The Experts were wrong about all things C19.

SOME ADDITIONAL REFERENCES

Why COVID-19 is more deadly in people with obesity—even if they’re young

“The stickiest blood I’ve ever seen” and other weight-related factors worsen the coronavirus disease

When the first wave of coronavirus hit the state of Vermont in the spring, patients from all corners of the state came to the intensive care unit at the University of Vermont Medical Center. There, critical care physician MaryEllen Antkowiak quickly saw a tragic pattern: Patients arrived at the hospital after a few days of flulike symptoms and fever. They tested positive for COVID-19. They grew increasingly short of breath. Many ended up on ventilators, and many died.

In addition to this course of disease, patients frequently shared one additional attribute: obesity. “These were otherwise healthy, hard-working people,” Antkowiak says. “Their major risk factor for getting this sick was obesity.”

Since the pandemic began, dozens of studies have reported that many of the sickest COVID-19 patients have been people with obesity. In recent weeks, that link has come into sharper focus as large new population studies have cemented the association and demonstrated that even people who are merely overweight are at higher risk. For example, in the first metaanalysis of its kind, published on 26 August in Obesity Reviews, an international team of researchers pooled data from scores of peer-reviewed papers capturing 399,000 patients. They found that people with obesity who contracted SARS-CoV-2 were 113% more likely than people of healthy weight to land in the hospital, 74% more likely to be admitted to an ICU, and 48% more likely to die.

A constellation of physiological and social factors drives those grim numbers. The biology of obesity includes impaired immunity, chronic inflammation, and blood that’s prone to clot, all of which can worsen COVID-19. And because obesity is so stigmatized, people with obesity may avoid medical care.

“We didn’t understand early on what a major risk factor obesity was. … It’s not until more recently that we’ve realized the devastating impact of obesity, particularly in younger people,” says Anne Dixon, a physician-scientist who studies obesity and lung disease at the University of Vermont. That “may be one reason for the devastating impact of COVID-19 in the United States, where 40% of adults are obese.”

People with obesity are more likely than normal-weight people to have other diseases that are independent risk factors for severe COVID-19, including heart disease, lung disease, and diabetes. They are also prone to metabolic syndrome, in which blood sugar levels, fat levels, or both are unhealthy and blood pressure may be high. A recent study from Tulane University of 287 hospitalized COVID-19 patients found that metabolic syndrome itself substantially increased the risks of ICU admission, ventilation, and death.

But on its own, “BMI [body mass index] remains a strong independent risk factor” for severe COVID-19, according to several studies that adjusted for age, sex, social class, diabetes, and heart conditions, says Naveed Sattar, an expert in cardiometabolic disease at the University of Glasgow. “And it seems to be a linear line, straight up.”

The impact extends to the 32% of people in the United States who are overweight. The largest descriptive study yet of hospitalized U.S. COVID-19 patients, posted as a preprint last month by Genentech researchers, found that 77% of nearly 17,000 patients hospitalized with COVID-19 were overweight (29%) or obese (48%). (The Centers for Disease Control and Prevention defines overweight as having a BMI, which is calculated as one’s weight in kilograms divided by the square of one’s height in meters, of 25 to 29.9.)

Another study captured the rate of COVID-19 hospitalizations among more than 334,000 people in England. Published last month in the Proceedings of the National Academy of Sciences, it found that although the rate peaked in people with a BMI of 35 or greater, it began to rise as soon as someone tipped into the overweight category. “Many people don’t realize they creep into that overweight category,” says first author Mark Hamer, an exercise physiologist at University College London.

The physical pathologies that render people with obesity vulnerable to severe COVID-19 begin with mechanics: Fat in the abdomen pushes up on the diaphragm, causing that large muscle, which lies below the chest cavity, to impinge on the lungs and restrict airflow. This reduced lung volume leads to collapse of airways in the lower lobes of the lungs, where more blood arrives for oxygenation than in the upper lobes. “If you are already starting [with] this mismatch, you are going to get worse faster” from COVID-19, Dixon says.

