Tag: antioxidants

The Pall Protocol for Treating CFS/ME

Dr. Martin Pall’s NO/ONOO– (“No! Oh, no!”) hypothesis is probably the most comprehensive explanation of cellular dysregulation in CFS and other oxidative stress illnesses. His model proposes that the chronic stage of CFS is driven by a vicious cycle of oxidative stress, in which the basic mechanisms that are meant to control pathogens don’t turn off. The result is oxidants run amok, creating havoc in the cell’s energy cycles, and increasing inflammation.

The protocol described here was originally put together by Dr. Pall and by Dr. Grace Ziem. It is based on antioxidant treatments which break the vicious cycle of oxidative stress as well as other agents that act to lower other parts of the cycle, such as lowering inflammatory responses, improving mitochondrial function and lowering excessive NMDA activity. However, taking large quantities of single antioxidants can actually increase oxidative stress. Once antioxidants such as tocopherols (vitamin E), vitamin C, and flavonoids react with free radicals, these antioxidants are themselves converted into free radicals. Other antioxidants are then needed to neutralize those newly formed free radicals. Therefore, a wide variety of antioxidants is optimal.

PLEASE NOTE: Dr. Pall emphasizes that he is a Ph.D., not an M.D., and none of these therapies should be viewed as medical advice.

Below is a list of Dr. Pall’s therapies. More detailed information follows.

  1. Nebulized reduced glutathione
  2. Nebulized inhaled hydroxocobalamin
  3. Mixed natural tocopherols
  4. Buffered C
  5. Magnesium, as malate
  6. Four flavonoids: gingko, cranberry extract, silymarin and bilberry
  7. Selenium, as selenium-grown yeast
  8. CoQ10
  9. Folic acid
  10. Carotenoids including lycopene, lutein and B carotene
  11. Alpha lipoic acid
  12. Zinc (modest dose), manganese (low dose), copper (low dose)
  13. Vitamin B6, as pyridoxal phosphate
  14. Riboflavin 5′-phosphate
  15. Betaine (trimethylglycine)
  16. Acetyl-carnitine
  17. Taurine

Detailed antioxidant protocol:

Vitamin C. Pall suggests doses on the order of 500 to 1000 mg/day, taken several times per day. Vitamin C can act to regenerate tetrahydrobiopterin (BH4) and, therefore, may act to lower nitric oxide synthase (NOS) uncoupling, and high doses of vitamin C can be useful in scavenging peroxynitrite (ONOO–), the most central element in his NO/ONOO– cycle hypothesis.

CoQ10. CoQ10 has been used in a number of diseases to improve mitochondrial function. It scavenges free radicals, protects against loss of mitochondrial respiratory function, increases energy metabolism, and down regulates NMDA activity. Take early in the day.

Magnesium. This mineral lowers NMDA activity, reducing excitotoxicity. Dr. Pall believes that “magnesium is one of the most promising agents for treatment of multisystem diseases, but, like other such agents, it produces modest responses and may best be used in a complex, combination therapy.”

Selenium. Selenium is considered an antioxidant because certain proteins that contain selenium have antioxidant properties. Selenium occurs in glutathione peroxidases, enzymes that eliminate peroxide in cells. Selenium is also essential in making T3, the most active form of thyroid hormone. The best form of selenium is selenomethionine, which is a selenium-grown yeast. (For those who are yeast-sensitive, there are non-yeast forms.)

Carotenoids. These are plant pigments which are quite active in scavenging free radicals. Lycopene is more active than beta-carotene as a peroxynitrite scavenger. Lutein and zeaxanthin, two carotenoids, may also have special roles as antioxidants because of the way they insert into biological membranes.

