Author Archives: lassesen

Unknown's avatar lassesen 6:35 am on February 27, 2013  

Thyroid and the gut

A correspondent raised some interesting questions about thryoid and gut bacteria. She wrote
“Thyroid disease is known to slow down the digestion” I find that I must ask the question, perhaps digestion slowed down FIRST, and the thyroid disease was a result! I don’t know the answer, but know that if we don’t examine both directions — we may miss a significant treatment approach.
Looking at some pubmed articles,

“thyroid hormones increase intestinal motility and transit rate, administration of cholecystokinin increases small bowel motility, diarrhoea occurs in adrenal failure, while mineralocorticoids increase salt and water absorption from the colon.Indeed aldosterone secretion may be increased by the loss of sodium in diarrhoea. The balance between the biochemical regulators is clearly complex, but study of certain endocrine abnormalities has demonstrated their importance in the control of intestinal function.” [1971]

Later studies report “Thyroid diseases may be related to gastrointestinal motility symptoms. Such symptoms can vary in degree and, sometimes, are the only clue of athyroid disease or, at least, the first…. thyroid diseases may be related to symptoms due to digestive motility dysfunction.” [2004]

In terms of demonstrating that the absence or prescence of a single bacteria species in the gut can cause thyroid problems is mentioned in this 2008 article.

“Perhaps the most celebrated example of the difference a single species can make is the ‘mimosine story’ in ruminants. Mimosine is a toxic amino acid found in the leguminous plant, Leucaena leucocephala. Mimosine can cause thyroid problems by being converted to the goitrogen, 3-hydroxy-4(1H)-pyridone, in the rumen.  Observations that mimosine-containing plants were toxic to ruminants in some countries but not others led to the discovery of Synergistes jonesii, which metabolises 3-hydroxy-4(1H)-pyridone and protects animals from toxicity.”[2008]

In other words,  a single species makes a major difference: Synergistes jonesii!

The sweetish article that I found comes from, BMJ in 1923: THE INFLUENCE OF INTESTINAL BACTERIA UPON THE THYROID GLAND, which is well worth a read.

I have talked with people that have thyroid issue run in their family.  Since both gut bacteria and DNA are inherited — (which means that the cross product[interaction between DNA and gut bacteria]  is also inherited) — this suggests the inheritance could be altered by gut flora alteration (speculation)

 

If this is the correct approach, then the question arises — how do we alter it? The 1923 articles suggest that lactose is not effective (and this implies that Lactobacillus species may not be effective), thus this leads us to the unusual probiotics. The easiest to obtain is Prescript-Assist which I have referred to earlier in this blog.

Unknown's avatar lassesen 1:31 am on February 24, 2013  

Autoimmune and Vitamin 1,25D

I thought that I should put together a collection on conditions that have been documented to have a high Vitamin 1,25D result(Calcitriol) when tested.

  • ” Results showed a strong positive association between these autoimmune conditions[ multiple sclerosis, lupus, psoriasis, osteoporosis, osteoarthritis, metabolic syndrome, fibromyalgia and chronic fatigue syndrome] and levels of 1,25-D >110 pmol/L. However, there was little association with vitamin D deficiency or the other inflammatory markers, meaning that the results challenge the assumption that serum levels of 25-D are a sensitive measure of the autoimmune disease state.” [2009]
  • “In granulomatous disease such as lymphoproliferative disorders, sarcoidosis, tuberculosis, and inflammatory bowel disease,”[emedicine]
  • “postural orthostatic tachycardia syndrome” – remission with calcitriol treatment [2012]

