We interviewed Dr. José Sabán, an internist with more than four decades of medical-professional experience, especially dedicated to persistent COVID, in addition to the most advanced anti-aging and cardiometabolism, both in Madrid and on the Costa del Sol.
You have recently been awarded the “Golden Stethoscope for Innovation in Medicine” by the European Association of Industry, Technology and Innovation (AEITI), what does this recognition mean to you?
An enormous satisfaction, and more than for me, for my former team and for my family, friends and patients. I studied Medicine in my native Cordoba, where I received the Extraordinary End of Career Award, the influence of two 12th century geniuses from Cordoba, Averroes and Maimonides, were always latent in my training and with them a spirit open to all kinds of knowledge, so when I went to the Hospital Ramón y Cajal, I did not do a conventional Residency (I did my doctoral thesis during the same), nor was my development as an Internist.
In 1990, when no one in Spain had a Cardiovascular Risk Unit, I had one; and when in 2000 the other hospitals opened theirs, I closed mine to open the Endothelial Unit (the tunic that lines the inside of our vessels), in which everything we did revolved around the functioning of this tissue. There I was (until I retired in April 2020) writing one of the most unique pages of the time in the Medicine of our country, since being the unit, without any doubt, less staffed of all major Spanish hospitals (for lack of institutional support) we were setting the standard for all others. As proof of what I am saying, there is our 2,500-page treatise on endothelial-based Cardiometabolic Medicine, entitled Global Control of Cardiometabolic Risk. The Endothelium as a Preferential Target, Volumes I and II, with forewords by Valentín Fuster. A text which, whenever I consult it, reminds me, due to its length, of Avicenna’s Canon, and Avicenna, whom I followed because he was a great musician (this will be better understood later), as well as a physician and philosopher, was the greatest influence that Averroes and Maimonides had.
When we founded our Unit in 2000, the study of the endothelium was used to prevent infarction, today, after my long experience, I would add two more applications without fear of being wrong: slowing down aging and alleviating many of the symptoms of persistent COVID (Long COVID). So much so that both areas of medicine are the ones in which I work the most, but already in private medicine, in addition to continuing to prevent heart attacks.
What are the latest advances in relation to Long COVID?
The immunological hypothesis of anti-idiotype antibodies, described in the December 2021 New England Journal Medicine, is postulated, at least in my opinion, as the most plausible hypothesis of persistent COVID, since it involves complexes formed by four components: viral protein S (the common nexus of all vaccines in a direct or indirect way), antibodies against said protein (idiotype) and antibodies against said antibodies (anti-idiotype). In addition, all this together with the ACE2 enzyme, the fourth component, which acts as a receptor as it is the only one capable of recognizing the S protein. Being the endothelium the major producer of ACE2 in the organism it is easy to deduce the role played by the endothelium as a “victim” (which explains the dysfunction we detected in the consultation), but best of all is that after being damaged, the endothelium “rebels against everything and everyone” and would act as “executioner” of a majority of tissues of the organism by awakening these complexes, anchored to four bands in its structure, a chronic/latent inflammatory response in this persistent phase of the disease and from it would derive most of the symptoms, since the capillary network reaches all areas of the organism, including the most recondite ones.
This hypothesis, at least for me, would be far superior to the so-called “viral hypothesis” for which there is no publication in any major journal, not only to confirm it, it would suffice to outline it in a minimally coherent way. To make matters worse, although many laboratories are determined to defend it tooth and nail, because their lives depend on it, the largest clinical trial with the use of antivirals, carried out by Patterson & Yogendra, is still underway and, moreover, holds a surprise in terms of the endothelium. This trial associates an antiviral (Maraviroc 300) with a statin (Atorvastatin 20). The latter can only be understood if it is used to protect the endothelium by its “pleiotropic” (anti-inflammatory) effects, a fact that underlines the importance given to the endothelium by these authors, even though they are virologists and not clinicians. It is curious that clinicians, with some exceptions, give hardly any chance to the endothelium in persistent COVID, while virologists do.
How do you approach the treatment of patients with Long COVID?
Very simple as far as its general approach is concerned and at the same time very complex and detailed, because we leave nothing to chance, making a precise and personalized medicine.
The first thing is to know what the patient’s previous health was like, since that is the objective, and if we can then improve it, then even better. The second thing is for the patient to tell us in their own language how they experience their illness. We do not agree with the effort that others show in translating into common symptoms what the patient tells us and even in our opinion it is a mistake, because this disease produces sensations and nuances never seen before, and if we misrepresent what the patient tells us simply because we do not understand it well, we may be tempted to think that he/she is a “functional” patient (translated in popular slang to mean that he/she is losing his/her sanity or is on the nerves), as has happened to many patients in my practice, who hardly anyone believes them, including many doctors and members of their own family. Hopefully the parents, a sibling or a close friend take the initiative and are the ones who bring or encourage them to consult us.
From there we do a thorough physical examination and a personalized analytical assessment depending on their history and the form of presentation of the disease, which is not the same for all patients, although in its most severe form, which is the one that usually comes to us, most of them agree that “they have suddenly aged from 10 to 20 years” or in colloquial terms, taken from one of our stories, “they have lost a lot of years from one day to the next”, logically longing for times not so long ago and for this they resort to expressions such as “with what I was” “I should have seen me” and things like that; a drama, let’s go…
From there we focus on the endothelium. It is not only important to know whether it is damaged or not, but also how much. Unless they are already treated with supplements or drugs that act favorably at the endothelial level, all, absolutely all of them have it affected and some of them much, more than any other disease (personal experience). Even those who are semitreated also have it affected, but not so much. The important thing is to define the starting point and, depending on how it is, we set ourselves some numerical objectives. Once we know where we start from and where we want to go, we choose between different groups of supplements that improve it. At 3, 6 and 9 weeks we make telematic readjustments (not face-to-face) of the doses according to the clinical response and at 3 months we see them face-to-face and repeat the endothelial study. It is as simple as that.
