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Defect in the MTHFR Gene is Present in CFS and most all other Autoimmune Diseases

Annikki

Senior Member
Messages
146
Defect in the MTHFR Gene is Present in CFS and most all Autoimmune Diseases
Autoimmune diseases have unique symptoms. It is easy to assume from this that each disease is unique one another and may not share a common cause. I have found this is not true, that frequently autoimmune diseases share root common biological traits. These can blossom into a variety of seemingly disparate disease symptoms in the human body.

Although, the symptoms of these diseases appear very different, they are likely related. This can be evinced by the fact these diseases are often comorbid to each other, meaning they occur once in the same person. This means I can have both Chronic Fatigue Syndrome and another autoimmune disease at the same time.

Understanding this, the next question, naturally, is why is this happening. I have studied not just CFS but a host of other autoimmune diseases, only to find that the same biological and biochemical processes are often at work. Based on this fact, I have a theory that some root anomalies in these autoimmune diseases are causing various different problems in different parts of the body. These problems seem unrelated when only looking at symptoms. However, it’s easy to deduce all autoimmune diseases are all related, since these diseases are frequently comorbid to one another.

Other researchers have made the connection between MTHFR and autoimmune disease. Yet no one has done a full survey of all the various autoimmune diseases for the MTHFR gene polymorphism. I have a done a survey of every major autoimmune disease and lesser known ones for the MTHFR polymorphism.

Consistently, in every autoimmune disease I looked at, including obscure ones, a polymorphism in the MTHFR gene can be found. MTHFR stands for methylenetetrahydrofolate reductase. It plays a role in folate metabolism and leads to a build up of glutathione and homocysteine in the blood. Insufficient folate metabolism leads to deficits in energy production.

The MTHFR defect explains some of the stranger quirks of CFS, such as the frequent appearance of the Eptein-Barr Virus in patients. The reason for this, is that the low levels of methylation caused by the MTHFR polymorphism, create a good climate for viral infections. It is also worth noting that viruses have been found in other autoimmune diseases, such as findings of BK virus in interstitial cystitis patients. Methylation is an important biological process and effects multiple systems in the body. The MTHFR defect causes a host of problems.

Listing all of these would require more space than what I have available here. I suggest going to various support websites for people with the MTHFR defect to learn more about the ramifications of possessing it.

There are also other comorbidities to autoimmune diseases such as the common occurrence of certain cancers. Research into these cancers has also found the MTHFR present. Most importantly, there have been studies which have found that treating for the MTHFR defect lessens the symptoms of not only CFS, ME, but fibromyalgia and others.

Fortunately, I learned more about my family history as far as disease, including cancers and thyroid problems and this led me to stumble upon MTHFR. I was already researching some other biological anomalies in comorbid diseases. I was researching this, when I recognized MTHFR from some unrelated research I was doing. I hope this information can be helpful.

I have broken down this article into two parts. I thought I should start with demonstrating the relationship between different autoimmune diseases by listing their comorbidities. Please note that these lists are incomplete, since it requires a full scale research project to list every comorbidity. These lists are short lists, used to prove my point. I encourage you to explore this subject further. I went for just the short lists available on some websites. Still, I have heard that thyroid disorders are always comorbid for all the main autoimmune diseases. I have as yet to research that.

Autoimmune Disease Comorbities List:

Chronic Fatigue Syndrome (Myalgic Encephalomyelitis):
*Study: “Comorbid Clinical Conditions in Chronic Fatigue”
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1495162/
Above article lists the following conditions which occur in tandem with CFS/ME:

fibromyalgia
irritable bowel syndrome,
multiple chemical sensitivities,
temporomandibular disorder,
interstitial cystitis,
postconcussion syndrome,
tension headache,
chronic low back pain,
chronic pelvic pain (women),
chronic nonbacterial prostatitis (men)

Ehler-Danlos Syndrome:
Study: “Chronic Fatigue Syndrome in Ehlers-Danlos syndromes and Hypermobility Spectrum Disorders”
https://strengthflexibilityhealthed...ions-to-eds/chronic-fatigue-syndrome-and-eds/

Thyroid Disease:
Article, “HSV, EBV, Methylation, and Functional Approaches for Healing Chronic Latent Viral Infections,”-https://www.truenaturehealthconsulting.com/blog/2017/11/27/chronic-viral-infections-methylation-and-functional-approaches-for-healing , says:

“Approximately 85% of people with CFS have thyroiditis.”

Interstitial Cystitis Comorbities:
Lupus
Sjogren’s
Irritable bowel syndrome: Source: Article: “Non‐bladder conditions in female Taiwanese patients with interstitial cystitis/hypersensitive bladder syndrome”
https://www.onlinelibrary.wiley.com/doi/10.1111/iju.12456
“Interstitial cystitis/hypersensitive bladder syndrome patients were more likely to meet diagnostic criteria for irritable bowel syndrome than controls (37.5% vs 11.5%), and tension/migraine headache (38.7% vs 15.7%; all P < 0.001.”

IBS
fibromyalgia (FM)
chronic pain
migraine
gastrointestinal symptoms suggestive of IBS and dyspepsia
sleep abnormalities with delayed onset of sleep
feeling poorly refreshed in the morning
waking up before needed
severe chronic fatigue and chronic generalized pain
migraines
Source: Study: “Co-Morbidities of Interstitial Cystitis,”-https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3415690/

Study: "COMORBIDITY OF INTERSTITIAL CYSTITIS WITH OTHER UNEXPLAINED CLINICAL CONDITIONS" by C.A. Tony Buffington
https://www.auajournals.org/doi/full/10.1097/01.ju.0000137953.49304.6c


Endometriosis Comorbities:
Article: “Endometriosis Linked to Autoimmune and Other Chronic Diseases Including Chronic Fatigue Syndrome & Fibromyalgia,”
https://www.prohealth.com/library/e...g-chronic-fatigue-syndrome-fibromyalgia-21072

systemic lupus erythematosus
Sjögren’s syndrome
multiple sclerosis
rheumatoid arthritis
inflammatory bowel diseases (such as Crohn’s disease and ulcerative colitis)
coeliac disease
chronic pancreatitis
chronic renal failure
nephrotic syndrome
interstitial cystitis
eczema
hay fever
food sensitivities
asthma
myocardial infarction
angina
increased chances of needing coronary artery surgery
Ovarian cancer
Breast cancer
Endometrial and cervical cancer
Melanoma skin cancer
Ovarian cancer
Other Cancers
Source: Article: Endometriosis.org named, “Endometriosis and co-morbidities,”
http://endometriosis.org/news/research/endometriosis-and-comorbidities/

Interstitial cystitis
Source: Article: “Endometriosis,” by the Interstitial Cystitis
https://www.ichelp.org/about-ic/associated-conditions/endometriosis/

Source: Article: “Comorbidity Risks Among Women with Endometriosis,”
https://www.endonews.com/comorbidity-risks-among-women-withendometriosis

“The highest risk comorbidity in women with endometriosis was the diagnosis
pelvic inflammatory disorder
Source: Article: “Comorbidity Risks Among Women with Endometriosis,”
https://www.endonews.com/comorbidity-risks-among-women-withendometriosis


