Author Archives: lassesen

Unknown's avatar lassesen 2:34 pm on July 13, 2013  

Lactobacillus Reuteri and recommendations on how to take it

Update: 2018 Summary on L Reuteri.

Lactobacillus Reuteri is near the top of my list of probiotics. The reason is simple, in almost all mammals it is the species that is usually most seen in healthy individuals. Often studies reported something like 55% of the Lactobacillus species are Reuteri. It is NOT in most probiotics. L.Reuteri is by far the Lactobacillus that is most likely to persist in the gut, most Lactobacillus are literally flow-thru, they have an impact, (in fact, one antibiotic (not used much today) is extracted from Lactobacillus Acidopholus), but do not establish a colony. It produces reuterin and cobalamin (B12), which no other Lactobacillus does.

My own practice is to buy as many different strains of L.Reuteri that I can find. For maintenance, I do a week of it every 2-3 months. It should be taken before meals and with some fat, see this post for details.

For a more technical description of L.Reuteri, see

Glutathione

Glutathione is one of L.Reuteri essential foods (http://www.ncbi.nlm.nih.gov/pubmed/21585317 ) so make sure that you supplement with it (I would suggest taking that 1 hr before the L.Reuteri) . This feeding of L. Reuteri may be one reason that it has positive effects on CFS patients (although the why of taking it comes from a different model).

The reason that some people may be non-responders to Gluthathione could be as simple as having no L.Reuteri left to feed!

Bottom line:  L Reuteri and Glutathione should be taken together – taking one without the other may result in little or no effect.

Unknown's avatar lassesen 2:00 pm on July 12, 2013  

Finally! Someone verified the 1999 Studies – Thank you Kenny!

I have been running my Microbiome Hypothesis after a study from 1999 which no one had attempted to replicate for 14 years. Finally in the Anaerobe journal on 18 June 2013, High-throughput 16S rRNA gene sequencing reveals alterations of intestinal microbiota in myalgic encephalomyelitis/chronic fatigue syndrome patients confirms that there is a distinct alteration!

Many thanks to

 

Available online 18 June 2013

In Press, Corrected Proof — Note to users

Cover image
Clinical microbiology

High-throughput 16S rRNA gene sequencing reveals alterations of intestinal microbiota in myalgic encephalomyelitis/chronic fatigue syndrome patients ☆

Open Access Article
  • a R.E.D Laboratories NV, Z-1 Researchpark 100, 1731 Zellik, Belgium
  • b Biostatistics and Medical Informatics Department, Vrije Universiteit Brussel, Laarbeeklaan 103, 1090 Brussels, Belgium
  • c DNAVision SA, Av. Georges Lemaitre 25, 6041 Gosselies, Belgium
  • d Department of Human Physiology, Vrije Universiteit Brussel, Pleinlaan 2, 1051 Brussels, Belgium

Highlights

•

We looked for alterations of gut microbiota in chronic fatigue syndrome patients.

•

Patients and controls from two geographical origins were included in the study.

•

Gut flora composition differed between people from different geographical origins.

•

Significant alterations of gut microbiota composition were observed in patients.

 

Abstract

Human intestinal microbiota plays an important role in the maintenance of host health by providing energy, nutrients, and immunological protection. Intestinal dysfunction is a frequent complaint in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) patients, and previous reports suggest that dysbiosis, i.e. the overgrowth of abnormal populations of bacteria in the gut, is linked to the pathogenesis of the disease.

We used high-throughput 16S rRNA gene sequencing to investigate the presence of specific alterations in the gut microbiota of ME/CFS patients from Belgium and Norway. 43 ME/CFS patients and 36 healthy controls were included in the study. Bacterial DNA was extracted from stool samples, PCR amplification was performed on 16S rRNA gene regions, and PCR amplicons were sequenced using Roche FLX 454 sequencer.

The composition of the gut microbiota was found to differ between Belgian controls and Norwegian controls: Norwegians showed higher percentages of specific Firmicutes populations (Roseburia, Holdemania) and lower proportions of most Bacteroidetes genera. A highly significant separation could be achieved between Norwegian controls and Norwegian patients: patients presented increased proportions of Lactonifactor andAlistipes, as well as a decrease in several Firmicutes populations. In Belgian subjects the patient/control separation was less pronounced, however some abnormalities observed in Norwegian patients were also found in Belgian patients.

