HomeHealth Update on Long COVID; Social Stress on the Immune System

Update on Long COVID; Social Stress on the Immune System

by admin

TTHealthWatch is a weekly podcast from Texas Tech. In it, Elizabeth Tracey, director of electronic media for Johns Hopkins Medicine in Baltimore, and Rick Lange, MD, president of the Texas Tech University Health Sciences Center in El Paso, look at the top medical stories of the week.

This week’s topics include a long COVID update, viral illnesses and neurodegenerative diseases, social stresses and their effects on the immune system, and the relationship between eating, sleeping, and weight change.

0:33 An update on long COVID

1:32 Almost a third had acute respiratory syndrome

2:30 A lot of viral infections have sequelae

3:30 Most resolve in a year

3:42 Viral illnesses and neurodegenerative diseases

4:42 Viral encephalitis and Alzheimer’s disease

5:43 Decreases Parkinson’s and dementia

6:46 Social stresses, T lymphocytes and older age

7:45 Naive or terminal T lymphocytes

8:45 Can do anything?

9:28 Eating, sleeping and weight change over time

10:28 Restricted timing did not help

11:30 App helped with research

12:18 End


Elizabeth: What do viruses have to do with neurodegenerative diseases?

Rick: Do social stresses affect our immune system?

Elizabeth: How about the association of eating and sleeping intervals with weight change over time?

Rick: And an update on long COVID symptoms.

Elizabeth: That’s what we’re talking about this week on TTHealthWatch, your weekly look at the medical headlines from Texas Tech University Health Sciences Center in El Paso. I’m Elizabeth Tracey, a Baltimore-based medical journalist.

Rick: And I’m Rick Lange, president of Texas Tech University Health Sciences Center in El Paso, where I’m also dean of the Paul L. Foster School of Medicine.

Elizabeth: Rick, why don’t we turn right to Clinical Infectious Diseases? This is a look at, “Oops, who is getting long COVID in the U.S.?”

Rick: This is an update titled “The Epidemiology of Long COVID in U.S. Adults.” What they attempted to do was to estimate the prevalence of long COVID and the impact on daily living among a representative sample of adults in the United States.

They conducted a population representative survey that was done over June and July of 2022, a random sample of over 3,000 U.S. adults aged 18 years and older. They used a questionnaire that was developed by the United Kingdom Office of National Statistics to estimate the prevalence of long COVID, adjusting for age and gender. Here is what they found out.

An estimated 7.3% of all the respondents reported long COVID. That means there were approximately 18.8 million adults that have long COVID symptoms. One quarter of the respondents with long COVID reported that their day-to-day activities were impacted a lot, and almost a third had severe acute respiratory syndrome related to COVID infection that was more than 12 months ago, so the long COVID symptoms persisted.

They had a higher incidence of long COVID symptoms among females, among those that had comorbidities, among those that did not receive boosters, and of course among those that were not vaccinated. Blacks, Asian Americans, and Hispanics had about a 40% to 50% less incidence of long COVID symptoms than the white U.S. population.

Elizabeth: I am really kind of curious about what you consider to be action points relative to long COVID. I have made the suggestion to you before in the course of the pandemic that if we had really examined long-term sequelae of even things like the flu or pneumonia, other common infectious diseases, I suspect that we would see abnormalities that remain. So I am wondering about the uniqueness of this with regard to COVID.

Rick: I would agree with you that a lot of viral infections — like we’re going to talk about neurodegenerative diseases in just a moment and their association with viral infections — viruses can cause long-standing symptoms. For example, Epstein-Barr virus is associated with chronic fatigue syndrome.

But what’s unique about the coronavirus is such a large number of individuals were infected, so the absolute numbers are just large. As I mentioned, 18.8 million individuals. I think the most disappointing thing is we know that vaccination and boosters decrease the incidence of severe COVID symptoms and long COVID symptoms, yet people are still reticent to get vaccinated or get boosted.

Elizabeth: Then comment, if you would, on when people ought to seek help for this and what you think might be helpful in terms of managing these symptoms.

Rick: Other than recognition right now and hopefully allowing time for these to go away, there is no treatment specific for long COVID symptoms at this time. That’s why prevention is so important.

Elizabeth: As I recall, I think we’ve covered studies that suggest that almost all of these resolve within a year on their own.

Rick: Most do. Unfortunately, some of the individuals here continue to have long COVID symptoms longer than a year. Now, this 7.3% is lower than previous estimates of about 20%.

Elizabeth: Okay. Let’s turn to Neuron since you’ve already foreshadowed this notion of, “Gosh, what do viral diseases do to us anyway?”

These folks took a look at two different databases, a database that’s called FinnGen and then also the U.K. Biobank. They had a discovery cohort that was from FinnGen — that’s a nationwide Finnish biobank with genotyping data available for over 300,000 individuals.

What they looked at in there was, “Let’s look at viral exposures and a variety of common neurodegenerative diseases.” These include Alzheimer’s disease, ALS, generalized dementia, which I’m not really sure exactly what that is, vascular dementia, Parkinson’s disease, and multiple sclerosis.

Then, they examined what are the links between these viral exposures and the neurodegenerative disease risk? Then they used the U.K. Biobank to replicate that data or validate it. They were able to replicate 22 of these associations.

Their largest effect association was between viral encephalitis exposure and Alzheimer’s disease, and that really increased somebody’s likelihood of developing Alzheimer’s several times. They also found sort of some of the usual suspects, the Epstein-Barr virus and MS, they used as a positive control. This is a really interesting association study, but it sure isn’t, as you’re so fond of saying, proving anything right now.

One thing that they do note is that a large number of these viral diseases are, as you’ve already said in the previous study, preventable using vaccines. So why not go ahead and get vaccinated and reduce your risk of a neurodegenerative disease?