Chronic Lyme Disease Comorbidities:
infertility/subfertility
ovarian cyst
uterine fibroids
pelvic inflammatory disorder
interstitial cystitis
irritable bowel syndrome
constipation/dyschezia
ovarian cancer
endometrial cancer
ovarian cancer
breast cancer
endometrial cancer
autoimmune diseases, and gastrointestinal diseases such as irritable bowel syndrome and constipation/dyschezia
Source: Article: “Comorbidity of hypercholesterolemia and Lyme disease.”
http://grantome.com/grant/NIH/R21-AI125806-01A1

Systemic Lupus Erythematosus Comorbidities:

Migraine headache
Source: Study: “Is migraine really comorbid with systemic lupus erythematosus?”
https://journals.sagepub.com/doi/pdf/10.1111/j.1468-2982.2004.00786.x

32.5% anemia
26.0% Chronic Kidney Disease
7.1% end-stage renal disease
17.9% rheumatoid arthritis
Source: Study: “Prevalence of Systemic Lupus Erythematosus (SLE) and Associated Comorbidities in the 2011-2015 Medicare Population” -https://acrabstracts.org/abstract/p...idities-in-the-2011-2015-medicare-population/

cardiovascular disease
osteoporosis
malignancies
myocardial infarction
congestive heart failure or stroke
Source: Study: “The second hit: comorbidities in systemic lupus erythematosus.”

https://www.openaccessjournals.com/...rbidities-in-systemic-lupus-erythematosus.pdf

Interstitial Cystitis:
Source: Article: “Lupus”
-https://www.ichelp.org/about-ic/associated-conditions/lupus/
“Research has found that interstitial cystitis (IC) patients are 30 times more likely than the general population to have systemic lupus erythematosus (SLE).”


Multiple Sclerosis Comorbidities:
hyperlipidemia
hypertension
gastrointestinal disease (inflammatory bowel disease (Crohn’s disease or ulcerative colitis)
thyroid disease
Source: Article: “Comorbidity in US patients with multiple sclerosis”
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5815483/


Irritable Bowel Syndrome Comorbidities:
Interstitial Cystitis
Chronic Lyme Disease
Elevated urinary norepinephrine


Fibromyalgia: between 35 and 70 percent of patients with fibromyalgia also have IBS

Chronic fatigue syndrome: 14% of these patients have IBS

Gastro-esophageal reflux disorder (GERD): 36% of these patients have IBS

Chronic pelvic pain: 30-80% of women with chronic pelvic pain have IBS

Source: Article: “Irritable Bowel Syndrome (IBS) Comorbidities”
https://www.news-medical.net/health/Irritable-Bowel-Syndrome-(IBS)-Comorbidities.aspx


Ehlers-Danlos Syndrome Comorbidities:

Chronic Fatigue Syndrome

“Chronic Fatigue Syndrome in Ehlers-Danlos syndromes and Hypermobility Spectrum Disorders”
https://strengthflexibilityhealthed...ions-to-eds/chronic-fatigue-syndrome-and-eds/


Vulvodynia Comorbidities:
A study, “Relationship Between Vulvodynia and Chronic Comorbid Pain Conditions” found the following comorbidities in Vulvodynia, at these percentages:

7.5% (95% CI 6.2, 9.0) for interstitial cystitis,
8.7% (95% CI 7.3, 10.4) for vulvodynia,
9.4% (95% CI 8.1, 11.0) for irritable bowel syndrome,
11.8% (95% CI 10.1, 13.7) for fibromyalgia.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3566870


Sjogrens Disease Comorbities:
Fibromyalgia:
Article: “Sjogren's Syndrome in Fibromyalgia & Chronic Fatigue Syndrome, A Common Overlapping Condition.”
https://www.verywellhealth.com/sjogrens-syndrome-fibromyalgia-3973018

Study: “Comorbidity Burden in Primary Sjögren’s Syndrome: A Long-Term Observation in Clinical Practice”- https://acrabstracts.org/abstract/c...a-long-term-observation-in-clinical-practice/ observed these comorbidities:
osteoporosis (53/112, 47.3%),
autoimmune thyroiditis (35/112, 31.3%)
arterial hypertension (27/112, 24.1%)
dislipidemia (19/112, 17%)
diabetes (9/112, 8%)
cerebrovascular disease (8/112, 7,1%)
myocardial infarction (4/112, 3.6%)
interstitial cystitis-
Article: “Sjogren’s Syndrome”
https://www.ichelp.org/about-ic/associated-conditions/sjogrens-syndrome/

cardiovascular comorbidity-
Article: “Sjögren's syndrome linked to increased cardiovascular comorbidity”
https://www.healio.com/rheumatology...inked-to-increased-cardiovascular-comorbidity

Migraine Headache
Article: “Migraine Triggers and Comorbidities: Sjogren’s Syndrome”
https://migraine.com/blog/migraine-triggers-and-comorbidities-sjogrens-syndrome/


Fibromyalgia Comorbidities:

irritable bowel syndrome (32.5%)
chronic pelvic pain (15.3%)
plantar fasciitis (24.8%)
temporomandibular joint disorder (17.4%)
restless leg syndrome (20.3%)
chronic joint pain/degenerative arthritis was the most common comorbidity in 88.7% of patients
migraines or chronic headaches in 62.4% of patients
Hyperlipidemia was seen in 51.3% of the patients
obesity in 48%
hypertension in 46.2%
type 2 diabetes in 17.9% of patients
resulting in 50.5% of all patients meeting criteria for metabolic syndrome

Study: ”More than Half of Patients with Fibromyalgia May have Comorbidities,” https://www.healio.com/rheumatology...ents-with-fibromyalgia-may-have-comorbidities

(30.8%) had endocrine diseases
(8.8%) had chronic lung diseases
(7.3%) had osteoporosis
deep vein thrombosis
hepatitis serology positivity
pulmonary thromboembolism
Source: “THU0478 Determination of comorbidities in fibromyalgia syndrome”
https://www.researchgate.net/publication/324656351_Prevalence_of_comorbid_diseases_in_patients_with_fibromyalgia_A_retrospective_cross-sectional_study

Migraine Headache Comorbidities
Sjogren’s
Fibromyalgia
Chronic Fatigue Syndrome

An article named, “Migraines, Chronic Fatigue Syndrome and Fibromyalgia: Treatment Options,” says:
“Two studies suggest as many as 75% of people with chronic fatigue syndrome experience migraines and that most migraines in ME/CFS are undiagnosed. Agreeing that migraines are common in ME/CFS, WebMD, which has very little to say otherwise about chronic fatigue syndrome, states ME/CFS is one of five disorders with high migraine rates.”
https://www.healthrising.org/treati...nd-chronic-fatigue-syndrome-and-fibromyalgia/

Multiple Chemical Sensitivity Comorbidities:
rhinitis
sinusitis
bronchitis
migraine headache
irritable bowel
multiple food intolerances
arthritis
Source: Article called, “Multiple Chemical Sensitivity”
https://www.sciencedirect.com/topics/medicine-and-dentistry/multiple-chemical-sensitivity

Footnote: All of these conditions, including migranes and multiple sclerosis were once considered “contested illnesses.”


