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e. When this happens, the person needs to inject extra insulin to manage the high levels of glucose in the blood, which can be dangerous.</p><p id="016b">Insulin resistance can lead to obesity because high basal levels of insulin in the blood will inhibit the fat burning process — so the body will store fat but have little or no opportunity to use that fat for energy.</p><p id="8f34">Insulin resistance can lead to high blood pressure due to increased renal sodium reabsorption. This is why many doctors advise a low-sodium diet. A LCHF diet results in the kidneys releasing a lot of water and sodium. When eating a LCHF diet, one typically needs to be sure to eat enough salt.</p><p id="49ff">Insulin resistance can lead to cardiovascular disease via several paths: it can create an imbalance in glucose metabolism that leads to chronic high blood sugar, which then creates oxidative stress and causes an inflammatory response that leads to cell damage. Insulin resistance can also alter lipid metabolism which in turn leads to the development of dyslipidemia and the combination of: A) low levels of high-density lipoprotein B) the appearance of small dense low-density lipoproteins and C) high levels of plasma triglycerides. This combination can contribute to atherosclerotic plaque formation.</p><p id="0538">Clearly, when I weighed 365 pounds, I was not metabolically healthy. Like many obese people, I avoided going to the doctor back then. I knew he was going to tell me to lose weight. But I also knew the “eat less/move more” advice he would always give me — and I always followed — never worked. So I don’t know how bad my health markers were back then. Now, my health markers are well within the normal range. The exception is my percentage body fat, which is just over the upper limit for normal. On the plus side, my percentage visceral fat (the fat around the organs) is within the normal range.</p><p id="b035">The relevance here is that suboptimal levels of any of these health markers is associated with impaired immunity response — an impaired ability to fight off a virus like SARS-CoV-2.</p><p id="ef95"><b>How SARS-CoV-2 Works</b></p><p id="b774">The typical way SARS-CoV-2 enters our body is through the inhalation or swallowing of droplets containing the virus. The virus then sticks to the tissue in the throat. If the virus can be successfully defeated at this point, the person will not likely experience severe symptoms. If, however, the virus makes it down to the lungs and takes hold there, much more severe issues can arise — as we’ve all seen on the news.</p><p id="8d34">The ability of the body to deal with SARS-CoV-2 early — while still in the throat — depends, on two factors:</p><p id="4941">· The ability of the virus to enter cells</p><p id="f39e">· The strength of the immune system which will fight the virus</p><figure id="efa2"><img src="https://cdn-images-1.readmedium.com/v2/resize:fit:800/1*Jn0dIFvT6UrRQVhEVLbN_Q.jpeg"><figcaption></figcaption></figure><p id="b349">In order to enter a cell in our body, SARS-CoV-2 needs a (figurative) doorway. That doorway is called an ACE2 receptor. ACE2 receptors have other functions besides allowing SARS-CoV-2 into a cell, but SARS-CoV-2 exploits these receptors to barge into cells. The relevance here is that insulin resistant people have more of these ACE2 receptors on their cells — giving the SARS-CoV-2 virus more doorways to enter any given cell. Smoking also increases the number of ACE2 receptors — which is likely why metabolically healthy individuals who smoke are also at high risk for a severe COVID-19 reaction.</p><p id="73a8">Once SARS-CoV-2 gets into a cell, our last line of defense is our immune system. The relevance here is that insulin resistance, as mentioned earlier, impairs our immune response to threats like SARS-CoV-2. For example, if there is a high level of glucose in the blood, glucose molecules can attach themselves to immune system “killer cells,” ren

