Diet

If it's on your mind and it has to do with multiple sclerosis in any way, post it here.
User avatar
Petr75
Family Elder
Posts: 1615
Joined: Sat Oct 19, 2013 10:17 am
Location: Czech Republic
Contact:

Re: Diet

Post by Petr75 »

2021 Jan 19
Yunnan University, School of Medicine and College of Life Sciences, China
Activation of FXR by Ganoderic Acid A Promotes Remyelination in Multiple Sclerosis via Anti-inflammation and Regeneration Mechanism
https://pubmed.ncbi.nlm.nih.gov/33482151/

Abstract

Multiple sclerosis (MS), as an inflammatory demyelinating disorder of central nervous system, is the leading cause of non-traumatic neurologic disability in young adults. The pathogenesis of MS remains unknown, however, a dysregulation of glia-neuroimmune signaling plays a key role during progressive disease stage. Most of the existing drugs are aimed at the immune system, but there is no approved drug by promoting remyelination after demyelination so far. There is a great interest in identifying novel agents for treating MS bytargeting to switch the immune imbalance from pro-inflammation and apoptosis to anti-inflammation and regeneration during remyelination phase. Here, we reported that ganoderic acid A (GAA) significantly enhanced the remyelination and rescued motor deficiency in two animal models of MS, including cuprizone-induced demyelination and myelin oligodendrocyte glycoprotein (MOG) 35-55-induced experimental autoimmune encephalomyelitis model. In these two independent MS animal models, GAA modulated neuroimmune to enhance the anti-inflammatory and regeneration markers IL-4 and BDNF, inhibited inflammatory markers IL-1β and IL-6, followed by down-regulation of microglia activation and astrocyte proliferation. Pharmacological and genetic ablation of farnesoid-X-receptor (FXR) abolished GAA-induced remyelination and restoration of motor deficiency in MS mice. Thus, GAA is a novel and potential therapeutic agent that can rescue MS neuroimmune imbalance and remyelination through an FXR receptor-dependent mechanism. Clinical investigation on the therapeutic effect of GAA in improving remyelination of the MS patients to rescue the motor function is warranted.

----------------------------------------
wiki https://en.wikipedia.org/wiki/Lingzhi_(mushroom)

https://www.eboro.cz
User avatar
Petr75
Family Elder
Posts: 1615
Joined: Sat Oct 19, 2013 10:17 am
Location: Czech Republic
Contact:

Re: Diet

Post by Petr75 »

2021 Feb
Institute of Neuronal Cell Biology, Technical University Munich, Munich, Germany
Diet-dependent regulation of TGFβ impairs reparative innate immune responses after demyelination
https://pubmed.ncbi.nlm.nih.gov/33619376/


Abstract

Proregenerative responses are required for the restoration of nervous-system functionality in demyelinating diseases such as multiple sclerosis (MS). Yet, the limiting factors responsible for poor CNS repair are only partially understood. Here, we test the impact of a Western diet (WD) on phagocyte function in a mouse model of demyelinating injury that requires microglial innate immune function for a regenerative response to occur. We find that WD feeding triggers an ageing-related, dysfunctional metabolic response that is associated with impaired myelin-debris clearance in microglia, thereby impairing lesion recovery after demyelination. Mechanistically, we detect enhanced transforming growth factor beta (TGFβ) signalling, which suppresses the activation of the liver X receptor (LXR)-regulated genes involved in cholesterol efflux, thereby inhibiting phagocytic clearance of myelin and cholesterol. Blocking TGFβ or promoting triggering receptor expressed on myeloid cells 2 (TREM2) activity restores microglia responsiveness and myelin-debris clearance after demyelinating injury. Thus, we have identified a druggable microglial immune checkpoint mechanism regulating the microglial response to injury that promotes remyelination.
https://www.eboro.cz
User avatar
Petr75
Family Elder
Posts: 1615
Joined: Sat Oct 19, 2013 10:17 am
Location: Czech Republic
Contact:

Re: Diet

Post by Petr75 »

2021 Feb 9
Salk Institute for Biological Studies, 10010 N. Torrey Pines Rd., La Jolla, CA
Preventing and Treating Neurological Disorders with the Flavonol Fisetin
https://pubmed.ncbi.nlm.nih.gov/33782648/

