Part 1: Cholesterol Isn’t the Villain
Why your body needs it (hormones, brain, repair)
For decades, “cholesterol” has been framed as the boogeyman of modern health. If your lab report shows an elevated number, the script often feels automatic: fear → urgency → medication → “see you next year.”
But here’s the truth from a terrain-first lens:
Your body makes cholesterol on purpose. Not as a mistake. Not as a glitch. As a feature.
Cholesterol is a foundational molecule used for structure, signaling, repair, and resilience—especially as we age. And while cholesterol markers can be part of a bigger risk conversation, cholesterol itself is not the simplistic villain it’s been made out to be.
A Bedrock reminder:
At Rooted Faith Wellness by Bedrock, we don’t worship numbers and we don’t demonize molecules. We look at context. We ask better questions. And we pursue stewardship over fear.
What cholesterol actually does (that most people never hear)
Cholesterol isn’t just “something in your blood.” It’s a critical component of your cell membranes, helping regulate membrane structure and function. PMC+1 It also helps create and stabilize lipid rafts—specialized membrane “platforms” that organize receptors and signaling proteins so your cells can communicate, respond to stress, and coordinate immune and repair processes. JCI+1 Translation: cholesterol is part of how cells work, not just something that “causes problems.”
Cholesterol and hormones: the raw material for steroid hormone production
If you care about hormones, you care about cholesterol.
Your adrenal glands and reproductive tissues use cholesterol to make steroid hormones, beginning with the conversion of cholesterol into pregnenolone—a precursor for downstream hormones like progesterone, testosterone, estrogen, cortisol, and others. PMC+1 And it’s not just about enzymes—cholesterol availability itself is crucial for steroid synthesis, which is why modern endocrinology reviews still emphasize cholesterol supply and trafficking as a core part of steroidogenesis. OUP Academic Bedrock take: When someone is struggling with perimenopause/menopause symptoms, low libido, low testosterone, chronic stress dysregulation, or “burnout biology,” it’s medically shallow to pretend cholesterol is irrelevant.
Cholesterol and the brain: protection, myelin, and function
The brain is one of the most cholesterol-rich organs in the body—but here’s the part that matters:
Brain cholesterol is largely its own protected pool. The blood–brain barrier limits exchange with circulating cholesterol, and much of the brain’s cholesterol comes from local synthesis. AHA Journals+2PMC+2 Cholesterol is deeply involved in:
- myelin (the insulating sheath around nerves)
- membrane integrity and synaptic function
- long-term brain maintenance (with low turnover in the adult brain) PMC+1
And in disease/repair contexts, emerging research continues to examine how cholesterol synthesis and handling relates to nervous system resilience and remyelination processes. Cell Bedrock take: If you want to talk about brain health and aging, cholesterol needs to be discussed as a biological asset—not a disposable toxin.
Cholesterol, aging, and longevity: why the conversation gets complicated
This is where nuance matters.
The “192 countries” world graphs (WHO data)
Zoë Harcombe is widely cited for graphing WHO country-level data across 192 countries (later updates use fewer countries depending on the dataset year), showing an inverse association in those ecological plots: populations with higher average cholesterol tended to show lower mortality rates in those charts. zoeharcombe.com+1 The WHO Global Health Observatory hosts the indicator Harcombe references: mean total cholesterol (age-standardized estimate). World Health Organization Important: ecological plots can be thought-provoking, but they do not prove cause-and-effect. Country-level patterns are confounded by many variables (poverty, infectious disease burden, medical access, smoking trends, malnutrition, and more). Harcombe herself flags this kind of limitation. zoeharcombe.com LDL-C and mortality in older adults (observational evidence)
A 2016 BMJ Open systematic review (Ravnskov et al.) reported that in many cohorts of adults ≥60, LDL-C showed no association or an inverse association with mortality outcomes in those datasets. BMJ Open+2PubMed+2 Also important: observational findings in older adults can be influenced by reverse causality (frailty, chronic disease, inflammation, and undernutrition can lower cholesterol and raise mortality risk). So the takeaway isn’t “LDL never matters.” The takeaway is: Cholesterol biology is context-dependent, especially with aging.
