Hello, a few months ago I saw a comment at the ME-Research Forum in which a sick commented that a doctor in Spain is prescribing hidroaltesona to the sick as palliative treatment for the ME.
I have tried to investigate about it since I have been taking 10 mg of hidroaltesona daily for a year having improved my intestinal problems (swelling and diarrhea, about 6 times a day in the last 15 years) passing to a Normal frequency.
My doctor put me the treatment for hipocortisolismo but the intestinal improvement was immediate.
Do you know studies or testimonies of people who have maintained this long-term treatment? 

From a reader

Hidroaltesona [C21H29Na2O8P] is related to Cortisol [
] (chemically different) containing two sodium atoms. Searching PubMed did not find any studies — I have never seen this happen before! I checked Hydrocortisone [C21H30O5] and found studies but the absence of sodium and phosphate atoms left me with a feeling that it was only vaguely similar.

Image result for hidroaltesona
Available only in Spain

From Manufacturer Site

All indications of oral corticotherapy, except in states that involve life-threatening and require intravenous route. The most important ones are:

  • Replacement therapy in primary or secondary adrenocortical insufficiency.
  • Congenital adrenal hyperplasia.

Other indications are:

  • Rheumatic and collagen diseases: treatment of exacerbations and / or maintenance therapy of rheumatoid arthritis, juvenile arthritis, ankylosing spondylitis and psoriatic arthritis when conservative treatments have been shown ineffective; Polymyalgia rheumatica; acute rheumatic fever; systemic lupus erythematosus; severe dermatomyositis; noia periarteritis; cranial arteritis and Wegener’s granulomatosis; scleroderma and dermatomyositis.
  • Dermatological diseases: allergic eczema, bullous pemphigoid pemphigus, generalized exfoliative dermatitis, severe erythema multiforme, erythema nodosum and severe psoriasis.
  • Serious allergic diseases: allergic rhinitis, contact dermatitis and bronchial asthma refractory to conventional therapy.
  • Lung diseases: sarcoidosis with pulmonary disease, extrinsic allergic alveolitis (organic dust pneumoconiosis), desquamative interstitial pneumonia (idiopathic pulmonary fibrosis).
  • Eye pathology: keratitis, choroiditis, chorioretinitis, iritis and iridocyclitis.
  • Hematological diseases: idiopathic thrombocytopenia, hemolytic anemias and palliative treatment of leukemia and lymphomas.
  • Gastrointestinal and hepatic pathology: ulcerative colitis, Crohn’s disease and hepatitis.

More Information

I found some experience from MDs with it at https://www.doctoralia.es/medicamentos/hidroaltesona/preguntas

That may be the best source to get solid information.

  • “long-term corticosteroid treatments, and depending on the dose, can induce changes and side effects in practically the entire economy of the organism, affecting almost any “
  • What is the relationship between hydroaltesona and prednisone? Both active ingredients are corticosteroids, with different potency and are used in many processes and diseases. “
  • ” In principle, in adrenal insufficiency, the doses range between 25 and 40 mg per day. ” – so this patient is on a low dosage.

PubMed on Hydrocortisone and ME/CFS

  • ” Cortisol levels, before or after dex, did not differ between CFS and Healthy Controls (HCs). Cortisol levels were more variable in CFS than HCs. ” [2018]
  • ” we found an inverse relationship between cortisol reactivity and symptom severity. There was no relationship between cortisol reactivity and illness duration. ” [2016]
  • Low-dose Hydrocortisone in Chronic Fatigue Syndrome: A Randomised Crossover Trial [1999] ” Interpretation: In some patients with chronic fatigue syndrome, low-dose hydrocortisone reduces fatigue levels in the short term. Treatment for a longer time and follow-up studies are needed to find out whether this effect could be clinically useful. “
  • ” The anti-inflammatory effect of cortisone at an adequate dose has, to my knowledge, not been investigated so far. I am left with the impression that the potential effect of cortisone on myalgic encephalopathy / chronic fatigue syndrome has been rejected on the basis of three studies that have investigated only low-dose hydrocortisone therapy of an hypocortisolism presumed and which are believed to have too little potency to conclude. with something. ” [2016]

Bottom Line

This drug is prescribed for ulcerative colitis, Crohn’s disease and is known to impact the entire body. We know that it inhibits many bacteria (list here).

Checking predictions on this page, it is predictive to help ME/CFS without IBS, but worsen ME/CFS with IBS and basic CFS. On the flip side, it is predictive to help IBS. The predictions are based on a naive estimate of it’s impact on the many reported shifts with these conditions.

