I was on a call with a client recently who said something I hear more and more often.
She told me her labs had come back normal, yet she didn't feel normal. Her energy had changed. Her body composition was shifting before her eyes. The things that used to work weren't working the same way anymore. She was doing many of the things she'd always been told to do, and yet something felt different.
That gap between "normal labs" and a body that feels increasingly unfamiliar has been sitting with me lately.
Especially when it comes to lipids. Most women have been given a very simplified story about cholesterol and cardiovascular health -- a story that sounds clean and straightforward on the surface, but leaves out much of the nuance that makes human physiology so fascinating.
The more I study metabolism, hormones, cardiovascular health, and aging, the more I find myself coming back to the same realization ... the body behaves less like a machine and more like an ecosystem. And ecosystems are rarely explained well by a single number.
Most people use the words cholesterol and lipids interchangeably. They're related, but they're not the same thing. Cholesterol is one molecule within a much larger lipid system. It's used to build hormones, maintain cell membranes, support brain function, and participate in countless physiological processes that keep us alive. Yay, cholesterol!
Lipids are the broader family. They include cholesterol, triglycerides, fatty acids, and the lipoproteins that transport these substances throughout the body. This means that when we're talking about cholesterol on a lab report, we're often talking about a transportation network moving resources through a living, adaptive system. That transportation network is far more interesting than most of us were ever taught.
Most standard lipid panels measure total cholesterol, LDL, HDL, and triglycerides. Those numbers provide useful information, sure, but they don't tell the entire story. One reason is that cholesterol itself travels through the bloodstream inside particles called lipoproteins. LDL functions as one of the primary delivery vehicles, transporting cholesterol and fat to tissues that need support for hormone production, repair, cellular maintenance, and structural integrity.
When we look deeper into lipid physiology, we're interested in understanding not only how much cholesterol is being transported, but also how many particles are circulating through the bloodstream. This is where ApoB becomes valuable.
ApoB is a protein found on atherogenic lipoproteins. Measuring ApoB provides insight into particle number, which many researchers and clinicians consider an important piece of cardiovascular risk assessment.
One way to think about it is this ...
Imagine looking at a shipping company. You could count how much cargo is being transported. Or you could count how many trucks are on the road. Both pieces of information matter. Sometimes they tell slightly different stories.
This is also where the conversation about 'normal' vs. 'optimal' enter the chat. Most laboratory reference ranges are based on population averages. They help identify values that are common within a population. Optimal health, however, doesn't always align perfectly with what is common. This is one reason we need to look beyond whether a marker falls inside a reference range and instead examine patterns across multiple markers.
One of the first places I look for myself and my clients is the relationship between triglycerides and HDL. Specifically, the ratio. Triglycerides often provide clues about how the body is handling and storing energy, while HDL can provide additional context around metabolic health and lipid transport. Looking at either marker independently can be useful, but examining the relationship between them often reveals much more.
The triglyceride-to-HDL ratio is an underutilized proxy for insulin sensitivity + metabolic flexibility. A lower ratio is generally associated with better metabolic health, while a higher ratio can sometimes signal that the body is struggling to regulate energy efficiently.
This relationship becomes even more interesting when we consider body composition. Visceral fat — the fat stored around the organs — is metabolically active tissue. It influences inflammation, insulin sensitivity, hormone signaling, and the way fats are processed throughout the body. As visceral fat accumulates, we often see changes in triglycerides, HDL, blood sugar regulation, and lipid particle patterns.
When elevated triglycerides, lower HDL, increasing waist circumference, insulin resistance, and shifting body composition appear together, they're often reflecting different aspects of the same underlying metabolic environment.
And for many women, that environment shifts significantly during perimenopause and menopause. Many women notice lipid changes seemingly out of nowhere during their 40s and 50s. LDL rises. ApoB rises. Triglycerides may climb. Fat distribution often changes, with more weight accumulating around the midsection. These shifts make sense when we consider the role estrogen plays throughout the body. Estrogen influences vascular function, insulin sensitivity, inflammation regulation, body fat distribution, and lipid metabolism. As estrogen fluctuates and eventually declines, the entire metabolic environment begins to change.