More reading about autoimmune disease comorbidities:
“The Relationship Between Interstitial Cystitis and Endometriosis in Patients With Chronic Pelvic Pain.” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3015716/
“The Connection Between Fibromyalgia and Thyroid Disease”
https://www.verywellhealth.com/the-thyroid-fibromyalgia-connection-3231681
“ Are All Chronic Fatigue Syndrome/Fibromyalgia Patients Low Thyroid? ,”
https://www.holtorfmed.com/download...ome_and_Fibromyalgia_Patients_Low_Thryoid.pdf
“The Link Between Interstitial Cystitis and Lyme Disease”
https://rawlsmd.com/health-articles/link-between-interstitial-cystitis-and-lyme-disease
“Boiling Point: The Lyme + Fibromyalgia + Chronic Fatigue Connection”
https://rawlsmd.com/health-articles/chronic-immune-dysfunction-lyme-disease”


A Genetic Polymorphism Common to the Majority of Autoimmune Diseases: Methylenetetrahydrofolate reductase (MTHFR)

Let me start with an explanation of the MTHFR genetic mutation. An article titled, "Genes Play a Role In Lupus? MTHFR"says:
“MTHFR mutation is an inability to process folic acid (vitamin B9) which is commonly discussed during pregnancy to prevent neural tube defects in the fetus. Folate deficiency can result in fatigue, impaired cognitive function, and mood disorders.”
Source: "Genes Play a Role In Lupus? MTHFR "
https://lupusrebel.com/genes-and-lupus-mthfr/

This gene mutation appears to be a common thread in autoimmune diseases, including CFS. MTHFR also has a relation to cancers, and these are listed here as well. This list is incomplete. I still need to see if the MTHFR polymorphism is present in other autoimmune diseases not listed here.
I provide here some basic information on the adverse affects of the MTHFR Polymorphism:

•chronic low glutathione
•leaky gut and food allergies
•Chronic viruses
•high serum B12 levels
•low serotonin and melatonin
•high serum ferritin and HFE mutation
•Thalassemia and hepatorenal failure
•FSG and renal failure
•autoimmunity frequency in women
•chronic dysbiosis/ chronic yeast infections
•estrogen dominant cancers..
and
Low Glutathione.
Source: “Why MTHFR Is Only A Part of Methylation”
https://mthfrsupport.com/2013/05/why-mthfr-is-only-a-part-of-methylation/


List of Diseases found to be associated with the MTHFR Polymorphism:

Chronic Fatigue Syndrome:
MTHFR:


MTHFR and resulting folate deficiency in Chronic Fatigue Syndrome

MTHFR Polymorphism and Epstein-Barre Virus
*Study: “MTHFR gene expression in EB virus transformed human B lymphoblasts”
https://www.ncbi.nlm.nih.gov/pubmed/12520914
https://www.ncbi.nlm.nih.gov/pubmed/12520914
Article: “MTHFR and Viral Infections; December 3, 2017 Home Slider, Introduction to Methylation and MTHFR”
http://www.beyondmthfr.com/mthfr-viral-infections/
http://www.beyondmthfr.com/mthfr-viral-infections/
Article: “What’s the Big Deal About Methylation?!”
https://www.jillcarnahan.com/2013/1...lation-update-of-the-popular-mthfr-blog-post/
https://www.jillcarnahan.com/2013/1...lation-update-of-the-popular-mthfr-blog-post/
Article: “MTHFR Genetic Mutations and Epstein Barr Virus”
https://kireland57.wordpress.com/2014/09/15/mthfr-genetic-mutations-and-epstein-barr-

Fibromyalgia
Article: “MTHFR RESOURCE CENTER: CHRONIC FATIGUE SYNDROME (CFS) & FIBROMYALGIA (FM)”
http://www.lookinguntojesus.info/MTHFR-Related/MTHFR-Pg10.html

Article: “A Functional Medicine Approach to Fibromyalgia,” https://www.amymyersmd.com/2016/06/a-functional-medicine-approach-to-fibromyalgia/

Article: "MTHFR Living: Things That Plague Us: Fibromyalgia"
http://mthfrliving.com/health-conditions/fibromyalgia/

Article: "MTHFR And Fibromyalgia."
https://blog.agapenutrition.com/mthfr-and-fibromyalgia/

Article: “A Functional Medicine Approach to Fibromyalgia,”
https://www.amymyersmd.com/

"MTHFR C677T/A1298C"
https://www.flatironsintegrative.com/mthfr-polymorphisms/

"MTHFR And Fibromyalgia,"
https://blog.agapenutrition.com/mthfr-and-fibromyalgia/

Fibromyalgia
Osteoporosis
Source: Study: “Association of the MTHFR C677T polymorphism and bone mineral density in postmenopausal women: a meta-analysis”
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3596689/

“Solving Fibromyalgia and Muscle Pain,”
https://www.patrickholford.com/advice/solving-fibromyalgia-and-muscle-pain

Interstitial Cystitis
MTHFR
“The potential role of folate metabolism in interstitial cystitis,” 
https://www.researchgate.net/public...of_folate_metabolism_in_interstitial_cystitis (MTHFR mutation causes change in folate metabolism)

  • Gene p53. This has been found to be the creator of the siagloglycopeptide found in interstitial cystitis patients’ urine, but not in the urine of control groups and or healthy populations.

  • Inflammatory cytokines, mast cell activation
  • Hormonal abnormalities
  • Estrogen receptor β abnormality
    Study on interstitial cystitis in animals, found inducing a Estrogen receptor β deficiency in female mice results in bladder damage identical to IC in those mice:
    *Study: “Estrogen receptor β-deficient female mice develop a bladder phenotype resembling human interstitial cystitis,” https://www.pnas.org/content/104/23/9806
  • Elevated urinary norepinephrine
    “Elevated urinary norepinephrine in interstitial cystitis.”
    https://www.ncbi.nlm.nih.gov/pubmed/10367842

    “MTHFR Polymorphism in Interstitial Cystitis and Evidence of Abnormal Folate Metabolism in Interstitial Cystitis”
  • Article: *Study: “The potential role of folate metabolism in interstitial cystitis”
    https://www.researchgate.net/public...of_folate_metabolism_in_interstitial_cystitis
Chronic Lyme
MTHFR
“How Learning I Had an MTHFR Mutation Changed How I Treat My Lyme Disease,”
https://themighty.com/2017/05/mthfr-gene-mutation-and-lyme-disease/

“MTHFR and Lyme disease MTHFR gene mutation. Lower levels of glutathione. Inefficient detoxification,”
https://www.tiredoflyme.com/mthfr-and-lyme-disease.html

“MTHFR Living, Things That Plague Us: Lyme Disease,”
http://mthfrliving.com/health-conditions/lyme-disease/

Article: "How Learning I Had an MTHFR Mutation Changed How I Treat My Lyme Disease."
https://themighty.com/2017/05/mthfr-gene-mutation-and-lyme-disease/

“LYME DISEASE, MTHFR, and LOW GLUTATHIONE,” https://www.nutritionandyourgenes.com/lyme-mthfr-and-low-glutathione
Sjogren’s Disease:
MTHFR

