Vitamin D3, Lamin A, and Nuclear Envelope Integrity

Abstract

Multiple lines of evidence suggest that high-dose vitamin D3 (cholecalciferol) can profoundly influence nuclear envelope integrity by modulating the expression and processing of lamin A—an essential nuclear scaffold protein that silences unneeded genes and maintains normal nuclear morphology. These effects are of particular interest in Hutchinson-Gilford progeria syndrome (HGPS), where a faulty lamin A (called progerin) drives accelerated aging, as well as in cancer cells that often downregulate lamin A to gain nuclear pliability. Recent in vitro work has shown that active vitamin D3 (1,25-dihydroxyvitamin D3 or calcitriol) reduces progerin production in HGPS cells while stabilizing critical DNA repair proteins such as BRCA1 and 53BP1, underscoring vitamin D’s broader role in genomic integrity. Furthermore, correcting lamin A deficits may force a shift from fermentative glycolysis (the Warburg effect) toward oxidative phosphorylation—supporting the metabolic theory that compromised mitochondrial function and a lax nuclear envelope go hand in hand in both cancer and progeria. This article also emphasizes the importance of supplementing vitamin K2 and magnesium when using high-dose vitamin D3 to avoid hypercalcemia.

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Posted in: D3

Back to the Future: How Cancer Cells and Stem Cells Recapture Their Ancestral Past.

Abstract
What if cancer cells are more than just rogue mutations—what if they represent a startling evolutionary throwback to our single-celled ancestors? In this paper, we uncover striking parallels between embryonic stem cells (ESCs) and cancer cells, focusing on their shared reliance on glycolysis (the Warburg effect), absence or minimal expression of lamin A, and capacity for indefinite self-renewal. We further reveal how these features mirror primordial life forms that predate Earth’s oxygenation. By exploring the evolutionary sequence—mitosis first, followed by sophisticated DNA repair and apoptosis—we illuminate how metabolic insufficiency in mitochondria can stall the apoptosis program, unleashing unregulated proliferation reminiscent of ancient single-celled behaviors. Building on Thomas Seyfried’s metabolic theory of cancer, we posit that restoring robust mitochondrial function might reverse cancer cells’ atavistic shift or even trigger their long-delayed cell death. From the subtle epigenetic changes that accompany mitotic chromosome segregation to the universal vulnerability of DNA under conditions of compromised energy, our synthesis bridges molecular biology, evolutionary theory, and clinical oncology. Readers will discover compelling evidence that cancer may be, at its core, a metabolic disease—one that seizes upon ancestral cellular states to circumvent modern-day apoptotic defenses. This perspective not only reframes our understanding of cancer’s origins but also promises novel therapeutic avenues targeting mitochondrial metabolism, inspiring us to look backward in order to move medicine forward.

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