Author Archives: lassesen

Unknown's avatar lassesen 2:51 pm on August 20, 2017  

Post #700 – Roles in Treating CFS

This is my 700th post and at the same time, a reader asked

“Ken I’m writing my final degree project in CFS and I would like to know, in some phrases, what you think about the role of “official medicine” in the treatment of the disease.
What’s your goal with the blog and how it can help the patients”

Role of Official Medicine

I need to answer this based on my model and observations. Medicine is looking for simple cookbook solutions to a complex condition. Most practicing MDs are also greatly constrained by several nasty things:

  • “Standards of Care” –  “Practice guidelines assist the health care practitioner with patient care decisions about appropriate diagnostic, therapeutic, or other clinical procedures for specific clinical circumstances.” [NIH]
  • “Medicare Insurance” – this is very closely tied to above
  • “Peer pressure” – What would other doctors do in their region.

A professor once told me: “The ideal doctor or engineer is the person with a fantastic memory, strong sense of conformity and zero creativity”.

Give them a cookbook on how to treat an issue by a medical association, and they will follow it. Give them a ton of studies with conflicting results and they will either say “We will wait until there is clarification” or “It is probably psychological or best handled by a specialist”. Often the excuse can become “We need more studies”…. studies that may never happen. Most MDs do not want their rear side exposed to fellow MDs, local medical organizations and insurance companies  for some very hard financial kicks.

Bottom Line: Official Medicine will stay in a holding pattern for years, likely decades. They will provide symptom relief and ad hoc  random experiments (often repeating things tried unsuccessfully decades ago!). Only an extreme few would read any research on CFS regularly.

Research

My opinion based on seeing enough studies is that CFS/FM/IBS symptoms are interactions between DNA/SNP and microbiome (which has more DNA than a human). The appropriate research approach would be to take a large sample of patients (likely 100,000 or more) and record:

  • DNA
  • Microbiome
  • Symptoms and Lab results

Then push all of this data in appropriate artificial intelligence algorithms to break down/discover the associations. In the comments of my last post,  you would see that I identified several bacteria groups that are very high. When the reader tried any suggested herbs, they became severely depressed in days and stopped. A little research on PubMed discovered that most of these bacteria groups are strongly associated with depression. The die-off from the herbs was triggering the depression. One type of symptom==> a group of bacteria (and likely DNA also).

Current Researchers

Most researchers are trained in specialties. They do excellent work examining the leaves and twigs around their focus of interest.  The problem with CFS is that the issue is bigger, not just the branches of the tree or the whole tree — rather the entire forest. IMHO, an ideal CFS researcher would be trained in medicine, DNA/SNP, microbiology and machine learning. They would need to be a world class data scientist besides being an MD. They will also need a big budget and cooperative clinics to get an adequate data sample (I am talking 100,000 patients needing their DNA and microbiome done).

To me, one of the greatest problems with CFS research is that successful results from studies are rarely repeated. My favorite soap box is pointing out the Berg’s studies finding a high (80-90%) of CFS patients having an inherited coagulation condition have never been repeated. Having a single study results in those results being ignored because “they have not been repeated” — ignoring the fact that no one tried to repeat them…

My Role

What is my role? Basically, it is as a recovered former patient who remembers the pain and hurt that this condition caused. I looked at my strengths and weaknesses and realized that my best service to the community is simple:

  • Someone with a clear head who can read thru the literature, understand generally what the article actually says (i.e. cut thru researchers’ double speak). This arose from experience and training.
    • I started reading medical articles and presentations at 14 years old because I was one of 15 students from my grade level in one of the largest school districts in Canada for a special enrichment program, Berg Science Seminars.
    • I did an undergraduate and graduate degree in Statistics
    • My Master’s topic was working with the Justice Institute of BC looking at how various medical treatments influenced survival during medical transport.
    • I worked for many years as an Industrial Statistician and was a member of the American Statistical Association, as well as the American Mathematical Association, and a few other professional organizations.
  • My day-to-day job deals with very complex systems and data – literally world class Information Technology Systems including Microsoft, Amazon and Starbucks. I am one of those few people who doesn’t suffer from information or complexity saturation, rather, I sit down and slowly shift and re-shift the information to build out and then test a model as to cause and solution. I have been (and still am) successful in this area.  In July, 2017 I was the Edison Award Winner for the Starbucks Digital Platform Team.