From an evolutionary perspective, this is fascinating.
Female physiology evolved within environments that included abundant movement, natural light exposure, strong social structures, seasonal variation, periods of food scarcity (hellooooo famines!), and dramatically different stress patterns than most women experience today. Menopause represents a major biological transition, yet many women are navigating it while sleeping less, sitting more, experiencing greater chronic stress, spending less time outdoors, and living in environments their biology never specifically evolved to encounter.
The interaction between those ancient biological systems and modern living may help explain why the menopause conversation often feels more complicated than conventional advice suggests.
Advanced lipid testing can sometimes add additional clarity. Markers such as ApoB, LDL particle number (LDL-P), Lipoprotein(a), and LDL particle size can help create a more detailed picture of cardiovascular risk. Particle size is particularly interesting because it often reflects the broader metabolic environment. Smaller, denser LDL particles tend to appear more frequently alongside insulin resistance, elevated triglycerides, inflammation, and lower HDL. Larger, more buoyant particles often appear in different metabolic contexts. What's fascinating is that particle size frequently reflects the environment surrounding the particles as much as the particles themselves.
Which brings us back to a theme that appears throughout physiology ...
Context matters.
One of the reasons lipid conversations become so confusing is that different people can arrive at similar-looking lab results through very different pathways.
One woman may have elevated ApoB primarily because of genetics. Another because she's entering menopause. Another because years of insulin resistance have altered her metabolic environment.
And yet another because of some combination of all three.
The destination may look similar on paper while the underlying drivers are entirely different. This is one reason one-size-fits-all solutions often fall short.
Genetics deserve special attention here. Familial Hypercholesterolemia (FH) is one example of how powerfully genetics can influence lipid physiology. Individuals with FH often have significantly elevated LDL and ApoB levels from a young age due to inherited differences in how cholesterol-containing particles are cleared from circulation. In these situations, lifestyle still matters A LOT, but the conversation often shifts from attempting to erase genetics to creating the healthiest possible environment around those genetics.
Sleep quality matters.
Exercise matters.
Blood pressure.
Body composition.
Insulin sensitivity.
Inflammation.
Nutrition quality + balance + timing.
Stress resilience.
Medication may become part of the strategy for some individuals.
The goal becomes reducing overall risk while supporting the health of the entire system.
A similar conversation occurs with Lipoprotein(a), or Lp(a). This is heavily influenced by genetics and can meaningfully affect cardiovascular risk. Elevated levels often encourage a stronger focus on the factors we can influence -- metabolic health, exercise, blood pressure, smoking avoidance, inflammation management, sleep, and overall cardiovascular resilience.
The presence of genetic risk factors doesn't eliminate the importance of lifestyle. It makes lifestyle even more important.
As I dug deeper into lipid science over the years, I found myself becoming increasingly fascinated by a question that remains surprisingly difficult to answer:
What is the ideal cholesterol level for a human being?
The more I read, the less convinced I become that this question can be separated from the environment in which the human is living.
Human physiology evolved under conditions that included abundant movement, sunlight exposure, nutrient-dense food, darkness at night, strong social connection, and significantly lower levels of chronic psychological stress.
Modern humans live in a very different world. We move less. Sleep less. Spend more time indoors. Experience greater chronic stress. Encounter more environmental pollutants. Eat more ultra-processed foods. Live under artificial lighting. Spend more time disconnected from the rhythms that shaped human biology for hundreds of thousands of years.
And that raises a fascinating possibility (at least, to me anyway)...
Cholesterol levels may not exist independently of the biological environment they're operating within.
After all, cholesterol participates in hormone production, cellular structure, brain function, repair processes, and countless aspects of human physiology. It serves important purposes. Maybe cholesterol levels that function beautifully within a metabolically healthy, physically active, low-inflammatory environment carry different implications than those same levels operating inside an environment characterized by insulin resistance, chronic stress, poor sleep, sedentary behavior, nutrient deficiencies, and inflammation.
We don't yet have complete answers. My guess is that a wider range of cholesterol / lipid levels make sense and would be healthy if we weren't dropped into these modern times. But since we are right here in 2026, we may need to be more careful / conservative than we would've otherwise had to be.