General Vitamin D level and symptoms

  • “A significant negative correlation between vitamin D level and widespread pain index was found.”[2012]
  • ” improvement became more significant when their blood level of 25(OH) D exceeded 50 ng/ mL.”[2011]
  • ” a positive association of vitamin D deficiency with a variety of nonspecific bone pain, particularly in women” [2010]
  • “Musculoskeletal pain is associated with very low levels of vitamin D in men” [2010]
  • “Resolution of hypersomnia following identification and treatment of vitamin d deficiency.” [2010]
  • “Vitamin D deficiency is a major risk factor for central nervous system (CNS) demyelinating diseases including multiple sclerosis (MS)” [2012]
  • “This study demonstrates for the first time a direct antiviral effect of vitamin D in an in vitro infectious virus production system.”[2011]
  • “vitamin D can suppress intracellular growth of M tuberculosis in vitro. Vitamin D also induced the expression of cathelicidin, which is involved in the first line of defense in TB patients” [2011]
  • “Vitamin D(3) skews cytokine responses toward an antiinflammatory profile,.. Candida albican” [2011]
  • Interesting that Epstain-Barr interfers with Vitamin D actions!!!! [2010]

For general information on Vitamin D and autoimnmune disease:

  • “Studies have shown evidences of 1,25(OH)D in inhibiting disease induction in autoimmune encephalomyelitis, thyroiditis, type-1 diabetes mellitus, inflammatory bowel disease (IBD), systemic lupus  erythematosus, and collagen-induced arthritis and Lyme  arthritis, as reported by Hayes et al and Adorini et al.  Vitamin D deciency could accelerate the occurrence of autoimmune encephalomyelitis” [2007]
Unknown's avatar lassesen 3:21 pm on February 19, 2013  

Reflections on Recovery from CFS

Having fully recovered three times over 40 years: the first time due to misdiagnosis that resulted in appropriate treatment (before CFS or Lyme existed); the second time due to a treatment approach that claimed 75+% recovery (and 3 of the 4 of us did recover!). This last time due to an approach of what CFS may be that is likely far closer than prior models.

The question of whether I had CFS is really moot this time, SPECT scans were abnormal in the manner the chronic Lyme and CFS are; Vitamin 1,25D was sky high – seen with FM, CFS, and many autoimmune disease (and returned to normal due to treatment).

The model is simple to describe — but difficult to create a “simple” treatment plan for because the key factors are inherited (not in your DNA but in you gut bacteria DNA). CFS is a stable gut bacteria dysfunction that impacts metabolites (B12, magnesium, and possible bad stuff etc) that are produced by the gut bacteria.

Contrary to urban myth, antibiotics do not kill ALL of your gut bacteria, only selected species (depending on which antibiotics). Conventional probiotics usually contain species that will out compete or impact(by producing their own natural antibiotics) a few other species. The typical example is Lactobacillus Acidophilus reducing E.Coli populations.

Gut bacteria tests only covers a handful of species and rarely identify if the species that are there are good or bad. Auzzie studies did find a common pattern (Low E.Coli, High levels for a half dozen other species).

Treatment will often make you sicker for a while, typically 7-14 days before any improvement. Sometimes, massively sick with extremely nasty headaches.

My latest recovery illustrated to me that addressing specific species shifts (killing or supplementing) impacts subsets of symptoms. Dry eye, dry mouth disappear with E.Coli supplementation. Cognitive improvement increased greatly within 10 days by killing other species off with Neem and Tulsi at 3 gms/day.

The real problem is that each of us has about 150 species out of 1500 “good bacteria” species when we are healthy. Effectively, they are as unique as finger prints! When CFS hits, the species shift is unique (hence the unique symptoms). Even if we knew the exact species shift, treating that shift is complex. The herb haritaki kills some of the high species, but also kills some of the low species (and normal species). The same applies to all of the antibiotics and herbs.

I targeted the low species by finding the right supplemental probiotics (not easy to obtain) and searching through hundreds of antibiotics and antibiotic-like herbs to find ones that had the right profile for those species that were high but did not severely impact the low species.

My game plan was derived from:
http://www.ahmf.org/98access/98butt3.html

So the problems for recovery are:

  • Herx /feeling sicker for a while
  • Not being able to tell if there is an improvement (forgetting how you were!) — I test myself with Wii Fit every day. When I herx, test performance drops badly then it returns to normal
  • Getting the RIGHT probiotics needed (cost, and for the most critical one, having the hassle of having to import it into the US because the FDA deems it to be a drug!)
  • Getting the antibiotics Or natural herbs/spices that are antibiotic like (MD issues for the first, ND issues for the second — my ND, who is a specialist for CFS, did not have that knowledge when I started).