Flavonoids. Anthocyanidins, which are found in purple plants, lower inflammatory activity, act as potent chain-breaking antioxidants, and regenerate other chain-breaking antioxidants after they have been converted to free radicals. Flavonoids also act as chelators for free iron, protecting cells from oxidative damage. Many flavonoids are soluble in both water and lipids. Flavonoids from green tea, citrus, grape seed extract, gingko, soy, olive, hawthorn, blueberry, and purple rice are effective antioxidants. Silymarin scavenges peroxynitrite, and increases the synthesis of SOD (superoxide dismutase), which makes it especially important. Flavonoids are rapidly absorbed in foods, and are quickly excreted through the kidneys, so they need to be eaten (or taken) throughout the day.

Acetyl-L-carnitine. Carnitine transports fatty acids into mitochondria, and is therefore essential for providing cellular energy. Acetyl-L-carnitine is more effective than L-carnitine because most oral L-carnitine ends up being excreted by the kidneys before it can be transported through the blood-brain barrier. Acetyl-L-carnitine is transported more efficiently. Recently, it has been shown that acetyl-L-carnitine lowers excessive NMDA activity and this may well be more important than the effects on mitochondrial function for lowering the NO/ONOO– cycle.

Reductive Stress Agents. Reductive stress causes oxidative stress. Methyl groups – SAMe, betaine, and carnitine – act as protective agents. Dr. Pall’s preference for a methylated compound is betaine (TMG.) It is cheaper and more stable than SAMe.

Hydroxocobalamin form of B12. B12 is a potent nitric oxide scavenger, but it is difficult to absorb. Oral absorption of B12 is limited by intrinsic factor. [Independent of intrinsic factor, the absorption rate of B12 is less than 1% of the total amount ingested.] Hydroxocobalamin taken as a nasal spray or injection is more effective.

Folate (folic acid). Reduced folate decreases uncoupling of NOS activity. Reduced folate in the form of 5-methyltetrahydrofolate (5-MTHF) is a potent scavenger of peroxynitrite and may well turn out to be among the most useful agents for lowering the NO/ONOO– cycle. Optimal dosage may well vary among different individuals but, in general, it should be taken along with quite a bit of vitamin C (at least 500 mg and preferably perhaps twice this amount). The reaction between peroxynitrite and 5-MTHF is important not only because it can be used to lower peroxynitrite levels. It is also important because in NO/ONOO– diseases, elevated peroxynitrite will act to lower the levels of 5-MTHF, lowering methylation cycle activity, and will also act to lower all reduced folates in the body. In this way, lowered methylation activity may be caused by the NO/ONOO– cycle.

B6, as P5P. B6 minimizes neurotoxicity. The best form is pyridoxine phosphate (P5P).

Riboflavin. Riboflavin is important for the production of reduced glutathione. It is also useful in the treatment of migraine.

Alpha Lipoic Acid (ALA) scavenges free radicals. As an added benefit, it can regenerate other antioxidants by reducing oxidized and free radical forms of glutathione, tocopherols, vitamin C and flavonoids. It can maintain glutathione pools by turning oxidized glutathione into its active form, reduced glutathione. ALA can cross the blood-brain barrier, making it an effective tool for reducing damage due to oxidative stress in the brain.

Zinc, Manganese and Copper. These minerals are components of superoxide dismutases (SOD), the enzymes that convert the oxidant superoxide into hydrogen peroxide and oxygen. Zinc, copper and manganese deficiencies can produce oxidative stress, part of which may be due to the lowered ability to produce SODs. Doses of these metals can be tricky. Excessive levels of copper and manganese can themselves produce oxidative stress. Excessive zinc lowers copper levels. Dr. Pall suggests “modest levels.”

Taurine is an unusual amino acid, because it is an antioxidant as well as a neurotransmitter. Taurine acts to stimulate the synthesis of GABA, and is transported easily across the blood-brain barrier, allowing it to work in the brain. Taurine stimulates several inhibitory receptors, leading to lowered NMDA activity. It also acts to lower intracellular calcium levels, thus lowering NO synthesis.

Long-chain omega-3 fatty acids. Polyunsaturated fatty acids (PUFAs) are more susceptible to lipid peroxidation than are other fatty acids, and consequently they tend to be depleted whenever there is oxidative stress. Fish oil, borage oil and flaxseed oil are sources of long-chain omega-3 fatty acids.