Other issues compound these mechanical problems. For starters, the blood of people with obesity has an increased tendency to clot—an especially grave risk during an infection that, when severe, independently peppers the small vessels of the lungs with clots. In healthy people, “the endothelial cells that line the blood vessels are normally saying to the surrounding blood: ‘Don’t clot,'” says Beverley Hunt, a physician-scientist who’s an expert in blood clotting at Guy’s and St. Thomas’ hospitals in London. But “we think that signaling is being changed by COVID,” Hunt says, because the virus injures endothelial cells, which respond to the insult by activating the coagulation system.

============================================================

Tried out Keto, High Carb, High Fiber, Calorie Restrictive Diets and/or Hours of Running on a Treadmill - But STILL Can't Seem to Lose Those Pounds?

Well Hallelujah! Finally We Know - It's Not Your Fault!

A Recent Japanese Study Found that ONE Simple Enzyme's Over-Activity Might Be To Blame.

Causing You to Gain Weight, Like a Bear Getting Ready to Hibernate, Rather Than Optimizing Your Metabolism to Efficiently Handle Carbs AND Fats.

DISCOVER What This Enzyme is AND How You Can 'Reboot' Your Stalled Metabolism Starting Today.

============================================================

Why Do Some People Get Sicker Than Others from COVID?

New study of virus in the lung suggests 11 “protection-defining genes” may help many avoid worst symptoms

COVID-19 vaccines have saved at least a million lives in the United States alone, but for many people, a lingering fear remains: if—or when—they get hit by the coronavirus, just how bad will it be? Will they breeze through with little more than a sore throat—or will it saddle them with long-term complications, perhaps even push them to the brink of death?

Since SARS-CoV-2 first began storming around the world in early 2020, COVID-19 has claimed six million lives and counting, according to the World Health Organization. And yet, the vast majority of people who’ve contracted COVID—some 99 percent of the more than 500 million confirmed cases—have survived their brush with the disease.

So, why is it that some people are so badly affected by COVID when many are barely scratched by it?

Age and other health conditions increase the risk of getting really sick, but a new study suggests that those who escape the worst symptoms might also have the right balance of a type of immune cells called macrophages.

White blood cells found in every tissue, macrophages—part of a group of cells called myeloid cells, the guards of the immune system—are healers. They’re crucial in wound repair, streaming to an injury to help the body patch itself up. They also take on invaders, gobbling up and digesting anything that looks like it doesn’t belong in the body, from dead cells to harmful bacteria. That attack mode helps keep us healthy, but it also seems to be a factor in severe COVID-19 cases. Evidence has been growing that many COVID deaths are caused by a hyper-immune response: rampaging macrophages attacking not just the virus, but also our bodies, causing excessive inflammation and damaging heart and lung tissue.

In a study published in Cell Reports, a team of researchers at Boston University’s National Emerging Infectious Diseases Laboratories (NEIDL) and Princeton University looked at why that was happening, examining COVID’s impact on those who get dangerously sick—and those who don’t. By studying lungs that seem to easily deflect SARS-CoV-2 or quickly bounce back from infection, they found a set of genes that determine whether immune cells mount a solid defense—or turn rogue and land someone on a ventilator. The findings could help efforts to develop new drugs that better prime immune systems for taking on the virus.

“If you can understand why most people are protected against COVID and how their body protects them, then you could potentially harness this knowledge to develop therapeutics and other advances,” says Florian Douam, a BU School of Medicine assistant professor of microbiology who coled the study.

Why Are Some Lungs Protected against COVID?

After two years of sickness and swabbing, there’s a lot scientists know about how SARS-CoV-2 is transmitted and how our bodies react when we get it—but there’s also a lot they don’t understand. Take the lungs: we know COVID-19 can leave lungs full of liquid and inflamed, sometimes scarred by sepsis. But most of what’s known about COVID in the lungs is driven by samples taken from those who died from the disease—not those who lived through it.

