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Food · lesson 6 of 12

Vitamin D — the sunshine hormone you're probably low on

Why D is the most common shortfall, D3 vs D2, the K2 + magnesium team, and how to test it.

7 min read · reviewed October 2026

Vitamin D is barely a "vitamin" at all — it behaves like a hormone. Your skin makes it when UVB sunlight hits cholesterol in the skin, your liver and kidneys then convert it into the active form, and that active form switches genes on and off in nearly every tissue you have.

It's the single most common micronutrient shortfall in the modern world, for one simple reason: we evolved outdoors and now live indoors.

Make a guess

Roughly what fraction of adults are below the commonly used vitamin D sufficiency threshold (~30 ng/mL / 75 nmol/L)?

Somewhere between 5 and 90 %.

Reveal the answer →

~40% (estimates vary by cutoff, season, latitude, skin tone)

Estimates range from roughly a quarter to well over half of adults depending on the threshold and population — ~40% is a defensible middle figure. The drivers are consistent: indoor life, sunscreen, higher latitudes, darker skin (more melanin = less synthesis), age (skin makes less with time), and the fact that almost no foods carry meaningful amounts.

What vitamin D actually does

In plain terms

Vitamin D lets you absorb calcium from food and tells your immune system how to behave. Too little and your bones suffer and your immunity gets dysregulated.

How it works →

UVB converts 7-dehydrocholesterol in skin to vitamin D3. The liver hydroxylates it to 25-hydroxy-vitamin D (25-OH-D, the storage form measured on blood tests), and the kidney converts that to 1,25-dihydroxy-vitamin D (calcitriol), the active hormone. Calcitriol binds the vitamin D receptor (VDR) — present in bone, gut, immune cells, muscle and more — acting as a transcription factor that regulates calcium absorption in the gut, bone remodeling, and immune-cell signaling.

What the studies show →

The bone role is rock-solid: severe deficiency causes rickets in children and osteomalacia in adults, and D is required for dietary calcium absorption. Beyond bone, observational data link low 25-OH-D to many conditions, but large randomized trials (e.g. broad supplementation trials in already-replete populations) have mostly failed to show big reductions in cancer or cardiovascular events — the strongest case for supplementing is correcting a genuine deficiency, not megadosing a normal level.

D3 vs D2 — and its teammates

D3 (cholecalciferol)

The form your skin makes and the form in animal foods (fatty fish, egg yolk). In supplements it raises and maintains blood 25-OH-D more effectively than D2 — the preferred choice for most people. Sourced from lanolin (sheep wool) or, for vegans, lichen.

D2 (ergocalciferol)

The plant/fungal form, also the older prescription high-dose form. It works but is generally less potent at sustaining blood levels than D3. Fine if it's what you have, but D3 is the better default.

Vitamin K2 — the traffic cop

D raises calcium absorption; K2 helps direct that calcium INTO bone and away from arteries (by activating proteins like osteocalcin and matrix Gla protein). Many people pair D3 with K2, especially at higher D doses. Food sources of K2: natto, hard cheeses, egg yolk.

Magnesium — the enabler

Every enzyme that activates and uses vitamin D depends on magnesium. If you're magnesium-deficient, supplementing D works less well. Correcting magnesium alongside D is sensible — and magnesium is itself widely under-consumed.

RDA vs the level clinicians target — and the upper limit

In plain terms

The official RDA (600–800 IU) is set to protect bones for most people. Many doctors aim a bit higher to hit a target blood level, but there's a real ceiling — more is not safer.

How it works →

The RDA assumes minimal sun exposure and targets the intake that keeps the population's bones healthy. Because D is fat-soluble and stored, chronic excess accumulates: very high intakes drive calcitriol up, over-absorbing calcium and causing hypercalcemia (raised blood calcium) — the mechanism behind D toxicity. This is why dosing is anchored to a blood level (25-OH-D), not a fixed milligram for everyone.

What the studies show →

The RDA is 600 IU for adults to ~70 and 800 IU after 70; the tolerable upper limit is 4,000 IU/day. Toxicity (hypercalcemia) is documented almost exclusively from sustained high-dose supplements, not sun or food — sunlight self-limits because excess pre-vitamin D in skin degrades. The practical takeaway: dose to a measured level rather than chasing ever-higher amounts.

Check yourself

Why is D3 usually preferred over D2 in supplements?

  1. D3 is always plant-derived and vegan
  2. D3 raises and maintains blood 25-OH-D more effectively
  3. D2 is toxic at normal doses
  4. D2 can only be obtained from sunlight
Show the answer →

B.D3 raises and maintains blood 25-OH-D more effectively

D3 (cholecalciferol) is the form your skin makes and tends to raise and sustain blood 25-OH-D better than D2 (ergocalciferol). Both work, but D3 is the better default. (D3 is usually animal-derived from lanolin, though lichen-sourced vegan D3 exists.)