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dering these killer cells “busy” when it’s time to battle the virus.</p><p id="d76a">So, having been and continuing to eat a low-carb/high-fat diet acted to reduce my insulin resistance, thereby improving my metabolic health, which in turn boosted my immune response to invaders like SARS-CoV-2.</p><p id="faa5">Fasting also acts to reduce insulin resistance. The insulin that gets secreted into the blood as a response to eating carbohydrate takes some time to get used up. Eating a lot of carbohydrate causes more insulin to be secreted — and therefore, it takes longer to get back to a low level. When you have a typical snack — even a piece of fruit — you will put more insulin into your system. The 16-hour fasting period allows insulin levels to drop — as does not snacking between meals. As we saw, lower levels of insulin reduce insulin resistance and bolster the immune system.</p><figure id="94a0"><img src="https://cdn-images-1.readmedium.com/v2/resize:fit:800/1*STglfp8gcZhTb9JmNJGKUA.jpeg"><figcaption></figcaption></figure><p id="14f5">When I experienced the COVID-19 symptoms, I took my fasting to a higher level — I only ate a bowl of bone broth in the evening. I fasted for over 23 hours a day and only ate about 2 grams of carbohydrate. I also sat on our balcony when I was awake, taking in as much sun as I could — since Vitamin D also boosts the immune system. I also drank a lot of water and slept maybe 15 hours a day — which are also immune system boosters.</p><p id="f0b2">In the end, I had a lot of factors going for me and my immune system. But given the scientific evidence, I think my low-carb/high-fat diet, along with fasting played a big part in beating COVID-19 and the virus that caused it.</p><p id="efd3"><b><i>Thank you for reading this article — hopefully it contained something you found useful.</i></b></p><p id="0510">If you aren’t a member of Medium but are thinking of joining, please join through my page! If you do <a href="https://santhony4649.medium.com/membership">sign up to Medium through my page,</a> some of your membership fee goes to me (but you still pay the normal membership price).</p><p id="5daa">With a paid membership to Medium, you will get to read more of my work plus you get unlimited access to thousands of Medium writers. And it’s only about $5.00 a month!</p><figure id="fe86"><img src="https://cdn-images-1.readmedium.com/v2/resize:fit:800/1*Ym5aHNcBTA8-FazE96fUWw.jpeg"><figcaption></figcaption></figure><p id="92d5"><i>References</i></p><p id="1e2e">Special thanks to <a href="undefined">Julian Parge</a> for clarifying the difference between SARS-CoV-2 (the virus) and COVID-19 (the disease caused by the virus).</p><p id="d124"><i>CDC Morbidity and Mortality Weekly Report of April 13, 2020.</i></p><p id="6c82"><i>Andersen and Murphy, Impact of obesity and metabolic syndrome on immunity.</i></p><p id="a5c5"><i>Salvetti, A. et al, (1993) The inter-relationship between insulin resistance and hypertension. Drugs, 46, 149–159.</i></p><p id="5ff9"><i>Ormazabal, V. et al, (2018) Association between insulin resistance and the development of cardiovascular disease. Cardiovascular Diabetology 17: 122.</i></p><p id="497e"><a href="http://www.newyorktimes.com/interactive/2020/03/11/how-corona-virus-hijacks-your-cells.html"><i>www.newyorktimes.com/interactive/2020/03/11/how-corona-virus-hijacks-your-cells.html</i></a></p><p id="68c9"><i>Brake, SJ et al, (2020) Smoking upregulates antiotensin-converting enzyme-2 receptor: A potential adhesion site for novel coronavirus SARS-CoV-2 (COVID-19). Journal of Clinical Medicine, 9(3). 841.</i></p><p id="f7d7"><i>Zhou, W. et al, (2019) Longitudinal multi-omics of host-microbe dynamics in prediabetes. Nature, 569(7758), 663–671.</i></p><p id="7904"><i>Rosenstock, P. et al, (2019). Glycation interferes with natural killer cell function. Mechanisms of Ageing and Development.</i></p><p id="22bf"><i>All images licensed via freepik.com</i></p></article></body>

I Survived COVID-19

Science suggests my diet helped

I celebrated my 61st birthday just before we heard about the existence of COVID-19. Then, a week after we went into lockdown here in Italy, I got sick — likely infected by someone who didn’t know they carried the virus. In terms of symptoms, I had a fever, cough, body aches, fatigue and the signature symptom of the loss of my sense of taste and smell.

These symptoms lasted a couple of weeks during which time I closely monitored my breathing and made a list of all my various passwords for my wife, in case everything turned south. As this very article exhibits, however, I survived!

Why?