“You can only access the lung when the patient dies,” says Douam, who’s based at NEIDL. “You cannot obviously get someone who had a mild disease and tell them, ‘Oh, give me your lung.’ In contrast to lung autopsy samples from diseased patients, the lungs from milder or asymptomatic patients are just much harder to access. When you have the diseased lung, you get a snapshot of the end-stage disease.”

To get around this challenge, Douam and the research team developed a new model—a mouse engrafted with human lung tissue and bolstered with a human immune system derived from stem cells—for monitoring the different stages of SARS-CoV-2 infection and COVID-19 disease. Douam says that mice with human lung tissue, but without the human immune system, don’t react well to infection—the lung tissues are damaged in a similar way to people with a severe case of the disease. But when they studied mice that also had a humanized immune system, it was different. “We were barely seeing any virus in the lungs,” he says. “The lung was protected. Then we asked the question, ‘Why is the lung protected?’ And this is where we found the macrophages.”

“Protection-Defining Genes”

According to Devin Kenney, a PhD student in Douam’s lab and lead author on the latest paper, one signature of lungs that were more severely impacted by COVID was a lack of macrophage diversity. They were dominated by a pro-inflammatory macrophage—the cells that usually respond to viruses and bacteria—called M1.

“It seems they drive this hyper-inflammatory response,” says Kenney (MED’27), “and it leads to a more severe disease state.”

By contrast, those immune systems that mixed in more of the cells that typically help in wound repair—M2 or regulatory macrophages—fared better.

“If you have a more diverse macrophage population that has both regulatory and inflammatory macrophages, you can more effectively regulate the signals driving antiviral responses, shutting them off when appropriate,” he says. “Then, the immune system can clear the virus really rapidly, protect the tissue.”

The researchers tied this positive antiviral response to a set of 11 genes they called “protection-defining genes.”

In cases of effective resistance, these genes were working harder, or what’s known as upregulated.

“We now know not only that macrophages can promote protection in the lung tissue,” says Douam. “We also know the key set of genes that these macrophages need to express to protect the lung.”

What they don’t know yet is why some people can put a diverse mix of macrophages to work while others can’t. That’s a target for future studies.

“What we’re doing here is really upstream,” says Douam. “If you can generate knowledge and better understand the molecular processes driving lung protection from COVID-19, then once you get this really good comprehensive picture of what’s happening, you can start designing potential immunotherapy strategies.”

And that’s the end goal of this work. Knowing that some genes are critical in the COVID fight gives potential fresh targets for drugs.

With new coronavirus variants springing up and taking root at a rapid rate, says Douam, it’s important that scientists find alternatives to medications that target the virus itself.

“The virus, over time, can start escaping these types of drugs,” he says. “It’s not the virus itself that makes you critically ill, it’s an overreaction of the immune system.”

Finding drugs that help patients have a more balanced immune response could “complement the antiviral strategy.”

Add obesity to the mix, and the clotting risk shoots up. In COVID-19 patients with obesity, Hunt says, “You’ve got such sticky blood, oh my—the stickiest blood I have ever seen in all my years of practice.”

Immunity also weakens in people with obesity, in part because fat cells infiltrate the organs where immune cells are produced and stored, such as the spleen, bone marrow, and thymus, says Catherine Andersen, a nutritional scientist at Fairfield University. “We are losing immune tissue in exchange for adipose tissue, making the immune system less effective in either protecting the body from pathogens or responding to a vaccine,” she says.

The problem is not only fewer immune cells, but less effective ones, adds Melinda Beck, a co-author of the Obesity Reviews metaanalysis who studies obesity and immunity at the University of North Carolina, Chapel Hill. Beck’s studies of how obese mice respond to the influenza virus demonstrated that key immune cells called T cells “don’t function as well in the obese state,” she says. They make fewer molecules that help destroy virus-infected cells, and the corps of “memory” T-cells left behind after an infection, which is key to neutralizing future attacks by the same virus, is smaller than in healthy weight mice.