These results show that intestinal microbiota is altered in ME/CFS. High-throughput sequencing is a useful tool to diagnose dysbiosis in patients and could help designing treatments based on gut microbiota modulation (antibiotics, pre and probiotics supplementation).

<Nag>I hate to say it, but I am already attempting by this blog and cortjohnson.org blog trying to do just that based on my own experience of going into remission by doing exactly that!</Nag>

The methods need to be improved, bigger sample populations and using tests that identify the specific strains — but it is a start!

We have a Ken and a Kenny on the same page!

 

 

 

 

Unknown's avatar lassesen 3:22 am on July 12, 2013  

How vaccines can cause Chronic Fatigue Syndrome – a Model

I saw this in the news today:
The vaccine known as hepatitis B has been ruled by a United States Court of Federal Claims that “a dose of the hepatitis B vaccination caused [a patient] to develop chronic fatigue syndrome.”  Article

This type of claim has been asserted many times and view skeptically by many (including me, once upon a time).

How do vaccine work? Usually they provoke a minor version of the disease or a close relative (for example, one of the first vaccines used cow-pox to protect from smallpox).  This is now it happens… whether you have a mild form or a severe form, the infection causes some alteration of the microbiota. If the microbiota returns to its prior state, there is no problems. If the microbiota does not return but stays in it’s altered state then we slide into Chronic Fatigue Syndrome.  It is that simple!!!

Should you avoid vaccines? In general, vaccines are good for the general population and result in a significant benefit from having less deaths and illnesses. I went to school and later taught with someone that had Polio as a child and apparently recovered fully. She later was confined to a wheelchair (a too common occurrence with those that recovered from polio as a child).  Would I tell anyone not to get a Polio shot?  Absolutely not, unless there is autoimmune in the person’s  blood relatives. If there are, then I would say avoid it — the risks are significantly higher for problems.

This is the conclusion of a 2005 study:
In genetically susceptible individuals or together with some other triggers such combination might confer the risk of developing a continuous autoimmune response in an individual. Anti-phospholipid antibodies following vaccination with recombinant hepatitis B vaccine.

NOTE:  a variation of anti-phospholipid syndrome (Hughes Syndrome) is what Dave Berg (Hemex) described the coagulation issues he saw in CFS patients.

One recent study is interesting:

Transiently or persistently increased levels of autoantibodies or appearance of new autoantibodies was demonstrated in up to 15% of apparently healthy adults after the influenza vaccination. http://www.ncbi.nlm.nih.gov/pubmed/18700173

Microbiota tend to be inherited in families, thus the presence of autoimmune in blood relatives implies (but does not prove) a greater risk of the microbiota not returning to normal.

So, do I believe that vaccine can cause CFS — yes, because there is both a model to explain how and published studies describing the the appropriate changes do occur.

Unknown's avatar lassesen 4:23 pm on July 10, 2013  

Un resumen de mis experiencias y modelo de ME / CFS

“He estado en el mundo ME / CFS por unos 20 años”. Los síntomas cada vez fueron diferentes, pero con algunas coincidencias. Las pruebas de laboratorio y la exploración cerebral confirmaron que cada vez que se trataba de EM / SFC.

Mi formación: soy un científico con un gran énfasis en modelar sistemas e interacciones (con varios cursos de nivel de doctorado completados). Comencé con la creencia popular del día, hace unos 20 años, y encontré tratamientos que funcionaron para mí (pero el razonamiento de que el tratamiento funcionó fue ligeramente incorrecto, en mi humilde opinión). Esos eran el Protocolo de Hemex y el Protocolo de Jadin.

Los mismos tratamientos no funcionaron para otros. Soy curioso por naturaleza y probé docenas de modelos para explicar los síntomas y el éxito / fracaso del tratamiento. Estaba en un programa para niños muy talentosos y comencé a leer revistas médicas a los 14. También tengo una maestría en estadística y sé cómo las revistas pueden hacer un giro de sus resultados. En otras palabras, puedo clasificar el valor actual para el tratamiento de cada estudio.