*Study:“Contribution of MTHFR Gene Polymorphisms in Sjogren’s Syndrome Related Lymphomagenesis,”
Sofia Fragkioudaki1, Adrianos Nezos2, Aristea Papageorgiou3, Michael Voulgarelis3, Mary K. Crow4, Haralampos M. Moutsopoulos3 and Clio Mavragani1, 1Department of Physiology, School of Medicine, University of Athens, Athens, Greece,
https://acrabstracts.org/abstract/c...in-sjogrens-syndrome-related-lymphomagenesis/

Endometriosis:
MTHFR:

Article: “Endometriosis and MTHFR: A Connection,”
http://mthfr.net/endometriosis-mthfr/2012/03/24/

*Study: “MTHFR gene polymorphisms (C677T, A1298C and G1793A) in infertile women with endometriosis and its correlation with follicular fluid and serum homocysteine: pilot study,”
https://www.fertstert.org/article/S0015-0282(12)01523-3/abstract

“Endometriosis and MTHFR: A Connection,” http://mthfr.net/endometriosis-mthfr/2012/03/24/

*Study: “MTHFR gene polymorphisms (C677T, A1298C and G1793A) in infertile women with endometriosis and its correlation with follicular fluid and serum homocysteine: pilot study,”
https://www.fertstert.org/article/S0015-0282(12)01523-3/abstract


Multiple Sclerosis





Lupus:

MTHFR
*Study: “Contribution of MTHFR gene variants in lupus related subclinical atherosclerosis.”
https://www.ncbi.nlm.nih.gov/pubmed/29501539

*Study: “BMJ: 07.11 Contribution of mthfr gene variants in lupus related subclinical
Ehlers-Danlos syndrome:

MTHFR
*Study: “Investigation of detoxification polymorphisms genes, methylenetetrahydrofolate-reductase (MTHFR) and P53 in the radiosensitive human cells,” https://www.ncbi.nlm.nih.gov/pubmed/20464958

*Study: “Methylenetetrahydrofolate Reductase Polymorphism in the Etiology of Ehlers-Danlos Syndrome, Hypermobility Type: Connecting the Dots”
https://www.mthfrheds.com/


Irritable Bowel Syndrome:

MTHFR
Study: “The association of the MTHFR C677T polymorphism with inflammatory bowel diseases in the Israeli Jewish population”
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5181816/


Article: “MTHFR LIVING: Things That Plague Us: Gut Issues”
http://mthfrliving.com/health-conditions/gut-gi-issues-leaky-gut/

Article: “The Gene Mutation That Affects 40% of People”
https://www.parsleyhealth.com/blog/mthfr-mutation/

Article: “MTHFR Mutation: A Missing Piece in the Chronic Disease Puzzle”
https://www.holisticprimarycare.net...a-missing-piece-in-the-chronic-disease-puzzle


Migrane Headache

MTHFR
*Study: “Methylenetetrahydrofolate Reductase Gene Variant (MTHFR C677T) and Migraine: A Case Control Study and Meta-analysis”
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3120667/

Article: “What We Know About MTHFR Gene Mutation and Migraine”
https://migraineagain.com/what-we-know-about-mthfr-gene-mutation-and-migraines/
Article: “MTHFR and Migraines”

https://www.geneticlifehacks.com/mthfr-and-migraines/

Multiple Chemical Sensitivity
How to prevent chemical sensitivities, or TILT”
http://drflannery.com/how-to-prevent-chemical-sensitivities-or-tilt/

Vulvodynia:

Celiac Disease
MTHFR

Thyroid Disease:

MTHFR

“MTHFR mutations in female patients with autoimmune thyroiditis,”
https://www.endocrine-abstracts.org/ea/0026/ea0026p110

“Methyl tetrahydrofolate Reductase (MTHFR): The Thyroid Connection”
https://www.holtorfmed.com/mthfr-gene-thyroid-connection/
https://www.holtorfmed.com/mthfr-gene-thyroid-connection/
Article: “PART ONE: the problem with the MTHFR gene,”
https://stopthethyroidmadness.com/mthfr/


The same genes such as MTHFR and p53 which are involved in autoimmune disease, are involved in cancer:

Cancer
___________________________________________
MTHFR, Chronic Fatigue Syndrome, Epstein-Barr and other viruses


MTHFR is a gene which controls methylation. Methylation plays a major role in the behavior of viruses.
"Epstein Barr and Chronic Fatigue"
“Acclaimed researchers Dr. Judy Mikovits and Dr. Frank Ruscetti brought great advances in the field of viral immunity and retroviral science. In particular, their work with Chronic Fatigue Syndrome (CFS) and its associations with the Herpes viruses and certain cancers was ground-breaking. While many doctors and practitioners have climbed onto the methylation bandwagon, unfortunately, CFS and its associated immune disorders are largely still considered to be psychosomatic problems with little understanding of the impacts the syndrome has upon methylation. Dr. Robert Naviaux stated very cleasrly in this Science Daily publication in March, 2013: "When cells are exposed to classical forms of danger, such as a virus or infection or toxic-environmental substances, a defense mechanism is activated. This causes changes to metabolism and gene expression, and reduces the communication between neighboring cells."

Dr's Mikovits and Ruscetti made scientific correlations between CFS and the XMRV retrovirus. In 67% of CFS patients, XMRV-like retroviruses and its telltale compromises of NKCs (natural killer cells) and T-cell rearrangements were identified. (1) A retrovirus is an RNA virus containing the enzyme reverse transcriptase. When the virus enters the cell, it utilizes reverse transcriptase to direct the cell to create viral DNA. This viral DNA becomes integrated into the host cell DNA. Once the DNA becomes impacted by this change in DNA transcription, the infected person is susceptible to numerous genetic mutations, including MTHFR and many other genes which control methylation. (Of note here also is the fact that once retroviruses become integrated into parents' DNA, they may become integrated into children's DNA in conception as well.)

New research indicates that as many as 55% of people with CFS have a defective form of EBV, making it difficult for the body to recognize the virus and to produce antibodies and cell-mediated immunity against it. (2) Most doctors are of the mind that EBV is "everywhere", that virtually all of the population has been exposed and will carry antibodies to the disease but are not affected by the virus unless it is active. While this may be true in some cases, it is not a reason to dismiss the notion that defective viruses may have pathogenic consequences, causing chronic inflammation and immune compromise in many people. As also emphasized by Drs. Mikovits and Ruscetti, viral latency and aberrant viral behavior can prevent detection and be coupled with the chronic stimulation of many host systems. (3) Viruses may hide in tissues rather than floating in the blood stream. In the process of integrating into body tissues, they may evade and/or silence normal T and B cell functions which would normally attack and purge the virus. A very close affinity for thyroid tissue has been observed with Herpes viruses, especially HHV-6A. (4) Approximately 85% of people with CFS have thyroiditis - EBV is a Herpes family virus.

