Kynurenine Pathway Hypothesis: The Nature of the Chronic Fatigue Syndrome (CFS) Revisited

Blankfield, Adele

doi:10.4137/ijtr.s7898

Cited by 3 publications

(12 citation statements)

References 4 publications

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“…Significant substrate deficiencies can be created by the additional demands1,17,40,69 imposed on the body by neoplastic cells,83 micro-organisms (eg, gut saprophytes84–86 and B-12 requirements of the blind loop syndrome),53 undue physical exertion by the ill patient, and interference by metabolic activity of medications (eg, isoniazid) 16,17,40,53. The resultant upregulation of the tryptophan kynurenine pathway offers an explanatory model for an immunological connection between malnutrition and infection, and for the pathophysiological and neurological complications of severe trauma and illness, CFS/FM included 1,2…”

Section: Resultsmentioning

confidence: 99%

“…CFS/FM is a complex autoimmune spectrum disorder which is frequently familial 2,3,41,47. The onset is either acute or insidious and has a variable and unpredictable course and outcome.…”

Section: Cfs/fm—the Metabolic Enigmamentioning

confidence: 99%

“…Genetic disorders of tryptophan and Vitamin B-12 status should be tested for, to exclude neurologic PA and other aberrations. Search for unexpected silent or chronic infections is required 2,48–50. In conclusion, the presence of nutritional3,31,68 and thyroid deficiencies and unsuspected infections offer a rational explanation as to the etiology of the patient’s signs and symptoms, such as ataxia, pain, paresthesias, and dysphorias 55…”

Section: Cfs/fm—the Metabolic Enigmamentioning

confidence: 99%

“…Aspects of some of the putative precipitating factors have been previously outlined 2,3. An analysis of the areas of metabolic dysfunction will focus on future directions for research and management.…”

mentioning

confidence: 99%

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Article Commentary: Kynurenine Pathway Pathologies: Do Nicotinamide and Other Pathway Co-Factors have a Therapeutic Role in Reduction of Symptom Severity, Including Chronic Fatigue Syndrome (CFS) and Fibromyalgia (FM)

Blankfield¹

2013

Int J�Tryptophan�Res

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The definition of dual tryptophan pathways has increased the understanding of the mind-body, body-mind dichotomy. The serotonergic pathway highlights the primary (endogenous) psychiatric disorders. The up-regulation of the kynurenine pathway by physical illnesses can cause neuropathic and immunological disorders1 associated with secondary neuropsychiatric symptoms.Tryptophan and nicotinamide deficiencies fall within the protein energy malnutrition (PEM) spectrum. They can arise if the kynurenine pathway is stressed by primary or secondary inflammatory conditions and the consequent imbalance of available catabolic/anabolic substrates may adversely influence convalescent phase efficiency. The replacement of depleted or reduced NAD+ levels and other cofactors can perhaps improve the clinical management of these disorders.Chronic fatigue syndrome (CFS) and fibromyalgia (FM) appear to meet the criteria of a tryptophan-kynurenine pathway disorder with potential neuroimmunological sequelae. Aspects of some of the putative precipitating factors have been previously outlined.2,3 An analysis of the areas of metabolic dysfunction will focus on future directions for research and management.

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Section: Resultsmentioning

confidence: 99%

“…CFS/FM is a complex autoimmune spectrum disorder which is frequently familial 2,3,41,47. The onset is either acute or insidious and has a variable and unpredictable course and outcome.…”

Section: Cfs/fm—the Metabolic Enigmamentioning

confidence: 99%

Section: Cfs/fm—the Metabolic Enigmamentioning

confidence: 99%

mentioning

confidence: 99%

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Article Commentary: Kynurenine Pathway Pathologies: Do Nicotinamide and Other Pathway Co-Factors have a Therapeutic Role in Reduction of Symptom Severity, Including Chronic Fatigue Syndrome (CFS) and Fibromyalgia (FM)

Blankfield¹

2013

Int J�Tryptophan�Res

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“…Nicotinamide absorption can be reduced through severe diarrhea. These listed observations imply that tryptophan, nicotinamide and B12 deficiencies can become a complication of CFS/FM 40,42,60–63. Evidence for the requirement of L-carnitine, zinc42 and intravenous vitamin solutions64 is circumstantial.…”

Section: Tryptophan Status In Cfs/fmmentioning

confidence: 99%

A Brief Historic Overview of Clinical Disorders Associated with Tryptophan: The Relevance to Chronic Fatigue Syndrome (CFS) and Fibromyalgia (FM).

Blankfield¹

2012

Int J�Tryptophan�Res

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Last century there was a short burst of interest in the tryptophan related disorders of pellagra and related abnormalities that are usually presented in infancy.1,2 Nutritional physiologists recognized that a severe human dietary deficiency of either tryptophan or the B group vitamins could result in central nervous system (CNS) sequelae such as ataxia, cognitive dysfunction and dysphoria, accompanied by skin hyperpigmentation.3,4 The current paper will focus on the emerging role of tryptophan in chronic fatigue syndrome (CFS) and fibromyalgia (FM).

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Endothelial Senescence and Chronic Fatigue Syndrome, a COVID-19 Based Hypothesis

Sfera

Osorio

Campo

et al. 2021

Front. Cell. Neurosci.

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Myalgic encephalomyelitis/chronic fatigue syndrome is a serious illness of unknown etiology, characterized by debilitating exhaustion, memory impairment, pain and sleep abnormalities. Viral infections are believed to initiate the pathogenesis of this syndrome although the definite proof remains elusive. With the unfolding of COVID-19 pandemic, the interest in this condition has resurfaced as excessive tiredness, a major complaint of patients infected with the SARS-CoV-2 virus, often lingers for a long time, resulting in disability, and poor life quality. In a previous article, we hypothesized that COVID-19-upregulated angiotensin II triggered premature endothelial cell senescence, disrupting the intestinal and blood brain barriers. Here, we hypothesize further that post-viral sequelae, including myalgic encephalomyelitis/chronic fatigue syndrome, are promoted by the gut microbes or toxin translocation from the gastrointestinal tract into other tissues, including the brain. This model is supported by the SARS-CoV-2 interaction with host proteins and bacterial lipopolysaccharide. Conversely, targeting microbial translocation and cellular senescence may ameliorate the symptoms of this disabling illness.

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Kynurenine Pathway Hypothesis: The Nature of the Chronic Fatigue Syndrome (CFS) Revisited

Cited by 3 publications

References 4 publications

Article Commentary: Kynurenine Pathway Pathologies: Do Nicotinamide and Other Pathway Co-Factors have a Therapeutic Role in Reduction of Symptom Severity, Including Chronic Fatigue Syndrome (CFS) and Fibromyalgia (FM)

Article Commentary: Kynurenine Pathway Pathologies: Do Nicotinamide and Other Pathway Co-Factors have a Therapeutic Role in Reduction of Symptom Severity, Including Chronic Fatigue Syndrome (CFS) and Fibromyalgia (FM)

A Brief Historic Overview of Clinical Disorders Associated with Tryptophan: The Relevance to Chronic Fatigue Syndrome (CFS) and Fibromyalgia (FM).

Endothelial Senescence and Chronic Fatigue Syndrome, a COVID-19 Based Hypothesis

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