Abstract

Neurological disorders, including neurodegenerative diseases, have a significant negative impact on both patients and society at large. Since the prevalence of most of these disorders increases with age, the consequences for our aging population are only going to grow. It is now acknowledged that neurological disorders are multi-factorial involving disruptions in multiple cellular systems. While each disorder has specific initiating mechanisms and pathologies, certain common pathways appear to be involved in most, if not all, neurological disorders. Thus, it is becoming increasingly important to identify compounds that can modulate the multiple pathways that contribute to disease development or progression. One of these compounds is the flavonol fisetin. Fisetin has now been shown in preclinical models to be effective at preventing the development and/or progression of multiple neurological disorders including Alzheimer's disease, Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis, stroke (both ischemic and hemorrhagic) and traumatic brain injury as well as to reduce age-associated changes in the brain. These beneficial effects stem from its actions on multiple pathways associated with the different neurological disorders. These actions include its well characterized anti-inflammatory and anti-oxidant effects as well as more recently described effects on the regulated cell death oxytosis/ferroptosis pathway, the gut microbiome and its senolytic activity. Therefore, the growing body of pre-clinical data, along with fisetin's ability to modulate a large number of pathways associated with brain dysfunction, strongly suggest that it would be worthwhile to pursue its therapeutic effects in humans.


-------------------
https://www.eboro.cz/ms/
https://www.eboro.cz
User avatar
Petr75
Family Elder
Posts: 1615
Joined: Sat Oct 19, 2013 10:17 am
Location: Czech Republic
Contact:

Re: Diet

Post by Petr75 »

2021 Mar 29
Institute of Clinical Immunology, Yue-Yang Hospital of Integrative Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, China
Remyelination is enhanced by Astragalus polysaccharides through inducing the differentiation of oligodendrocytes from neural stem cells in cuprizone model of demyelination
https://pubmed.ncbi.nlm.nih.gov/33794147/

Abstract

Demyelination is the hallmark of multiple sclerosis (MS). Promoting remyelination is an important strategy to treat MS. Our previous study showed that Astragalus polysaccharides (APS), the main bioactive component of Astragalus membranaceus, could prevent demyelination in experimental autoimmune encephalomyelitis mice. To investigate the effects of APS on remyelination and the underlying mechanisms, in this study we set up a cuprizone-induced demyelination model in mice and treated them with APS. It was found that APS relieved the neurobehavioral dysfunctions caused by demyelination, and efficaciously facilitated remyelination in vivo. In order to determine whether the mechanism of enhancing remyelination was associated with the differentiation of neural stem cells (NSCs), biomarkers of NSCs, astrocytes, oligodendrocytes and neurons were measured in the corpus callosum tissues of mice through Real-time PCR, Western blot and immunohistochemistry assays. Data revealed that APS suppressed the stemness of NSCs, reduced the differentiation of NSCs into astrocytes, and promoted the differentiation into oligodendrocytes and neurons. This phenomenon was confirmed in the differentiation model of C17.2 NSCs cultured in vitro. Since Sonic hedgehog signaling pathway has been proven to be crucial to the differentiation of NSCs into oligodendrocytes, we examined expression levels of the key molecules in this pathway in vivo and in vitro, and eventually found APS activated this signaling pathway. Together, our results demonstrated that APS probably activated Sonic hedgehog signaling pathway first, then induced NSCs to differentiate into oligodendrocytes and promoted remyelination, which suggested that APS might be a potential candidate in treating MS.
https://www.eboro.cz
User avatar
NHE
Volunteer Moderator
Posts: 6227
Joined: Sat Nov 20, 2004 3:00 pm
Contact:

Re: Diet

Post by NHE »

Total flavonoids of astragalus attenuates experimental autoimmune encephalomyelitis by suppressing the activation and inflammatory responses of microglia via JNK/AKT/NFκB signaling pathway
Phytomedicine. 2021 Jan;80:153385.

Background: Microglia-mediated neuroinflammation is one of the most prominent characteristics of multiple sclerosis (MS), a chronic demyelination disease. As one of the main active ingredients in Astragali radix, total flavonoids of Astragalus (TFA) has multiple pharmacological effects such as immunomodulation, anti-inflammation and and anti-tumor. However, little is known about whether TFA could inhibit microglia-mediated neuroinflammation in MS.

Purpose: This study was aimed to elucidate whether TFA could inhibit microglia-mediated neuroinflammation in MS.

Study design: In the present study, we explored the protective effect of TFA on experimental autoimmune encephalomyelitis (EAE), an animal model of MS, in mice for the first time, and discussed its mechanism from the aspect of anti-microglia-mediated neuroinflammation.

