Helminth therapy?
ME/CFS in the Era of the Human Microbiome: Persistent Pathogens Drive Chronic Symptoms...
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gbells
Improved ME from 2 to 6
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Honestly, I don't think it's a big deal. The main thing you're getting out of the VDR are those antibiotic chemicals. As long as you can find a way to kill the virally infected cell or transform it into a normal one with CRISPR (and add a dummy chain to prevent EBV reinfection) then the VDR is irrelevant. Besides, antibiotics don't touch viruses.
uglevod
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google: defensin VDR viruses, cathelicidin VDR viruses
Viruses obviously mess around VDR to establish their own persistence, not to help "fellow" bacteria:
Hepatitis B virus downregulates vitamin D receptor levels in hepatoma cell lines, thereby preventing vitamin D-dependent inhibition of viral transcription and production
https://molmed.biomedcentral.com/articles/10.1186/s10020-018-0055-0
Recently studies (Chan et al., 2015; Wong et al., 2015; Chen et al., 2015) demonstrated a correlation between low serum vitamin D levels in chronic HBV patients and high levels of viral replication. These studies raised the possibility that vitamin D levels inhibit HBV replication. In contrast, our in-vitro study showed that Vitamin D does not affect the rate of HBV replication, and downregulates VDR levels in the presence of the virus, thereby attenuating vitamin D signal transduction.
Vitamin D plays a crucial role in the regulation of genes central to protection against microbe invasion, such as the induction of the expression of antimicrobial peptides (also known as host defense peptides) such as CAMP and defensin. These peptides were demonstrated to disrupt the integrity of the microbe membrane, resulting in its death (Gombart, 2009). In addition, Vitamin D regulates the immune system by managing the expression of TNFα (Golovko et al., 2005), one of the most important pro-inflammatory and pro-immune cytokines. Therefore, downregulation of the vitamin D signaling pathway by viruses, can result in decreased production of antimicrobial peptides and cytokines and as a result, to attenuation of the immune response. Several studies have previously indicated that certain viruses can inhibit the Vitamin D signal transduction. In 2009, Yenamandra et al. demonstrated that VDR mRNA and protein levels were lower in EBV-transformed cells compared with primary B cells (Yenamandra et al., 2009). A few years earlier, Haug et al. reported a marked decrease in serum Calcitriol levels in human immunodeficiency virus (HIV)-infected patients, that correlated with the degree of immunodeficiency and patient survival (Haug et al., 1994). Therefore, in this study, we compared the activation of both TNFa and CAMP in HepG2 cell versus HepG2.2.15 cells following Cacitriol stimulation. Indeed, while the addition of Calcitriol upregulates both CAMP and TNFα expression in HepG2 cells, significantly less transcription of these genes was observed in HepG2.2.15 cells. These findings suggest that HBV can repress the activation of the immune system by downregulating the vitamin D signaling pathway.
etc
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uglevod
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Guys you should really try to figure/learn how to filter information sources - the successful young businessman behind selfhacked.com just hijacked parts of Marshall's work without even providing complete references to help promote his own pseudoscientific "stuff"(he is selling consultations, books, etc https://selfhacked.com/store/). No reason to quote him, when you have the original data over here: mpkb.org
No need to promote persons who is trying to make every possible $ on the sick ones.
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gbells
Improved ME from 2 to 6
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Still has no relevance. Even if you restore the VDR you are stuck with a cell that has the viral time bomb integrated into its DNA the next time it gets infected with a virus and has lowered immunity. It isn't a practical strategy to get well.
uglevod
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https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4498101/
Vitamin D is a steroid hormone with pleiotropic effects. Aside from its long-recognized role in regulating calcium and phosphorous balance, vitamin D can also influence cell differentiation and proliferation, as well as modulate the immune system. In the CNS, vitamin D can act as an immune-regulator, and as stimulator of neurotrophic factors and neurotransmitters expression (Di Rosa et al., 2011; Eyles et al., 2011; Gezen-Ak et al., 2011). Vitamin D has two main receptors, membrane-associated rapid response steroid-binding (MARRS) and vitamin D receptor (VDR), which are critical for its different regulatory properties (Khanal and Nemere, 2007; Meyer et al., 2010). MARRS is a membrane receptor that when bound to vitamin D induces rapid non-genomic responses, such as modulation of calcium concentrations and activity of protein kinase C (Khanal and Nemere, 2007). VDR, on the other hand, is a transcription factor that regulates the expression of multiple genes and is responsible for the non-classical responses of vitamin D (Meyer et al., 2010). Upon binding to vitamin D, VDR translocates to the nucleus and heterodimerizes with the retinoid X receptor (RXR). Subsequently, the VDR-RXR complex formed binds to vitamin D responsive elements in the DNA to activate or repress the expression of vitamin D target genes (Fetahu et al., 2014). Moreover, the VDR gene has large cytosine/guanine dinucleotide (CpG) repeats at the promoter region that are susceptible to epigenetic modifications. Conversely, VDR can also modulate the epigenome, inducing DNA methylation and chromatin modulation (Fetahu et al., 2014).
