabolic studies.

Toxicol Res Camb. Royal Society of Chemistry; ;7: — van der Sluis R, Ungerer V, Nortje C, van Dijk A A. New insights into the catalytic mechanism of human glycine N-acyltransferase.

Myhill S, Booth NE, Mclaren-howard J. Chronic fatigue syndrome and mitochondrial dysfunction. One of the most important routes for excretion is sweating. An exercise programme is important and effective in mobilising the fat into fuel, to release the fat-soluble chemicals.

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Infections may be a toxic foci, which until naturally resolved by the system or treated, may potentially contribute to chronic diseases.

The increased burden on the system can be fatiguing in a very general sense and affect the energy envelope available to the patient. Our combination of detoxification therapies is comprehensive in that toxic metals may be pulled out of the tissues and excreted intravenous chelation therapy , low-grade infections may be treated, organic toxins can be identified in case there is an increased body burden and addressed, and the liver, kidneys, and lymphatic system may be supported.

A temporary low-allergen diet may recommended in patients. Support of liver detoxification comes from recognizing the biochemistry of natural detoxification in this organ. Medical foods and supplements may be used to support Phase I reactions and Phase II liver detoxification pathways. There are also herbal drainage remedies that are commonly used which seem to give additional help.

Detoxification can often be broken down into a three-step process when dealing with either heavy metal toxins organic toxins. The 1st is to focus on intracellular mobilization of the toxins: the analogy here is to go through a deep spring cleaning of the house.

The 2nd is to focus on excretion of those toxins by mobilization of the lymphatics, kidney and liver support. The analogy can be thought of as making sure that the garbage and recycling pickup is operating so that what is removed in the deep spring cleaning does not simply accumulate elsewhere.

The 3rd important component is to ensure that there is no reabsorption of the toxins, which typically happens in the enterohepatic recirculation system between the gut and the liver. This is where fibers, binders can be useful to ensure that toxins stay in the gut and get excreted.

Again, and analogy is that we want to make sure that the garbage and recycling does not make its way back to the house after the spring cleaning.

In conclusion, detoxification is one of the fundamental ways in which we can support body. We are not speaking of acute toxicity but rather are trying to lower the burden on the body.

Stimulation of the body's natural healing ability may involves removing these toxic obstacles to cure; thus detoxification may be indicated. aggravation of symptoms with even the slightest departure from a very clean diet.

onset of symptoms after a more acute chemical or toxin exposure. aggravation of symptoms in certain environments such as the workplace or home. Evidence for role of infections in Auto-immune diseases, heart disease only a few of many more :. Issa OM1, Roberts R2, Mark DB2, Boineau R3, Goertz C4, Rosenberg Y5, Lewis EF6, Guarneri E7, Drisko J8, Magaziner A9, Lee KL2, Lamas GA Effect of high-dose oral multivitamins and minerals in participants not treated with statins in the randomized Trial to Assess Chelation Therapy TACT.

Am Heart J. Diaz D1, Fonseca V2, Aude YW3, Lamas GA1. Chelation therapy to prevent diabetes-associated cardiovascular events. Curr Opin Endocrinol Diabetes Obes.

Alessandro Fulgenzi and Maria Elena Ferrero EDTA Chelation Therapy for the Treatment of Neurotoxicity Int. Bamonti, F. Metal chelation therapy in rheumathoid arthritis:. A case report: Successful management of rheumathoid arthritis by metal chelation therapy. Biometals Fulgenzi, A. A case of multiple sclerosis improvement.

Biometals , 25, — Aluminium involvement in neurotoxicity. Efficacy of chelation therapy to remove. aluminium intoxication. Improvement of oxidative and metabolic parameters.

by cellfood administration in patients affected by neurodegenerative diseases on chelation treatment. Roussel, A. EDTA Chelation. therapy, without added vitamin C, decreases oxidative DNA damage and lipid peroxidation.

Evidence for detoxification improving risk factors and healing chronic disease brief examples of many :.

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