It’s hard to know for sure. But there is scientific evidence that suggests my low-carb/high-fat (LCHF) diet and my practice of intermittent fasting (IF) helped me beat SARS-CoV-2 (the virus that causes COVID-19 (the disease)).

Backstory

For most of the last 40 years, I’ve struggled with my weight. At my heaviest, I had a BMI of 49, weighing in at 365 pounds (166 kg) — I was morbidly obese. As of my 61st birthday, I was just a few kilos away from a “normal” BMI at 190 pounds (86 kg). I achieved this dramatic reduction in weight by cutting my intake of carbohydrate to under 30 grams per day, eliminating sugar from my diet, and practicing intermittent fasting. For those not familiar with intermittent fasting, I do a practice called 16/8 fasting: I eat 2 meals a day within an 8-hour window (for me it is between 1:00PM and 9:00PM) and the rest of the time I don’t eat anything. So, I basically skip a morning meal and I don’t snack. I do drink black coffee and water during the periods of fasting.

The result of the LCHF diet and IF practice is that my body has strong metabolic health.

In their Morbidity and Mortality Weekly Report of April 13, 2020, the CDC noted that there is an increased risk of a severe reaction to the SARS-CoV-2 virus in people with the underlying conditions of:

· Diabetes

· High blood pressure

· Obesity

· Heart disease

While age has been noted as a risk factor, the four conditions listed above (which are indications of poor metabolic health) have also been noted in younger people having severe reactions to this new virus.

Good Metabolic Health Defined

Metabolic health is typically measured by 5 markers:

· Body fat percentage (especially visceral fat)

· Blood glucose control

· Blood pressure

· Blood triglycerides

· Serum HDL cholesterol level

All these markers have a normal or “ideal” level/range. While poor metabolic health can present itself in any of the four medical conditions listed above, these conditions all have the same root cause: Insulin resistance.

Insulin resistance is a condition where cells in the body need more and more insulin to be receptive to what insulin is trying to do. One of the major roles of insulin is to help the body regulate blood glucose.

Insulin resistance can lead to Type 2 diabetes because the pancreas can’t produce enough insulin on its own to deal with the amount of glucose in the blood after a typical meal following the USDA dietary guidelines that recommends a high percentage of calories come from carbohydrate — which is broken down into glucose. When this happens, the person needs to inject extra insulin to manage the high levels of glucose in the blood, which can be dangerous.

Insulin resistance can lead to obesity because high basal levels of insulin in the blood will inhibit the fat burning process — so the body will store fat but have little or no opportunity to use that fat for energy.

Insulin resistance can lead to high blood pressure due to increased renal sodium reabsorption. This is why many doctors advise a low-sodium diet. A LCHF diet results in the kidneys releasing a lot of water and sodium. When eating a LCHF diet, one typically needs to be sure to eat enough salt.

Insulin resistance can lead to cardiovascular disease via several paths: it can create an imbalance in glucose metabolism that leads to chronic high blood sugar, which then creates oxidative stress and causes an inflammatory response that leads to cell damage. Insulin resistance can also alter lipid metabolism which in turn leads to the development of dyslipidemia and the combination of: A) low levels of high-density lipoprotein B) the appearance of small dense low-density lipoproteins and C) high levels of plasma triglycerides. This combination can contribute to atherosclerotic plaque formation.

Clearly, when I weighed 365 pounds, I was not metabolically healthy. Like many obese people, I avoided going to the doctor back then. I knew he was going to tell me to lose weight. But I also knew the “eat less/move more” advice he would always give me — and I always followed — never worked. So I don’t know how bad my health markers were back then. Now, my health markers are well within the normal range. The exception is my percentage body fat, which is just over the upper limit for normal. On the plus side, my percentage visceral fat (the fat around the organs) is within the normal range.

The relevance here is that suboptimal levels of any of these health markers is associated with impaired immunity response — an impaired ability to fight off a virus like SARS-CoV-2.

How SARS-CoV-2 Works

The typical way SARS-CoV-2 enters our body is through the inhalation or swallowing of droplets containing the virus. The virus then sticks to the tissue in the throat. If the virus can be successfully defeated at this point, the person will not likely experience severe symptoms. If, however, the virus makes it down to the lungs and takes hold there, much more severe issues can arise — as we’ve all seen on the news.