VDR is expressed in more than 38 types of cells, including immune cells (e.g., monocytes, dendritic cells, activated B and T cells) and CNS cells (e.g., neurons, astrocytes, and microglia; Di Rosa et al., 2011; Cui et al., 2013; Smolders et al., 2013). VDR activation was reported to regulate the innate immune response by inducing tolerogenic dendritic cells, inhibiting type 1 T helper (Th1) cell responses, as well as downregulating TLR2, TLR4, and TLR9, inducing decreased expressions of IL-6 (Dickie et al., 2010). Studies with neurons also showed that VDR can regulate the expressions of nerve growth factor and iNOS (Gezen-Ak et al., 2011; Dursun et al., 2013). In addition, the VDR gene has been reported to be associated with viral and bacterial infections. In one study, Epstein-Barr virus nuclear antigen 3 (EBNA-3; produced by EBV) was demonstrated to bind to VDR inducing blockage of VDR-dependent genes, thus protecting cells from VDR-induced growth arrest and/or apoptosis (Yenamandra et al., 2010). Another study showed downregulation of VDR expression in monocytes by Borrelia burgdorferi infection (Salazar et al., 2009). In addition, human immunodeficiency virus (HIV) was proved to downregulate VDR expression by inducing its hypermethylation in T cells. This event resulted in the activation of the renin angiotensin system and generation of reactive oxidative species, consequently leading to T cell apoptosis (Chandel et al., 2013). Moreover, vitamin D elicits the expression of the anti-microbial peptides cathelicidin and defensin, important for counteracting infection (Gombart, 2009).
Despite the substantial amount of evidence linking VDR and the immune response, its role in the regulation of the inflammatory response in mood disorders remains to be elucidated.
Vitamin D is a steroid hormone with pleiotropic effects. Aside from its long-recognized role in regulating calcium and phosphorous balance, vitamin D can also influence cell differentiation and proliferation, as well as modulate the immune system. In the CNS, vitamin D can act as an immune-regulator, and as stimulator of neurotrophic factors and neurotransmitters expression (Di Rosa et al., 2011; Eyles et al., 2011; Gezen-Ak et al., 2011). Vitamin D has two main receptors, membrane-associated rapid response steroid-binding (MARRS) and vitamin D receptor (VDR), which are critical for its different regulatory properties (Khanal and Nemere, 2007; Meyer et al., 2010). MARRS is a membrane receptor that when bound to vitamin D induces rapid non-genomic responses, such as modulation of calcium concentrations and activity of protein kinase C (Khanal and Nemere, 2007). VDR, on the other hand, is a transcription factor that regulates the expression of multiple genes and is responsible for the non-classical responses of vitamin D (Meyer et al., 2010). Upon binding to vitamin D, VDR translocates to the nucleus and heterodimerizes with the retinoid X receptor (RXR). Subsequently, the VDR-RXR complex formed binds to vitamin D responsive elements in the DNA to activate or repress the expression of vitamin D target genes (Fetahu et al., 2014). Moreover, the VDR gene has large cytosine/guanine dinucleotide (CpG) repeats at the promoter region that are susceptible to epigenetic modifications. Conversely, VDR can also modulate the epigenome, inducing DNA methylation and chromatin modulation (Fetahu et al., 2014).
VDR is expressed in more than 38 types of cells, including immune cells (e.g., monocytes, dendritic cells, activated B and T cells) and CNS cells (e.g., neurons, astrocytes, and microglia; Di Rosa et al., 2011; Cui et al., 2013; Smolders et al., 2013). VDR activation was reported to regulate the innate immune response by inducing tolerogenic dendritic cells, inhibiting type 1 T helper (Th1) cell responses, as well as downregulating TLR2, TLR4, and TLR9, inducing decreased expressions of IL-6 (Dickie et al., 2010). Studies with neurons also showed that VDR can regulate the expressions of nerve growth factor and iNOS (Gezen-Ak et al., 2011; Dursun et al., 2013). In addition, the VDR gene has been reported to be associated with viral and bacterial infections. In one study, Epstein-Barr virus nuclear antigen 3 (EBNA-3; produced by EBV) was demonstrated to bind to VDR inducing blockage of VDR-dependent genes, thus protecting cells from VDR-induced growth arrest and/or apoptosis (Yenamandra et al., 2010). Another study showed downregulation of VDR expression in monocytes by Borrelia burgdorferi infection (Salazar et al., 2009). In addition, human immunodeficiency virus (HIV) was proved to downregulate VDR expression by inducing its hypermethylation in T cells. This event resulted in the activation of the renin angiotensin system and generation of reactive oxidative species, consequently leading to T cell apoptosis (Chandel et al., 2013). Moreover, vitamin D elicits the expression of the anti-microbial peptides cathelicidin and defensin, important for counteracting infection (Gombart, 2009).