In my practice, I hear some very common themes being repeated by clients arriving in a state of frustration and lack of success working with their conditions...Here are the top 3:
  • "My doctor says I have "MTHFR", but I feel worse since I started taking the supplements."
  • "My doctor says everyone has had EBV, and it does not matter to my symptoms."
  • "My doctor has been treating my thyroid but nothing is changing."
All of these statements are reflective of the lack of understanding of inter-relatedness of certain conditions and physical functions, as well as a lack of proper investigation into a person's functional biochemistry. I caution against seeing "MTHFR" as the problem rather than the expression of an underlying problem, or problems. I have cautioned the same against seeing the thyroid as the root cause of one's disturbance - in fact, I refer to the thyroid as "the canary in the coal mine". And now, I wish to caution against the belief that any virus, whether Herpes family or retrovirus, is no threat to the body if it is not in active expression and also against the assumption that these viral sequences and proteins should be dismissed as agents in chronic disease. Again, any toxin or pathogen can derail the body's fine balance and ability to maintain homeostasis. The likelihood of a CFS sufferer to contract non-Hodgkins lymphoma was deemed to be 250 times higher than a typical healthy person. (5) The association of the XMRV with prostate cancer was discovered in 23% of patients with the cancer. The researching team on this discovery, led by Dr. Ila Singh of the University of Utah, reported,

research recently conducted by a team of scientists at the Cincinnati Children’s Hospital found links between EBV and seven other major diseases: systemic lupus erythematosus (SLE), multiple sclerosis (MS), rheumatoid arthritis (RA), juvenile idiopathic arthritis (JIA), inflammatory bowel disease (IBD), celiac disease, and type 1 diabetes. These seven diseases combined affect nearly 8 million people in the U.S. The links between EBV and these major diseases were defined as a result of the researchers’ discovery of the unique way in which viral cells hijack the immune system. This action occurs specifically by its invasion of B cells and the reprogramming of those cell functions through the use of tiny proteins called transcription factors. This reprogramming leads to to a potentially massive disruption of normal cell function across multiple points in the body.

Herpes Simplex Virus
HSV 1 & 2 are also viruses which place significant stress upon the immune system and therefore can also be in the category of pathogens which upset balances in the methylation pathways. Herpes viruses are very large, double-stranded viruses. They have multiple mechanisms in the immune system by which they are able to avoid cell death. HSVs may persist in a quiescent but persistent form known as latent infection, notably in the neural ganglia. HSV-1 tends to reside in the trigeminal ganglia, while HSV-2 tends to reside in the sacral ganglia, but these are tendencies only, not fixed behavior. During latent infection of a cell, HSVs express latency associated transcript (LAT) RNA. LAT regulates the host cell genome and interferes with natural cell death mechanisms. By maintaining the host cells, LAT expression preserves a reservoir of the virus, which allows subsequent, usually symptomatic, periodic recurrences which are characteristic of non-latency. (8) Let us remember that every single cell in the body is dependent upon ATP for its energy source. ATP allows a cell to do its job, no matter what it is, just like gas in a car engine. When ATP is being used to fight a chronic latent virus, it is potentially diverted from other cells working to complete other tasks. The modulation of the immune system and efficient management of HSVs is critical to a person's overall health and ability to maintain successful completion of other physical tasks in the body.”

Article: “DNA Methylation Has a Local Effect on Transcription and Histone Acetylation”
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC134040/

MTHFR and HIV/AIDS
“I'll thank Fred Greenwood for educating me on the issue this year, he's a 70 year old HIV+ who is missing the MTHFR1 gene which is needed to process folic acid. He tells me that the forms of Folic acid we take are unmethylated and possibly dangerous in that they can accelerate cancer growth. The gene is apparently missing in up to 20% of caucasians. And there's another called MTHFD1 which if not working means there's too much hypomethylation going on due to Folate and B12 loss.

“When I tell people that the HIV virus sits over chromosome 1 where MTHFR is located the freak out and think I am telling them they have HIV. No you don't it is just a fact that is sits on chromosome 1 over the MTHFR enzyme and causes hypomethylation after repeated replication. ~~Sterling”
Source: https://www.facebook.com/mthfrsuppo...mosome-1-where-mthfr-is-loca/445139578860736/

The following article goes into further depth about this:
Article: “The Eyes Never Lie Gene: Explanation of the Mthfr 677 C / A Cytogenic Location 1p 363, Short (P) Arm of Chromosome 1”
https://medcraveonline.com/IJCAM/IJCAM-03-00101.pdf

Article: "Retroviruses : Rethinking Mast Cell Activation", July 23, 2018
https://alisonvickery.com.au/retroviruses/

Article: “HSV, EBV, Methylation, and Functional Approaches for Healing Chronic Latent Viral Infections,”

: “In contrast, retroviruses work their way backward via the reverse transcriptase enzyme, from the RNA to DNA. From there they work forward again to the RNA where they create viral proteins.
They change our DNA to make us a good host and once in our DNA can be passed onto future generations. For example, retroviruses can change our MTHFR (or any other) genetic status. Virulent and chronic latent viruses have become a significant threat to health and homeostasis for millions of people. Any significant pathogen or toxin can impair the body's neurological and immune systems, mitochondrial energy, and subsequently, methylation function and gene expressions. Dozens of viruses are capable of posing this threat, but in this article, I will focus primarily on EBV (Epstein Barr Virus), CFS (Chronic Fatigue Syndrome), and the Herpes family of viruses.”
Source: https://www.truenaturehealthconsult...ylation-and-functional-approaches-for-healing


Article: “Retroviruses: Poorly Understood Agents of Change”

“Although retroviruses have been an important part of human evolution as the placenta evolved from ancestral retroviral envelope genes 25-40 million years ago, envelope genes from both exogenous and endogenous retroviruses, aberrantly expressed in humans, have been shown to be responsible for the development of many chronic diseases. The incidence rates of these diseases are skyrocketing in 21st century America and include prostate cancer, breast cancer, leukemia lymphoma, multiple sclerosis, and amyotropic lateral sclerosis (Lou Gherig’s disease).”

Source: https://worldmercuryproject.org/news/retroviruses-poorly-understood-agents-of-change/


Annikki
https://stopthethyroidmadness.com/mthfr/
 

PatJ

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There is an old poll here on PR asking what MTHFR mutations people have.

According to 23andme I'm +/+ for MTHFR A*372C, MTHFR A1298C, MTHFR A1572G, MTHFR C-137T, MTHFR C10318T, MTHFR C24909T.
 

Hip

Senior Member
Messages
17,874
To show that the MTHFR C677T mutation or the MTHFR A1298C mutation might be playing a role in any given disease, you would need to demonstrate that the prevalence of these mutations is higher in that disease than it is in the general population.

This article gives the prevalence of MTHFR in the general population:
  • C677T. Some 30 to 40 percent of the American population may have a mutation at gene position C677T. Some 25 percent of people of Hispanic descent, and 10 to 15 percent of Caucasian descent are homozygous (have two mutations) for this variant.
  • A1298C. Around 20 percent of the American population may have a homozygous mutation at gene position A1298C.
  • It’s also possible to acquire both C677T and A1298C mutations (one copy of each).
 

