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<\/a>And it didn\u2019t happen quietly. It wasn\u2019t a minor tweak, a footnote, or an incremental update. It was a full reversal of a doctrine that has dominated labs, clinics, public-health brochures, and countless biomarker panels for decades. A classical paper even claimed that 50% of the world population<\/a> is vitamin D insufficient. For years, we had to\u00a0 live with the tidy triplet:<\/p>\n That middle category \u201cinsufficiency\u201d became a diagnosis in itself. It justified mass screening<\/a>. It justified supplementation campaigns. It justified entire clinical cultures built around chasing numbers.\u00a0 And then 2024 arrived.<\/p>\n Because after reviewing all high-quality randomized trials, the Endocrine Society concluded something truly astonishing:<\/p>\n there is no reliable evidence that people with 25(OH)D levels between 20 and 30 ng\/mL derive any clinically meaningful benefit from raising those levels<\/p><\/blockquote>\n In fact, the guideline panel found that even below 20\u201324 ng\/mL, evidence for clear benefit is surprisingly weak or uncertain \u2014 except perhaps in the very elderly, and even there the benefit didn\u2019t map neatly to a threshold. Vitamin D physiology makes the whole \u201cinsufficiency\u201d concept biologically dubious, because serum 25(OH)D is only an external storage marker of an intracellular prohormone system \u2014 a tank that appears \u201cempty\u201d only in true deficiency like rickets. Let me put that differently: The category of \u201cvitamin D insufficiency,\u201d introduced in 2011 and used worldwide, is now considered *scientifically unsupported*. The Society explicitly withdraws it.<\/p>\n That is not merely unusual. In the world of clinical guidelines, this is as close as you get to a scientific earthquake. Why did they withdraw it? Because the evidence never really showed what everyone assumed.<\/p>\n The new communication explains the problem with striking clarity:<\/p>\n 1. Observational associations misled us. 2. Surrogate markers were overinterpreted. 3. Large RCTs showed no special benefit in \u201clow\u2013normal\u201d ranges. 4. Across thousands of participants aged 50\u201374, supplementation beyond the RDA made essentially no difference \u2014 including in those below the supposed thresholds. We rarely see a major medical society openly dismantle one of its own most influential guidelines \u2014 not because of scandal, not because of politics, but because the evidence finally matured and said: we were wrong<\/em>. And they didn\u2019t hedge. They didn\u2019t massage the language. They called the new stance what it is: epistemic humility<\/em>.<\/p>\n Still not convinced? For key readings google for the approx 10 vitamin D “umbrella reviews<\/a>” and the 20 studies that “vitamin D is a marker of inflammation<\/a>” and not vice versa.<\/p>\n <\/p>\n\n <\/p>\n Vitamin D insufficiency? Gone! I can’t even remember how many vitamin D studies I did, explaining how the prohormone has been discovered, how stupid guidelines came on to the scene. And it didn\u2019t happen quietly. It wasn\u2019t a minor tweak, a footnote, or an incremental update. It was a full reversal of a doctrine that … Continue reading The biggest turning point in medical science that I have probably ever encountered<\/span> \r\n<20 ng\/mL = deficiency\r\n20\u201330 ng\/mL = insufficiency\r\n\u226530 ng\/mL = sufficiency\r\n<\/pre>\n
\nMany early threshold claims came from correlations \u2014 low vitamin D and higher PTH, low vitamin D and lower bone density, etc. But none of this proved causality, and much of it turned out to be non-informative once RCTs were performed.<\/p>\n
\nCalcium absorption, PTH suppression, even bone mineral density \u2014 these are *indirect* signals. They don\u2019t automatically translate into fewer fractures, fewer falls, fewer infections, or longer life. And when RCTs finally tested real outcomes, the expected clinical benefits simply weren\u2019t there.<\/p>\n
\nVITAL \u2014 one of the biggest vitamin D trials ever \u2014 found no difference in fractures even in participants below 24 ng\/mL, and even those below 12 ng\/mL did not exhibit the dramatic benefit everyone predicted (though the subgroup was very small).<\/p>\n
\nThe forest plots in the guideline communication make this visually obvious: the <20\u201324 ng\/mL subgroups almost never differ from the overall population in any meaningful direction. (See page 5 of the document: identical risk-change estimates for falls, fractures, cancer, CVD, etc.)<\/p><\/blockquote>\n