Simon Murray, MD

This month is American Heart Month. I could begin by telling you that heart disease is the leading cause of death for men, women, and people of most racial and ethnic groups in the United States.

One person dies every 36 seconds in the United States from cardiovascular disease. 

About 655,000 Americans die from heart disease each year

I could also tell you the risk factors for coronary artery disease: LDL cholesterol elevation, diabetes, family history of premature heart disease, hypertension, and smoking. But you already know that or haven't given it much attention.

Maybe you did not consider heart disease a possibility at your age or that your family was immune or perhaps you thought getting heart disease was the natural consequence of aging—None of these are true.

When it comes to evaluating risk, humans are relatively poor at predicting probability. You may be more worried about being bitten by a shark (1/ 370,000,00)

, but forget that the lifetime risk of dying from the cardiac disease is just 1-in-4.

Consider this: research from analysis of the Framingham Heart Study demonstrates multiple important points:

The average lifetime risk of developing cardiovascular disease in Americans was around 52% for men and 39% for women.

Lifetime risk jumped to 69% for men and 50% for women who had two or more cardiovascular risk factors by age 50.

Lifetime risk was just 5% among men and 8% among women who had optimal risk factors for cardiovascular disease at age 50. That meant that they lacked risk factors like being overweight, did not smoke and did not have diabetes, high cholesterol, and high blood pressure.

People in the low-risk group tended to live into their nineties, while those in the higher risk groups died decades earlier.

ust 3% of men and 4% of women in the analysis fell into this very low-risk category at age 50! 

But the Risk of Dying from Cardiac Disease is Declining.

We have done better in our "war against cardiac disease." The death rate from heart disease over the past two decades declined by 18.6% and for coronary heart disease we saw the rate decrease by 31.8%.7 Using a combination of surgery, multiple drugs, and other interventions, we have improved our risk, but at what cost?

The amount of money spent on health care last year in the U.S. was 3.6 trillion dollars, much of it for heart disease. (Consider this: If you spent one dollar per second, it would take you over 32,000 years to spend one trillion dollars.)

In 2019, I had the opportunity to speak to Dr. Dean Ornish, a leading proponent of lifestyle changes to treat and reverse cardiac disease, about his book "Undo It."

 I became interested in his work with Bill Clinton, who had been told after having a heart attack in 1993 that he had a genetic predisposition to having heart disease. There was nothing that could help him.

Ornish worked with him and Clinton's cardiac conditions improved, and he remains vigorous and healthy. Nonetheless, I was dubious that lifestyle could help reverse and prevent heart disease. I also knew there here was little financial incentive for physicians to promote prevention over treatment of illness. Lastly, patients in my experience were often resistant towards at following treatment plans that required major changes in lifestyle, (Even if they did work).

Dr. Ornish is the founder and president of the nonprofit Preventive Medicine Research Institute and a medicine professor at the University of California, San Francisco. He is the author of six books, including Dr. Dean Ornish's Program for Reversing Heart Disease; Eat More, Weigh Less; Love & Survival; The Spectrum, and his most recent book, "Undo It." He has created hundreds of centers around the United States to teach people how to change their lives.

He was convinced that high tech medicine had reached its limitations for treating chronic medical conditions like cardiac disease. Ornish commented that, "As doctors we are trained to act quickly when something bad happens. We call in the calvary for quick fixes, to patch things up, but don't consider how the situation might have been avoided." Someone once told me that, "Bad things happen quickly; good things take time."

As Americans, we don't like things that take time to get results. We want quick cures, and it cost 3.6 trillion dollars last year to follow this course. We were able to reduce death from heart disease by 18%, but what happened to the other 72%?

Dr. Ornish cited his 39 years of research with randomized trials documenting that lifestyle changes could not only treat cardiac disease but could prevent and reverse it at very little cost. 

He noted that 80% of the money spent on health care is for chronic diseases that are mostly preventable. 

In his book, he cited four proven lifestyle choices to prevent cardiac disease.

It seemed a bit too simple for me. But as I learned, there are many proponents of lifestyle management of chronic diseases. And it is not a new idea. Herophilus, a Greek physician who practiced medicine in Alexandria in 300 B.C. defined the art of medicine as a triad consisting of knowledge of the things concerning health, knowledge of things pertaining to disease, and knowledge of neutral things.