Methods: The mice received oral administration of TFA (25 and 50 mg/kg) daily from two days before immunization and continued until day 21 post-immunization. The effect of TFA on EAE in mice and its mechanism were investigated by ELISA, Western blot, real-time PCR, luciferase reporter assay, histopathology and immunohistochemistry.

Results: TFA were shown to alleviate the severity of EAE in mice. It inhibited the excessive activation of microglia both in spinal cords of EAE mice and in LPS-stimulated BV-2 cells, evidenced by weakening the production of inflammatory mediators such as NO, TNF-α, IL-6, and IL-1β markedly at either protein or mRNA level. Further study demonstrated that TFA repressed the phosphorylation, nuclear translocation and transcriptional activity of NFκB, and inhibited the activation of AKT and JNK signaling in BV-2 cells induced by LPS. The agonists of AKT and JNK, anisomycin and SC79, could partly abolish the inhibitory effect of TFA on the production of inflammatory mediators in BV-2 cells induced by LPS.

Conclusions: Taken together, our results clarified that TFA inhibited microglia-mediated inflammation in EAE mice probably through deactivating JNK/AKT/NFκB signaling pathways. The novel findings may lay a theoretical foundation for the clinical application of TFA in the treatment of MS.
User avatar
Petr75
Family Elder
Posts: 1615
Joined: Sat Oct 19, 2013 10:17 am
Location: Czech Republic
Contact:

Re: Diet

Post by Petr75 »

2021 Apr 8
Centre for Genetic Engineering and Biotechnology, Ave., Havana. Cuba
C-Phycocyanin-derived Phycocyanobilin as a Potential Nutraceutical Approach for Major Neurodegenerative Disorders and COVID-19-induced Damage to the Nervous System
https://pubmed.ncbi.nlm.nih.gov/33829974/

Abstract

The edible cyanobacterium Spirulina platensis and its chief biliprotein C-Phycocyanin have shown protective activity in animal models of diverse human health diseases, often reflecting antioxidant and anti-inflammatory effects. The beneficial effects of C-Phycocyanin seem likely to be primarily attributable to its covalently attached chromophore Phycocyanobilin (PCB). Within cells, biliverdin is generated from free heme and it is subsequently reduced to bilirubin. Although bilirubin can function as an oxidant scavenger, its potent antioxidant activity reflects its ability to inactivate some isoforms of NADPH oxidase. Free bilirubin can also function as an agonist for the aryl hydrocarbon receptor (AhR); this may explain its ability to promote protective Treg activity in cellular and rodent models of inflammatory disease. AhR agonists also promote transcription of the gene coding for Nrf-2, and hence can up-regulate phase 2 induction of antioxidant enzymes such as HO-1. Hence, it is proposed that C-Phycocyanin/PCB chiefly exert their protective effects via inhibition of NADPH oxidase activity, as well as by AhR agonism that both induces Treg activity and up-regulates phase 2 induction. This simple model may explain their potent antioxidant/anti-inflammatory effects. Additionally, PCB might mimic biliverdin in activating anti-inflammatory signaling mediated by biliverdin reductase. This essay reviews recent research in which C-Phycocyanin and/or PCB, administered orally, parenterally, or intranasally, have achieved marked protective effects in rodent and cell culture models of Ischemic Stroke and Multiple Sclerosis, and suggests that these agents may likewise be protective for Alzheimer's disease, Parkinson's disease, and in COVID-19 and its neurological complications.


----------------------------------------------
https://www.eboro.cz/ms/
https://ereska.net/viewtopic.php?f=17&t ... 8604#p8604
https://www.eboro.cz
User avatar
Petr75
Family Elder
Posts: 1615
Joined: Sat Oct 19, 2013 10:17 am
Location: Czech Republic
Contact:

Re: Diet

Post by Petr75 »

2021 Apr 16
School of Life Sciences, Zhengzhou University, Henan, China
Fucoidan: a promising agent for brain injury and neurodegenerative disease intervention
https://pubmed.ncbi.nlm.nih.gov/33861265/


Abstract

Brain injury and neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis are urgent medical problems, which severely threaten the life quality of patients and their carers. However, there are currently no effective therapies. Fucoidan is a natural compound found in brown algae and some animals, which has multiple biological and pharmacological activities, such as antioxidant, anti-tumor, anti-coagulant, anti-thrombotic, immunoregulatory, anti-viral, and anti-inflammatory effects. A growing number of studies have shown that fucoidan also exerts a neuroprotective function. Particularly, recent findings have indicated that fucoidan could slow down the neurodegenerative processes and show protective effects against brain injury, which might be of therapeutic value for intervening in brain injury and neurodegenerative diseases. In this review, we have discussed the pharmacokinetics of fucoidan as well as the molecular mechanisms by which fucoidan exerts its neuroprotective effect on some neurological disorders. Along with this, we have also summarized the potential benefits of fucoidan in combination with other drugs in the treatment of neurodegenerative diseases and brain injury. Although the extraction process of fucoidan has been improved well, more efforts should be devoted to the translational research and clinical trials of fucoidan in the near future.