Curcumin, honokiol (from magnolia), cat’s claw, vinpocetine and feverfew all reduce inflammation by lowering NF-kappaB activity, as do a number of conventional pharmaceuticals.

Vitamin E should not be taken as synthetic alpha-tocopherol, which is the most commonly taken form, Pall argues. Rather, it should be taken as relatively high doses of gamma-tocopherol and tocotrienols with modest amounts of natural alpha-tocopherol. These other forms of vitamin E have important functions, such as lowering inflammation, scavenging an important breakdown product of peroxynitrite, lowering excessive NMDA activity and improving mitochondrial function, all important for lowering NO/ONOO– cycle diseases.

Algal supplements. Both chlorella and blue-green algae are rich in antioxidants. Blue-green algae contain phycocyanin, which is a potent free radical scavenger.

FURTHER READING:

Pall, Martin. Explaining “Unexplained Illnesses”: Disease Paradigm for Chronic Fatigue Syndrome, Multiple Chemical Sensitivity, Fibromyalgia, Post-Traumatic Stress Disorder, Gulf War Syndrome and Others. New York: Harrington Park Press, trade division of Haworth Press, Inc. 2007.

This book is technical, but well worth reading. Dr. Pall has made a remarkable contribution to the study of “unexplained illnesses.”

“How Can We Cure NO/ONOO– Cycle Diseases: Approaches to Curing Chronic Fatigue Syndrome/Myalgic Encephalomyelitis, Fibromyalgia, Multiple Chemical Sensitivity, Gulf War Syndrome and Possibly Many Others.” Martin Pall. Townsend Letter. Feb/March 2010.

Excellent paper by Martin Pall on agents that lower parts of the NO/ONOO? cycle. Contains detailed information on protocols and potential therapeutic agents. 

Martin Pall – MEPedia’s comprehensive page on Dr. Pall includes publications, talks, interviews, papers, and more.

Antioxidant Suggestions from Dr. Martin Pall, Ph.D.  Tables of supplements recommended by Dr. Pall, along with mechanisms and comments.

Potential Beneficial Effects of Naringin and Naringenin on Long COVID—A Review of the Literature

Abstract:

Coronavirus disease 2019 (COVID-19) caused a severe epidemic due to severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). Recent studies have found that patients do not completely recover from acute infections, but instead, suffer from a variety of post-acute sequelae of SARS-CoV-2 infection, known as long COVID.
The effects of long COVID can be far-reaching, with a duration of up to six months and a range of symptoms such as cognitive dysfunction, immune dysregulation, microbiota dysbiosis, myalgic encephalomyelitis/chronic fatigue syndrome, myocarditis, pulmonary fibrosis, cough, diabetes, pain, reproductive dysfunction, and thrombus formation. However, recent studies have shown that naringenin and naringin have palliative effects on various COVID-19 sequelae. Flavonoids such as naringin and naringenin, commonly found in fruits and vegetables, have various positive effects, including reducing inflammation, preventing viral infections, and providing antioxidants.
This article discusses the molecular mechanisms and clinical effects of naringin and naringenin on treating the above diseases. It proposes them as potential drugs for the treatment of long COVID, and it can be inferred that naringin and naringenin exhibit potential as extended long COVID medications, in the future likely serving as nutraceuticals or clinical supplements for the comprehensive alleviation of the various manifestations of COVID-19 complications.
Source: Liu S, Zhong M, Wu H, Su W, Wang Y, Li P. Potential Beneficial Effects of Naringin and Naringenin on Long COVID—A Review of the Literature. Microorganisms. 2024; 12(2):332. https://doi.org/10.3390/microorganisms12020332 https://www.mdpi.com/2076-2607/12/2/332 (Full text)

Improving Quality of Life in Chronic Fatigue Syndrome using Antioxidant Complex Twendee M®.