Annikki

Senior Member
Messages
146
To show that the MTHFR C677T mutation or the MTHFR A1298C mutation might be playing a role in any given disease, you would need to demonstrate that the prevalence of these mutations is higher in that disease than it is in the general population.
No. The reason some 40% of the population is found to have the MTHFR polymorphism, is that this genetic mutation is found not only in autoimmune disease patients, but in a vast, vast array of other different diseases. Here is a complete list of diseases associated with the MTHFR polymorphism, from MTHFR.net:
MTHFR gene mutations can cause absolutely no symptoms at all. They can also cause severe irreversible health conditions such as Down’s syndrome.


Research is still pending on which medical conditions are caused by, or at least partially attributed to, the MTHFR gene mutations.


From the partial list I recently went through on Medline, these are the current symptoms, syndromes and medical conditions relating to the MTHFR gene mutations:


I will continue to add to this list as I find new conditions and symptoms caused by the MTHFR gene mutations.


Updated: December 6, 2012

  1. Autism
  2. Addictions: smoking, drugs, alcohol
  3. Down syndrome
  4. Miscarriages
  5. Pulmonary embolisms
  6. Depression in Post-Menopausal Women
  7. Schizophrenia
  8. Fibromyalgia
  9. Chronic Fatigue Syndrome
  10. Chemical Sensitivity
  11. Parkinson’s
  12. Irritable Bowel Syndrome
  13. Pre-eclampsia
  14. Stroke
  15. Spina bifida
  16. Esophageal Squamous cell carcinoma
  17. Acute Lymphoblastic Leukemia
  18. Vascular Dementia
  19. Bipolar disorder
  20. Colorectal Adenoma
  21. Idiopathic male infertility
  22. Blood clots
  23. Rectal cancer
  24. Meningioma
  25. Glioma
  26. Congenital Heart Defects
  27. Infant depression via epigenetic processes caused by maternal depression
  28. Deficits in childhood cognitive development
  29. Gastric Cancer
  30. Migraines with aura
  31. Low HDL
  32. High homocysteine
  33. Post-menopausal breast cancer
  34. Atherosclerosis
  35. Oral Clefts
  36. Type 1 Diabetes
  37. Epilepsy
  38. Primary Closed Angle Glaucoma
  39. Alzheimer’s
  40. Tetralogy of Fallot
  41. Decreased telomere length
  42. Potential drug toxicities: methotrexate, anti-epileptics
  43. Cervical dysplasia
  44. Increased bone fracture risk in post-menopausal women
  45. Multiple Sclerosis
  46. Essential Hypertension
  47. Differentiated Thyroid Carcinoma
  48. Prostate Cancer
  49. Premature Death (not associated)
  50. Placental Abruption
  51. Myocardial Infarction (Heart Attack)
  52. Methotrexate Toxicity
  53. Nitrous Oxide Toxicity
  54. Heart Murmurs
  55. Tight Anal Sphincters
  56. Tongue Tie
  57. Midline Defects (many are listed above)
  58. Behcet’s Disease
  59. Ischemic Stroke in Children
  60. Unexplained Neurologic Disease
  61. Asthma
  62. Shortness of Breath
  63. Bladder Cancer
  64. Anecephaly
 

Hip

Senior Member
Messages
17,874

Well that answer suggests you perhaps do not really grasp the concept of causality in the context of epidemiology.

If any factor is playing a causal role in a disease, it will be found more frequently in patients with the disease than in the population as a whole. That's how epidemiology uncovers causal factors of a disease.
 
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Hip

Senior Member
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17,874
I should add that it is interesting to study comorbid diseases, as examining the comorbidities may throw some light on the main disease.
 

Annikki

Senior Member
Messages
146
I think you are mincing the problem. Causality in epidemiology is irrelevant to the problem, because you are assuming that 40 percent of MTHFR defect carriers are all healthy. They are not. This is because the MTHFR mutation causes such a large amount of different common diseases, the total population sick with all of these could easily equate to 40 percent of the population. Look at my list above; there are 64 diseases associated with the MTHFR mutation. These diseases include common conditions, including a host of cancers, Parkinsons, Spina bifida, Type 1 diabetes, schizophrenia, epilepsy, autism, (see list in my above post). If I were to get the numbers of people sick with this long list of diseases, total them and then compute a percentage of the population sick with all of these, I could easily reach or exceed 40%. Really, this sounds like you are rehashing the old argument for ignoring "contested diseases" like CFS. For years, the medical community insisted that because it didn't know the cause of these diseases, that meant these diseases didn't exist. Well, we don't know what caused the Big Bang- that doesn't mean the universe doesn't exist. I think we have a good culprit for the cause here. As to why anyone would want people to not look for the cause is beyond me. CFS is a real disease, therefore, there is a cause- don't stick pins in that.
 

Hip

Senior Member
Messages
17,874
I am not denying the possibility that MTHFR mutations might play a role in ME/CFS and some of the other diseases you listed.

Just pointing out that if MTHFR mutations are playing a causal role in a given disease, you will find those mutations at a higher prevalence in patients who have the disease compared to the prevalence in the general population. The higher the relative prevalence in the disease, the stronger the causal effect.

In fact, a quick bit of Googling leads to this article about a genetic study which indeed found a higher prevalence of MTHFR in ME/CFS. So that indicates MTHFR mutations may be a causal factor in ME/CFS. Just how strong a causal effect would depend on the relative prevalence in ME/CFS in relation to the general population.



The idea that MTHFR mutations might be a factor in ME/CFS has been discussed on this forum for years. Lots of patients have tried the methylation protocol, which includes active folate to try to make up for any MTHFR C677T mutations. Those with this mutation don't convert folic acid into active folate very well.

I am +/+ for MTHFR C677T, but the methylation protocol did not help in my case. There is a whole sub-forum dedicated to methylation.
 
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MTpockets

Senior Member
Messages
202
Location
AZ, USA
I agree with Hip. My husband has the exact same mutation as me and he is healthy as a horse. He gets one cold per year. He has never done a MTHFR protocol. I have been on one for years now and it didn't make a lick of difference to my ME.
 

Hip

Senior Member
Messages
17,874
Personally, @Annikki, I am a fan of the pathogen theory of disease — the idea that behind many chronic illnesses of currently unknown etiology, there is a low-level infection of the tissues that causes the disease.

As you know, in the case of interstitial cystitis (IC), which I understand is the condition you suffer from, this has been linked to polyomavirus infection of the epithelial cell lining of the bladder, and that intravesical antiviral treatment (squirting a solution into the bladder) with cidofovir leads to substantial improvement in IC symptoms — see here.

I have something similar to IC, which is overactive bladder (OAB), also called irritable bladder. Unlike IC there is no pain in OAB, but there is the same urinary urgency symptom, due to involuntary nervous contractions of the bladder muscles. I believe I developed OAB from catching an infection during sex.

Talking about IC/OAB has reminded me that I always wanted to start a poll about these diseases and their possible connection to sex, which I have now done here:

POLL: Did your interstitial cystitis or overactive bladder appear after starting a new sexual relationship (it may be due to catching a virus)?
 
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Belbyr

Senior Member
Messages
602
Location
Memphis
I believe Dr Chia does a lot of work on chronic viral infections. If he is connected with Stanford, then the guy have some legitimacy.
 

