The Covid Era Has More Diabetes and Brain Fog

uk vaccinated covid cases

By Therese Raphael and Sam Fazeli | Bloomberg

Commenting on Britain’s near-record-high number of Covid cases, the U.K.’s chief medical officer, Chris Whitty, said last Wednesday that we should expect seasonal peaks for the next few years, interspersed with new variants of SARS-CoV-2.

As we move into the post-pandemic, living-with-the-virus era, more research is surfacing about the ways even mild Covid cases leave lingering effects on health in some people. Three conditions in particular are capturing scientists’ attention due to the large number of sufferers: increased rates of diabetes, neuropsychological problems, and the illness known as long Covid. Researchers have found associations between Covid infections and each of these issues, but we don’t know enough yet to establish causality.

Bloomberg Opinion columnist Therese Raphael and Bloomberg Intelligence senior pharmaceutical analyst Sam Fazeli look at why the long tail of Covid is hard to pin down.

uk vaccinated covid cases

Therese Raphael:  Let’s start with diabetes. Early in the pandemic, it became clear that diabetes (and obesity, which is often linked to Type 2 diabetes) was a risk factor for developing more severe illness. Some recent research, including a study in the U.S. and another by German researchers, shows a higher incidence of diabetes in those who had Covid but were at low risk of diabetes up to that point. That seems significant, given that 11.5% of all global health spending is on diabetes and it’s been growing rapidly.

Sam Fazeli:  The U.S. study showed there was a greater risk of being diagnosed with diabetes after a Covid-19 infection, especially among those people who needed hospitalization or intensive care. There was also a clear link to age, prior conditions and obesity.

Another study, at Mass General, found that of the patients with diabetes hospitalized for Covid during March to September 2020, 13% had newly diagnosed diabetes. Yet, contrary to the above study, they found that new diagnosis was more common in younger individuals and, critically, those with higher inflammatory markers. The fact that one-third had known pre-diabetes before admission, and half regressed to pre-diabetes or were normal at follow-up, suggests the actual incidence of truly new, enduring diagnoses may be lower.

uk vaccinated covid cases

The German study you mention showed a 28% increase in the risk of being diagnosed with diabetes, closer to the Mass General study risk increase, but all three had limitations that make it difficult to draw firm conclusions.

TR: So are we any closer to understanding how Covid triggers diabetes in these patients?

SF:  That’s still unclear. The question is whether this apparent amplified risk is driven by the infection itself or a secondary effect. For example, there is a possibility that the diabetes is triggered by a more sedentary lifestyle, which may follow more severe cases. This may be enough to push someone who is already borderline diabetic (defined as an HbA1c of 6 or 6.5) over the line. This wasn’t assessed in the two recent studies you mentioned. In the German study, stress-induced diabetes is not accounted for.

TR: There is also data showing increased risk of diabetes in children after Covid.

SF: The research by the Centers for Disease Control and Prevention showed that new diabetes diagnoses were 166% higher in those under the age of 18 with Covid-19. The problem is that only a 31% higher risk was observed when the analysis was done using different data. This undermines the value of the CDC study.

There was also no data on prior illness or body weight. Obesity can raise the risk of both Covid-19 and diabetes. Without these details, the data is hard to interpret.

TR: Do we have diabetes diagnosis data on patients who have been fully vaccinated, including with a booster shot?

SF: Sadly, that is one area where a lot more work needs to be done, not just on the risk of diabetes, but on all long-term consequences of Covid. There have been a smattering of research papers on the subject. For example, a U.S. study showed that patients who were vaccinated before being diagnosed with Covid were seven to 10 times less likely to report two or more symptoms after their infection had cleared than unvaccinated patients. Also, patients who were vaccinated for the first time within four weeks of an infection were four to six times less likely to report multiple long-term symptoms.

