antivirals Pharmacy and Health Blog from myGenericPharmacy.com

Iron dysregulation linked to long COVID development

March 15, 2025 blogadmin Comments 0 Comment

According to new research, SARS-CoV-2 infection-related issues with blood iron levels and the body’s capacity to control this vital nutrient may be a major cause of protracted COVID-19. The finding may help explain why symptoms resembling those of long-term COVID are also frequently observed in a variety of post-viral disorders and chronic inflammation, in addition to suggesting potential preventative or therapeutic measures.

Although estimates vary greatly, up to three out of ten individuals infected with SARS-CoV-2 may develop long-term COVID-19, which manifests as memory and concentration issues (also known as “brain fog”), exhaustion, shortness of breath, and muscle aches. As of March 2023, the Office of National Statistics estimates that 1 in 9 people in the UK alone were suffering from self-reported long COVID-19.

Researchers at the University of Cambridge started adding individuals who had tested positive for the virus to the COVID-19 cohort of the National Institute for Health and Care Research (NIHR) BioResource shortly after the COVID-19 pandemic began. These ranged from patients admitted to the Cambridge University Hospitals NHS Foundation Trust, some of whom were admitted to the intensive care unit, to asymptomatic medical personnel found through routine screening.

Participants gave blood samples for a year, which allowed researchers to track changes in the blood after infection. As it became evident that many patients would experience long-lasting COVID symptoms, researchers were able to follow up on these samples to determine whether any blood changes were associated with the patients’ subsequent health. Researchers from the University of Cambridge’s Cambridge Institute of Therapeutic Immunology and Infectious Disease (CITIID), along with colleagues from Oxford, examined blood samples from 214 people for their findings, which were published in Nature Immunology. When asked about their recovery, about 45% of respondents said they experienced long-term COVID-19 symptoms three to ten months later.

Having recruited a group of people with SARS-CoV-2 early in the pandemic, analysis of several blood samples and clinical information collected over 12 months after infection has proven invaluable in giving us important and unexpected insights into why, for some unfortunate individuals, initial SARS-CoV-2 infection is followed by months of persistent symptoms, said Professor Ken Smith, who was Director of CITIID at the time of the study and will start a new role as Director of the Walter and Eliza Hall Institute of Medical Research (WEHI) in Melbourne, Australia, in April.

As early as two weeks after COVID-19, the team found that in those who reported long COVID many months later, persistent inflammation—a normal component of the immune response to infection—and low blood iron levels, which lead to anemia and interfere with the production of healthy red blood cells, could be observed. Regardless of age, sex, or the initial severity of COVID-19, early iron dysregulation was found in the long COVID group. This suggests that recovery may be impacted even in individuals who were not at high risk for severe COVID-19 or who did not need hospitalization or oxygen therapy when ill. It took a very long time to recover from the early disruption of iron levels and the body’s ability to regulate iron during SARS-CoV-2 infection, especially for those who reported long COVID months later.

In the face of persistent inflammation, we observed evidence that the body was not doing a very good job of producing more red blood cells in an attempt to address low iron availability and the ensuing anemia. It’s interesting to note that individuals who developed long COVID after a milder course of acute COVID-19 displayed comparable blood patterns, even though iron dysregulation was more severe during and after severe COVID-19. Although symptoms tended to persist long after iron levels had recovered, the most notable correlation with long COVID was the speed at which inflammation, iron levels, and regulation returned to normal after SARS-CoV-2 infection. stated that iron dysregulation is a normal reaction to infection and a frequent result of inflammation.

The body eliminates iron from the bloodstream in response to an infection. This shields us from potentially fatal bacteria that quickly grow and absorb iron from the blood. The body redistributes iron as a result of this evolutionary response, turning the blood plasma into an iron desert. On the other hand, if this continues for a long period, there will be less iron for white blood cells, which require iron to function properly, and red blood cells, which means oxygen is transported less effectively, impacting metabolism and energy production. In the end, the protective mechanism becomes problematic.

The results could help explain why long-term COVID-19 and some other post-viral syndromes with persistent symptoms frequently exhibit symptoms like fatigue and exercise intolerance. By correcting iron dysregulation in early COVID-19, the study suggests possible strategies to prevent or lessen the effects of long COVID-19 to avoid negative long-term health outcomes, according to the researchers.

One strategy could be to manage the severe inflammation as soon as possible before it affects the regulation of iron. Iron supplementation could be another strategy, but as Dr. Hanson noted, this might not be simple. People may not actually have insufficient iron in their bodies; rather, it may simply be stored in the wrong location. The iron must be remobilized and drawn back into the bloodstream so that the red blood cells can use it more effectively.

The study also confirms “accidental” findings from other research, such as the IRONMAN study, which examined the potential benefits of iron supplements for heart failure patients. The study was interrupted by the COVID-19 pandemic, but initial results indicate that trial participants had a lower risk of experiencing serious side effects from COVID-19. People who have beta-thalassemia, a blood disorder that can lead to excessive iron production in the blood, have seen similar effects.