And I suspect this is one reason the cholesterol conversation remains controversial.
Human biology is extraordinarily context-dependent. Heart disease remains the leading cause of death in women. And yet, the underlying process is far more dynamic than many people realize.
The inside of a blood vessel functions as an active biological environment. Cells communicate. Repair mechanisms activate. Immune responses occur. Blood flow patterns influence signaling. Hormones exert effects. Inflammatory pathways interact with metabolic pathways. Plaque develops within this environment. It consists of cholesterol-containing particles, immune cells, fibrous tissue, calcium, and repair-related materials that accumulate within the vessel wall over time.
One analogy I like to use with clients is biological spackle.
Plaque formation also isn’t just a cholesterol story — it’s more like a layered response inside the vessel wall. Early changes tend to be “soft plaque” (lipid-rich, more dynamic, more reversible-feeling in nature), which can gradually transition into “harder” plaque as inflammation persists and calcium gets involved, and eventually more “stabilized” plaque that’s fibrous and calcified (not always the most dangerous type, but a marker of long-term vascular stress and remodeling). This is also where things like ApoB and LDL particle number start to matter more than total cholesterol, and where CAC scores (coronary artery calcium scans) give a snapshot of calcified plaque burden specifically — not early soft changes, not inflammation, just the later-stage footprint. Particle size gets discussed a lot here too, but it’s easy to over-focus on it and miss the bigger picture, which is that particle number + metabolic environment (insulin sensitivity, blood pressure, glucose stability, inflammation) tend to drive risk more consistently than size alone. And this is also where prevention becomes less about one lever and more about the whole system -- oral health and the oral microbiome (gum inflammation matters here!), nasal breathing, sleep quality, resistance training and muscle mass, blood pressure regulation, blood sugar stability, HRV and nervous system tone, vitamin K2 (for calcium handling), vitamin D from sunlight exposure, nitrates from plants for nitric oxide signaling, sauna for vascular conditioning, grounding, daily movement, plus the basicsssss that sound boring but are very not boring — hydration, minerals, and consistent cardiovascular output.
When tissues experience irritation, injury, or stress, the body activates repair mechanisms. The repair itself serves a purpose. It helps maintain integrity and function.
Over time, repeated activation of those repair processes can contribute to plaque development.
There's another fascinating layer of this conversation ... what is often called the fourth phase of water, structured water, or exclusion-zone (EZ) water.
Water adjacent to hydrophilic surfaces — such as the inner lining of blood vessels — organizes differently than other water. This has implications for flow dynamics, charge separation, cellular signaling, and vascular function.
What interests me most is the broader reminder it give us ...
Blood vessels function as highly organized biological environments where structure, flow, signaling, metabolism, inflammation, and repair are occurring simultaneously. Sleep influences that environment. Hydration. Minerals. Movement. Nutrition. Stress.
EVERYthing participates in the conversation. Isn't that wildddddddd?!
This is also why I don't view medication and lifestyle as opposing forces.
There are absolutely situations where lipid-lowering medications are evidence-based, appropriate, and potentially life-saving. Medicine has helped countless people.
But perhaps they're overprescribed? I think so. But your plan is between you, your doctor, and your biology.
How do medications fit into the larger system? Statins aren't the only guys on the market, but they're common and provide a good example. They reliably lower LDL cholesterol and reduce cardiovascular events in specific populations. At the same time, the pathways they influence connect to broader aspects of human physiology, including CoQ10 production (reduction) and cellular energy systems. Some people tolerate them exceptionally well. Others experience side effects like the increased risk of diabetes or earlier onset of diabetes and muscle pain.
One of the most valuable lessons physiology has taught me is that everything carries tradeoffs. Everything! Every intervention. Every medication. Every dietary strategy. Every exercise program. Every physiological adaptation.
It's all one giant, biological butterfly effect. Pull one lever and multiple gears move elsewhere. Sometimes that leads to a stacking of amazing and beneficial "side effects" and sometimes it's more of the adverse kind. Now-you-need-meds-for-the-side-effects-of-your-meds stuff.
So when ApoB is elevated, my thinking often extends beyond simply lowering ApoB. I want to understand why it may be elevated. I want to improve insulin sensitivity. Body composition. Sleep. Fitness. Metabolic flexibility. Stress resilience. Inflammation regulation.