My role is a citizen scientist modeler. It is “citizen” because I am not receiving any money for doing it. I have worked professionally as a scientist modeler.

My role is not:

  • CFS Life Coach
  • Action for getting more funding
  • Social Support
  • Treatment support

I could easily get involved with the above, but there are others who are more capable. My gifts are dealing with data and sketching out how the thousands of dots are connected. Taking these sketches and converting them into studies, treatment plans should be a role for the medical professionals. For example, Neem fits the model, but no one has done a clinical study on whether it is actually effective.

Bottom Line for Me

  • Continue to review studies, cutting thru the medical double talk
    • I am grateful for many readers who forward new studies to me for early review.
  • Continue to test and refine the model that seems to fit best against all of the data: microbiome x DNA/SNP interactions
    • Doing uBiome reviews help evolve the model
  • Continue to identify items which may help — based on applying the model to known literature.
    • Producing posts on these items with links to the research that I based it on (the keyword here is transparency)
    • Advising patients that these items should be discussed with their medical professionals before starting. I have blinkers on and have no idea if the same item may cause a different medical condition to get worse. Only your medical professional can determine if it is safe to try or not. I do not want to get sucked into time-consuming understanding of interactions, I would rather spend that time connecting more dots.

 

Unknown's avatar lassesen 4:54 am on August 17, 2017  

uBiome from a Hep Triggered CFS patient

Another uBiome result, as with other patients, low or no bifidobacterium and lactobacillus. Similar to most other patients, biodiversity was very high, 97%ile, with the usual many families at a very low (0.01 or 0.02) (trace) level compared to controls with the same families.

bb

Again, many rare ones show up

rare

Firmicutes to Bacteroidetes ratio was low 1.1: 1 instead of the normal 2.1:1. (about 1/3 have low ratios so far, and 2/3 have high ratios).

  • Akkermansia level is high (6.83) -seen in about 25% of the uBiome, the other 75% are low.
    • This subset of high patients also tend to be high in:
      • Alistipes, Bilophila, Intestinibacter,  Oscillospira, Intestinimonas,  Butyricimonas
      • This hints that 7 genus may be mutually beneficial to each other.

Notes on person: hepatitis triggered CFS over 20 years ago. Currently not doing any protocol.

The Low Amount of Abundance Bacteria Genus

I have been recording the relative percentage (compare to controls) of different uBiome that I have reviewed. I took the numbers at the Genus (lowest) level, counted and plotted them.

spread

The expectation for a normal group of patients would be a bell/Normal-curve with the top of the bell being at 100. With CFS patients we find a large number of genus with a very low level compare to control.  In other words we have high biodiversity but it is very fragmented and made up of nominal populations. If the tests being applied to the microbiome was less sensitive than uBiomes, then a result of low biodiversity could be reported on the same sample because all of the trace, 10%, 20% may not be recorded.

Bottom Line

My best suggestion (especially since information on reducing Alistipes, Bilophila, Intestinibacter,  Oscillospira, Intestinimonas,  Butyricimonas is almost non-existent) is to discuss with their medical professionals the items on my “Cookbook Summary for the Brain Fogged“. The items are linked (eventually) back to the PubMed studies that provided dosage information.

 

Unknown's avatar lassesen 4:10 am on August 16, 2017  

uBiome with bioscreen results and an unwelcomed surprise

Another reader shared their uBiome results with bioscreen results (done the old fashion was of culturing bacteria). First thing is the classic “where’s the bifo and lacto!!” result seen with CFS/

cat

Looking at: Firmicute to Bacteriodetes ratio: 3.8 (double the typical ratio of 2.1), the volume of Bacteriodetes was the cause of the shift (50% of typical).