-------------------------------------
wiki https://en.wikipedia.org/wiki/Fucoidan
https://www.eboro.cz
User avatar
Petr75
Family Elder
Posts: 1615
Joined: Sat Oct 19, 2013 10:17 am
Location: Czech Republic
Contact:

Re: Diet

Post by Petr75 »

2021 Apr 23
Department of Clinical Pharmacology, Xiangya Hospital, Central South University, Institute of Clinical Pharmacology, Central South University, Hunan Key Laboratory of Pharmacogenetics, China
Dietary nutrition for neurological disease therapy: Current status and future directions
https://pubmed.ncbi.nlm.nih.gov/33901506/

Abstract

Adequate food intake and relative abundance of dietary nutrients have undisputed effects on the brain function. There is now substantial evidence that dietary nutrition aids in the prevention and remediation of neurologic symptoms in diverse pathological conditions. The newly described influences of dietary factors on the alterations of mitochondrial dysfunction, epigenetic modification and neuroinflammation are important mechanisms that are responsible for the action of nutrients on the brain health. In this review, we discuss the state of evidence supporting that distinct dietary interventions including dietary supplement and dietary restriction have the ability to tackle neurological disorders using Alzheimer's disease, Parkinson's disease, stroke, epilepsy, traumatic brain injury, amyotrophic lateral sclerosis, Huntington's disease and multiple sclerosis as examples. Additionally, it is also highlighting that diverse potential mechanisms such as metabolic control, epigenetic modification, neuroinflammation and gut-brain axis are of utmost importance for nutrient supply to the risk of neurologic condition and therapeutic response. Finally, we also highlight the novel concept that dietary nutrient intervention reshapes metabolism-epigenetics-immunity cycle to remediate brain dysfunction. Targeting metabolism-epigenetics-immunity network will delineate a new blueprint for combating neurological weaknesses.

--------------------------------------------------
https://www.eboro.cz/ms/
https://www.eboro.cz
User avatar
Petr75
Family Elder
Posts: 1615
Joined: Sat Oct 19, 2013 10:17 am
Location: Czech Republic
Contact:

Re: Diet

Post by Petr75 »

2021 Apr 13
Department of Zoology, Ramjas College, University of Delhi, India
Microglia Specific Drug Targeting Using Natural Products for the Regulation of Redox Imbalance in Neurodegeneration
https://pubmed.ncbi.nlm.nih.gov/33927630/


Abstract

Microglia, a type of innate immune cell of the brain, regulates neurogenesis, immunological surveillance, redox imbalance, cognitive and behavioral changes under normal and pathological conditions like Alzheimer's, Parkinson's, Multiple sclerosis and traumatic brain injury. Microglia produces a wide variety of cytokines to maintain homeostasis. It also participates in synaptic pruning and regulation of neurons overproduction by phagocytosis of neural precursor cells. The phenotypes of microglia are regulated by the local microenvironment of neurons and astrocytes via interaction with both soluble and membrane-bound mediators. In case of neuron degeneration as observed in acute or chronic neurodegenerative diseases, microglia gets released from the inhibitory effect of neurons and astrocytes, showing activated phenotype either of its dual function. Microglia shows neuroprotective effect by secreting growths factors to heal neurons and clears cell debris through phagocytosis in case of a moderate stimulus. But the same microglia starts releasing pro-inflammatory cytokines like TNF-α, IFN-γ, reactive oxygen species (ROS), and nitric oxide (NO), increasing neuroinflammation and redox imbalance in the brain under chronic signals. Therefore, pharmacological targeting of microglia would be a promising strategy in the regulation of neuroinflammation, redox imbalance and oxidative stress in neurodegenerative diseases. Some studies present potentials of natural products like curcumin, resveratrol, cannabidiol, ginsenosides, flavonoids and sulforaphane to suppress activation of microglia. These natural products have also been proposed as effective therapeutics to regulate the progression of neurodegenerative diseases. The present review article intends to explain the molecular mechanisms and functions of microglia and molecular dynamics of microglia specific genes and proteins like Iba1 and Tmem119 in neurodegeneration. The possible interventions by curcumin, resveratrol, cannabidiol, ginsenosides, flavonoids and sulforaphane on microglia specific protein Iba1 suggest possibility of natural products mediated regulation of microglia phenotypes and its functions to control redox imbalance and neuroinflammation in management of Alzheimer's, Parkinson's and Multiple Sclerosis for microglia-mediated therapeutics.
https://www.eboro.cz
User avatar
Petr75
Family Elder
Posts: 1615
Joined: Sat Oct 19, 2013 10:17 am
Location: Czech Republic
Contact:

Re: Diet

Post by Petr75 »

2021 May 11
Retraction of High-dose ω-3 Fatty Acid Plus Vitamin D3 Supplementation Affects Clinical Symptoms and Metabolic Status of Patients with Multiple Sclerosis: A Randomized Controlled Clinical Trial. J Nutr 2018;148(8):1380-6
https://pubmed.ncbi.nlm.nih.gov/33974700/

No abstract available
https://www.eboro.cz
User avatar
NHE
Volunteer Moderator
Posts: 6227
Joined: Sat Nov 20, 2004 3:00 pm
Contact:

Re: Diet

Post by NHE »

Petr75 wrote: Wed May 12, 2021 6:03 am 2021 May 11
Retraction of High-dose ω-3 Fatty Acid Plus Vitamin D3 Supplementation Affects Clinical Symptoms and Metabolic Status of Patients with Multiple Sclerosis: A Randomized Controlled Clinical Trial. J Nutr 2018;148(8):1380-6
https://pubmed.ncbi.nlm.nih.gov/33974700/

No abstract available
Retraction of High-dose ω-3 Fatty Acid Plus Vitamin D3 Supplementation Affects Clinical Symptoms and Metabolic Status of Patients with Multiple Sclerosis: A Randomized Controlled Clinical Trial. J Nutr 2018;148(8):1380–6.

The Editor-in-Chief is retracting this article due to concerns about the validity of participant data in the study.

https://academic.oup.com/jn/article/151/5/1362/6273770
User avatar
Petr75
Family Elder
Posts: 1615
Joined: Sat Oct 19, 2013 10:17 am
Location: Czech Republic
Contact:

Re: Diet

Post by Petr75 »

2021 May 6
Danish Multiple Sclerosis Center, Department of Neurology, Copenhagen University Hospital, Rigshospitalet, Glostrup, Denmark
Serum Short-Chain Fatty Acids and Associations With Inflammation in Newly Diagnosed Patients With Multiple Sclerosis and Healthy Controls
https://pubmed.ncbi.nlm.nih.gov/34025661/

Abstract

Multiple sclerosis (MS) is a chronic immune-mediated disease characterized by demyelination and neuroaxonal damage in the central nervous system. The etiology is complex and is still not fully understood. Accumulating evidence suggests that our gut microbiota and its metabolites influence the MS pathogenesis. Short-chain fatty acids (SCFAs), such as acetate, propionate and butyrate, are metabolites produced by gut microbiota through fermentation of indigestible carbohydrates. SCFAs and kynurenine metabolites have been shown to have important immunomodulatory properties, and propionate supplementation in MS patients has been associated with long-term clinical improvement. However, the underlying mechanisms of action and its importance in MS remain incompletely understood. We analyzed serum levels of SCFAs and performed targeted metabolomics in relation to biomarkers of inflammation, and clinical and MRI measures in newly diagnosed patients with relapsing-remitting MS before their first disease modifying therapy and healthy controls (HCs). We demonstrated that serum acetate levels were nominally reduced in MS patients compared with HCs. The ratios of acetate/butyrate and acetate/(propionate + butyrate) were significantly lower in MS patients in a multivariate analysis (orthogonal partial least squares discriminant analysis; OPLS-DA). The mentioned ratios and acetate levels correlated negatively with the pro-inflammatory biomarker IFNG, indicating an inverse relation between acetate and inflammation. In contrast, the proportion of butyrate was found higher in MS patients in the multivariate analysis, and both butyrate and valerate correlated positively with proinflammatory cytokines (IFNG and TNF), suggesting complex bidirectional regulatory properties of SCFAs. Branched SCFAs were inversely correlated with clinical disability, at a nominal significance level. Otherwise SCFAs did not correlate with clinical variables or MRI measures. There were signs of an alteration of the kynurenine pathway in MS, and butyrate was positively correlated with the immunomodulatory metabolite 3-hydroxyanthranilic acid. Other variables that influenced the separation between MS and HCs were NfL, ARG1 and IL1R1, D-ribose 5-phosphate, pantothenic acid and D-glucuronic acid. In conclusion, we provide novel results in this rapidly evolving field, emphasizing the complexity of the interactions between SCFAs and inflammation; therefore, further studies are required to clarify these issues before supplementation of SCFAs can be widely recommended.
https://www.eboro.cz
User avatar
Petr75
Family Elder
Posts: 1615
Joined: Sat Oct 19, 2013 10:17 am
Location: Czech Republic
Contact:

Re: Diet

Post by Petr75 »

2021 May 18
Department of Ophthalmology, West China Hospital, Sichuan University, China
Green leafy vegetable and lutein intake and multiple health outcomes
https://pubmed.ncbi.nlm.nih.gov/34034049/

Abstract

Green leafy vegetables (GLVs) are a key element of healthy eating patterns and are an important source of lutein. To clarify the evidence for associations between GLVs and lutein intake and multiple health outcomes, we performed a review. A total of 24 meta-analyses with 29 health outcomes were identified by eligibility criteria. Dose-response analyses revealed that, per 100 g/d GLV intake was associated with a decreased risk (ca. 25%) of all-cause mortality, coronary heart disease and stroke. Beneficial effects of GLV intake were found for cardiovascular disease and bladder and oral cancer. Dietary lutein intake was inversely associated with age-related macular degeneration, age-related cataracts, coronary heart disease, stroke, oesophageal cancer, non-Hodgkin lymphoma, metabolic syndrome, and amyotrophic lateral sclerosis. Caution was warranted for contamination with potentially pathogenic organisms, specifically Escherichia coli. GLV consumption and lutein intake therein are generally safe and beneficial for multiple health outcomes in humans.
https://www.eboro.cz
User avatar
Petr75
Family Elder
Posts: 1615
Joined: Sat Oct 19, 2013 10:17 am
Location: Czech Republic
Contact:

Re: Diet

Post by Petr75 »

2021 Jul 9
Interdisciplinary Graduate Program in Immunology, University of Iowa, IA, USA
Isoflavone diet ameliorates experimental autoimmune encephalomyelitis through modulation of gut bacteria depleted in patients with multiple sclerosis
https://pubmed.ncbi.nlm.nih.gov/34244137/


Abstract

The gut microbiota is a potential environmental factor that influences the development of multiple sclerosis (MS). We and others have demonstrated that patients with MS and healthy individuals have distinct gut microbiomes. However, the pathogenic relevance of these differences remains unclear. Previously, we showed that bacteria that metabolize isoflavones are less abundant in patients with MS, suggesting that isoflavone-metabolizing bacteria might provide protection against MS. Here, using a mouse model of MS, we report that an isoflavone diet provides protection against disease, which is dependent on the presence of isoflavone-metabolizing bacteria and their metabolite equol. Notably, the composition of the gut microbiome in mice fed an isoflavone diet exhibited parallels to healthy human donors, whereas the composition in those fed an isoflavone-free diet exhibited parallels to patients with MS. Collectively, our study provides evidence that dietary-induced gut microbial changes alleviate disease severity and may contribute to MS pathogenesis.

Free full text.
https://www.eboro.cz
User avatar
Petr75
Family Elder
Posts: 1615
Joined: Sat Oct 19, 2013 10:17 am
Location: Czech Republic
Contact:

Re: Diet

Post by Petr75 »

2021 Aug 14
Neuroepidemiology Unit, Melbourne School of Population & Global Health, The University of Melbourne, Melbourne, Australia (George Jelinek)
Higher quality diet and non-consumption of meat are associated with less self-determined disability progression in people with multiple sclerosis: a longitudinal cohort study
https://pubmed.ncbi.nlm.nih.gov/34390078/

Conclusions: These results show that better quality of the diet, as well as not consuming meat, were associated with reduced disability progression in people with MS. Substantiation of these findings in other settings may inform opportunities to manage disability progression in people with MS using dietary modifications.
https://www.eboro.cz
Post Reply
  • Similar Topics
    Replies
    Views
    Last post

Return to “General Discussion”