And if ApoB comes down, I also want to continue supporting the systems cholesterol participates in — brain health, hormone production, muscle maintenance, cellular repair, and long-term resilience.
The goal is evolving as the healthiest, most resilient human possible in all of our various stages and iterations. This is the form that allows us to feel our best, squeeze more life out of our years, and help others most.
Coronary artery calcium scoring can sometimes add another piece to this puzzle. A calcium score helps assess calcified plaque burden and can provide additional context alongside ApoB, Lp(a), inflammatory markers, metabolic markers, and clinical history.
Each test offers a different photograph. The real challenge is assembling those photographs into a coherent story.
And that's where I find myself landing after years of studying metabolism, hormones, behavior change, fitness, nutrition, and physiology. The body behaves less like a machine and more like an ecosystem. Ecosystems are constantly adapting. Constantly communicating and responding to changes in resources, stressors, environments, and demands.
Lipids participate in that conversation. Hormones. Inflammation. Sleep, movement, nutrition, genetics, relationships, stress, light exposure, body composition, and aging all participate in that conversation. You name it! Every lab marker tells part of the story. But no single marker tells the whole story. And no single marker should be evaluated as a stand-alone.
Health emerges from interactions between systems over time. This is why I find myself asking fewer questions about whether a number is good or bad and more questions about what the body may be communicating through that number in the first place.
Biology is remarkably intelligent. Adaptation is rarely random. Understanding why the body is doing something often brings us closer to meaningful answers than simply trying to force it to do something else.
Your lipid panel is one page from a very long book. The real story is how well the system maintains resilience, adaptation, repair, and internal order over time. And that story is always bigger than a single number.
If you want a place where all of this starts to feel more connected — where lab work, metabolism, hormones, body composition, and behavior actually start talking to each other instead of feeling like separate puzzles, that’s what we do inside The Metabolic Edge. It’s a private community of women who are all learning how to understand their own physiology in real time, with the support + guidance to actually apply it. Inside, you’ll find not just education and coaching, but the practical tools that make it usable in daily life — meal ideas, recipes, workouts, and structure that takes things from “hmm, interesting” to “this is what I do this week.” Enrollment will open briefly on June 30th for July. Learn more + hop on the waitlist.
If you want individualized support — where labs, symptoms, training, nutrition, stress physiology, and life context are all interpreted together and in a custom way to fit your life — I also work 1:1 with a small number of clients. Learn more and apply here. I'll be in touch to discuss what availability and timing looks like right now and next steps to make sure it's the right fit.
Stay wild + well,
Tara
P.S. In case you missed it
A problem with DEXA scans
A hot take on what aging really means
P.P.S. What I'm loving lately
Psyllium husk -- (no affiliation to this brand) this is a great supplement to add to a balanced nutrition plan if the goal is to lower ApoB / LDL.
These oral care products (use code Allen10 for my affiliate discount of 10% off) -- fluoride exposure has been hypothesized to influence thyroid function / LDL receptor activity in the liver, which can influence LDL and ApoB levels. This wouldn't be my first lever to pull, but it's one nonetheless. I choose non-fluoride products for many other reasons as well. But not any non-fluoride products as we need active ingredients to remineralize still since the fluoride is not present. That's where hydroxyapatite comes into the picture. I use their non-nano versions to avoid crossing the blood-brain barrier (which happen to be their least expensive too.... win win!) Their floss has hydroxyapatite too, so remineralizes between the teeth as you floss. LOVE that!
Gardening while grounding has become oddly satisfying. lately. Bare feet in the dirt, hands in soil, pleading with the weeds… and my population of garden gnomes. The grounding is helping to build 4th phase water, so part of my lipid / heart health protocol. Also, I’m turning 43 in two days, which seems to mean I’ve entered my old, quirky nature-lady era. Birds, a few quiet minutes in the mornings, tea / coffee rituals, earlyish bedtimes, emotionally intelligent conversations or no thank you, and a growing appreciation for mom jokes, bits, and crochet tops. I think ... I've made it?? My 14-year old self would be mortified.
