r/science • u/Wagamaga • Feb 03 '25
Neuroscience Scientists discover that even mild COVID-19 can alter brain proteins linked to Alzheimer’s disease, potentially increasing dementia risk—raising urgent public health concerns.
https://www.imperial.ac.uk/news/260553/covid-19-linked-increase-biomarkers-abnormal-brain/
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u/StreetWiseBarbarian Feb 05 '25 edited Feb 05 '25
Scientists also discovered that vitamin d alone in large, infrequent doses can prevent many of the inflammatory impacts of most common viruses, even preventing infection outright, as well as their spread, even though calcitriol and vitamin d’s uses as effective immune system modulators are well studied, most folks still won’t educate themselves cus it counters what they think they know about how our immune systems function. So I put together a brief summary of some of the research that is available.
Here’s a comprehensive guide to understanding why having high enough (70-80nl/mg) blood levels of d vitamin can keep you from getting covid, and most other common viruses as well as helping quickly end the systemic inflammation caused by them if you’re already sick, in a short timeframe:
..This is how vitamin D interacts with the immune system; specifically, what directly influences immune activity based on the amalgamation of several clinical trials as well as a meta study on dozens of others:
The Role of Vitamin D in Immune System Modulation
Vitamin D is a critical modulator of immune function, but it does not act on the immune system in isolation. Its effects are mediated through a complex network of hormones, enzymes, and signaling molecules that directly influence immune cell behavior. While vitamin D initiates or amplifies certain immune responses, it relies on intermediaries and supporting systems to achieve the effects ascribed to it.
How Vitamin D Functions
Vitamin D is primarily obtained through sunlight exposure (via the skin) or diet and exists in an inactive form. After conversion in the liver to 25-hydroxyvitamin D (25D), it is further hydroxylated in the kidney to its active form, 1,25-dihydroxyvitamin D (calcitriol), by the enzyme 1-alpha-hydroxylase (CYP27B1). This active form binds to the vitamin D receptor (VDR), a transcription factor present in various immune cells, including T cells, B cells, macrophages, and dendritic cells.
Vitamin D acts locally in immune environments (paracrine/autocrine activity) and systemically through endocrine signaling. Immune cells like macrophages and dendritic cells produce their own calcitriol via localized 1-alpha-hydroxylase, allowing for targeted modulation of immune responses.
When calcitriol binds to VDR, the complex forms a heterodimer with the retinoid X receptor (RXR). This dimer translocates to the cell nucleus, where it binds to vitamin D response elements (VDREs) on the DNA, regulating genes involved in immune function, including those encoding for antimicrobial peptides like cathelicidin and beta-defensin 4, which enhance innate immunity.
Direct Factors Influencing the Immune System
While vitamin D plays a key role, its actions are dependent on or complemented by other factors:
Cytokines like IL-10, IL-6, IL-17, and TNF-α are directly responsible for modulating immune activity. For example:
PTH stimulates renal production of calcitriol, ensuring sufficient systemic levels of active vitamin D for immune and skeletal functions.
Immune cells directly respond to pathogens through receptors like Toll-like receptors (TLRs), which recognize microbial components (e.g., lipopolysaccharides). TLR activation triggers a cascade of events, including the upregulation of cathelicidin and other antimicrobial peptides, which is amplified by vitamin D.
The transcription factor NF-kB is essential for inflammatory signaling. While vitamin D modulates NF-kB activity, NF-kB directly binds to genes involved in immune activation, driving processes like inflammation and pathogen clearance.
Vitamin D’s effects on adaptive immunity are indirect. It inhibits B cell proliferation and promotes T regulatory cells (Tregs), which maintain immune tolerance. Additionally, it shifts T cell phenotypes from inflammatory (Th1 and Th17) to anti-inflammatory (Th2), reducing autoimmune tendencies.
Protective Immunity and Infection Prevention
The articles I’ve studied emphasize vitamin D’s role in reducing infection susceptibility through its effects on protective immunity:
Vitamin D increases the production of antimicrobial peptides like cathelicidin, which disrupt bacterial cell membranes and neutralize infections. TLR signaling is amplified by vitamin D to produce these peptides efficiently.
Studies show a correlation between low vitamin D levels and increased respiratory infections, including influenza and tuberculosis. For example, military recruits with higher vitamin D levels had fewer respiratory infections.
Vitamin D administration has been linked to reduced infection rates in controlled studies, such as a 42% reduction in influenza incidence in one clinical trial.
Vitamin D and Autoimmune Disease
Low vitamin D levels are associated with increased risk and progression of autoimmune diseases like multiple sclerosis (MS), rheumatoid arthritis (RA), and type 1 diabetes (T1D).
Vitamin D deficiency correlates with higher disease activity and severity in lupus, MS, and RA. For example, lupus patients often exhibit severe vitamin D deficiency, which aligns with increased disease activity.
Vitamin D is not directly responsible for every immune modulation effect. Instead, it operates dynamically within a network of hormones, enzymes, and signaling molecules that collectively influence immune function. Factors like cytokines, PTH, NF-kB, TLRs, and other hormones interact with or respond to vitamin D signaling, amplifying or complementing its effects. Thus, while vitamin D is a key regulator, it relies on this broader system to achieve its protective and modulatory roles in immunity and disease prevention.