CONDITIONS • WESTMINSTER, ARVADA, BROOMFIELD, THORTON & DENVER METRO
High Cholesterol Pressure Treatment in Westminster, CO
The standard cholesterol test gives you a total number and a recommendation for medication. What it does not give you is an accurate picture of your actual cardiovascular risk — because total cholesterol is one of the least predictive markers available.
Millions of people are on statin medication to lower a cholesterol number that may not accurately reflect their true risk of heart disease. Millions of others have been told their cholesterol is fine when the markers that actually predict cardiovascular events were never tested. Understanding what cholesterol actually does in the body — and what is actually driving it up — changes the entire picture of what treatment should look like.
Same-Day & Same-Week Appointments Available
WE UNDERSTAND WHAT YOU'RE GOING THROUGH
You went in for a routine checkup, felt perfectly fine, and came out with a diagnosis and a prescription. And now you have questions nobody took the time to answer.
High cholesterol is one of the most common diagnoses in primary care — and one of the least explained. You were told your LDL is above the target range. You were told to eat less saturated fat and possibly prescribed a statin. You may have accepted the prescription, tried to change your diet, and found either that the medication helped but came with side effects you were not fully warned about, or that your dietary changes made surprisingly little difference to the number. What you probably were not told is that LDL cholesterol alone is a poor predictor of cardiovascular risk, that the particle size and quality of your LDL matters far more than the total amount, that inflammation is the actual mechanism of arterial damage and cholesterol is more a bystander than a villain, and that the most powerful modifiable driver of your cholesterol profile is almost certainly not the saturated fat in your diet. We want to give you the full picture — and the tools to address the actual drivers.
COMMON CONCERNS THAT BRING PEOPLE IN
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Elevated LDL or total cholesterol found on routine blood work
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A family history of heart disease and a desire to understand and manage risk proactively
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Statin medication causing muscle pain, fatigue, or cognitive effects they want to reduce or eliminate
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Wanting to understand whether their cholesterol actually represents elevated risk — or whether they are being treated for a number rather than a genuine cardiovascular threat
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Elevated triglycerides alongside the cholesterol — a pattern pointing clearly toward metabolic syndrome
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Low HDL — the "good" cholesterol — that dietary changes have not improved
THE CONNECTION TO PAIN
Statin medications — the most commonly prescribed cholesterol treatment — are associated with muscle pain and weakness in a significant proportion of patients. This statin-induced myopathy ranges from mild achiness to debilitating muscle damage. Many patients attribute their muscle pain to age, overuse, or other causes when their statin is the actual driver.
Statins deplete CoQ10 — a nutrient essential for muscle energy production. If you are on a statin and have new or worsened muscle pain, CoQ10 depletion is almost certainly contributing — and it is almost never mentioned or supplemented by the prescribing physician.
WHAT YOU PROBABLY HAVEN'T BEEN TOLD
Cholesterol does not cause heart disease. Inflamed, oxidized cholesterol lodging in damaged blood vessel walls causes heart disease. That distinction changes what you should actually be treating.
WHAT CHOLESTEROL ACTUALLY IS — AND WHY TOTAL LDL IS THE WRONG NUMBER TO FOCUS ON
Cholesterol is not a poison your body accidentally produces. It is a critically important substance that every cell membrane is made from, that your body uses to produce sex hormones and stress hormones, that is essential for bile production and fat digestion, and that is the primary building block of brain and nerve tissue. The liver produces roughly 80 percent of the cholesterol in your bloodstream — dietary cholesterol has a much smaller effect on blood cholesterol than most people believe. When your LDL is elevated, it is most often a signal that the liver is responding to something: chronic inflammation, insulin resistance, oxidative stress, or thyroid dysfunction. The elevated number is not the problem — it is pointing toward something the body is trying to compensate for.
Here is what actually predicts cardiovascular risk: not total LDL, but the size and density of the LDL particles. Small, dense LDL particles are dangerous — they penetrate blood vessel walls easily, oxidize readily, and trigger the inflammatory cascade that produces arterial plaques. Large, buoyant LDL particles are essentially harmless — they circulate without damaging vessel walls. Two people can have identical total LDL numbers and completely different cardiovascular risk profiles depending on their particle size. Standard cholesterol testing does not distinguish between these patterns. Advanced lipid testing — which measures particle size, particle number, and oxidized LDL — gives the actual risk picture. Without it, many people are being treated unnecessarily, and many others with dangerous patterns are being reassured falsely.
What actually drives small dense ldl — and it is not saturated fat
The dietary advice most people receive for high cholesterol — reduce saturated fat and replace it with vegetable oils and whole grains — is based on research that is now understood to have been incomplete. The primary driver of the dangerous small, dense LDL pattern is not saturated fat. It is elevated triglycerides from excess refined carbohydrates and sugar. When triglycerides are high, the body produces more small dense LDL particles. When triglycerides are low and HDL is high — regardless of total LDL — the cardiovascular risk profile is generally favorable. This is why many people on low-fat, high-carbohydrate diets see their LDL number drop but their cardiovascular risk actually increase — because the particle pattern has worsened while the total number has improved.
A triglyceride-to-HDL ratio above 2.0 is a more reliable indicator of cardiovascular risk and insulin resistance than LDL alone. It is rarely the focus of standard cholesterol counseling.
Inflammation — the actual mechanism of arterial damage
Cholesterol does not deposit on blood vessel walls randomly. It deposits specifically at sites of existing inflammation and endothelial injury — where the vessel wall has been damaged by oxidative stress, elevated blood sugar, chronic immune activation, or mechanical stress. The process that produces arterial plaques is fundamentally an inflammatory process, not a lipid-excess process. This is why markers of inflammation — high-sensitivity C-reactive protein (hsCRP) and homocysteine in particular — predict cardiovascular events more accurately than LDL cholesterol in many studies. And it is why reducing systemic inflammation through diet, gut health, and metabolic optimization reduces cardiovascular risk in ways that simply lowering the cholesterol number does not.