Despite the substantial amount of evidence linking VDR and the immune response, its role in the regulation of the inflammatory response in mood disorders remains to be elucidated.
uglevod
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Symptom changes in 90% of patients with autoimmune conditions when EMF blocked
http://www.greenmedinfo.com/blog/gr...ows-shielding-emf-improves-autoimmune-disease
References T. Marshall paper.
http://www.greenmedinfo.com/blog/gr...ows-shielding-emf-improves-autoimmune-disease
References T. Marshall paper.
Hip
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uglevod
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Hehe, as soon as anyone do a formally "improper" study there is always a feedback like this as if the anti inflammatory drugs people use to copy with their symptoms passed any proper double-blind studies... 
Guys, a time has come to question the effectiveness of your own "helpful" supplements and face the reality: the sooner the better...
Guys, a time has come to question the effectiveness of your own "helpful" supplements and face the reality: the sooner the better...
Hip
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There is no excuse for not having a control group. If you really believe that EMF an issue in chronic illness, then you should be alerting the scientific community. The scientific community will only take notice if you perform your study properly. It would have been very easy to create a control group, just by using a material that looked the same, but which was not electrically conductive.
uglevod
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There is no excuse for nit-picking either: the article is far from being a 100% Marshall data: there are in fact some links to papers over there too and scientific community is already well alerted hence more and more studies and talks like this:
p.s. usually I don't quote doctors(since for me their "knowledge" and "insights" are of zero practical value) but this one is specific case: he went as far as started to talk about actual measurements of our environments - what a giant step forward.
p.s. usually I don't quote doctors(since for me their "knowledge" and "insights" are of zero practical value) but this one is specific case: he went as far as started to talk about actual measurements of our environments - what a giant step forward.
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Hip
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That's not nit-picking; it's pointing out a fundamental flaw. Do you actually know why double-blinded studies with control groups are so important in medical research? If not, you might want to investigate the placebo effect, and how it's vital to control for in any proper medical study.
I am not denying the possibility of adverse effects from EMF, especially in those with chronic diseases. However, it should be mentioned that out of 33 proper studies that tried to find evidence of health effects of EMF in people who complained of experiencing adverse effects, none of those studies found a positive result. See here:
One the other hand, Prof Martin Pall believes electrosensitivity exists, and has a theory that electrosensitivity might in some people be caused by electromagnetic radiation triggering voltage gated calcium channels. He suggests that calcium channel blocker drugs (like nimodipine) may thus reduce electrosensitivity.
More research is needed, but we need high quality research.
uglevod
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https://www.ncbi.nlm.nih.gov/pubmed/28659302
Objective: We investigated the influence of food and nutrient intake on H. pylori eradication therapy.
Factors associated with the failure of eradication therapy included increased age (P = 0.02), higher CRP concentrations (P < 0.01), higher dietary cholesterol (P < 0.01) or egg intake (P < 0.01), higher ω-3 (n-3) fatty acid (P = 0.02) or fish intake (P = 0.01), and higher vitamin D intake (P = 0.02). Moreover, the higher vitamin D intake was strongly linked to higher fish intake.
Daily Nutritional Supplementation with Vitamin D3 and Phenylbutyrate to Treatment-Naïve HIV Patients Tested in a Randomized Placebo-Controlled Trial
https://www.researchgate.net/public...sted_in_a_Randomized_Placebo-Controlled_Trial
Objective: We investigated the influence of food and nutrient intake on H. pylori eradication therapy.
Factors associated with the failure of eradication therapy included increased age (P = 0.02), higher CRP concentrations (P < 0.01), higher dietary cholesterol (P < 0.01) or egg intake (P < 0.01), higher ω-3 (n-3) fatty acid (P = 0.02) or fish intake (P = 0.01), and higher vitamin D intake (P = 0.02). Moreover, the higher vitamin D intake was strongly linked to higher fish intake.
https://www.researchgate.net/public...sted_in_a_Randomized_Placebo-Controlled_Trial
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uglevod
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