Beck’s work suggests the same thing happens in people: She found that people with obesity vaccinated against flu had twice the risk of catching it as vaccinated, healthy weight people. That means trials of vaccines for SARS-CoV-2 need to include people with obesity, she says, because “coronavirus vaccines may be less effective in those people.”

Beyond an impaired response to infections, people with obesity also suffer from chronic, low-grade inflammation. Fat cells secrete several inflammation-triggering chemical messengers called cytokines, and more come from immune cells called macrophages that sweep in to clean up dead and dying fat cells. Those effects may compound the runaway cytokine activity that characterizes severe COVID-19. “You end up causing a lot of tissue damage, recruiting too many immune cells, destroying healthy bystander cells,” says Ilhem Messaoudi, an immunologist who studies host responses to viral infection at the University of California, Irvine. Of the added risk from obesity, she adds: “I would say a lot of it is immune-mediated.”

The severity of COVID-19 in people with obesity helps explain the pandemic’s disproportionate toll in some groups. In American Indians and Alaska Natives, for example, poverty, lack of access to healthy food, lack of health insurance, and poor exercise opportunities combine to render “rates of obesity … remarkably high,” says Spero Manson, a Pembina Chippewa who is a medical anthropologist at the University of Colorado’s School of Public Health. And obesity “is connected to all these other [illnesses], such as diabetes and cardiovascular disease, rendering us susceptible” to severe COVID-19, Manson says.

In addition, a large body of literature shows that people with obesity may delay seeking medical care due to fear of being stigmatized, increasing their likelihood of severe disease or death. “Patients that experience weight stigma are less likely to seek care and less likely to seek follow up because they don’t feel welcome in the health care environment,” says Fatima Cody Stanford, an obesity medicine physician-scientist at Harvard Medical School and Massachusetts General Hospital.

COVID-19–specific research on this question is urgently needed, she adds. “We don’t know how many people are dying in the community that are never making it in,” Stanford says. “Maybe that was [due] to their weight or to their race, the two most prevalent forms of stigma in the U.S.”

For people with obesity, the extra risk adds a psychological burden, says Patty Nece, vice chair of the Obesity Action Coalition. “My anxiety is just totally ramped up,” she says, adding that because of stress eating she’s recently regained 30 of the 100 pounds she lost before the pandemic. “You have the general anxiety of this pandemic … and then you layer on top of it: ‘You in particular, you could get really sick.'”

Data on how to treat COVID-19 patients with obesity are scant. Published evidence supports giving such patients higher doses of anticoagulants, says Scott Kahan, an obesity medicine physician who directs the National Center for Weight and Wellness. But very little is known about whether and how to adjust other treatments such as remdesivir and dexamethasone, partly because patients with obesity “are often excluded from clinical trials,” he says. He urges that COVID-19 treatment trials include people with high BMIs wherever possible.

People with obesity should take extra care to avoid getting sick, Messaoudi says. “If you are a person with obesity, be extra, extra cautious,” she says. “Wear your mask. Wash your hands. Avoid large gatherings.”

In addition, exercising and, separately, losing even a little weight can improve the metabolic health of a person with obesity, and, in doing so, reduce their chances of developing severe COVID-19 if they become infected, says Stephen O’Rahilly, a physician-scientist who directs the MRC Metabolic Diseases Unit at the University of Cambridge. “If you’re 300 pounds, even losing a modest amount is likely to have a disproportionate benefit on how well you do with coronavirus infection. You don’t have to become a slim Jim to benefit.”

HIGH INTENSITY HEALTH’s THOUGHTS

Policymakers and the media are on the wrong side of history for ignoring solutions that actually improve health. I have a new study that reviewed over 12 million scientific articles related to all things Covid-19 disease severity and risk factors increasing the risk for disease severity. And guess what this paper found. So we’ve heard over and over that this is the pandemic of the unvaccinated.