Herophilus, who became the most influential anatomist of his time, practiced in Egypt where human dissection was allowed, unlike Greece. Dr. Von Staden, an emeritus scholar at the Institute for Advanced Study told me that Herophilus and other Greek philosophers believed that the knowledge of things concerning health was the most essential part of the art of medicine triad. Von Staden wrote, "Medicine in Hellenistic times, like earlier medicine, is concerned with the dietetics of the health. Indeed at this time the doctrine of health is considered to be not only as important as therapeutics, it seems to be even more important than healing of the sick." 

 (Dietetics is the science of applying nutrition principals to aid in preservation of health, and can loosely include exercise. )

Ornish may be one of the most influential modern thought leaders who have connected heart health and emotional health, but he is not the only one.

In a recent article in Psychiatric Times, Dr. Lawson Wulsin and Dr. Juliana Zambrano stated, "Psychosocial factors, especially recurrent depressive symptoms, severe mental illness, and high numbers of adverse childhood experiences, contribute substantially to both the onset and progression of CHD. Its effect size is as strong as that of the traditional CHD risk factors, such as smoking and high cholesterol".

They state, "The most robust psychosocial interventions for CHD are intensive lifestyle medicine programs."

Dr. Ornish has established a nonprofit group to promote and teach his ideas. He reported that 85% of his patients could comply with the program, and he has reduced their health care costs by 50%. Medicare now covers treatment at one of his centers. The affordable health care act mandated even more preventative measures to promote health that are covered by insurance. As Ornish commented to me, it is unfortunate that the programs didn't become popular until they were reimbursable by insurance.

The major point is that many chronic diseases, including cardiac disease, are significantly influenced by our wellness state. Modern medicine is good at intervening once we are sick but has for too long has neglected the simple things that can make a more significant impact on health. These things include following a Mediterranean diet, moderate exercise (150 hours a week), stressing less (Meditation, yoga, turn off the news), loving more (especially loving yourself enough to avoid unhealthy behaviors like smoking, drugs, drinking to excess, and the unhealthy pursuit of wealth, career, fame ). Practicing gratitude is especially helpful at reducing stress. Being kind and forgiving yourself for perceived personality defects will allow you to forgive others. If you seek revenge, you dig two graves.

Change doesn't come quickly. We seek progress, not perfection. Choose to change your life. Learn more about formulating a plan. (Ornish's book 'Undo It' is a good start.) The desire to make a change is a wish, and without a plan is only a dream.

Lastly, learn to do with less. I have had the privilege of spending the final hours of life with hundreds of patients, and not one ever said, "My only regret is that I didn't work more hours and have more money." My father used to say that a man is not wealthy for what he has, but for what he can do without.

1. Centers for Disease Control and Prevention. Underlying Cause of Death, 1999–2018. CDC WONDER Online Database. Atlanta, GA: Centers for Disease Control and Prevention; 2018. Accessed March 12, 2020.

2. Virani SS, Alonso A, Benjamin EJ, Bittencourt MS, Callaway CW, Carson AP, et al. Heart disease and stroke statistics—2020 update: a report from the American Heart Association. Circulation. 2020;141(9):e139–e596.

3. Fryar CD, Chen T-C, Li X. Prevalence of uncontrolled risk factors for cardiovascular disease: United States, 1999–2010 NCHS data brief, no. 103. Hyattsville, MD: National Center for Health Statistics; 2012. Accessed May 9, 2019.

4. Sources: All accidental death information from National Safety Council. Disease death information from Centers for Disease Control and Prevention. Shark fatality data provided by the International Shark Attack File.

5. Sources: All accidental death information from National Safety Council. Disease death information from Centers for Disease Control and Prevention.

6. Sources: All accidental death information from National Safety Council. Disease death information from Centers for Disease Control and Prevention.

7. Lloyd-Jones DM, Leip EP, Larson MG, D'Agostino RB, Beiser A, Wilson PW, Wolf PA, Levy D. Prediction of lifetime risk for cardiovascular disease by risk factor burden at 50 years of age. Circulation. 2006 Feb 14;113(6):791-8. doi: 10.1161/CIRCULATIONAHA.105.548206. Epub 2006 Feb 6. PMID: 16461820.

9. Reverón RR. Herophilus and Erasistratus, pioneers of human anatomical dissection. Vesalius. 2014 Summer;20(1):55-8. PMID: 25181783.

10. Von, S. H. (1989). Herophilus: The art of medicine in early Alexandria: edition, translation, and essays. Cambridge: Cambridge University Press.