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Can antibiotics, vaccines, and antivirals help lower dementia risk?

January 23, 2025 blogadmin Comments 0 Comment

A recent systematic review found that anti-inflammatory medications such as ibuprofen, as well as antibiotics, antiviral drugs, and vaccines, were linked to a lower risk of dementia. Up to 70% of those with dementia have Alzheimer’s disease, and the condition affects over 55 million people globally at an estimated cost of over $1 trillion. Before drawing any conclusions about repurposing current medications for the treatment of dementia, experts point out that more research is necessary due to the complexity of dementia in various individuals. In a recent systematic review, researchers from the Universities of Cambridge and Exeter in the United Kingdom found that anti-inflammatory drugs like ibuprofen, antibiotics, antiviral drugs, and vaccines, were linked to a lower risk of dementia.

Published in Alzheimer’s and Dementia: Translational Research and Clinical Interventions, the review examined data from 14 studies that included 1 million dementia cases and over 130 million people. Antimicrobials, vaccinations, and anti-inflammatory drugs (NSAIDs) were linked to a lower risk of dementia. In contrast, vitamins, supplements, antipsychotics, and diabetes medications were somewhat linked to a higher risk, according to the researchers’ analysis of medical and administrative records as well as large clinical datasets. Evidence regarding antidepressants and certain blood pressure medications was inconclusive. The authors observed that overall, there was a lack of consistency across studies in identifying specific medications that alter the risk of Alzheimer’s disease or all-cause dementia and that some limitations and false positives may have impacted findings.

It’s crucial to keep in mind that dementia, which merely characterizes a collection of progressive symptoms, can result from a variety of pathological conditions. Furthermore, according to Dr. Dot MacSweeney, Alzheimer’s disease, the most prevalent cause of dementia as we age, is not a single illness. It is complicated and has a lot of aberrant biomarkers. However, it is widely acknowledged that the majority of conditions that eventually lead to dementia do, in large part, have a neuroinflammatory origin, just like many other diseases. Large-scale, longitudinal, randomized controlled trials (RCTs) are required to prove a causal relationship between dementia risk and particular medications, according to MacSweeney.

Confounding variables such as age, gender, and comorbidities should be controlled for, and lifestyle and genetic data should be included to find effects specific to subgroups, and biomarkers (e.g. G. levels of tau or amyloid) to gauge how drugs affect the body. She also suggested that they concentrate on long-term results to verify a lower incidence of dementia. Given how common these drugs are already worldwide, Clifford Segil, DO, a neurologist at Providence Saint John’s Health Center in Santa Monica, CA, who was not involved in the review, expressed some skepticism to MNT regarding its findings: Studies frequently surface expressing concern for prescription and over-the-counter medications causing dementia that are not clinically observed. For instance, studies have shown that taking allergy drugs like Benadryl/diphenhydramine increases the risk of dementia; however, in my clinical neurology practice, I have never observed this to be the case.

Although sleep aids are frequently linked to deteriorating memory loss in the elderly, I think the advantages of getting a good night’s sleep exceed any possible hazards. According to him, there are too many cooks in the kitchen these days, and if dementia is a concern, you should speak with a specialist like me who makes it their career to diagnose and treat dementia patients. The best strategy to lower one’s risk of dementia, according to Segil, is to alter one’s lifestyle, since middle-aged habits shape one’s later years. He informed us that some tests related to the genetics of dementia do not ensure the onset of dementia and that false-positive test results are common. I would suggest leading a healthy lifestyle to prevent the need for a doctor’s prescription medication. If medication is required, I would suggest consulting a board-certified neurologist for guidance on which medications to take as you age.

Over 55 million people worldwide suffer from dementia, which is estimated to cost more than $1 trillion. Up to 70% of those affected have Alzheimer’s disease, which is typified by the accumulation of two proteins, tau and amyloid. Adults with early symptomatic Alzheimer’s disease, including those with mild cognitive impairment (MCI) and mild dementia with confirmed amyloid plaques, can now receive treatment with the monoclonal antibody donanemab, which was approved by the Food and Drug Administration (FDA) in July 2024. In 2024, the FDA granted accelerated approval to two additional monoclonal antibodies, lecanemab and aducanumab, after encouraging trial outcomes.

Alzheimer’s disease can be managed with the help of current treatments, but the disease’s progression is unaffected. In a global phase 3 clinical study, donanemab reduced cognitive decline in individuals with low/medium tau levels by 35% when compared to a placebo. There is broad agreement that multiple approaches are likely required to provide maximally effective treatment and the authors of the new review point out that these treatments target a single pathway in a complex condition and carry a significant risk of severe side effects. Although they emphasize that repurposing current medications for potential dementia treatment is a global priority, experts argue that, given the complexity of dementia and Alzheimer’s disease, more research is necessary to determine the specific effects of such medications.