Hace unos ocho años, tuve que recaer debido al estrés laboral (trabajando para Amazon en Data Science). Al releer toda la literatura / artículos publicados de ME / CFS, me encontré con el estudio de Australia de 1999 que informaba los cambios en el microbioma.

Esto hizo que intentara construir un modelo para que el EM / SFC sea un trastorno microbiológico. Con un modelo, obtienes la capacidad de predecir y, por lo tanto, probar si el modelo parece correcto. Mirando lo que funcionó para mí, vi que lo que hice alteraría mi microbioma. A lo largo de los años, cada vez más estudios confirmaron que el modelo parece ser correcto.

Es una explicación simple, y explica que diferentes personas tengan diferentes síntomas (ya que es probable que los síntomas estén agrupando bacterias específicas). También da cuenta de diferentes reacciones a diferentes cosas. Tiene un alto contenido de bacterias ‘sensibles al gluten’, es sensible al gluten, tiene un alto contenido de bacterias productoras de histamina, tiene problemas de histamina.

Para el brote en el que estoy actualmente, he pasado de estar enfermo durante toda la semana con una lista masiva de síntomas a la planificación para trabajar 6 horas al día la próxima semana con solo unos pocos síntomas restantes. Los síntomas restantes incluyen que mi cutis se vuelva gris si voy más allá de los límites evolutivos (por ejemplo, visitar a un amigo demasiado tiempo en una cafetería). Esto es durante un período de cinco semanas. No tengo antibióticos ni medicamentos recetados: solo obtengo los resultados de mi microbioma y los probióticos (Bacillus Clausii, SymbioFlor-2 principalmente) y muchas nueces (tomar un puñado de Almendras para el desayuno es mi norma actual).

Acabo de sentir en una nueva muestra de microbioma y probablemente tendré que volver a modificar las cosas cuando lleguen los resultados.

Sí, muchas cosas por ahí son correctas. Cosas como los cambios de TH1 / TH2. Como científico, mi formación es clara:

El modelo más simple que explica la mayoría de las observaciones, cuanto más preferido es.
Un modelo debe tener la capacidad de predecir, generar experimentos para probar que se prueben. El éxito repetido en experimentos construye confianza.
Ningún otro modelo viene a explicar los síntomas y las respuestas con ME / CFS. El modelo también proporciona una explicación clara y aceptada para un cambio TH1 / TH2.

Para mí, no diré que otros modelos están equivocados, son posibles. Cuando se trata de la probabilidad de ser correcta, las probabilidades son similares a las de un boleto de lotería.

Unknown's avatar lassesen 5:04 am on July 9, 2013  

Icelandic Disease, Polio and Up-regulation of Immune System.

Recently I saw on Facebook:

“Reading a book about CFS and although I knew there was a big outbreak of CFS in a region of Iceland in the 1940’s (over 1000 cases, mostly high school students), I didn’t know that 7 years later the same region of Iceland had a serious Polio outbreak and for some reason all of those who had gotten CFS were immune to the Polio virus. This led some researchers to believe that there is a virus that causes at least some cases of CFS and it may be closely related to Polio.”

I recall reading this in Osler’s Web: Inside the Labyrinth of the Chronic Fatigue Syndrome Epidemic(1996) back in 2000. I also read of the appearance of the immune system being up-regulated because CFS patient rarely catch other illness. Iceland or Akureyri Disease and polio is described in this study.

The light went on today that the microbiota hypothesis would explain both of these observations perfectly.

If we assume that most infections reprogram the microbiota by sending deceptive chemical signals to produce the chemicals it needs, or to surpress the chemicals it does not want then things become obvious.

If another infection comes along, it’s attempt to reprogram will likely fail. Without the chemicals to supply it’s reproduction the infection fails to get established.

This actually leads to the stable microbiota dysfunction being of evolutionary advantage. Having 2-4% of the population in this state means that if a nasty nasty deadly infection hits a population, this group will survive while all around them the healthy microbiota folks are being reprogrammed to eventually kill the person.