COVID19 is not elderly death sentence. Exercise. Can Clonidine limit COVID-19 cytokines storm?



This is an article for medical practitioners to consider. 

Clinicians are reaching some similar suspicions to what FPMag’s partners observed:

Elderly patients have a good outcome battling COVID-19 disease if their chronic illnesses have been well-managed, plus other observations.

“That sounds like an obvious statement, but unfortunately many patients need to be reminded about the obvious,” notes Dr. Anderson of The RINJ Foundation.

“Older women and the family members they care for when she is the center of the family, can benefit from being reminded that they must take particular care during lock down to maintain their healthy diet, exercise and chronic illness medications,” adds the doctor.


“Dropping their daily exercise during ‘lock-down’ is one dangerously unhealthy mistake of people during their social distancing ‘stay-home/stay-safe’ regime. The benefits of modestly increasing exercise include positive impacts on depression, glucose tolerance, high blood fat like cholesterol, hypertension, joint mobility and flexibility, parkinson’s disease, respiratory conditions such as asthma, and weight management.”


by Micheal John


 

Having a good outcome fighting CIVID19 may depend on good management of Chronic illness

Having a good outcome fighting CIVID19 may depend on good management of chronic illness and other important observations, like the way exercise boosts a healthy immune system better able to prevent serious COVID-19 infection. Photo Credit: Melissa Hemingway. Photo Art/Cropping/Enhancement: Rosa Yamamoto FPMag

People around the world have been learning about the vulnerability of seniors to COVID-19 infection, particularly those who suffer hypertensive heart disease and diabetes.

This article will share clinical observations but is not an intended clinical study of significance but is indeed random observation of real world clinical situations.

Note: Readers who may not be following doctor’s orders need to contact their medical care provider and update their advice. (If this applies, monitor your blood sugar and your blood pressure, if you can, and have this data ready, but nevertheless, contact your practitioner. Why? Because we are all learning that chronic illness management is crucial to good outcomes fighting the coronavirus.)


Warning: Readers are prohibited from using this article as medical advice and should contact their doctor for information about their case.


Seniors who have followed their doctor’s orders fare best with COVID-19.

The best outcomes for seniors encountered by clinicians working in RINJ Foundation nurse-led clinics around the world are being noted as ones where elderly patients have done two important things;

  1. Maintained a steady adherence to their proven chronic illness management of healthy prescribed diet and doctor-prescribed pharmacological therapy; and
  2. Exercised daily at least one hour. Walking is sufficient, but more varied exercise is better.

 

Should humans be looking to do what the bat can do (sometimes): Manage Immune System Overreaction

Bats have learned to manage what some scientists call the *cytokines storm. Bats carry a number of dangerous viruses but seem to manage the viral load by quashing their immune system’s propensity to overreact. Concomitantly, bats have encountered illness caused by fungus (white nose fungus, pseudogymnoascus destructans, as scientists would say) that they cannot manage. Meanwhile, the COVID-19 variant of the bat’s coronavirus loads, humans cannot manage. (* Cite: COVID-19: consider cytokine storm syndromes and immunosuppression)

Bats have been known as repositories of a wide range of viruses, among other things. Two of them are a close match to the SARS-CoV-2 virus which is somewhat evolved since transferring to human mammals.

Scientists believe bats have evolved methods of suppressing viruses, detecting DNS tampering and dampening inflammation in their bodies by not overreacting to DNA tampering by viruses.

In the past  few years, bats, particularly in North America, have been suffering and dying from a parasitic fungus (pseudogymnoascus destructans) which causes their ordinarily restrained immune system to go overboard in much the same way as the human system overreacts to the SARS-CoV-2 attacking the DNA of its cells.

Humans do not die from the COVID-19 disease, they die from the human body’s hyperinflammatory reaction to the SARS2 virus.

This is a vampire bat. The inset is a little brown bat with white nose syndrome

This is the  vampire bat. The inset is a little brown bat with white nose syndrome. Photo Credit: Uwe Schmidt
Photo Art/Cropping/Enhancement: Rosa Yamamoto FPMag

Read id you wish: Global cooperation collapsed, endangering humanity.

It’s worth noting that both mammals are respectively stalked by the microorganisms referenced hence a solution to the hyper reaction is essential for both species to survive the onslaught. Some scientists believe we humans need the bat as a healthcare ally. Our help for the bat, the only flying mammal, would be climate change mitigation and an end to fossil fuel burning.

The cytokine storm has captured the attention of the public and the scientific community alike, and while the general notion of an excessive or uncontrolled release of proinflammatory cytokines is well known, the concept of a cytokine storm and the biological consequences of cytokine overproduction are not clearly defined.” Cite: “Into the Eye of the Cytokine StormJennifer R. Tisoncik, Marcus J. Korth, Cameron P. Simmons, Jeremy Farrar, Thomas R. Martin,and Michael G. Katze

In a 16 March study published in the Lancet the authors point our that “Current management of COVID-19 is supportive, and respiratory failure from acute respiratory distress syndrome (ARDS) is the leading cause of mortality.”

