Current evidence that vitamin D is effective against COVID-19 neurological sequelae
Current evidence that vitamin D is effective against COVID-19 neurological sequelae

Current evidence that vitamin D is effective against COVID-19 neurological sequelae

In a recent Life sciences study, researchers are analyzing the available scientific evidence that supports vitamin D as a neuroprotective agent against the neurological sequelae of coronavirus disease 2019 (COVID-19).

Examination: COVID-19 and neurological sequelae: Vitamin D as a possible neuroprotective and / or neurore repair agent. Image credit: Komarina /


The infectious capacity of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is not limited to the respiratory system. In fact, SARS-CoV-2 can also invade other vital organs, including the central nervous system (CNS), which can result in several neurological consequences.

Some of the neurological manifestations of SARS-CoV-2 infection may include immune-mediated demyelinating disease, anxiety, stroke, depression, and neurodegeneration. Two possible reasons why SARS-CoV-2 attacks the CNS include its ability to remain latent in cells for long periods, as well as its association with the induction of cytokine storm.

These neurological medical conditions may be exacerbated in COVID-19 patients with underlying chronic medical conditions such as hypertension, diabetes, or coronary heart disease. As a result, this subgroup of COVID-19 patients is more likely to experience neurovascular sequelae of this disease.

There is considerable scientific evidence that vitamin D down-modulates the effects of neuroinflammatory cytokines, thus attenuating the negative consequences of COVID-19. In particular, vitamin D also has other anti-inflammatory / immunomodulatory effects.

In the current meta-analysis, which covers 54 independent studies examining the literature on COVID-19 and vitamin D, the researchers found that patients with low 25-hydroxyvitamin D levels showed higher susceptibility to SARS-CoV-2 infection and related hospitalization. . These patients also had an increased risk of acute respiratory disease, hospitalization, and SARS-CoV-2-related mortality.

Neuroinflammation and neurodegeneration in COVID-19

Due to the cytokine storm, some COVID-19 patients have reported acute necrotizing haemorrhagic encephalopathy. During SARS-CoV-2 invasion of dendritic cells, monocytes, macrophages, and proinflammatory cytokines are overexpressed, including tumor necrosis factor-alpha (TNF-α), interleukin-1, and 6 (IL-1 and IL-6).

As these biomarkers are associated with increased COVID-19 severity and its derived neurological pathologies, monitoring of these biomarkers may help to categorize the most severely ill patients and select appropriate therapeutic options.

In a study of more than 30,000 healthy individuals, autoantibody titers targeting type-1 interferon (IFN) increased with age. This finding shows why older people tend to have a poorer prognosis for COVID-19 and its neuropathological consequences.

Since brain cells in some cases act as latent reservoirs of SARS-CoV-2, such latency may be associated with delayed apoptosis and oxidative stress pathways in the cells of the nervous system, leading to neurodegenerative pathologies such as Alzheimer’s disease (AD). Other reports suggest that SARS-CoV-2 increases alpha-synuclein synthesis, which triggers the release of various cytokines and chemokines that are characteristic of Parkinson’s disease (PD).

The SARS-CoV-2-induced neuroinflammatory response is associated with a marked reduction in human angiotensin-converting enzyme 2 (hACE2) activity. hACE2 regulates neuroprotective and neuroimmunomodulatory functions in the host and potentially neutralizes cellular inflammation and oxidative stress.

Furthermore, SARS-CoV-2-ACE2 binding alters gamma-aminobutyric acid (GABA) neurotransmission in the amygdala and possibly in other parts of the brain. Alternatively, it may produce changes in dopaminergic neurotransmission, representing other neurodegenerative sequelae associated with COVID-19.

Antibodies to SARS-CoV-2 epitopes have also been shown to react with receptors at the neuromuscular junction, including the nicotinic acetylcholine. Thus, this activity could accelerate COVID-19-associated neurodegenerative pathologies, such as myasthenia gravis.

Vitamin D supplementation minimizes COVID-19-related neurological sequelae

Several studies have explored vitamin D and 25-hydroxyvitamin D3 (calcifediol) as new therapeutic options for COVID-19-related neurological conditions. In fact, this type of supplement has been shown to improve innate immunity, such as early macrophage response to mucosal invasive viruses and bacteria, thereby reducing the incidence and severity of acute respiratory infections.

Adequate plasma levels of 25-hydroxyvitamin D are converted to the hormone 1,25-dihydroxyvitamin D, which activates genes encoding antimicrobials against fungi, bacteria and viruses, including SARS-CoV-2.

In their study, Durrant et al. showed that vitamin D3 supplementation effectively induced gene expression associated with type I and type II IFN activity, which is crucial for the innate response to bacterial and viral infections. Similarly, 1,25 (OH) 2D helps to inhibit the effect of renin by increasing the production of hACE2, while reducing the cellular immune response induced by the cytokine storm during SARS-CoV-2-induced pneumonia.

Several clinical studies are also underway to evaluate the possible optimization of the SARS-CoV-2 vaccine efficiency by supplementation of vitamin D.


Taken together, data from several studies support the use of vitamin D supplements as well as its role in improving disease prognosis and preventing fatal consequences.

In the future, longitudinal studies should follow up with COVID-19 patients in order to gather the necessary data to evaluate the diagnosis, prognosis and treatment of COVID-19 related neurological sequelae. Meanwhile, studies should also monitor vitamin D supplementation in current COVID-19 patients and in those who have recovered from the disease.

To conclude, vitamin D may be a valuable addition to the current therapeutic arsenal against COVID-19 neurological sequelae.

Leave a Reply

Your email address will not be published.