Abstract:

Chronic fatigue syndrome (CFS) is a disease in which fatigue that interferes with daily life persists for six months or longer. The number of patients with CFS is increasing, as CFS-like symptoms have been reported to occur in the sequelae of both COVID-19 infection and the SARS-CoV-2 vaccine, both of which have become significant issues in recent years. While the pathogenesis mechanism is not yet fully understood, research suggests that oxidative stress (OS) may play a role in the development of CFS.
In this paper, we discuss the antioxidant potential of the antioxidant formulation Twendee M® (TwM) and the results of a questionnaire that monitored changes in symptoms before and after TwM in a total of 23 men and women diagnosed with CFS. TwM is a supplement containing 15 different ingredients, and has a strong antioxidant capacity that cannot be achieved with a single antioxidant ingredient.
The results of the questionnaire showed that TwM significantly improved all of the major symptoms of CFS, including fatigue, muscle pain, joint pain, sleep disturbance, decreased memory and concentration, and headache. TwM was shown to alleviate various symptoms of CFS and improve quality of life.
Source: You, F.; Harakawa, Y.; Yoshikawa, T.; Inufusa, H. Improving Quality of Life in Chronic Fatigue Syndrome using Antioxidant Complex Twendee M®.. Preprints 2024, 2024020373. https://doi.org/10.20944/preprints202402.0373.v1 https://www.preprints.org/manuscript/202402.0373/v1 (Full study available as PDF file)

Advancing Research and Treatment: An Overview of Clinical Trials in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) and Future Perspectives

Abstract:

Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a chronic, debilitating, and multi-faceted illness. Heterogenous onset and clinical presentation with additional comorbidities make it difficult to diagnose, characterize, and successfully treat. Current treatment guidelines focus on symptom management, but with no clear target or causative mechanism, remission rates are low, and fewer than 5% of patients return to their pre-morbid activity levels. Therefore, there is an urgent need to undertake robust clinical trials to identify effective treatments.
This review synthesizes insights from clinical trials exploring pharmacological interventions and dietary supplements targeting immunological, metabolic, gastrointestinal, neurological, and neuroendocrine dysfunction in ME/CFS patients which require further exploration. Additionally, the trialling of alternative interventions in ME/CFS based on reported efficacy in the treatment of illnesses with overlapping symptomology is also discussed. Finally, we provide important considerations and make recommendations, focusing on outcome measures, to ensure the execution of future high-quality clinical trials to establish clinical efficacy of evidence-based interventions that are needed for adoption in clinical practice.
Source: Seton KA, Espejo-Oltra JA, Giménez-Orenga K, Haagmans R, Ramadan DJ, Mehlsen J on behalf of the European ME Research Group for Early Career Researchers (Young EMERG). Advancing Research and Treatment: An Overview of Clinical Trials in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) and Future Perspectives. Journal of Clinical Medicine. 2024; 13(2):325. https://doi.org/10.3390/jcm13020325 https://www.mdpi.com/2077-0383/13/2/325 (Full text)

Clinical Rationale for Dietary Lutein Supplementation in Post COVID-19 and mRNA Vaccine Injury Syndromes

Abstract:

Lutein, a plant-derived xanthophyl-carotenoid, is an exceptional antioxidant and anti-inflammatory constituent found in food. Elevated concentrations of lutein found in human blood and plasma, due to high dietary intake, are beneficial against eye disease and improve cardiometabolic health.

Lutein plays an important protective role against the development of neurological disorders, including Alzheimer’s disease (AD), multiple sclerosis (MS) and Parkinson’s disease (PD). It has also been shown to be beneficial for liver, kidney and respiratory health. Lutein, acting as a very strong antioxidant, can alleviate oxidative stress and downgrade reactive oxygen species (ROS). Oxidative stress is one of the key pathogenic mechanisms in post-COVID and mRNA vaccine injury syndromes.

Recent in silico studies suggest that lutein and other naturally derived antioxidants, by docking at the site where the SARS-CoV-2 spike protein (SP) binds to the angiotensin enzyme type 2 (ACE2) receptor, may neutralize the SP-ACE2 interactions. Lutein can be added to a detoxification regimen to aid in clearing Spike protein and relieving symptoms.