An elevated hsCRP alongside elevated cholesterol represents dramatically more cardiovascular risk than elevated cholesterol with normal hsCRP. Standard care tests one; we test both.
Statin side effects and coq10 depletion
Statins lower cholesterol by blocking an enzyme in the liver called HMG-CoA reductase. This same enzyme also produces CoQ10 — a nutrient essential for energy production in every muscle cell in the body, including the heart. When statins block this enzyme, CoQ10 production falls alongside cholesterol production. The result in susceptible patients is muscle pain, muscle weakness, fatigue, and cognitive effects — the well-documented statin side effect profile. CoQ10 supplementation is supported by research as a mitigation strategy for statin myopathy, and is routinely recommended in some countries as a standard co-prescription with statins. In the United States it is almost never mentioned, let alone prescribed, despite the strong biological rationale and supportive clinical evidence.
If you are on a statin and have developed muscle pain since starting it, CoQ10 should be one of the first interventions tried — before stopping or changing the medication.
OUR APPROACH
Conventional care versus our approach
We support medication when it is genuinely indicated — particularly for people with established cardiovascular disease, very high genetic risk, or very high-risk lipid patterns. Our role is to assess actual cardiovascular risk more accurately, identify and address the underlying drivers of the lipid pattern, reduce inflammation as the primary mechanism of arterial damage, and support patients on statins in managing side effects and achieving better results from the medication they are already taking.
The conventional approach
What most patients experience
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Standard lipid panel: total cholesterol, LDL, HDL, and triglycerides
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Advised to reduce saturated fat, eat more fiber, exerci
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Statin prescribed when LDL is above guideline threshold
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Dose adjusted until LDL is within target range — medication typically continued indefinitely
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Particle size, oxidized LDL, hsCRP, homocysteine, and insulin resistance rarely tested
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Statin side effects managed by changing drug or dose — CoQ10 supplementation rarely discussed
Standard lipid management is appropriate for reducing documented cardiovascular risk, particularly in high-risk patients. Its limitation is that it reduces one number without investigating the quality of the lipid pattern, the inflammatory state of the arteries, or the metabolic drivers of the pattern.
What we do differently
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Advanced lipid testing: LDL particle number and size, oxidized LDL, hsCRP, homocysteine, lipoprotein(a), and apolipoprotein B — the markers that actually predict cardiovascular events
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Metabolic assessment: fasting insulin, HbA1c, and triglyceride-to-HDL ratio — identifying insulin resistance as the primary driver of the dangerous lipid pattern in the majority of patients
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Targeted dietary guidance based on the specific lipid pattern — not generic low-fat advice, but specific carbohydrate and fat quality guidance tailored to the patient's metabolic picture
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Evidence-based natural interventions with clinically meaningful effects on lipid profiles: therapeutic omega-3s, plant sterols, red yeast rice, berberine, and soluble fiber
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Systemic inflammation reduction — addressing the gut health, dietary, and metabolic drivers of the arterial inflammation that is the actual mechanism of cardiovascular damage
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For statin patients: CoQ10 supplementation for muscle side effects, thyroid assessment for lipid-thyroid interactions, and collaborative physician communication about medication optimization
We do not discontinue patients' medications. We give them a more accurate picture of their actual cardiovascular risk, address the drivers of their lipid pattern, and support the best possible outcomes from any medication they are already taking.
WHAT MAKES OUR APPROACH DIFFERENT — IN A SINGLE PARAGRAPH
Standard cholesterol care lowers the LDL number. Our approach investigates what your cholesterol is actually doing — the particle size, the oxidation level, the inflammatory markers that determine whether your LDL is causing arterial damage or simply circulating. It identifies the insulin resistance and carbohydrate overconsumption that is driving the dangerous small dense LDL pattern in most patients — which dietary fat restriction does not address. It reduces the systemic inflammation that is the actual engine of arterial plaque formation. And for patients on statins, it addresses the CoQ10 depletion causing their side effects. The result is not just a better number. It is a genuinely lower cardiovascular risk — which is what the treatment is supposed to achieve.
ADVANCED CARDIOVASCULAR ASSESSMENT
The markers that actually predict cardiovascular risk — and that standard testing does not include
A complete cardiovascular risk picture requires looking beyond the standard four-number lipid panel. These are the markers we assess that give the actual picture of what your cholesterol is doing and what is driving your cardiovascular risk.
LDL particle size and number
Small dense LDL particles are dangerous. Large buoyant particles are not. Two people with identical total LDL can have completely different cardiovascular risk. Particle testing identifies which pattern you have — information that changes the treatment strategy fundamentally.
hsCRP and homocysteine
High-sensitivity C-reactive protein measures arterial inflammation — the actual mechanism of plaque formation. Homocysteine is an independent cardiovascular risk factor that damages blood vessel walls and is driven by B vitamin deficiency. Both are often more predictive of cardiovascular events than LDL.
Fasting insulin and HbA1c
Insulin resistance is the most powerful modifiable driver of the dangerous small dense LDL pattern. Identifying it through fasting insulin and long-term blood sugar markers (HbA1c) identifies the root cause of the lipid abnormality in most middle-aged patients — one that statin medication does not address but dietary and metabolic intervention does.
TAKE THE NEXT STEP
Your LDL number is one piece of a much larger picture. We look at the whole picture — and treat what actually matters.
Advanced lipid testing, inflammatory markers, metabolic assessment, and targeted interventions that address actual cardiovascular risk.
Not sure where to begin? Give us a call and we'll help you choose the best first step.