Well, this is really the pandemic of the unhealthy.

Now, I know for some of you that might be offensive because perhaps you’ve ignored your health over the years. So this video is not to shame you. We have designed this video and this podcast to encourage you and inspire you to make the modifiable lifestyle factors and nutrition changes necessary to improve your health.

Let’s dive into the data. I think you’ll find this quite interesting. The title of the paper here is modifiable contributing factors to Covid-19.

A comprehensive review by scientists in Chronic diseases have similar origins to covid-19, according to a recent study. This means that if we ignore the underlying health conditions in a population, we can expect the same outcome from Covid-19.

The current approach is not working because it is not addressing the root cause of the problem. The root cause is exposure to toxic stimuli and toxic lifestyle behaviors. We need to address these root causes in order to make a lasting impact on the health of our population.

We’re finding contributable, modifiable factors that worsen chronic disease. The same factors that are causing severe Covid.

They’re two sides of the same coin. So we can no longer run and hide from pathogens. We need to continue to implement policies that will keep us safe. You might think my Covet’s over, but it’s not. If you work at Google, Amazon, Facebook, if you go to University Of Washington or Harvard, you need to not only wear a mask in most places, but you also need to be up to date on your immunizations. These are the same emanations that people that have been dying in the hospital have gotten by the way. I’m just throwing it out there. So why are we focusing with the same degree of intensity about lessening the immune system dysfunctionality. Because these are things that are sustainable if we’re serious about saving lives.

We should be serious about this now. I just want you to know the areas that are modifiable that you have tangible control over.

Over the past three years, researchers have looked at factors that make it harder for the body to fight off infection.

They found that some of these factors include poor sleep, iron deficiency, and exposure to painkillers.

Vulnerable to severe infectious disease, it turns out. And so, they looked at that. As well, what’s interesting about this paper is they also looked at biotoxins. So, we’re talking about mycotoxins like Mold, cytomegalovirus, herpes simplex Virus, and also occupational and food Exposure to persistent organic Pollutants or the pops. The pops are endocrine disrupting chemicals including but not limited to arsenic, Benzene, Benzodine, BPA, cadmium, lead, and much more. And this, I think, is the most important category: the psychosocial aspect of it. Stress, living in isolation – remember how it was such a brilliant idea to lock everyone in their homes and isolate people. Well, guess what that does. When you’re isolated, my friends, that leads to feelings of angst.

I shared a study on Monday’s live video about HIV Positive individuals who are homosexual. The men who are still in the closet had, after controlling for other factors, worse outcomes compared to people who are living lies are more likely to get sick with Covid.

Because when you lie you are stressing, your immune system gets weaker.

So, if you want to stay healthy, live with integrity and be honest.

One major public health official recently gave a policy speech in El Salvador. In the speech, he talked about a video (promoted in 2021).

He said that the video was about exercising outdoors, eating healthy foods, getting enough sleep, and reducing sugar intake.

He also said that this message needs to be spread to more people. The article concludes with the idea that any long-term strategy for addressing either Covid-19 or the associated co-morbidities must involve reducing or eliminating exposure to toxic stimuli and modifying toxic behaviors.

I think Jim Rohn was the first person to talk about this. Other folks have talked about it too, so we need to focus on the root cause. And addressing the root cause, instead of continuing to ignore it. We literally put masks on ourselves every day and throw them away. I mean, at some point we have to think about the global waste we’re creating. And focus on the root cause. So let me know what you think about that in the comments below. I’ll share links to this article in the description. Please share this with a friend and help them conceptualize how they can reduce the underlying health conditions with diet, exercise, toxin exposure and toxin avoidance.

The links above are affiliate links, so I receive a small commission every time you use them to purchase a product. The content contained in this video, and its accompanying description, is not intended to replace viewers’ relationships with their own medical practitioner. Always speak with your doctor regarding the content of this channel, and especially before using any products, services, or devices discussed on this channel or website.