Articles

Dr. Simon Murray reflects on the ongoing fight against cardiovascular disease in the US as part of our coverage of American Heart Month. 

Reflecting on The Fight Against Cardiovascular Disease in 2021 with Simon Murray, MD

“The art of medicine is keeping the patient amused while the disease runs its own course.”

If this quote, attributable to Voltaire, made you think of diabetes, you wouldn’t be wrong… until the last decade. Recently, new advances in diabetic medicines have improved the outcomes for people with diabetes, particularly those with cardiovascular disease.

Trends show declining mortality from diabetes with patients with cardiovascular disease in wealthy countries.

 SGLT2 inhibitors developed for type 2 diabetes have shown a cardioprotective effect due to reduction of plasma volume from continuous urine glucose excretion without activating renin-angiotensin system and sympathetic nervous system—recent trials demonstrate this improvement in heart failure risk is even seen in nondiabetic patients.

Due to previous failures among glucose-lowering medications, the US FDA mandated that new diabetes medications undergo trials for cardiac safety in 2008. The unexpected benefit of this was the discovery of several new diabetic medicines that worked by unique mechanisms other than simply lowering glucose levels. Traditional hypoglycemic drugs through various mechanisms of action lower blood glucose and effectively reduce microvascular target end-organ damage like retinopathy, nephropathy, and neuropathy. However, they do not improve macrovascular end organs like coronary arteries. Worse yet, some agents like thiazolidinediones increased the risk of congestive heart failure and myocardial infarction.

A pair of landmark trials, CANVAS and EMPA-REG outcome, both showed reductions in all-cause mortality, cardiac mortality, and admissions for congestive heart failure using SGLT2 inhibitors.

 The demonstrated benefit was independent of the favorable effect on serum glucose levels, and the low risk of hypoglycemia.

Glucagon-like peptide 1 (GLP-1) analogues are a class of injectable hypoglycemic drugs that activate the endogenous GLP-1 receptor. They promote glucose-dependent insulin release, inhibit glucagon secretion, and delay gastric emptying.

 The LEADER trial showed that liraglutide was superior to placebo in reducing the primary composite outcome of CV death, MI, and stroke (13% vs 14.9% in placebo; 

=.01). The reduction in the primary endpoint was driven by significantly lower CV mortality (4.7% vs. 6%; 

=.007). Moreover, liraglutide reduced all-cause mortality as well (8.2% vs. 9.6%; 

 SUSTAIN-6, also showed composite CV event reduction (6.6% vs 8.9%; 

=.02) with semaglutide, which was driven by a significant reduction in strokes (1.6% vs. 2.7%; 

Since most of the risk reduction is due to cardiac disease reduction, it raises the question: who should manage diabetes?

Several studies have shown that patients with diabetes fare better when treated by endocrinologists compared to primary care doctors. A retrospective, 4-year study was done comparing several measures of compliance with diabetes guidelines between primary care doctors and endocrinologists. In this study, the endocrinologists were better on every measure.

That study came as no great surprise since endocrinologists are better trained to treat diabetes.

Changing views about diabetes have begun to shift the focus on diabetes care from merely controlling blood sugar to treating all the metabolic dysfunctions that accompany diabetes. The protein adipsin, which is produced in body fat, helps protect insulin-secreting cells called pancreatic beta cells from destruction in type 2 diabetes, according to a study by researchers at Weill Cornell Medicine and New York-Presbyterian. By targeting this protein, beta cell function could be preserved, and insulin would remain normal.

So, should diabetes be managed by cardiometabolic specialists?

In practice, most people with diabetes are treated by their primary care doctor either by default or with whom they have a long-term relationship. They are better able to spot status changes and keep better track of complications. Shouldn’t the internist oversee managing diabetes? The following medical axioms may shed some light on this mostly theoretical discussion.

Good doctors treat people, not diseases. It makes the case that maybe we are all different and there is no right choice.

Patients do better with physicians they know and trust and who make them comfortable. People with long term relationships with primary care doctors generally live longer.

Until recently, the outcome in type 2 diabetes was dismal and many physicians, including some endocrinologists, didn’t want to treat diabetes. It is time-consuming and pays poorly. The outcome of people with type 1 diabetes changed dramatically in 1922 with the discovery of insulin but results for type 2 diabetes stagnated for decades. An endocrinologist told me the worst thing that happened to the treatment of Type 2 diabetics was insulin discovery. We thought insulin would solve all our problems, not realizing that T1D and T2D are completely different diseases and lowering blood glucose was not the only way to prevent complications. Four decades passed before new research into the pathophysiology of diabetes began. We now think of diabetes as a cardiometabolic syndrome, not just a blood sugar issue.