Will I get CFS? Again, given what it is, it is possible. At the first signs of it, I do have a varied supply of supplements on hand that may stop it from becoming established….

Best to you all!

Ken

 

 

Unknown's avatar lassesen 5:31 pm on February 16, 2013  

CFS Low Blood Pressure, High Blood pressure and gut bacteria

This week’s Economist had another article dealing with the microbiome (gut bacteria, microflora), “Sniffing out hypertension Gut bacteria help regulate blood pressure“. A major drop in blood pressure (often with dizziness and other symptoms) is common in CFS – but the mechanism for this happening has been unclear. On the other side, there is an increasing problem with high blood pressure in society.
There are two proteins that may be produced Olfr78, and Gpr41. The presence (or absence) impacts how the body responded to metabolites produced by the microbione.

  • ” in normal, healthy mice propionic acid regulates this process, causing blood pressure to drop.”
  • “the blood pressure of those in which Olfr78 had been reduced, dropped more than it did in normal mice.”
  • “reducing Gpr41, by contrast, blood pressure did not fall at all.”
  • “she treated some mice with an antibiotic, to kill off their gut bacteria. Mice so treated that had no gene for Olfr78 showed a significant rise in blood pressure. Those that were genetically normal did not.”

While this does not confirm the role of gut bacteria dysfunction in CFS causing low blood pressure and other symptoms — it does suggest that this may be a viable mechanism.

Unknown's avatar lassesen 8:13 am on February 9, 2013  

Cystic Fibrosis and Microflora / Gut Bacteria / Microbiota

Today I had a conversation with an old friend and he asked if I had any insight to cystic fibrosis from my readings. I had to say no — but stated that it would be worthwhile to examine whatever research may apply.

Cystic fibrosis is a genetic disorder, so the initial assumption would be that it had nothing to do with the microbiota. From my readings, both the DNA of the body and the DNA of the bacteria that inhabits the body are inherited — so there is a possibility that it may take a double inheritance to cause the condition to develop fully. While altering the microbiota may not stop or prevent the disease — it may have an impact of the rate of progression or side-effects — this is the hypothesis that I am exploring in this post.

As a starting point in this 2010 article,Comparing the microbiota of the cystic fibrosis lung and human gut which states “the typically mutually beneficial relationships usually found in the GI tract from the injurious relationships in the CF lung.” This is a familiar situation of the disease altering the microbiotia, with the microbiotia then supporting the disease. This was  illustrated in the diagram below.

For CF, this is reported in this 2004 article, Intestinal inflammation is a frequent feature of cystic fibrosis and is reduced by probiotic administration

The authors go on to say, “demonstrated that pathogenically important behaviors of Pseudomonas aeruginosa can be impacted by the presence of bacterial species that are routinely disregarded by most treating clinicians.” In terms of the general relationship (not CF specific), “association between changes in the composition of gut microbes and changes in the normal functioning of the nervous system” speaks to the neurological issues seen with the shift of the microbiota seen with Chronic Fatigue Syndrome.

The article does a nice discussion of some of the issues and ends with “The challenge that remains for the study both of chronic infections affecting CF airways and of gut microbiota is to construct theoretical frameworks in which the implications of these data can be understood.” – in other words, we have a concept but not sufficient evidence to suggest a study supported therapy.

Other Studies

Almost all of the studies raised the question that it is unclear if the effect is due to reduce inflammation because of the probiotics or because it inhibited the CF process.

  • Lactobacillus Rhamnosus was found to improve CF patients [2010] [2007] [2008] [2004]
  • A non-CF study finding that Lactobacillus casei reduces Pseudomonas aeruginosa [2001]
  • Azithromycin and other antibiotics improves CF patients [2003] [2011]
    • The issue is always whether it is because they alter gut bacteria, or impact the other infections seen in CF.

What I would love to see is a well designed study done of CF patients with the two commercially available (and unusual) probiotics:

  • Mutaflor (E.Coli Nissle 1917)
  • Prescript Assist (mixture of 29 non-Lactobacillus species)