Are the custom probiotics from your 16s Provider right?

I have often been asked that question. The general answer is “it depends”. This post gives you a science based answer.

Enter the probiotic Mixture

Once you are logged in, a new item appears on the menus as shown below

On the next screen enter a name (including the provider), for example

Or do Thryve/ L. Reu,Rha, being an abbreviated list

Now go back and get your suggestions.. What you just entered will be shown,

Their recommendations is a NEGATIVE in the mixed results, In the Humble Opinion of the Artificial Intelligence behind this page, a poor choice.

Bottom Line

A simple process. If you have your thryve (or other providers) custom probiotic mixtures handy, run them thru add add the results as a comment on this page.

Antibiotic Treatment of ME/CFS

A reader asked me to compile a list of of published studies and articles on the use of antibiotics with ME/CFS. Note that with gut dysbiosis as the model, the choice of antibiotics may depend on the details of the dysbiosis (this a 16s or shotgun GI report is suggested. Xenogene.es offers excellent reports).

At the Whittemore Peterson Institute (WPI) is a non-profit medical research institute dedicated to the support of those with a spectrum of neuro-immune diseases (NIDs) including: myalgic encephalomyelitis, (ME), fibromyalgia, and similar complex chronic diseases of the immune system and the brain. Dr. De Meirleir earned his medical degree from the Vrije Universiteit Brussel in 1977, and completed an internal medicine residency in the Department of Internal Medicine, University Hospital of Vrije Universiteit Brussel. His current research focuses on a subgroup of ME patients who show evidence of chronic bacterial infection and gut dysbiosis. These patients are responding to specific antibiotic/ probiotic therapy.


A treatment plan (Cecile Jadin’s is similar)

Treatment with antibiotics is difficult because drugs have to penetrate the host cell wall as well as the intracellular organisms. Treatment needs to be prolonged and pulsed, because of continual replication of the intracellular forms. Until adequate diagnostic facilities are readily available treatment needs to be in two stages: the first stage, which is diagnostic, involves the use of two long-term bacteriostatic antibiotics for 6 weeks, and the second, meant to be curative, involves the introduction of a third bactericidal antibiotic.

One possible choice of antibiotics for the first stage is a combination of Doxycycline and Azithromycin. Initially, the Doxycyline needs to be given alone in low dosage for two weeks, because of the risk of a Herxheimer reaction resulting from the release of toxins by damaged bacteria. Such reactions are usually mild and short-lived. If stable after two weeks, Azithromycin in low dosage is added for 4 weeks. Roxithromycin can be used in place of Azithromycin. . Improvement of symptoms, or the occurrence of a Herxheimer reaction, confirms the diagnosis.

Chronic fatigue syndrome or myalgic encephalomyelitis (2007) in British Medical Journal

From Published Books

Chronic Fatigue Syndrome: A Treatment Guide, Second Edition
By Erica Verrillo 2002
In this summary by two of the leading researchers

Bottom Line

There is a high success rate reported with antibiotics. Recent research suggests that the failures may be selection of inappropriate antibiotics for the person’s specific gut dysbiosis. IMHO, a 16s or shotgun (Xenogene) microbiome report should be done and carefully analyzed prior to selecting the various antibiotics needed.

The microbiomePrescription site supports evaluation of antibiotics against a microbiome, as well as other prescription drugs.

Unfortunately, there has been only one comprehensive study done, so relative ranking may not apply for many samples (i.e. do a show all and scan for the ones that are most acceptable)

With hand-picking against ME/CFS profiles, results can get quite good. All of the antibiotics involved with prior successful treatment were listed.

So which theory of ME/CFS?

A reader wrote me asking about the different theories of ME/CFS, and I just read Cort’s The Best, the Most, the Strangest and the Worst of 2019 in ME/CFS and Fibromyalgia. I have used different models over the years (going with the best available usually). Often it seems that both patients and researchers are lost in the forest strictly following a compass bearing and crossing over paths (and ignoring) that may lead them out of the forest.

My academic training is modelling. A model is a hypothesis with some extra criteria:

  • Must be predictive
  • Must be testable
  • Must explain existing observations
  • Should be as simple as possible

A good model is one that explains more observations than other models. A good model is one that is easy to test. A good model predicts possible findings (which if the findings comes in correct, confirms the model).

The most challenging set of observations

The following is known to every ME/CFS patient and treating physician: The huge variation of symptoms. For a list of non-lab symptoms, see MEpedia Page, CDC Page, Review of the Evidence on Other ME/CFS Symptoms and Manifestations, and Review of the Evidence on Major ME/CFS Symptoms and Manifestations.