There are 6400 endocrinologists in the US with 123 new graduates every year. The supply is shrinking. These doctors are the best trained to treat diabetes, but they can’t do it and some may not want to treat diabetes. The CDC reports there are 25 million Americans with diabetes in the US and 79 million more with prediabetes. Endocrinologists are the lowest paid of all Internists, and it is challenging to attract top American students.

Cardiologists in the US are, generally, more interested in interventions than the prevention of cardiac disease. I know that comment may be unsettling to some, but, unfortunately, in my experience it is true. How will the cardiologist deal with a patient with urinary frequency, blurred vision, or unexplained weight loss? The answer is most likely that the patient will be referred to a urologist, an ophthalmologist, or a gastroenterologist, respectively, and all three of those conditions are common symptoms in diabetes.

The person most likely to see the big picture is the primary care doctor. People with diabetes get all kinds of odd symptoms, involving many organ systems. They are best managed by being seen by the same physician regularly with scheduled monitoring of the toenails, circulation in the feet, the urine albumin, the health of the retina, sexual functioning, body fat, mental status, blood pressure, lipoproteins, Adiponectin, TMAO, A1c, dietary habits, the 46 miles of nerves that feel like fire or being stung by a thousand bees when damaged, or the 6-8 meters of intestine that can be paralyzed by autonomic dysfunction. It’s a lot to remember and it takes regular follow-up—having the cooperation and trust of your patient will make this easier

Even asking which specialist should manage diabetes highlights the main problem facing people with chronic disease in our medical system. The question itself shows how little many physicians value collaboration and communication. Patients with diabetes ultimately see dozens of specialists who are slow to communicate their findings or quick to change medications and treatment plans, which fragments care and causes confusion. There has been a gradual deterioration in collegiality and respect between primary care and specialists. It is pervasive and real.

Many times, specialists communicate through a third party like a physician assistant or nurse practitioner because they are too busy to talk directly to the primary care doctor. There may not be any intentional disrespect, but I am offended when a doctor only speaks to me through a third party. If there were ever a disease that epitomized the need for all players to be on the same page, it’s diabetes. The patients do best with a primary care doctor for their quarterback who knows the game, understands the rules and cooperates, and communicates cohesively with his teammates of dieticians, nurse educators, psychologists, cardiologists, endocrinologists, and surgeons. No one can do it alone. Teamwork. That’s the way it works best.

There is one essential caveat. The primary care doctor must keep up with the quickly changing technology by reading, attending meetings, and asking questions. If the quarterback can’t call the right play at the right time, the game will indeed be lost. Diabetes is very patient and a rapacious predator that methodically destroys people’s lives right under the nose of the ill-informed physician; however, good his intentions.

In the last of our 3-part series examining the idea of a cardiometabolic subspecialty, Simon Murray, MD, offers his thoughts on who should be treating patients with type 2 diabetes. 

Simon Murray, MD: Who Should Be Treating Patients with Diabetes?

Polymerase chain reaction (PCR) testing for 

 is currently the most effective frontline test to detect exposure and infection. A positive test, taken from a nasal sample, is presumptive evidence of disease. But a negative test does not rule out infection for a variety of reasons. As many as 25% of the nasal swab tests are likely false negatives.

Causes of false-negative tests include improper collection, improper handling or storage, the prolonged time between collection and testing, or laboratory error.

Since the PCR swab test gives us no information about a person’s immunity to infection, we have been anxiously waiting for a method to test for antibodies to the virus. From experience with other infectious agents, we know that the presence of IgG antibodies indicates that immunity exists, and a presumption can often be made that the patient cannot be re-infected.

If this were, in fact, the case with SARS-CoV-2, we could send people with antibodies back to work, expecting that they will be protected. Unfortunately, not all enzyme-linked immunoassay (ELISA) tests are alike in their ability to reliably predict immunity.

Abbott Labs has been at the forefront of developing an ELISA test for COVID-19. The company has been reluctant to disclose much about its technology on the grounds that plans for deployment are still not finalized.

 it had received emergency clearance from the US Food and Drug Administration (FDA) to begin shipping the first point-of-care diagnostic test for the SARS-CoV-2 virus. The platform, called ID NOW, is the size of a toaster and can provide results in as little as 13 minutes. The ID NOW platform had been used to detect influenza and strep and was designed to be used by point-of-care providers.