Annikki

Senior Member
Messages
146
The MTHFR defect results in decreased methylation. According an article from a MTHFR support website, methylation is required to keep viruses silent: "MTHFR and Viral Infections Introduction to Methylation and MTHFR." http://www.beyondmthfr.com/mthfr-viral-infections/
I will quote what the author says about MTHFR and viral infections:
Why Methylation Matters

What I am about to explain to you is simply why people with MTHFR issues are more likely to have serious chronic viral issues when they are under stress. Remember that while the subject of methylation is complicated, you can how to use it to improve your life. One of the big things to remember with MTHFR-related issues is that people with these genes are slower at producing the active form of Vitamin B9. If there is one single thing to pound into your brain about methylation this is it – people with MTHFR issues are SLOW at producing the activated folate molecule. This is the whole reason why supplements which support MTHFR provide the active form of folate – 5-MTHF. As long as people with MTHFR issues take vitamins or eat foods with activated folate they bypass the genetic problem. Pretty simple.

While supplementing the diet with extra sources of methylation support (folate, choline, B12, TMG, etc.) is a good strategy to optimize methylation, sometimes stress makes the picture more complicated. When we are stressed our bodies burn through resources at an accelerated rate. This means people will become vitamin deficient regardless of their gene SNPs when under stress. If the stress is brief and short-lived then the effect on your vitamin pathways and your methylation status is small. However when stress is chronic, the impact on your methylation pathways becomes severe. This process impacts all people – it literally doesn’t matter if you have MTHFR issues or not; being under chronic stress will create the same problems in all people. You see stress is the great equalizer as it harms everyone without regard to age, sex, genes, etc. Of course it goes without saying that the people with MTHFR issues are going to be MORE impacted by stress because they run out of the one-carbon methyl groups faster (remember the “methyl” in methylation refers to one carbon atom with three hydrogen atoms attached. This is why it is also referred to as the one-carbon cycle.)
Naturally, Hip, you remind me that yes, I have IC. Yes, IC is caused by viral infection in ulcerative cases of the disease. This virus is BK virus, which most people are infected with, and yet don't get sick. No, BK virus isn't spread by sex. People normally become infected at age 3 or 4. BK virus lives in various parts of the body, not just the urinary system. It infects the lungs and a number of other places in the body. It is likely transmitted by coughing and or sneezing. BK virus, prior to it's discovery in IC cases, was only known to cause disease in kidney transplant patients on immunosuppressant drugs. This indicates something suppresses the immune system of IC patients or is giving viruses a better chance to proliferate and cause damage. That's why I'm intrigued by the MTHFR finding. MTHFR accounts for this. And I highly expect, MTHFR defects found in CFS patients gives rise to some CFS patients having EBV. We know EBV isn't found in all CFS patients. A deficient MTHFR gene probably is what allows EBV to remain active in CFS patients. In healthy people, EBV goes dormant in other people after getting Mono. I could also argue the same for Chronic Lyme Disease, that if you have a MTHFR defect, the Borrelia burgdorferi infection likely can't be cleared out. So no, sex doesn't have anything to do with it, and don't see what you are getting out of bringing sex into the discussion. Maybe check out an HIV thread if that's an area that interests you.
 
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Hip

Senior Member
Messages
17,874
This virus is BK virus, which most people are infected with, and yet don't get sick.

The same applies to enterovirus, EBV, and all other ME/CFS-associated viruses. Most people have these, but are healthy. So clearly there are other causal factors involved that determine whether a virus causes a given disease or not.

In the case of ME/CFS, it may be only when these viruses enter certain tissue compartments or certain cells, such as the brain, that ME/CFS develops.



BK virus lives in various parts of the body, not just the urinary system.

That's also true of other viruses, that they can live in multiple areas of the body. Enterovirus can live in multiple organs, but for example if it enters the heart, it may cause myocarditis. Often the disease precipitated depends on which parts of the body the virus infects.



No, BK virus isn't spread by sex.

Sexual transmission of BK virus is considered a possibility, according to this study:
Many different routes for the transmission of BK virus have been hypothesized. According to many authors, respiratory transmission is the most likely route.
...
Sexual transmission has been proposed as another mechanism. Monini et al. detected BK virus in 57% of specimens of genital tissues and 95% of sperm samples. Because primary infection generally occurs before the age of sexual activity, this hypothesis would assume a sexually transmitted trigger for reactivation of BK disease.

But BK virus may not be the cause of interstitial cystitis in all cases; other viruses and pathogens may also be involved. Quite a few disease are linked to more than one suspected causal pathogen; ME/CFS for example is linked to EBV, enterovirus, cytomegalovirus and others.

As you point out, BK virus is linked to the ulcerative form of interstitial cystitis; other forms of IC might conceivably be caused by other pathogens.

And OAB may be due to different pathogens again.



This indicates something suppresses the immune system of IC patients or is giving viruses a better chance to proliferate and cause damage. That's why I'm intrigued by the MTHFR finding. MTHFR accounts for this.

Where did you see that MTHFR leads to immunosuppression allowing viruses to proliferate?

When I Googled just now I could not find any evidence that MTHFR causes immunosuppression. In fact I found the opposite: this study found that in MTHFR knock-out mice, cytomegalovirus infection was better controlled. Thus the authors conclude that MTHFR mutations may have evolved because they lead to stronger immunity.

Of course, stronger immunity might be part of the problem: if the immune system is unable to eradicate a virus, but continually reacts to the presence of the virus in the body, a stronger immune response might make a disease like ME/CFS worse.

The study mentioned earlier found MTHFR mutations to be more common in ME/CFS, so that suggests these mutations may be playing some sort of causal role in this disease. But what that role might be is anybody's guess.



Annikki, could you please divide your posts into paragraphs no longer than around 3 or 4 lines, as lots of people on this forum have difficulty reading long blocks of text, due to the neurological issues of ME/CFS.
 
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Annikki

Senior Member
Messages
146
Methylation has a direct effect on inhibiting or encouraging viral l infections. I need not labor the point, the facts are there to support it and they aren't going anywhere.
Facts:
A defect in MTHFR has been found definitively in people with many different diseases, CFS included.
I have cited countless studies to confirm this. This is solid fact.
Reduced methylation is a consequence of MTHFR defects.
Reduced methylation is abnormal and has direct side effects, from expression of latent viruses, to hormonal imbalance, fatigue from lack of folate and other problems.
If you dispute these, then it's probably better you dispute it with all the organizations which provide information and support for people with the MTHFR defect.

A handful of healthy people having the defect doesn't change that a vast multitude of studies confirm there is a link between MTHFR polymorphism and disease.
Either tell me how every study ever done on MTHFR is wrong, and used flawed data, or don't belabor the point.

Go over every study which found the MTHFR defect in patient groups from Type 1 diabetes, to Parkinsons, to Multiple Sclerosis and explain how every study which found a MTHFR defect was wrong. This may take some time because the studies on MTHFR number greater than 50. Next you have to prove to us exactly how all these studies were flawed. I hope you aren't right because that would mean a vast number of researchers at prestigious institutions don't have a clue what they are doing.
If that many researchers screwed up on it, this would mean science and research as we know it are doomed.