Over on Bioscreen, we see the rest of the normal story for CFS patients: Zero E.Coli and overgrowth (remember this is cultured, so only a few results will be shown — most gut bacteria cannot be cultured).

catl

Going back to the uBiome results — we again see a fair number of rare bacteria appearing. There is no clear pattern beyond “a lot of rare ones appear”. For example, this is the first sample showing any of the Spirochaetia Phylum (The TOP level of bacteria tree). This family includes Borrelia burgdorferi, B. garinii, and B. afzelii, which cause Lyme disease.

cat3

Drill Down

Phylum Level

  • Lentisphaerae was 19.21x the average where as most CFS patients have zero
  • Tenericutes was 4.31x the average where as most CFS patients have zero

Class Level

  • Mollicutes (under Tenericutes) was 4.30x the average where as most CFS patients have zero. The best-known genus in the Mollicutes is Mycoplasma.

Order

Family

  • Victivallaceae (under Lentisphaerae) was 20.17x the average where as most CFS patients have zero

Genus

  • Victivallis (under Lentisphaerae) was 20.32x the average where as most CFS patients have none

Bottom Line

There was two major surprises in this uBiome — beyond seeing the usual CFS pattern:

  • Overgrowth of the class that contains mycoplasma – Mollicutes 
  • Overgrowth of the phylum that contains lyme bacteria – Spirochaetia

I do not know if one or the other have been tested for. The prescription antibiotics for both of these classes also overlap the generic CFS antibiotics and would likely reduce the overgrowth. My own preference (for myself), would be [with regular rotation]:

  • Tetracyclines: for example:
    • Doxycycline
    • Chlortetracycline.
    • Clomocycline.
    • Demeclocycline.
    • Lymecycline.
    • Meclocycline.
    • Metacycline.
    • Minocycline.
  • Macrolides:
    • azithromycin (brand name Zithromax),
    • clarithromycin (brand names Klacid and Klacid LA),
    • erythromycin (brand names Erymax, Erythrocin, Erythroped and Erythroped A),
    • spiramycin (no brand), and.
    • telithromycin (brand name Ketek).

Normally, lyme and mycoplasma are done by blood tests. If their “first cousins” and thriving in your gut, then the metabolites that they produce may be similar to those produce by lyme and mycoplasma — producing similar symptoms.

The lab results concluded “mild neutropenia” – WebMD cites for this condition

  • “Antibiotics for bacterial infections, if the underlying cause is an infection”
    • There appears evidence from the uBiome that there are atypical gut infections.

Again, this is not medical advise — just inferences from the data and the model that I am using. These inferences should be discussed with your knowledgeable medical professionals.

I will add to my backlog posts looking for herbs/spices etc that have been demonstrated effective for these two abnormalities.

 

Unknown's avatar lassesen 4:21 am on August 15, 2017  

Ubiome result after recent Ross River Virus

A reader was very kind to share with me their uBiome results. Ross River Virus is an infection (one of many) associated with the subsequent development of CFS. In March 2017, the reader was positive for Ross River Virus (6 months after symptoms started). We have someone in possible early CFS (less than 1 year from onset).

Does the ubiome fit the CFS Pattern?

rr1

  • Low Bifidobacterium – Check
  • Low Lactobacillus – Check
  • Akkermansia is very high: 8.27x.
    • This is the bacteria that reduces inflammation. This may be a response to this being a recent infection/onset (the very low level seen later in most CFS patients, could be a result of ‘exhaustion’, i.e. the metabolites that this bacteria needs were badly depleted).
    • One earlier result had higher values
  • Firmicutes/Bacteroidetes ratio: 0.45 (both high and low ratios are seen)
    • Bacteroidetes: 1.33x
    • Firmicutes: 0.6x

Looking at some prior uBiomes from prior posts:  B and F uBiomes are vary similar with shared spikes in the same groups (not seen with other CFS uBiome results):

  • High Genus: Odoribacter, Parabacteroides, Sarcina, Intestinibacter, Allermansia
  • High Family: Peptostreptococcaceae, Porphyromonadaceae, Clostridiaceae 