By redesigning software and integrating different reagents, ID NOW was repurposed to test for SARS-CoV-2. Abbott said it could produce about 50,000 tests a day, with the eventual ability to produce 1.5 million tests a month. Initially, the tests were deploying only to areas with the highest concentration of COVID-19 cases.

A week later, Abbott announced it had developed an ELISA test, the m2000 SARS-CoV-2 assay, to be used in large laboratories. The company expects to produce about 4 million tests a month.

 the launch of its third test for COVID-19, a serology test to be run on its laboratory-based Architect i1000 and i2000 instruments. More than 2000 of these machines are in use in the United States. The test will cost about $5. Abbott expects to process 100-200 tests per hour. According to published reports, the number of true positives will be almost 100% within 14 days after the onset of symptoms. Remarkably, Abbott claims the false-negative rate is 99% after 14 days. It is unclear whether the test detects only IgG, or both IgG and IgM immunoglobulins.

Abbott tested its device on a few thousand patients, but when applied to millions of patients in the real world, we will see how it performs.

Another critical question is, what does a positive test tell us? Typical ELISA tests provide results for 2 distinct immunoglobulins, IgM and IgG. Typically, the IgM antibody is the first one detected. It usually rises and falls quickly, followed by a rise in IgG, which is believed to confer immunity. It may remain elevated for years, or months as in the case of influenza.

I spoke recently to Elliot A. Krauss, MD, chair of the Department of Pathology at Penn Medicine Princeton Medical Center, who expressed some concerns about the test, specifically that it didn’t undergo the same scrutiny as a test would in normal times; it was released as part of an FDA agency process that allows companies to produce and market tests without an explicit Emergency Use Authorization, although the company says it plans to file for one. As such, the test may cross-react with other common forms of coronavirus that cause the common cold.

Secondly, we don’t know which antigen is being detected by the ELISA. We know the critical antigens necessary to penetrate human cells are the s, or spike, and n antigen. There are several other antigens on the virus, some of which may be insignificant, or not enough to produce immunity, but may give rise in IgG.

Third, we don’t yet know whether the presence of IgG does, in fact, confer immunity and, if so, for how long.

Lastly, ELISA is a screening test. It casts a wide net and picks up many unrelated proteins. A positive ELISA must be confirmed by another method. Lyme disease is a prime example of a disease that causes the ELISA to be positive in many cases where there is no Lyme disease present.

Krauss had several questions about the value of the test in clinical practice. He mentioned that the University of Pennsylvania is also close to developing an antibody test, as well as other large manufacturers like Siemens and BD.

After testing positive via the ELISA test, are we going to allow teachers to return to school and doctors to return to work before we are certain they are indeed immune with no possibility of being infectious?

Krauss said it will take some time to have these questions answered.

Once again, it comes down to getting a vaccine that works, or the development of herd immunity. It is likely that the test will prove to be valuable epidemiologically and will help us better understand the natural history. It will take some time to see the real value.

For now, we will need to do both the test for active infection and the serologic test and not let the results determine whether or not to give up what we are doing. Over time we will learn the best utility of the ELISA. SARS-CoV-2 is here to stay. Most importantly, what we learn here can help us prepare for future pandemics that are undoubtedly going to affect us.

Simon Murray, MD, is an internist based in Princeton, NJ. The piece reflects his views, not necessarily those of the publication.

Can positive ELISA test results better interpret for how much longer social distancing must continue?

Finally, an ELISA for COVID-19

What is the role of ACE inhibition or angiotensin receptor blockers (ARBs) within regard to the novel coronavirus (COVID-19)?

There has been some dissent lately about the role angiotensin-converting enzyme plays in the COVID-19 infections. The chemistry can be quite confusing, making it easy to see why it has caused controversy.

A very elegant system exists in humans to regulate blood pressure when there are sudden drops in renal blood flow or reduced sodium excretion, which could lead to hypotension. The system is called the renin-angiotensin system (RAS), which keeps us from fainting when we stand up quickly or when we are dehydrated.

Angiotensinogen is a protein formed in the liver and activated when renin, an enzyme secreted by the kidney in response to a drop in renal blood flow, cleaves it. The resulting protein is called Angiotensin 1, which has no known function except as an intermediary in the process of maintaining blood pressure. Angiotensin 1 is converted by angiotensin-converting enzyme-1 or ACE1 in the lung into angiotensin II.