In agreement with Hippocrates’ dictum to “Let food be thy medicine,” this review establishes dietary lutein as a valuable therapy in the treatment of post-COVID syndrome, mRNA vaccine injury syndromes, and a wide range of other chronic illnesses.

Source: Kyriakopoulos, A.M.; Nigh, G.; McCullough, P.A.; Seneff, S. Clinical Rationale for Dietary Lutein Supplementation in Post COVID-19 and mRNA Vaccine Injury Syndromes. Preprints 2023, 2023091385. https://doi.org/10.20944/preprints202309.1385.v1 https://www.preprints.org/manuscript/202309.1385/v1 https://www.preprints.org/manuscript/202309.1385/v1 (Full text available as PDF file)

The global challenges of the long COVID-19

Abstract:

COVID-19 may lead to a perseverance of symptoms after recovery from the disease, a condition known as long COVID, characterized by continual cognitive, somatic and behavioral symptoms. SARS-CoV-2 infection triggers different molecular to tissue level events, given by the inherent features of each patient. The potential pathological changes which determine the array of symptoms are arduous to anticipate.

There is an increasing interest to develop treatment strategies for survivors who experience a long COVID. In this respect, considering the anti-inflammatory, anti-oxidative and cytoprotective effects of melatonin (MEL) on viral infections, its potential links with COVID-19 should be researched. Several studies suggest that administration of MEL may prevent clinical deterioration and even death in patients with acute and long COVID-19.

This paper briefly reviews the current status of knowledge of the pathogenic, clinical, and therapeutic features of Long COVID-19 and forthcoming directions for research and implications for the management and therapy of the disease are analyzed.

Source: Leonor Chacin-Bonilla. The global challenges of the long COVID-19. Journal of Clinical Images and Medical Case Reports. ISSN 2766-7820 https://jcimcr.org/pdfs/JCIMCR-v4-2512.pdf (Full text)

Chronic inflammation, neuroglia dysfunction, and plasmalogen deficiency as a new pathobiological hypothesis addressing the overlap between post-COVID-19 symptoms and myalgic encephalomyelitis/chronic fatigue syndrome

Highlights:

  • Plasmalogens (Pls) are lipids containing a vinyl-ether bond in their glycerol backbone
  • Pls have antioxidant properties and are important for curved membrane assemblies
  • Post-COVID-19 symptoms are highly prevalent and share several features with ME/CFS
  • Pls depletion is a shared biological hallmark of ME/CFS and acute COVID-19 syndrome
  • Pls replacement is a promising tool against neuroinflammation in these two conditions

Abstract:

After five waves of COVID-19 outbreaks, it has been recognized that a significant portion of the affected individuals developed long-term debilitating symptoms marked by chronic fatigue, cognitive difficulties (“brain fog”), post-exertional malaise, and autonomic dysfunction. The onset, progression, and clinical presentation of this condition, generically named post-COVID-19 syndrome, overlap significantly with another enigmatic condition, referred to as myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS).

Several pathobiological mechanisms have been proposed for ME/CFS, including redox imbalance, systemic and central nervous system inflammation, and mitochondrial dysfunction. Chronic inflammation and glial pathological reactivity are common hallmarks of several neurodegenerative and neuropsychiatric disorders and have been consistently associated with reduced central and peripheral levels of plasmalogens, one of the major phospholipid components of cell membranes with several homeostatic functions.

Of great interest, recent evidence revealed a significant reduction of plasmalogens contents, biosynthesis, and metabolism in ME/CFS and acute COVID-19, with a strong association to symptom severity and other relevant clinical outcomes. These bioactive lipids have increasingly attracted attention due to their reduced levels representing a common pathophysiological manifestation between several disorders associated with aging and chronic inflammation. However, alterations in plasmalogen levels or their lipidic metabolism have not yet been examined in individuals suffering from post-COVID-19 symptoms.