If you are so sure about what causes CFS, then please tell us what it is. We would all love to know. And cite studies to prove your argument, just don't flail around with facts which seem to support your argument. Supply only studies, period or let it drop.
 

MTpockets

Senior Member
Messages
202
Location
AZ, USA
I wonder if they are finding the defect in so many disease types, because the defect is so common in EVERYONE though. You would need to take a huge sample from the healthy population to prove they DON'T have the defect to make the connection that the defect is responsible for disease. Not saying I know one way or the other but correlation does not always equal causation. Like I said before, my husband has the exact defect I do, and he has no health problems.

I think MTHFR is fairly common. But most people live and die without ever knowing of its existence, because it doesn't bother most people enough that they would notice. Their bodies are capable of compensating. Some people's bodies are not, and it causes problems. I think it is a piece of a very large puzzle, but not necessarily the key to unlocking the door. Just my thoughts.
 

Hip

Senior Member
Messages
17,874
Go over every study which found the MTHFR defect in patient groups from Type 1 diabetes, to Parkinsons, to Multiple Sclerosis and explain how every study which found a MTHFR defect was wrong.

These 4 studies you listed found MTHFR mutations more prevalent in the disease than the general population:

Sjogren's
multiple sclerosis
inflammatory bowel diseases
migraine

In other diseases you listed I could not see studies on MTHFR mutations prevalence (but I have not checked every single link).

So we should be in agreement that a higher prevalence of MTHFR mutations in a given disease shows that these mutations may be playing a causal role, because that's what the studies you listed are saying.

Just how much of a causal role MTHFR mutations are playing depends on how high the prevalence is in a given disease, compared to the general population.


It's worth pointing out that this poll suggests the methylation protocol rarely leads to any major improvement in ME/CFS (only 3% of patients found methylation made a major improvement), though 28% found it made a minor improvement. But that minor improvement may just come from the beneficial effects of B12 in the methylation protocol, as B12 on its own is known to be helpful for ME/CFS.



If you are so sure about what causes CFS, then please tell us what it is. We would all love to know. And cite studies to prove your argument, just don't flail around with facts which seem to support your argument. Supply only studies, period or let it drop.

My own view is that chronic viral infection is likley the primary cause of ME/CFS. If you look at these three brain autopsies on ME/CFS patients, all 3 had enterovirus in their brain.
 
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Annikki

Senior Member
Messages
146
I listed far more than four studies which found MTHFR defects in autoimmune patients. I listed over 24 studies, so I am far more correct in my thesis, than you are giving me credit for. Furthermore, there were also a vast many studies I didn't yet list verifying the presence of the MTHFR polymorphism in autoimmune diseases. My information is quite solid, it is there at the beginning of this thread.
You are also wrong that folate and vitamin B12 are ineffectual in treating ME/CFS. This study shows these both have been effected. Only the CFS patients in the study who were taking opioid pain medication received no benefit from taking B12 and folate to compensate for abnormally low levels caused by a bad MTHFR.
Study: "Response to Vitamin B12 and Folic Acid in Myalgic Encephalomyelitis and Fibromyalgia"
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4406448/
Quote:
"Conclusions
Dose-response relationship and long-lasting effects of B12/folic acid support a true positive response in the studied group of patients with ME/fibromyalgia. It’s important to be alert on co-existing thyroid dysfunction, and we suspect a risk of counteracting interference between B12/folic acid and certain opioid analgesics and other drugs that have to be demethylated as part of their metabolism. These issues should be considered when controlled trials for ME and fibromyalgia are to be designed."
Of course, these supplements don't cure ME/CFS, but if a ME/CFS patient- or all of them unilaterally possess the MTHFR polymorphism, then it is inevitable they are deficient in both folate and B12. Having deficiencies of these nutrients is the result of the MTHFR polymorphism. With this genetic defect, you have a root problem that effects a number of core, essential, biological processes. Hormonal imbalances, thyroid damage, and cancers are among the many things which happen as a consequence of a defective MTHFR.
Really you can argue the issue into the ground by your various arguments, which again, didn't take into account the amount of data out there from many studies which attest to the fact this genetic defect is causing problems in all autoimmune disease patients. Also, these studies, if anyone cares to read them, explain both the biological processes hindered by a bad MTHFR and how these exact hindered biological processes cause disease in autoimmune patients and others. It is also incorrect to consider other diseases unrelated to CFS and the autoimmune diseases. For example, Type 1 diabetes is considered an autoimmune condition. Migranes also occur in tandem with thyroid autoimmune diseases, and as such there is probably or likely an autoimmune component.
Finally, all the diseases on the list, save for the cancers, all have been diseases considered psychosomatic. Gee, I wonder why? So far, anyone who ever does research which shows there is a clear, biological cause to ME/CFS and all the psychosomatic, i.e., contested illnesses, get's a bunch of crap and has their findings trolled, belittled and allegedly "disproven," by fake or unfairly weighted studies.
In the same manner that global warming get's regularly disproven by "studies," which say mankind isn't doing it, so does CFS/ME get "debunked." Naturally, you can find half the climate change denial studies received funding from places like the American Petroleum Institute and Exxon-Mobile.
And if you go to really any forum where proof of the reality of ME/CFS is found, then you get trolls and others who discount. Since we know well from Trump and Russia, most troll outfits are funded by political and corporate interests. What I want to know is exactly what benefits are obtained by pharmaceutical and disability insurance companies, the British Government, and the heavily lobbied CDC in hiding all they can about ME/CFS.
Yes, when the British Government locked up it's records on it's ME/CFS research until 2070, it showed me that there are some big wigs who have an uncanny interest in keeping the public ignornant about the cause of ME/CFS. Isn't it funny how people who get too close to figuring it out get their findings manipulated and mauled by trolls. Welcome to the age where liars rule the roost and trolls mediate threatening political and social ideas into oblivion.
And if trolling doesn't work, just cite a few studies which were done poorly but sound official. I say to anyone here, the only thing you can do in this sort of climate is to check facts, rigorously and keep and open mind. If you don't idiots like Wessely will wind up selling you real estate in Florida, which is really just a swamp.
 

Rufous McKinney

Senior Member
Messages
13,388
I listed over 24 studies

thank you very much for this major information and all the work you've done summarizing this.

I didn't get tested: i just know I have this. (sorry if that sounds lame)

I've been slow to uptake all the latest but my foggy sense of the matter is: for whatever reason, that mutation happened and has been carried for a long time. I think it just pre-disposes those bodies to: having bit harder time of it, but not THAT hard. I was able to reproduce (in theory, two, in reality, only one made it). That one probably is a carrier but not homozygous. I will then bet money my husband who never gets any of this stuff: does not have the MTHFRE.

So back in Caveland, we were lucky to live to 30. We were subjected to stressors, to smoke, to parasites. Now its a planetary asssault, a fully loaded AK 47.

So then: the world changes into a much more toxic, stressful, overwhelming overpopulated state. Hello: unwell ness.

So: are we surprised THEY don't want to find out what REALLY CAUSES this level of sick. Its our SICK lifestyle. Its our entire Industrial Revolution. Its the loss of moments to view sunsets.