Angiotensin II can act on the adrenal to produce the hormone aldosterone, which increases sodium retention and promotes potassium excretion. Angiotensin II will bind a specific receptor in the heart, lung, and blood vessels called the AT1 receptor. There are 3 other receptors-AT2, AT3, AT4-but their roles remain unknown.

Once bound to AT1, angiotensin II causes vasoconstriction, fluid and sodium retention, stimulation of aldosterone, and cardiac stimulation. Free, unbound angiotensin II has direct proinflammatory properties in lung tissue.

There is a second angiotensin-converting enzyme called ACE2 that had remained rather obscure in literature until 2002 when it turned out to be the point of entry for SARS virus to enter lung cells.

The 2 angiotensin-converting enzymes, ACE1 and ACE2, are analogs of each other and structurally very similar. ACE2 protein exists as a soluble form but mainly resides on the epithelial surface of the lung, intestine, and heart. Not much was known about ACE2 until the SARS epidemic, but much has been learned since.

ACE2 plays a counterregulatory role in the classical RAS and causes vasodilation, reduction in sodium, and reduced levels of angiotensin II. It does so by reducing angiotensin II levels and converting angiotensin II into angiotensin (1,7), which are vasodilators. ACE2 levels are generally 200 times higher than ACE1 levels.

It also has a negative effect on aldosterone. The 2 proteins ACE1 and ACE2 each have very different actions on the RAS.

Chronic overactivity of the RAS is felt to be one cause of hypertension. It became logical to look for drugs to interfere with this system. In the late 70’s and 1980’s a class of drugs were developed called angiotensin-converting enzyme inhibitors after the discovery that cobra snakes have a large amount of angiotensin in their venom. The way that cobra snakes kill their prey is by causing shock from hypotension.

ACE inhibitors block the conversion of angiotensin 1 to angiotensin II by inhibiting ACE1. The inhibitors were not felt to have any role in blocking ACE2. But a few years later, the second class of drugs was developed, which blocked the action of angiotensin II further upstream at by preventing angiotensin II from binding to specific receptor sites on the blood vessel and heart.

These are ARBS, which have been shown to reduce the symptoms of congestive heart failure, lower blood pressure and protect the kidney from high blood pressure. They are often the first-line drugs used to treat these conditions.

And I said before: the role of ACE2 remained obscure until 2002, prior to the discovery that it binds SARS virus avidly and served as the point of entry of the virus into the cells that lined the surface of the lung.

Why is this important? We know that SARS-COV-2 is bound to ACE2 and serves as a portal of entry of the SARS-COV2 virus into cells-just as it was for the SARS and probably the MERS viruses. Theoretically, anything with increased ACE2 levels could make patients more susceptible to infection with coronavirus, and make their cases more severe.

A letter to the editor in The Lancet described the observation that Chinese patients who had high blood pressure or diabetes and who were taking ACE inhibitors and ARBS had worse outcomes, with more severe infections and more deaths.

The article implied that ARBS and ACE inhibitors elevated ACE2 levels and that increased ACE2 facilitated more viral penetration into lung tissue. The paper concluded that taking these medicines could increase the number and severity of infections. The authors suggested that people should stop taking these medications. On face value, it seemed like a logical conclusion.

For several days after publication, there was a firestorm of confusion about whether or not to take ACE inhibitors or ARBs. The European Society of Cardiology and several leading American cardiology societies all refuted the findings in The Lancet. They suggested that patients should continue their medications and that there was no proof that the COVID-19 infection was adversely affected by inhibition of the RAS. There is evidence that these medicines might make infections better.

It is complicated, but it has already been demonstrated that viral pneumonia improved faster when the patients were taking ACE inhibitors.

Did The Lancet article consider that the patients who did worse either had diabetes, hypertension, or obesity? That triad is part of the metabolic syndrome and would make any sick person worse, because the metabolic syndrome can produce the “cytokine storm” that generates damage to lung tissue.

I was drawn into this debate by several patients who had the quickly popularizing article. A few days later, when institutions refuted the findings, I saw more controversy stir.

This episode is an example of the ongoing issue we have during this pandemic-in which public announcements or declarations on the virus are later retracted. People in authority are making statements and decisions without certain and evidenced knowledge. The most present fact in this debate is that story is rapidly developing.

Of course, as we see the virus rapidly spread and take more lives, it is understandable to see people react quickly, rather than rationally.