Collagen: The “Glue” Holding You Together (And Why You’re Probably Not Thinking Big Enough About It) When most people hear collagen, they think “wrinkles” and maybe “creaky knees.” But collagen is far more than a beauty supplement or a joint helper. It’s literally the scaffolding that holds your entire body together – from your gut lining to your blood vessels to your bones and fascia. Let’s zoom out and look at collagen the way your biology “sees” it. What exactly is collagen? - Collagen is the most abundant protein in the body, making up about 30% of your total protein. - It’s the main structural protein in skin, bones, tendons, ligaments, cartilage, fascia, blood vessels, and the intestinal lining. - Think of it as a tough, rope-like triple helix that gives tissues strength and shape, while elastin gives them stretch. There are at least 28–29 types of collagen, but most of your body is built from a core few: - Type I – skin, bones, tendons, ligaments, teeth - Type II – cartilage and joints - Type III – blood vessels, hollow organs, skin (with type I) - Type V & X – support bone, joint surfaces, and specialized tissues When collagen is abundant and well-organized, tissues are strong, springy, and resilient. When it’s damaged or depleted, you feel it – not just on your face, but everywhere. Why collagen declines (and why midlife women feel it hardest) Starting in our mid-20s, collagen production naturally drifts downward. Sun damage, smoking, high sugar intake, chronic inflammation, and poor sleep all accelerate the breakdown of collagen fibers. For women, the big cliff is menopause. Estrogen normally stimulates fibroblasts (your collagen-making cells). As estrogen drops: - Up to ~30% of skin collagen can be lost in the first five years after menopause, followed by ~2% per year after that. - Skin gets thinner, drier, and less elastic. Joints, fascia, and pelvic tissues also feel the loss. On top of that, fibroblasts can shift from making more elastic type III collagen toward stiffer type I collagen, the kind found in ligaments and scar tissue. That’s one reason midlife can feel like a season of “tight, brittle, and creaky” instead of “bouncy and flexible.”

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First - let’s explain the allopathic interpretation of this study (study linked below): What the new AHA abstract ACTUALLY found - Adults with established heart disease who had their vitamin D dosed to reach and maintain 25-OH-D between ~40–80 ng/mL had a 52% lower risk of myocardial infarction vs. a usual-care group that did not manage vitamin D levels. Primary composite outcomes (death/HF hospitalization/stroke) were not reduced. It’s a preliminary conference abstract (TARGET-D), not yet peer-reviewed. - 52% of the treatment group needed >5,000 IU/day to hit >40 ng/mL, and dosing was titrated every 3 months with safety monitoring; doses were reduced/stopped if levels exceeded 80 ng/mL to avoid hypercalcemia. Why “normal” lab values are often too low - U.S. National Academies/NIH materials frame ≥20 ng/mL as “generally adequate” for bone outcomes, which is why some labs set the “normal” lower bound near 20. But that threshold was never meant to optimize non-skeletal outcomes. - The Endocrine Society’s 2024 guideline moved away from endorsing a single universal target like 30 ng/mL for everyone, acknowledging heterogeneous needs and advising routine RDA-level supplementation only for most healthy adults <75 without indications—reserving higher targets/doses for specific populations/indications. - Earlier (2011) guidance commonly sought ≥30 ng/mL, and many functional clinicians aim 40–60 ng/mL for broader physiology—aligning with the TARGET-D optimization approach rather than a one-size-fits-all dose. (Note: the 2011 target is now superseded, but it explains today’s differing “normals.”) What low vitamin D implies (condensed) - Cardiometabolic risk: Low 25-OH-D is consistently associated with higher CVD risk; however, in the general population the large VITAL RCT (2,000 IU/day) did not lower major CVD events, suggesting benefit may require targeted treatment of deficiency or higher-risk subgroups (like TARGET-D did). - Infectious disease/COVID-19: Observational and some interventional/meta-analytic data link low D to worse outcomes and suggest benefit to supplementation—especially with multiple/adequate doses—but it’s not accurate to claim “nearly 100% of COVID deaths are due to low vitamin D.” That overstates the evidence. - Musculoskeletal/immune: Low D compromises calcium homeostasis, bone, and immune function; very high levels can cause toxicity (hypercalcemia, renal issues, arrhythmias), which is why monitoring matters. UL for most adults is 4,000 IU/day (outside supervised care).