Chapter 5 ● ME|CFS New Scratches

Never go to a doctor whose office plants have died.

– Erma Bombeck

An impressive amount of information on?fibromyalgia, FMS, ME or?myalgic encephalomyelitis, CFS or?chronic fatigue syndrome, ME|CFS,?gulf war illness,?and several related diseases flood cyberspace and the medical literature. This data tsunami refers to a mysterious, often terrible disease, appearing scattered in the mid-19th century, initially affecting just a few but continually growing. It is a neuromuscular and immunoendocrine affection associated with fatigue, pain, dizziness, depression, and cognitive impairment; hence ME seems to be a more appropriate disease designation than CFS, but ME|CFS consolidates worldwide as the nosological preference.

In the early 20th century, already more expressive, the disease emerged as outbreaks among nurses and physicians, in hospitals and other healthcare and nursing facilities in the United States, the United Kingdom, and a few other countries. Followed then by the affection of other people living similar lifestyles or relatively confined, like the military, professional athletes, or people in certain institutions, including schools, industries, and even convents. Its epidemic power blossomed throughout the 20th century, while sporadic ME|CFS cases show geometric growth.

Then, somehow, disease focuses on a new target – the wealthy middle-aged women – and millions become affected throughout the industrialized nations. The condition evolves under an umbrella encompassing similar and related syndromes, victimizing other human groups. These illnesses exploded endemically almost worldwide in the late 20th century and booms in the nineties mingled with the astonishing Gulf War Illness phenomenon, a weird epidemic affecting around 160 thousand previously healthy soldiers, most American and British, males and females.

In the early 21st century, the ailment victimizes children, adults, and the elderly, of both genders, throughout the world's most developed regions: a new disease is set up over humankind. Just recently, it mingled with and increased its numbers during the COVID-19 pandemic and seems to participate in a previously unknown condition named long covid. Earlier I mentioned its possible involvement in other widespread human diseases.

Here we review and correlate enough historical, clinical, and scientific data to track disease origins; and show how it is generated, nested, and sustained on its expanding path.

The knowledge for this rationale traveled a problematic trail through 150 years, facing diverging tracks, narrow alleys, storms, obstacles, quicksand, and dead-ends. Now adversaries and ambushes are expected, as it destroys dogmas, contests scholars, imposes therapy changes, and interruption of some clinical trials. Innovation is disruptive.

The insight in solving the puzzle, partially at least, was not a gift but rather a dug concept, developed through careful clinical research and observations, aided by the bright minds of some extraordinary colleagues and friends. Some facts leading to our insight were whimsical; sprinkled through this work and its LinkedIn page, they make its reading more enjoyable.

Essential for the assembly of this theory was:

1. The unveiling of one possible ME|CFS pathophysiological pathway, after Marian Dix Lemle and her proposed concept, developed by De Meirleir et al., related to dysbiosis, overproduction of hydrogen sulfide [H2S] in the bowel, its absorption and reaction with metals in the body, in times of endemic metal poisoning;
2. The development of the Neurotoxic Metabolite? urine test and its behavior in our clinical studies;
3. Disease epidemiology, ecology, and economy;
4. New emerging scientific concepts; and
5. The reports of spontaneous cures.

Main cornerstones: 6) medical intervention can cure ME|CFS or place it in clinical remission if therapy is targeted to correct the main etiogenic factor and mitigate damage; 7) prevention is feasible through environmental adjustments and other measures.

This theory is validated by the fading of symptoms and reduction of the intestinal lesion as shown by a decrease in fecal calprotectin and the normalization of the Neurotoxic Metabolite? tests (NM) after treatment in previously suffering patients with Neurotoxic Metabolite? abnormal tests. This later achievement points to the possibility of effective ME|CFS prevention through medical intervention, new public health policies, guidelines, and programs. And very important, by the prospect of detecting and eliminating the very first clinical manifestations.

On a small control cohort of eligible patients in clinical remission, abnormal NM tests and syndromes returned upon therapy discontinuation.

It is important that although no patient exhibited significant clinical improvements while keeping high calprotectin and a REAGENT NM test, a few patients did not show consistent improvements when becoming NM test NEGATIVE; a piece of evidence that other pathogenic mechanisms operate in ME|CFS, probably related to the main etiogenic factor. Besides, increased calprotectin may exist in Neurotoxic Metabolite? NEGATIVE patients without ME|CFS-related symptoms. Also, unexplained recurrent infections in otherwise asymptomatic NM REAGENT ME|CFS patients suggest that immune dysfunction can precede and last longer than all other disease manifestations. Statistical data analysis shows ME|CFS and related syndromes are due to a unique environmental issue grassing on Earth mothership – demanding further research, better treatment, and logical preventive measures. Overall, my conclusions fit the available information about ME|CFS and explain its most known related facts.?

Chapter 6 >>