Training for “The COVID-19”

Today we welcome guest author Dr. Ronesh Sinha, internal medicine physician and expert on insulin resistance and corporate wellness, author of The South Asian Health Solution. He is a top rated speaker for companies like Google, Oracle, Cisco and more. Check out his media page for lectures, interviews and articles from Dr. Sinha.

Most of us have been sheltering-in-place for a few months now, and we have evolved into an unprecedented state of fear and hyper-vigilance in this pandemic. After a long period of being cooped up, we are now gradually released into the wild, which introduces us to a whole new level of anxiety. Public health recommendations appear to be flip-flopping regularly, and we are learning on the fly as the situation evolves.

In today’s post, I’d like to share some thoughts on how we can regain some control of our lives. Rather than duck and cover for several more months, we can face this beast head-on. I don’t mean being careless and reckless and not following social distancing and hygiene protocols. Instead, we can adopt a mindset that we will do what is necessary to minimize our risk of a severe COVID-19 outcome. I titled this post “Training for the COVID-19” to help you reframe this pandemic in your mind, and view it like a warrior approaches an enemy on the battlefield or an athlete faces an opponent in a competition.

Cognitive Reframing Coronavirus: From Fear to Readiness

Cognitive reframing isn’t just some touchy-feely behavioral technique. Viewing the world through a more positive lens has a beneficial impact on your immune system, which is potentially relevant to COVID-19. One study shows that participants who were cognitive reappraisers, identified by a 10-item Emotion Regulation Questionnaire, and then exposed to an experimental cold virus (rhinovirus not coronavirus) had reduced nasal cytokine release compared to individuals who were emotional suppressors.https://www.culturalhealthsolutions.com/beware-of-the-covesity-covid-obesity-pandemic/‘>² Specifically, it’s the central visceral fat (aka “belly fat”) that is an especially insidious storehouse of proinflammatory cytokines like IL-6 and TNF-alpha, which fuel the cytokine fire.

Another reason fat cells may increase risk is through the ACE-2 receptor shown in the above image. Fat cells have an abundance of these receptors, and their affinity for COVID-19 means they may serve as a viral storehouse. So fat cells not only provide more entry points for COVID-19 but also ready access to an ammunition supply of cytokines.

ACE-2 also puts the brakes on the enzyme angiotensin II, which, if left unrestrained, can contribute to the more severe manifestations of COVID-19 (like acute lung injury, heart damage, etc.). Angiotensin II levels appear to rise in severe COVID-19 infections due to a downregulation in ACE-2 (the “brake pedal” for Angiotensin II). In the case of obesity, angiotensin II increases further by visceral fat cells that secrete angiotensin II in addition to the cytokines we just discussed.

So fat cells provide the fuel to ignite the cytokine fire and release excess amounts of angiotensin II, which can further provoke damage and destruction of vital organs. We also know that obesity increases our risk of chronic health conditions like diabetes and high blood pressure, which are additional risk factors for a more severe COVID-19 infection.

Again, I don’t want this information to set you into a state of panic if you are struggling with extra weight or other COVID-19 health risks. I assure you that this is not a disease where the only people left standing at the end of the pandemic will have single-digit body fat percentages and 6-packs. Fit, lean individuals who are experiencing chronic stress and sleep issues might have a higher risk than slightly more substantial, less fit individuals who are physically active and better manage their sleep and stress. No matter where we are in our health journey, we need to identify our own gaps (physical, mental, social, etc.) and make key changes that will markedly reduce our cytokine load and overall risk.

One common question I get during lectures and in the clinic is, “how do I know if my fat is the inflammatory type?” This is an important distinction. Some of us might be above the recommended BMI (body mass index) cutoff, but not have as much inflammatory adipose tissue. In contrast, others might be underweight but have visceral fat cells packed with proinflammatory cytokines. This is why body weight and BMI can often be a misleading marker. Some clues that you might have more inflammatory adipose tissue are below. Just a reminder that NLRP3 is the alarm sensor that COVID-19 turns on and triggers the cytokine surge.

• Increased belly fat: ethnic waistline cutoffs are here and to learn more about body fat and the impact of ethnicity, read my post here.
• High triglycerides: aim for triglyceride levels to be closer to 100 mg/dL or below
• Low HDL (healthy cholesterol): males should target an HDL>40 mg/dL and for females, HDL>50 mg/dL
• High triglyceride/HDL ratio is even better than looking at individual triglyceride and HDL, aiming for a ratio of less than 3.0 (lower the better)
• Elevated blood glucose (prediabetes, diabetes)
• High blood pressure: More recent research is showing that hypertension may be an inflammatory condition and the NLRP3 inflammasome might be a key switch as discussed in this study.https://www.culturalhealthsolutions.com/is-your-liver-fat/‘>⁴ This mouse study ⁵ is linked to NAFLD (non-alcoholic fatty liver disease) and blockade of this pathway leads to regression of fatty liver.
• Elevated hsCRP: this is a test for inflammation that is not indicated in all patients and can give an elevated result for various reasons. Many of my patients with insulin resistance have elevated hs-CRP, and research https://www.culturalhealthsolutions.com/metabolic-syndrome-what-cholesterol-guidelines-should-really-focus-on/’>⁷ whose root cause is insulin resistance. Many of us have become disconnected from our health care providers and systems as a result of shelter-in. I strongly encourage you to track the risk numbers applicable to you. For example, I’m putting a growing number of my at-risk patients on continuous glucose monitors (CGMs), especially given studies const lazyloadRunObserver = () => { const lazyloadBackgrounds = document.querySelectorAll( `.e-con.e-parent:not(.e-lazyloaded)` ); const lazyloadBackgroundObserver = new IntersectionObserver( ( entries ) => { entries.forEach( ( entry ) => { if ( entry.isIntersecting ) { let lazyloadBackground = entry.target; if( lazyloadBackground ) { lazyloadBackground.classList.add( 'e-lazyloaded' ); } lazyloadBackgroundObserver.unobserve( entry.target ); } }); }, { rootMargin: '200px 0px 200px 0px' } ); lazyloadBackgrounds.forEach( ( lazyloadBackground ) => { lazyloadBackgroundObserver.observe( lazyloadBackground ); } ); }; const events = [ 'DOMContentLoaded', 'elementor/lazyload/observe', ]; events.forEach( ( event ) => { document.addEventListener( event, lazyloadRunObserver ); } );