Having the suspicion that endothelial damage could be behind many of the symptoms of persistent COVID, do you know if any studies have been launched at the official level on the relationship of the endothelium and persistent COVID?
This question is a bit uncomfortable for me, because I am no longer part, being retired from Social Security and from my position as Professor of Medi
cine, of what you call “official”. Anyway, I will answer you. In the acute phase, where the role of the endothelium is indisputable, I am only aware of one study in Spain that is being carried out in “critically ill patients” and with a drug never previously used in cardiovascular disease, which was my field of action. Why was this substance chosen over others that had been tested before? – Why was only a critically ill population chosen when the endothelium is involved from the initial stages of the disease, I do not know either. That study remains unpublished. Hopefully, it would be successful and would encourage further studies in other more common scenarios. If this was done in the acute phase, with the accumulation of evidence in favor, how can it be done differently in persistent IVOC where the study of the endothelium is not even contemplated in the clinical practice guidelines. And if its study is not contemplated, it is logical that its treatment is not contemplated either. In our clinical practice we act independently of the guidelines, which we only follow in certain aspects such as physiotherapeutic and socio-labor aspects, which are very good, by the way. Everything else, ignoring the endothelium, is of no interest to us. It can be said louder, but not clearer.
Outside Spain, I know that the Karolinska Institute in Stockholm is conducting studies on endothelium and persistent COVID. I am anxiously awaiting their results.
Do you consider yourself a pioneer in the COVID and endothelium relationship and did this help the recent award you received?
Among his strongest advocates without a doubt, and as for being a pioneer, judge for yourself and your readers. In the article I published with my colleague Dr Ly-Pen in the Journal Nutrition Health & Aging, which came out on-line on May 12 (although we submitted it on April 17), we were already talking about the possible endothelial involvement, because otherwise the disease could not be understood. Of course, no comment was made in the Spanish media about our article, even though it was one of the first articles published by a Spanish group on this subject in a journal of this level. Just on April 17, the day we submitted our article, the first biopsies showing endothelitis, i.e., inflammation of the endothelium at different levels (lung, kidney, small intestine) were published in the Lancet, no less. Around the same time, an Italian group also sent their liver biopsies for publication with identical results, but it took a few months for their publication to be accepted. If we go to the autopsies, they all agree that the most damaged tissue in the organism is the endothelial tissue. The first one published was that of the University of Texas on May 7. Then came that of a German/Swiss/American collaborative group on May 21, a curious study, because here the endothelium (inner tunica) was attacked from the inside (from the lumen) and from the outside (perivascular inflammation).
With these preambles, if when we submitted our article in April we pointed to the endothelium without objective data, based on logic, once its implication was demonstrated I wrote an opinion article on May 24, 2020 in a national newspaper, even anticipating the fantastic article by Petter Libby and Thomas Lüscher, who published it in July in a Lancet.This article should have sentenced this issue forever, but as human beings are very stubborn and hospitals do not have endothelial Units, it was preferred to look the other way and nothing changed.
After a reasonable time had passed, I hoped that they would call us for something serious and seeing that no, taking advantage of a musical interview published on January 24, 2021 about a double CD that I released in October 2021 with the music of the Beatles in Jazz format to help us investigate, I inserted in the course of the interview that phrase “The tuning of the endothelium could be key in the management of Covid-19”, a phrase that I tried to slip in as a wedge, but that the journalist liked it very much and used it as the headline of the interview. Incidentally, I said this phrase 10 months before Professor Maoz’s team at Tel Aviv University published an article on the subject in which not only viral protein S was implicated, but also 3 of the so-called NSPs (nonstructural proteins), all of which have the capacity to damage our endothelium and thus our vascular network. Hence the risk in the acute phase of clots in venous and arterial territories, high risk of myocardial and cerebral infarction, renal failure and especially bilateral pulmonary endothelitis, endothelitis that simulates in imaging techniques (radiography, scanner) a bilateral pneumonia, but which later turns out not to be such, hence its good response to high doses of steroids. Although in my opinion the term endothelitis (inflammation of the endothelium) should always have been used in situations like this, which is what it really is, as an alternative, pneumonitis should have been used in all cases, as is done in vasculitis/connectivopathies (e.g. systemic lupus erythematosus), but the term pneumonia should never have been used except in the first months of the pandemic when there was a great lack of knowledge of the disease.
I don’t know if all this, together with what I told you previously about the persistent COVID, helped the award or not. Mr. President certainly did not stop talking about COVID during the awards ceremony, so I deduce that it had some influence.
After having received in recent years the Dr. Gomez Ulla Awards for Healthcare Excellence 2019, European Award for Technology and Innovation in Anti-Aging Medicine 2021, European Golden Stethoscope Award for Innovation in Medicine 2022, what would be the next one?
My relatives and friends, already joke about it about the golden endothelium. With the influence of Averroes, Maimonides and Avicenna, I’m going for it, but the truth is that I already have my golden endothelium: it’s my patients.