There have also been anecdotal reports of people with long Covid being treated with Pfizer’s Paxlovid and reporting a resolution of their symptoms. This would suggest that, at least in some people, the problem is due to a persistent infection somewhere in the body. Whether it’s the virus directly or the ongoing inflammatory reaction to the infection which cause the issues is not known.

TR:  Now on to the brain. A recent study found an apparent reduction in grey matter thickness in regions of the brain involved in memory and cognition, as well as tissue damage in regions connected to olfaction, in subjects who had a Covid infection. What’s the research telling us?

SF:  It’s a “chicken and egg” quandary: Are people with faster brain degeneration more susceptible to Covid, or is this a result of Covid? Also, what would have happened if people with other respiratory infections had been studied? And what explains the gain in brain volume in older uninfected people (which was seen in the UK Biobank analysis)?

In a review of medical history, George Stefano showed that altered cognition was reported during prior pandemics, including that of influenza in 1889 and 1892 (Russian flu) and Spanish flu in 1918-1919. Symptoms included lethargy and chronic fatigue syndrome or post-viral fatigue syndrome. It’s also possible that social isolation which accompanied prior pandemics — as well as that of Covid-19 — is a factor in changes to the brain.

There was a study presented at the recent Alzheimer’s and Parkinson’s Diseases Conference showing a similar outcome to the U.K. Biobank study, but with one key difference: It followed patients for several months post-infection and found that those who didn’t “seek care for persisting symptoms” showed a recovery of brain loss and cognitive impairment.

The Swedish analysis, showing a recovery in brain volume after symptom resolution, raises the question of whether the effects are an imaging issue in people with a viral infection or are a real impact on the brain. Again, as in the U.K. study, there was no active control group, i.e. patients with other respiratory infections, aimed at proving that the issue was due to Covid rather than a viral infection more generally.

TR: That suggests that countries and localities where there is not high vaccine and booster coverage face a Catch-22 situation whereby they can lower infections with more restrictions but that could potentially lead to more secondary effects among those who get Covid.

SF: Exactly. The problem is in areas where people are either not vaccinated or less effective vaccines have been used, such as China. Research has shown an accelerated decline in patients suffering from various degrees of dementia before the pandemic started, likely the result of social restrictions.

TR: Finally, let’s turn to long Covid, the umbrella term of a post-Covid condition in which the body can be affected in a number of ways. One interesting piece of research published earlier this year identified four factors that could be associated with higher risk of developing long Covid: existing Type 2 diabetes (which also makes serious illness more likely); the presence of autoantibodies that can attack normal cells by mistake; a reactivation of the Epstein-Barr virus, which causes glandular fever and is often dormant after infection; and high level of coronavirus RNA in the blood.

Are we closer to understanding what causes long Covid or does it remain as mysterious as ever? Do we have any evidence that anti-viral treatments lowers the risk of any of these conditions?

SF:  The answer is no for now, even if we are making some headway. There is a lot of work to do still, especially in finding treatments. All of these findings are associations and don’t prove causation.

TR: All of this seems to reinforce the case for vaccines and boosters. But is more better? The FDA on Tuesday gave emergency-use authorization for a second booster of the Pfizer-BioNTech and Moderna shots for the over-50s. Is there data to suggest that’s going to help with either infections or any of the post-Covid issues we’re talking about?

SF: Not that we’ve seen. Data from Israel is not showing a significant effect of a fourth shot on the risk for infection, and if there is an impact, this is not long-lived. I think the decision on fourth shots should be based on the additional value of the shots for each age cohort and the cost, both economic and on the individual, as many still suffer for one or two days after the shots, which can impact their ability to work.

This column does not necessarily reflect the opinion of the editorial board or Bloomberg LP and its owners.

Therese Raphael is a columnist for Bloomberg Opinion. She was editorial page editor of the Wall Street Journal Europe.

Sam Fazeli is senior pharmaceuticals analyst for Bloomberg Intelligence and director of research for EMEA.

More stories like this are available on bloomberg.com/opinion

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