Rick: Specifically, Elizabeth, vaccines that are currently available with respect to the viruses you mentioned associated with neurodegenerative diseases are vaccines against influenza, shingles, which is varicella zoster, and vaccines against pneumonia. These are already currently available.

We know that the vaccines not only decrease hospitalization rates, but other studies have suggested that vaccination decreases the incidence of Alzheimer’s disease, Parkinson’s disease, and dementia. This association of viruses and neurodegenerative disease goes back to the Spanish Flu of 1918, when individuals that had encephalitis afterwards had a higher incidence of Parkinson’s disease. It’s not a long stretch to suspect that these viruses cause long-standing inflammation, and inflammation affects the neurons or the central nervous system.

The thing that was a little surprising to me, Elizabeth, is some of these presented up to 15 years after the viruses, but there is at least biologic plausibility.

Elizabeth: That’s furthered by the fact that these viruses — many of them are neurotropic and they do cross the blood-brain barrier.

Rick: This is another example with the COVID vaccine, where [it] not only can affect acute disease incidence, but also affect long-term diseases associated with viral infections.

Elizabeth: They also note in here that, of course, messenger RNA vaccine technologies could obviate a lot of these infections going forward. It sounds like it’s well worth doing.

Rick: Let’s switch gears and talk about a paper that’s published in PNAS that talks about social stressors associated with T-lymphocytes in older U.S. adults. We know that stress is a risk factor for poor health. It increases the risk of early-onset, age-related disease and even premature death.

Most of the studies that have looked at stress have focused on the hormonal system, like the adrenal system or the pituitary, and very few have actually centered on how stress can actually influence the immune system.

Usually when we talk about stress, we talk about acute stress, chronic stress, and is it intermittent stress. Few of these have actually looked at the different types of stressors. For example, traumatic life stress, even lifetime discrimination and lifetime trauma. That’s what these investigators did.

They looked at these five different stressors and they measured the number and percent of CD4 T cells and CD8 T cells, and also whether they were naïve, that is, whether they had the ability to differentiate to address different types of infections, or that they were differentiated, i.e. were terminal and just about dead.

To summarize, it didn’t matter what kind of stress they looked at. All of them were associated with some type of immune disorder, either lower CD4 cells, or lower CD8 cells, or fewer of the naïve type. These lifetime stressors do affect the immune system.

Elizabeth: How does this compare to so-called normal aging and the relative percentages of CD4s and CD8s? And, is there anything we can really do about this?

Rick: We know that as we age our immune system ages too. It becomes senescent. They used the nationwide sample of over 5,600 adults over the age of 50, some of whom have stress and some of them who didn’t. They were able to look at the immune system in aging individuals and that normal aging process, and then those that had additional stressors as well, to determine if these stressors provided additional immune senescence in addition to what happened with the normal aging process.

Elizabeth: Okay. What about modification? What can we do about this? Anything?

Rick: One would presume that if you can decrease the stressors, that you could favorably affect the immune system and health.

Elizabeth: I would just add another basic science intervention that I’m familiar with, where they used transfusion from younger animals into older animals, and they are able to reconstitute a lot of this immune response, which I think is really fascinating. I’m wondering if there might be some kind of strategy like that in the offing as this kind of research goes forward.

Rick: If there are ways to make our immune system more plastic and younger, that would be a different type of therapy. This just talks about one part of the immune system. It doesn’t talk about B-cells. It doesn’t look at absolute infections.

Elizabeth: Finally, let’s turn to the Journal of the American Heart Association. This is a look at eating and sleeping intervals and what those do to weight change over time.

They have a cohort that they call the Daily24 Cohort. They had 547 participants who downloaded and used a mobile application to record their own timing of meals and sleep. They got information on weight and comorbidities at each outpatient visit of these folks from their electronic medical record for up to 10 years before until 10 months after baseline.

What they found was that the number of meals per day was positively associated with weight change. They also characterized these meals as small meals, medium meals, or large meals and unsurprisingly, I think, they found if you ate more large meals you weighed more. There was some positive association there.

The thing that was a little disappointing is there has been a lot of energy behind the notion that if you just restrict your daily food intake — irrespective of how many calories you consume to a truncated time period — you could somehow manage your weight. In this case, they did not validate that particular hypothesis.

Rick: That was the focus of the study, because there has been a lot of interest in the timing of food intake. People have intermittent fasting or they restrict their food intake to 4 to 12 hours per day without changing the calories in the hopes that it would actually improve body weight. It doesn’t.

Time-restricted eating has had some benefits in randomized clinical trials. It improves the cardiometabolic risk factors, including abdominal fat loss, glucose regulation, insulin resistance, blood pressure, and lipid profile. But what this study shows is it doesn’t actually decrease weight.

Elizabeth: Unsurprising and a little bit disappointing. What did you think about the utility of the app with regard to this study?

Rick: I thought that the app was helpful for the investigators to look at not only the amount of food, but the timing. Now that we know that the timing of when you intake food doesn’t really matter, I’m not sure that it has general applicability. Your thoughts?

Elizabeth: I wonder if there is some utility in recording whether one is consuming a small, medium or a large meal at different times of the day — might be helpful over the long haul.

Rick: Elizabeth, that’s interesting because in the old days you didn’t need an app to do it. You just needed a little notebook and record what you ate. You’re right. Anything that decreases the frequency and the caloric intake, whether it’s an app or it’s a simple notebook, will help reduce weight.

Elizabeth: On that note then, that’s a look at this week’s medical headlines from Texas Tech. I’m Elizabeth Tracey.

Rick: And I’m Rick Lange. Y’all listen up and make healthy choices.

Source : MedPageToday

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