Here, we proposed a pathobiological model for post-COVID-19 and ME/CFS based on their common inflammation and dysfunctional glial reactivity, and highlighted the emerging implications of plasmalogen deficiency in the underlying mechanisms. Along with the promising outcomes of plasmalogen replacement therapy (PRT) for various neurodegenerative/neuropsychiatric disorders, we sought to propose PRT as a simple, effective, and safe strategy for the potential relief of the debilitating symptoms associated with ME/CFS and post-COVID-19 syndrome.

Source: Chaves AM, Braniff O, Angelova A, Deng Y, Tremblay MÈ. Chronic inflammation, neuroglia dysfunction, and plasmalogen deficiency as a new pathobiological hypothesis addressing the overlap between post-COVID-19 symptoms and myalgic encephalomyelitis/chronic fatigue syndrome. Brain Res Bull. 2023 Jul 7:110702. doi: 10.1016/j.brainresbull.2023.110702. Epub ahead of print. PMID: 37423295. https://www.sciencedirect.com/science/article/pii/S0361923023001272?via%3Dihub (Full text)

Ginkgo Biloba and Long COVID: In Vivo and In Vitro Models for the Evaluation of Nanotherapeutic Efficacy

Abstract:

Coronavirus infections are neuroinvasive and can provoke injury to the central nervous system (CNS) and long-term illness consequences. They may be associated with inflammatory processes due to cellular oxidative stress and an imbalanced antioxidant system. The ability of phytochemicals with antioxidant and anti-inflammatory activities, such as Ginkgo biloba, to alleviate neurological complications and brain tissue damage has attracted strong ongoing interest in the neurotherapeutic management of long COVID.
Ginkgo biloba leaf extract (EGb) contains several bioactive ingredients, e.g., bilobalide, quercetin, ginkgolides A–C, kaempferol, isorhamnetin, and luteolin. They have various pharmacological and medicinal effects, including memory and cognitive improvement. Ginkgo biloba, through its anti-apoptotic, antioxidant, and anti-inflammatory activities, impacts cognitive function and other illness conditions like those in long COVID. While preclinical research on the antioxidant therapies for neuroprotection has shown promising results, clinical translation remains slow due to several challenges (e.g., low drug bioavailability, limited half-life, instability, restricted delivery to target tissues, and poor antioxidant capacity).
This review emphasizes the advantages of nanotherapies using nanoparticle drug delivery approaches to overcome these challenges. Various experimental techniques shed light on the molecular mechanisms underlying the oxidative stress response in the nervous system and help comprehend the pathophysiology of the neurological sequelae of SARS-CoV-2 infection.
To develop novel therapeutic agents and drug delivery systems, several methods for mimicking oxidative stress conditions have been used (e.g., lipid peroxidation products, mitochondrial respiratory chain inhibitors, and models of ischemic brain damage). We hypothesize the beneficial effects of EGb in the neurotherapeutic management of long-term COVID-19 symptoms, evaluated using either in vitro cellular or in vivo animal models of oxidative stress.
Source: Akanchise T, Angelova A. Ginkgo Biloba and Long COVID: In Vivo and In Vitro Models for the Evaluation of Nanotherapeutic Efficacy. Pharmaceutics. 2023; 15(5):1562. https://doi.org/10.3390/pharmaceutics15051562 https://www.mdpi.com/1999-4923/15/5/1562 (Full text)

Exploring the Genetic Contribution to Oxidative Stress in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome

Abstract:

OBJECTIVES/GOALS: Strong evidence has implicated oxidative stress (OS) as a disease mechanism in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). The study aim was to assess whether a C>T single nucleotide polymorphism (SNP) (rs1800668), which reduces the activity of glutathione peroxidase 1 (GPX1), is associated with brain OS in patients with ME/CFS.