The ability of the body to deal with SARS-CoV-2 early — while still in the throat — depends, on two factors:

· The ability of the virus to enter cells

· The strength of the immune system which will fight the virus

In order to enter a cell in our body, SARS-CoV-2 needs a (figurative) doorway. That doorway is called an ACE2 receptor. ACE2 receptors have other functions besides allowing SARS-CoV-2 into a cell, but SARS-CoV-2 exploits these receptors to barge into cells. The relevance here is that insulin resistant people have more of these ACE2 receptors on their cells — giving the SARS-CoV-2 virus more doorways to enter any given cell. Smoking also increases the number of ACE2 receptors — which is likely why metabolically healthy individuals who smoke are also at high risk for a severe COVID-19 reaction.

Once SARS-CoV-2 gets into a cell, our last line of defense is our immune system. The relevance here is that insulin resistance, as mentioned earlier, impairs our immune response to threats like SARS-CoV-2. For example, if there is a high level of glucose in the blood, glucose molecules can attach themselves to immune system “killer cells,” rendering these killer cells “busy” when it’s time to battle the virus.

So, having been and continuing to eat a low-carb/high-fat diet acted to reduce my insulin resistance, thereby improving my metabolic health, which in turn boosted my immune response to invaders like SARS-CoV-2.

Fasting also acts to reduce insulin resistance. The insulin that gets secreted into the blood as a response to eating carbohydrate takes some time to get used up. Eating a lot of carbohydrate causes more insulin to be secreted — and therefore, it takes longer to get back to a low level. When you have a typical snack — even a piece of fruit — you will put more insulin into your system. The 16-hour fasting period allows insulin levels to drop — as does not snacking between meals. As we saw, lower levels of insulin reduce insulin resistance and bolster the immune system.

When I experienced the COVID-19 symptoms, I took my fasting to a higher level — I only ate a bowl of bone broth in the evening. I fasted for over 23 hours a day and only ate about 2 grams of carbohydrate. I also sat on our balcony when I was awake, taking in as much sun as I could — since Vitamin D also boosts the immune system. I also drank a lot of water and slept maybe 15 hours a day — which are also immune system boosters.

In the end, I had a lot of factors going for me and my immune system. But given the scientific evidence, I think my low-carb/high-fat diet, along with fasting played a big part in beating COVID-19 and the virus that caused it.

Thank you for reading this article — hopefully it contained something you found useful.

If you aren’t a member of Medium but are thinking of joining, please join through my page! If you do sign up to Medium through my page, some of your membership fee goes to me (but you still pay the normal membership price).

With a paid membership to Medium, you will get to read more of my work plus you get unlimited access to thousands of Medium writers. And it’s only about $5.00 a month!

References

Special thanks to Julian Parge for clarifying the difference between SARS-CoV-2 (the virus) and COVID-19 (the disease caused by the virus).

CDC Morbidity and Mortality Weekly Report of April 13, 2020.

Andersen and Murphy, Impact of obesity and metabolic syndrome on immunity.

Salvetti, A. et al, (1993) The inter-relationship between insulin resistance and hypertension. Drugs, 46, 149–159.

Ormazabal, V. et al, (2018) Association between insulin resistance and the development of cardiovascular disease. Cardiovascular Diabetology 17: 122.

www.newyorktimes.com/interactive/2020/03/11/how-corona-virus-hijacks-your-cells.html

Brake, SJ et al, (2020) Smoking upregulates antiotensin-converting enzyme-2 receptor: A potential adhesion site for novel coronavirus SARS-CoV-2 (COVID-19). Journal of Clinical Medicine, 9(3). 841.

Zhou, W. et al, (2019) Longitudinal multi-omics of host-microbe dynamics in prediabetes. Nature, 569(7758), 663–671.

Rosenstock, P. et al, (2019). Glycation interferes with natural killer cell function. Mechanisms of Ageing and Development.

All images licensed via freepik.com

Health
Diet
Covid-19
Keto
Lifestyle
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