Volcanic eruption => clouds (low vitamin D?) => Black death

Volcanic eruptions set off a chain of events that brought the Black Death to Europe

which refers to Climate-driven changes in Mediterranean grain trade mitigated famine but introduced the Black Death to medieval Europe (has PDF)

Possible Link Between the Black Death and Low Vitamin D Perplexity AI - Dec 2025

Yes, it is highly plausible that low vitamin D levels contributed to the severity and high mortality of the Black Death (1347–1351), although it was likely a contributing factor rather than the sole cause.

Recent research supports this hypothesis through three main lines of evidence: the environmental context of the "Little Ice Age," the biological mechanism of vitamin D in fighting Yersinia pestis, and skeletal evidence of chronic stress in plague victims.

1. The "Little Ice Age" and Reduced Sunlight

The Black Death arrived during the onset of the Little Ice Age, a period of global cooling that began in the early 14th century. This climate shift brought increased cloud cover, heavy rains, and shorter, cooler summers to Europe.^1 2

• Reduced UVB: Since the body creates vitamin D primarily through exposure to UVB rays in sunlight, persistent cloud cover and cooler temperatures (requiring more clothing) would have led to widespread population-level vitamin D deficiency.
• Famine Connection: These conditions also caused the Great Famine (1315–1317). Malnutrition exacerbates vitamin D deficiency, as dietary sources (like fatty fish) were not consumed in sufficient quantities to compensate for the lack of sunlight.³

2. Biological Mechanism: The Cathelicidin Connection

The strongest biological link is cathelicidin (LL-37), an antimicrobial peptide that your immune system uses to kill bacteria.

• Vitamin D Dependence: Vitamin D is the specific "key" that unlocks the gene to produce cathelicidin. Without sufficient vitamin D, your white blood cells (macrophages) cannot produce enough of this natural antibiotic.^4 5
• Battle against Yersinia pestis: Yersinia pestis (the plague bacterium) is a sophisticated pathogen that evolved to resist antimicrobial peptides. It modifies its outer membrane (specifically the Lipid A section) to repel these attacks. However, high levels of cathelicidin can still be effective or overwhelm these defenses. A population with low vitamin D would have had a "disarmed" innate immune system, producing insufficient cathelicidin to fight off the initial infection before it became systemic.^6 7 8

3. Skeletal Evidence from Plague Cemeteries

Bioarchaeological analysis of the East Smithfield Black Death cemetery in London provides physical evidence of this susceptibility.

• Stress Markers: Victims buried there show high rates of dental enamel hypoplasia, a defect in tooth enamel that forms during childhood stress, malnutrition, or disease.^9 3
• Interpretation: While this doesn't exclusively prove rickets (severe vitamin D deficiency), it confirms that the victims were physiologically stressed and nutritionally comprised before they caught the plague. A population with chronic nutritional deficiencies—likely including vitamin D—was significantly more likely to die when exposed to the pathogen.

The Seasonality Paradox

One counter-argument is the seasonality of the plague. The Black Death mortality often peaked in late summer and early autumn (August–October), a time when vitamin D levels are typically at their highest after a sunny summer.¹⁰

• Vector vs. Host: This suggests that the lifecycle of the rat flea (Xenopsylla cheopis)—which reproduces rapidly in warm, humid weather—was the dominant factor. The sheer number of infected fleas likely overwhelmed human immune systems regardless of vitamin D status.
• Immune Lag: However, if the preceding years had been unusually cloudy and wet (as historical records suggest), the population may have entered summer with already depleted reserves, meaning the "seasonal peak" of vitamin D never actually occurred.

Summary of the Connection

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