METHODS/STUDY POPULATION: Study population: The study enrolled 20 patients with ME/CFS diagnosed according to Canadian Consensus Criteria, and 11 healthy control (HC) subjects. Genotyping: DNA was extracted from whole blood samples, amplified by PCR, and purified. Sanger sequencing was used for genotyping. 1H MRS: Proton magnetic resonance spectroscopy (1H MRS) was used to measure levels of glutathione (GSH) a primary tissue antioxidant and OS marker in a 3x3x2 cm3 occipital cortex (OCC) voxel. GSH spectra were recorded in 15 minutes with the standard J-editing technique. The resulting GSH peak area was normalized to tissue water level in the voxel. Statistical Analysis: T-tests were used to compare OCC GSH levels between ME/CFS and HC groups, and between the study’s genotype groups (group 1: CC, group 2: combined TC and TT).

RESULTS/ANTICIPATED RESULTS: Clinical characteristics: ME/CFS and HC groups were comparable on age and BMI but not on sex (p = 0.038). Genotype frequencies: Genotype frequencies in the ME/CFS group were 0.55 (CC), 0.25 (TC) and 0.2 (TT); and 0.636 (CC), 0.364 (TC), and 0 (TT) in the HC group. GSH levels: There was a trend-level lower mean OCC GSH in ME/CFS than in HC (0.0015 vs 0.0017; p = 0.076). GSH levels by genotype group interaction: Within the ME/CFS group but not in the combined ME/CFS and HC group or HC group alone, GSH levels were lower in the TC and TT genotypes than in CC genotypes (0.00143 vs 0.00164; p = 0.018).

DISCUSSION/SIGNIFICANCE: This study found that the presence of a C>T SNP in GPX1 is associated with lower mean GSH levels and, hence, brain oxidative stress, in ME/CFS patients. If validated in a larger cohort, this finding may support targeted antioxidant therapy based on their genotype as a potentially effective treatment for patients with ME/CFS.

Source: Hampilos, N., Germain, A., Mao, X., Hanson, M., & Shungu, D. (2023). 474 Exploring the Genetic Contribution to Oxidative Stress in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome. Journal of Clinical and Translational Science, 7(S1), 137-138. doi:10.1017/cts.2023.488. DOI: https://doi.org/10.1017/cts.2023.488

A Review of Possible Supplements to Relieve the Symptoms of Fatigue after COVID-19

Abstract:

Background: The highly infectious coronavirus has become a global pandemic; the effective medication is yet to be developed. The health care system was strained; millions of people have been suffered from infection and complications. Post COVID-19 fatigue is a dominant characteristic of coronavirus infection. It affects general state of health, muscle strength, sleeping quality, mental health, and life quality. This paper is emphasizing and summarizing the potential beneficial supplementations of post COVID-19 fatigue symptoms.

Methods: The knowledge gained from PubMed and from the National Library of Medicine. Clinical studies and systematic review articles were collected in this topic.

Results: Herein, we discuss the possible therapeutic supplementations with anti-inflammatory, immunomodulatory and antioxidant effect. Vitamin complexes, trace elements, antioxidants, coenzymes, probiotics, essential fatty acids; one and creatine as amino acid derivatives have been appeared to be effective in relieving post COVID-19 fatigue symptoms.

Conclusions: Based on the data, these nutrients and supplements might be important to alleviate the post COVID-19 fatigue symptoms and they could be considered as a supportive therapy

Source: Boglárka Bernadett Tisza, Gyöngyi Iván, Viola Keczeli, Melinda Kóró, Patricia Szántóri, Zsófia Gyócsiné Varga, Henriett Müller, Olivia Pribéli, Zoltán Szabó, Zsófia Verzár, Monika Sélleyné Gyuró, Andrea Gubicskóné Kisbendek and Tímea Stromájer-Rácz. A Review of Possible Supplements to Relieve the Symptoms of Fatigue after COVID-19.  J Med Public Health. 2023;4(2):JMPH-04-1062. https://www.medtextpublications.com/open-access/a-review-of-possible-supplements-to-relieve-the-symptoms-of-1309.pdf (Full text)