The report goes on to say that, “Secondary haemophagocytic lymphohistiocytosis (sHLH) is an under-recognised, hyperinflammatory syndrome characterised by a fulminant and fatal hypercytokinaemia with multiorgan failure.”

The report concludes that, “All patients with severe COVID-19 should be screened for hyperinflammation using laboratory trends (eg, increasing ferritin, decreasing platelet counts, or erythrocyte sedimentation rate) and the HScore.”

Clinical observations are not proof but an observed effect of a medication used to manage hypertension that is suspected of some positive impact for COVID-19 pts by suppressing hyperinflammation. This is not a solution but an indication of an explorative direction.

This may be why. On a suspicion and as a precautionary step, patients with multiple medications for hypertensive heart disease were given an increased dosage of one particular medication sufficient to maintain a constant blood level of clonidine (used with calcium channel blocker or other medication) with good result.

“Better management of hypertension without adverse impact, is one result, and reduced or even preventing hyperinflammation as compared to patients not using the medication, is suspected but not conclusively proven,” says Michele Francis a nurse practitioner who relies on a medical directive now used by her organization to respond to (1) positively tested COVID-19 elderly patients with comorbid hypertensive heart disease; and (2) emergency hypertension levels with comorbid COFOVID-19.

“The small number of patients under observation is insignificant but clinicians in Venezuela, Syria, Iraq and other countries now apply with good result the same approach with positive tested elderly patients suffering comorbid hypertensive heart disease. These are normally indicated responses to patients presenting with clinical hypertension emergencies and comorbid COVID-19 but the injected or oral route of clonidine boost response is having additional positive benefits not noticed in patents using other pharmacological therapy for their chronic high blood pressure.”

“We immediately assign a chronic care specialist when an elderly patient presents with comorbid chronic illness following a positive COVID-19 test,” she added.


Warning: It’s worth discussing with patients during a full evidence-based (recent vitals)  case evaluation but altering these medications can have an enormous and sometimes mortal coronary event outcome, hence is something patients must not undertake on their own. Follow your doctor’s instructions only, even if you understand this article fully.


An effect of clonidine (Brain Behav Immun. 2007 Jul; 21(5): 569–580.)  is associated with a reduction in pro-inflammatory cytokines, as well as a reduction in local leukocyte numbers and their capacity to produce pro-inflammatory cytokines.

Clonidine is not the only solution but when the patient has an underlying hypertensive heart disease and is already taking Catapres, elevating the dosage to make certain blood levels are constant without peaks and valleys from casual oral routes seem to have a good outcome.

Olumiant (baricitinib) is also under test but is already an approved drug like clonidine. The object is to lower the levels of inflammatories like cytokine proteins. (See Lancet report.)

Coupled with  remdesivir which was developed for Ebola virus without much success but is showing promise with certain dosing and accompanying therapies such as the anti inflammatory  therapy.

Clinicians are reporting 6-day regimens having the best outcomes with IV removal at day 6 and patient release on the 7th day.

The author is in a location where there are limited means and one tries any basic treatment that is available. Eventually there will be a specific, approved, targeted treatment.  This is what has been seen to work. Stop the storm, protect t-cells and s-cells and disallow the virus. There are several anecdotal accounts that have hit the media. 

“This  may explain a perceived benefit to COVID-19 patients who have hypertensive heart disease. The effect of reducing pro-inflammatory cytokines seems only to present after two or three days of therapy, likely owing to the requirement to build up and maintain certain levels,” notes NP Francis.

“Dosing seems to be normal to achieve this effect although it needs to be maintained precisely in order not to cause a fluctuation of blood levels of the medication and its reduction of pro-inflammatory cytokines.”

“Curiously, clonidine antinociceptive effect appears with a 2–3-day delay. Previous observations have shown that α-adrenoceptor activation induces apoptosis in leukocytes, which would reduce leukocyte number. Additionally, macrophage scavenging of apoptotic cells results in a shift to an anti-inflammatory phenotype, with expression of transforming growth factor (TGF)-β1,” — “Clonidine reduces hypersensitivity and alters the balance of pro- and anti-inflammatory leukocytes…

 

Additional Reference:

Clinical predictors of mortality due to COVID-19 based on an analysis of data of 150 patients from Wuhan, China (With Errata).

Intensive Care Med. 2020; ( Ruan Q , Yang K. Wang W , Jiang L, Song J —published online March 3.DOI:10.1007/s00134-020-05991-x