New (not seen in others)

  • Class: Opitutae, Order: Puniceicoccalea, Genus: Butyricicoccus,

From Lab Reports

  • “Most essential and other elements are very low, suspected malabsorption issue. About half are below 16th percentile: calcium, magnesium, sodium, copper, manganese, lithium, phosphorus, strontium, cobalt, iron, zirconium.”
  • “Main symptom is fatigue. I can work on my computer from home 4 hours a day, … can walk comfortably in total in and around home about 1-1.5km in steps a day, 2km feels like a marathon. Wish I could sleep more, feel terrible in the mornings. Lately I’ve been feeling nauseous on and off. I need to rest regularly throughout the day. No pain thankfully, occasional headaches.”

Items to Discuss with Your Professional(s)

The nausea(and IBS) aspect is where I would start, and in that direction, I would suggest taking herbs and probiotics documented to work in this area. The goal is to adjust the gut while the dysbiosis is still fresh (and less stable). My short list would be:

  • Probiotics:
  • Herbs and Spices
  • Magnesium Malate
  • Consider Folinic Acid (the bioactive form of Folate), it may be more effective in the face of mal-absorption.

Bottom Line

You appear to match the uBiome of a subset of CFS patients. I recall from studies that lab tests for CFS start changing about 2 years after onset (the likely cause is cumulative mal-absorption). Given that it appears to be less than a year since you developed symptoms, there is a reasonable chance (likely 20-40%) that you may go into spontaneous remission over the next year. I believe that the above items will increase your odds.

If you can get Vitamin 1,25D measured, it will likely be very high (and should drop as you move towards remission). This is from my own personal experience and just 1 or 2 studies hinting at this.

 

 

Unknown's avatar lassesen 3:44 pm on August 12, 2017  

Gluten sensitivity and the microbiome

There is evidence suggesting that both lactose and gluten sensitivity may be the result of shifts in the microbiome. In this post I will explore gluten intolerance.

  • “The Mayo Clinic reports that intestinal problems such as lactose intolerance  may be present long after the parasites are gone.”[src]