When it comes to cholesterol numbers, here’s what we know:
The idea that total cholesterol must be under 200 is an oversimplification — and in some cases, it can actually be dangerous. Context matters. One of the most meaningful cholesterol markers is the HDL-to-total cholesterol ratio, not total cholesterol by itself.
- Goal: HDL ÷ Total Cholesterol = 0.24 or higher (higher is generally better)
For many adults — especially over age 40 — it’s also common to see total cholesterol naturally rise over time. In a terrain-focused approach, we often view cholesterol as part of the body’s support system for brain function, hormone production, and aging resilience, rather than something that automatically needs to be suppressed.
Triglycerides are often a clearer risk signal than LDL
Another major point: one of the clearest lab indicators of cardiometabolic risk is often triglycerides, not LDL.
A very useful ratio is Triglycerides-to-HDL:
- Goal: Triglycerides ÷ HDL = 1.5 or less (lower is better)
This ratio gives us insight into metabolic health, including insulin sensitivity and cardiovascular risk patterns.
Other markers that often matter just as much (or more) than total cholesterol include:
- Fasting insulin (often more informative than fasting glucose or A1c)
- Homocysteine
- C-reactive protein (CRP)
How we view LDL (the firefighter analogy)
LDL is often evidence that the body is doing a job.
That doesn’t mean LDL is irrelevant — it has value — but we don’t treat it as a standalone diagnosis or the single “cause” of risk. Instead, we ask:Why is the body sending more LDL into circulation right now?Is it responding to inflammation? Repairing damage? Adapting to stress, oxidation, or metabolic strain?
A simple way to understand LDL is this:
LDL is like a firefighter at the scene of a fire.
The firefighter is always present at the emergency — but the firefighter didn’t start the fire. The firefighter shows up because there’s a problem to address. In the same way, LDL is often part of the body’s response system — not automatically the root cause of the problem.
So we look at context, we listen to symptoms, and we interpret labs as signals — not verdicts.
What I care about more than “a cholesterol number”
In clinical reality, the question isn’t “Is cholesterol good or bad?”The question is: What is driving risk in this body right now?
In a terrain-first approach, I’m usually looking harder at:
- Triglycerides and TG/HDL ratio (often a metabolic signal)
- insulin resistance patterns (fasting insulin, A1c trends, CGM patterns)
- inflammation load (sleep, stress, training load, nutrient depletion, toxins)
- and when appropriate, deeper lipids like ApoB/non-HDL
This is why many metabolic-focused clinicians keep hammering the idea that insulin resistance changes the whole story—and why simplistic “lipids-only” thinking can miss the true driver. crossfit.com+1 Bottom line: cholesterol is useful—fear is not
Your body uses cholesterol because it’s necessary for:
So no—cholesterol is not automatically your enemy.And yes—your labs still matter, BUT they must be interpreted in context, alongside your metabolic terrain.
Ready to make this personal?
If you’re confused by your cholesterol labs, worried about your numbers, or you want a real “big picture” look at what your body is doing:
Take our complimentary health assessment today and let one of our Bedrock team members help you map out what’s driving your patterns—and what to do next.
Reply “ASSESSMENT” (or DM us “ASSESSMENT”) and we’ll get you started.
References
- Harcombe Z. Cholesterol & mortality – world graphs (WHO country-level cholesterol vs mortality plots; ecological analysis). zoeharcombe.com+1
- WHO Global Health Observatory. Cholesterol, mean total (age-standardized estimate) (indicator definition/metadata). World Health Organization
- Ravnskov U, et al. BMJ Open (2016). Lack of an association or an inverse association between LDL-C and mortality in the elderly: a systematic review. BMJ Open+2PubMed+2
- Noakes T. It’s the Insulin Resistance, Stupid: Part 8 (metabolic context critique; includes discussion referencing Harcombe’s WHO plots). crossfit.com+1
- Steroidogenesis and cholesterol → pregnenolone pathway (open-access reviews). PMC+2PMC+2
- Brain cholesterol is largely locally synthesized and separated by the blood–brain barrier (reviews). AHA Journals+2PMC+2
- Cholesterol’s role in membranes and lipid rafts/signaling (reviews). PMC+2JCI+2