We know that DNA/SNP plays a role – for example, ME/CFS people have smaller hearts, craniocervical instability and certain DNA mutations are more common. These are not causes (people with the same items do not have ME/CFS) but contributing factors that makes people more disposes to developing ME/CFS. Think of the “Perfect Storm”, you have a sea worthy boat — unfortunately you motor died in the middle of gale when you were close to a reef…. a series of unfortunate events.

My criteria for a hypothesis that has merit to investigate or fund — it must give an explanation for the different symptoms! A common response is there are different subsets and we need to identify each subset first, or ‘we have not had time to investigate that yet’ (and likely will never) or even a truthful, “I don’t know” or perhaps a dismissive “that’s not relevant”.

The Microbiome Model explains Symptoms

A rhetoric question — if all of your ME/CFS symptoms disappear do you have ME/CFS. At one time remission was defined as no longer having the minimum number of symptoms required for the CDC definition.

About a seven months ago, I tossed up an analysis page on symptoms to bacteria expecting weak results. I was shocked, Eureka! Specific bacteria are associated with specific conditions and symptoms. Since then the database have grown and the number of people entering symptoms have increased.

Alcohol Intolerance

This occurs in a very high percentage of M/E CFS patients. Our analysis found that there were specific microbiome shifts (high levels of certain bacteria)


Neurological: Difficulty reading

We find similar patterns, and can drill down to higher resolution (because of more data) and see a strong clustering with people with the highest 15% of some bacteria.


Neurocognitive: Difficulty paying attention for a long period of time

As we walk thru them, we notice overlaps of some bacteria. Look at what is below and alcohol intolerance above. We see the following in common

  • Butyricimonas (genus)
  • Deltaproteobacteria (class)
  • Desulfovibrionales (order)

These are the main players for some ME/CFS, the other bacteria likely cooperate with them to produce specific symptoms (which often have a DNA requirement to appear).


I should point out that a P-value of 0.05 or below is often the criteria for getting a finding published in a medical journal. Some of the values we came up with are 0.000194 and lower. Much much stronger evidence than is usually seen.


The criteria are below:

  • Must be predictive
  • Must be testable
  • Must explain existing observations
  • Should be as simple as possible

The microbiome model beats everything else (please add detail comments if you disagree of which model is better using these criteria).

This model is predictive, it can take a microbiome sample in and based on the content alone predict probable symptom (key word is probable) which from my own experience and other user feedback seems around 75% accurate.

This mode is testable, from a microbiome sample we can determine a list of items that would probably help. Some people have had outstanding results. Again, the key word is probable.

This model explain existing observations, the observations we used above in symptoms. Recent research studies also find that it explains many lab results seen with ME/CFS.

This model is simple to understand. It is a beast to work with because of the number of bacteria involved.

The last issues for me are treatment-actionable and available. Most of the research hypothesis do not have treatments to address the cause. A few that do are usually not available — often because it is a research protocol and not “standard of medical care” .. i.e. no one can use, especially the ordinary family physician sitting in a community clinic in the Australian Outback!

The microbiome can be manipulated without prescription drugs which removes the stumbling block of “standard of medical care”. It can even be done under quasi-medical supervision if a patient uses available tools and present the suggestions to their physician for review. Getting physicians up to speed on the microbiome is a different issue.

If you believe a different model is better — then please provide the details in the comments. I am open to changing models.

An ideal FMT Donor scenario for ME/CFS

A reader pointed me to this blog, our2ndbrain.com. He did a DYI FMT transplant using a donation from his daughter [post] and obtained remission.

” For many of you visiting this site, you may have wondered why I picked my daughter as the donor for Fecal Microbiota Transplant.   “


I say kudos because this is a very ideal choice of donor! (on the matter of DYI Fmt, I choose, for legal reasons, to keep mute). The whys are simple:

  • As close to the same DNA as possible (50%)
  • Same diet (which means that the bacteria mix has already been tuned to the diet)
  • A son could technically be better (since gender is a factor for the microbiome)
  • Same longitude (which is a factor)
  • Younger microbiome — which usually means stronger and more robust. The microbiome “has not slipped into old age”

Bottom Line

I am not advocating people to volunteer to change diapers of their kids and grandkids to get material for DYI FMT. I am advocating, if you have kids (if you do not have kids, if a sibling has children those are better candidates than a random person IMHO), and have a MD willing to go down the FMT path, to advocate for those people as donors, instead of doing the DYI approach on this site.

The following paper gives some background on FMT. There is still disagreement whether family members give better results ( I suspect those studies were done on siblings and not descendents).