Pub Med Studies

  • A commensal Bifidobacterium longum strain improves gluten-related immunopathology in mice through expression of a serine protease inhibitor [2017].
  • “114 bacterial strains belonging to 32 species were isolated; 85 strains were able to grow in a medium containing gluten as the sole nitrogen source, 31 strains showed extracellular proteolytic activity against gluten protein and 27 strains showed peptidolytic activity towards the 33 mer peptide, an immunogenic peptide for celiac disease patients. ” [2017]
  • Significantly higher faecal counts of the yeasts candida and saccharomyces identified in people with coeliac disease [2017].
    • “Candida sp. was detected in 33% of the CoeD group compared 0% of the control group (p = 0.000) and Saccharomyces sp. was detected in 33% of the CoeD group compared to 10% of the control group (p = 0.026).”
  • Dysbiosis a risk factor for celiac disease. [2017]
  • Changes in duodenal tissue-associated microbiota following hookworm infection and consecutivegluten challenges in humans with coeliac disease [2016].
    • ” Bacteroidia and Flavobacteriia (class) and Bacteroidales and Flavobacteriales (order) displayed a trend towards increased abundance in Trial subjects “
    • “Together, these data suggest that helminth infections and gluten exposure can significantly alter the composition of the tissue-resident and faecal microbiota, which has implications for the purported therapeutic efficacy of helminths in inflammatory disease.”
  • Effect of Bifidobacterium breve on the Intestinal Microbiota of Coeliac Children on a Gluten Free Diet: A Pilot Study. [2016]
    • ” The comparison between CD subjects and Control group revealed an alteration in the intestinal microbial composition of coeliacs mainly characterized by a reduction of the Firmicutes/Bacteroidetes ratio, of Actinobacteria and Euryarchaeota. Regarding the effects of the probiotic, an increase of Actinobacteria was found as well as a re-establishment of the physiological Firmicutes/Bacteroidetes ratio. Therefore, a three-month administration of B. breve strains helps in restoring the healthy percentage of main microbial components.”
  • “Conclusion. The probiotic formula[5 g of VSL#3 twice daily] when taken orally over the 12-week period did not significantly alter the microbiota measured in this population. ” [2016]
  • The Overlap between Irritable Bowel Syndrome and Non-Celiac Gluten Sensitivity: A Clinical Dilemma [2015].
    • “While the treatment of non-celiac gluten sensitivity is exclusion of gluten from the diet, some, but not all, of the patients with IBS also improve on a gluten-free diet. “
  • Intestinal microbiota modulates gluten-induced immunopathology in humanized mice.[2015]
    • ” Antibiotic treatment, leading to Proteobacteria expansion, further enhanced gluten-induced immunopathology in conventional SPF mice. Protection against gluten-induced immunopathology in clean SPF mice was reversed after supplementation with a member of the Proteobacteria phylum, an enteroadherent Escherichia coli isolated from a CD patient. The intestinal microbiota can both positively and negatively modulate gluten-induced immunopathology in mice. In subjects with moderate genetic susceptibility, intestinal microbiota changes may be a factor that increases CD risk.”
  • Novel players in coeliac disease pathogenesis: role of the gut microbiota [2015].
    • “Several studies point towards alteration in gut microbiota composition and function in coeliac disease, some of which can precede the onset of disease and/or persist when patients are on a gluten-free diet. Evidence also exists that the gut microbiota might promote or reduce coeliac-disease-associated immunopathology. “
  • “Approximately 30% of the general population carry the HLA-DQ2/8 coeliac disease susceptibility genes; however, only 2–5% of these individuals will go on to develop coeliac disease, suggesting that additional environmental factors contribute to disease development.[2010]  “
  • “Specifically, changes in the abundance of Firmicutes and Proteobacteria have been detected in children and adults with active coeliac disease.42,43 Other studies have reported decreases in the proportion of protective, anti-inflammatory bacteria such as Bifidobacterium, and increases in the proportion of Gram-negative bacteria such as Bacteroides and E. coli, in patients with active coeliac disease.44–46 Increases in the number of Staphylococcus44,46 and Clostridium,44,47 and decreases in Lactobacillus spp.46,48,49 have also been reported in children with coeliac disease.” [2015]
  • EFFECTS OF PROBIOTIC INTAKE ON INTESTINAL BIFIDOBACTERIA OF CELIAC PATIENTS[2017].
    • “Faecal bifidobacteria concentration before probiotic consumption was significantly higher in healthy individuals (2.3×108±6.3×107 CFU/g) when compared to celiac patients (1.0×107±1.7×107 CFU/g). “
    • “The probiotic supplementation significantly increased the number of bifidobacteria in the feces of celiac patients, although it was not sufficient to reach the concentration found in healthy individuals prior to its consumption.”

Bottom Line

The DNA risk of gluten sensitivity may exist in 30% of the population, however developing gluten sensitivity may be an epigentic event triggered by a shift in bacteria in the microbiome.

You have not become gluten/lactose sensitive — your microbiome has become gluten/lactose sensitive.

Correction of the microbiome shift appears likely to reverse the gluten sensitivity even with a DNA risk factor. We see studies suggesting that some bifidobacteria have a positive effect. Lactobacillus containing VSL#3 does not appear to be effective.  We do not know which families or strains are the problem (too high or too low is unclear).

The Dilemma: Going on a Gluten free diet does alter the microbiome. Does this change make it easier or harder to return to a healthy microbiome? Yes, it helps with symptom relief … but…

  • “A number of taxon-specific differences were seen during the gluten-free diet: the most striking shift was seen for the family Veillonellaceae (class Clostridia), which was significantly reduced during the intervention (p = 2.81 × 10(-05)). Seven other taxa also showed significant changes; the majority of them are known to play a role in starch metabolism. We saw stronger differences in pathway activities: 21 predicted pathway activity scores showed significant association to the change in diet. ” [2016]