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Cholesterol markers are often where doctors start when it comes to reducing your risk of heart disease, but they don’t tell the whole story. They’re the quick fix, a number we can more easily control with statins.
The thing is, many individuals with heart disease have normal cholesterol levels. Something else is happening in these patients that has nothing to do with the results on lipid panels. Focusing solely on cholesterol means we ignore factors like chronic inflammation and poor blood vessel health that are closely linked to heart attack and stroke risk as we age.
Heart health is multifaceted. Instead of isolating cholesterol as a primary focus, it’s essential to see it in context for better outcomes and a more preventative approach.
LDL Versus HDL
Your body needs cholesterol to function at its best. It's essential to healthy cell membranes, hormone production, and the absorption of nutrients like vitamin D.
Your liver does a great job of producing most of the cholesterol you need for these biological processes, but you can also increase your cholesterol from the foods you eat. That’s where some of the confusion sets in.
There are 2 types of cholesterol. We’re told that high-density lipoprotein (HDL) cholesterol is the “good” kind because it helps your body clear plaque buildup along your arteries.
LDL (low-density lipoprotein) cholesterol is often labeled as “bad” cholesterol because of its link to plaque buildup on your artery walls.
Lipid panels at your doctor’s office look at both types with the addition of triglycerides. These are a type of fat found in your blood that store energy. Elevated levels are often considered alongside LDL cholesterol as risk factors for heart disease down the line.
While low levels of LDL cholesterol over time are linked to a reduced risk of developing atherosclerosis, cholesterol levels on a blood test won’t give you the full picture. (1)
Dietary Cholesterol
For decades, we’ve been told that eating foods high in cholesterol — eggs got a particularly bad rap! — would raise your blood cholesterol levels and increase your heart disease risk. There was an assumption that high blood cholesterol and dietary cholesterol were directly linked.
The confusion likely arose because dietary cholesterol was often consumed alongside trans fats or trans-fatty acids. If LDL cholesterol is “bad” (we maintain this is debatable), trans fats are generally considered the “worst” because of their effects on lowering HDL cholesterol. (2)
Most recent research shows that for most people, dietary cholesterol has minimal to no effect on blood cholesterol levels. (3) Your body is good at keeping things in balance, even when you eat saturated fats. When dietary cholesterol goes up, your liver compensates by producing less.
Of course, there are always exceptions.
You may be genetically predisposed to hanging on to cholesterol more than others (e.g. those with familial hypercholesterolemia), so diet matters more. (4) Certain specialized diets cause bigger swings in your numbers.
Lean Mass Hyper-Responders (LMHRs), for example, are those with high LDL cholesterol, high HDL cholesterol, and low triglycerides, often thanks to low-carb or ketogenic diets. These are generally people with a lower body weight and a healthy metabolism.
Research so far suggests this shouldn’t be cause for alarm. (5) High levels of good cholesterol and low triglycerides seem to offset any potential effects of high LDL cholesterol for these dieters.
In addition to family history and diet, physical activity, pre-existing conditions, and how you manage chronic stress all matter, perhaps even more so than diet.
Today, experts recognize that foods like eggs, dairy products, and red meat can be a part of any heart-healthy diet, especially if you’re already consuming healthy fats like olive oil and avocados. It’s even more beneficial when you’re taking steps to respond to inflammatory triggers and arterial health, which are even bigger culprits behind plaque buildup.
Plaque
Atherosclerotic plaques are hardened deposits of cholesterol, fats, blood cells, and other debris (e.g. fibrous material from previous blood clots) that form along artery walls. Over time, they cause atherosclerosis, a narrowing of your arteries that can restrict blood flow and increase your risk of heart attacks and stroke. (6)
How these plaques form is a complex process, but it goes beyond the idea of managing high LDL cholesterol levels. Just looking at what they’re made of debunks that theory, as it’s more than just cholesterol.
While excess LDL cholesterol in the blood is a cause of atherosclerosis, research suggests that the progression of these plaques to a point of concern is caused by a combination of factors. (7)
It starts with your immune responses. Any damage to your arteries, whether that’s inflammation, cellular breakdown, or a history of blood clots, triggers an immune response. (8) Your white blood cells try to repair the damage, which only attracts more to the source of the problem.
LDL cholesterol plays an indirect role at best. When it becomes oxidized due to inflammation or oxidative stress, it triggers that same immune response. (9) This increases the size of the plaque’s fatty core and makes it more likely to rupture, increasing your risk of a cardiac event or stroke. (10)
Plaques can develop differently in each person. Some grow slowly and remain harmless. Others can become unstable. It’s that instability and plaque rupture that increases your risk of heart attack and stroke. (11)
This complex sequence shows how heart health goes well beyond the numbers on a lipid panel. Focusing on total cholesterol alone may not fully prevent heart disease. We need to look beyond cholesterol at strategies that reduce inflammation and improve blood vessel health.
The True Cause of Heart Disease
The true cause of heart disease starts with endothelial dysfunction. (12) The endothelium is a layer of cells (endothelial cells) that lines your blood vessels for healthy blood flow. When it’s damaged, this triggers the immune system responses we talked about above related to plaque formation.
That damage can be caused by any condition or biological state that increases inflammation in the body. That includes diabetes, obesity, smoking, or a history of infection. (13)
White blood cells cluster to the spot where the damage occurred, triggering arterial inflammation and the formation of blood clots, or thrombosis, as a repair mechanism. Over time, continued dysfunction and accumulation of debris that includes remnant clots narrow arteries, causing atherosclerosis.
These remnants include fibrin, a protein involved in clot formation. (14) Any residue of these proteins left behind can exacerbate inflammation along the endothelium, perpetuating this cycle of damage and eventual plaque buildup.
Cardiologists with the American Heart Association (AHA) have pointed to endothelial dysfunction as a primary risk factor for heart disease for decades. (15)
LDL cholesterol often gets blamed for plaque instability, but it’s not the root cause. Oxidized LDL cholesterol can certainly worsen things, but even so, it’s still a byproduct of an inflammatory process.
To fully understand the role of LDL, we need to consider the size and type of LDL particles. Light, fluffy LDL particles pose little risk to your health, whereas small, dense LDL particles are far more problematic. Since LDL-C only measures the total volume of LDL, it doesn’t reflect the actual number of particles in circulation.
When there is a higher number of small LDL particles, it takes longer for the liver and biliary system to efficiently clear. This increases the likelihood of oxidation and a triggered immune response.
This is why, in addition to monitoring LDL-C levels, it’s essential to evaluate ApoB. ApoB is a biomarker that directly measures LDL particle count. So, it’s a more reliable predictor of cardiovascular disease (CVD) risk than LDL-C alone.
Targeting the real culprits, meaning anything that damages your endothelial cells, means a more holistic, effective approach to managing heart health. It also turns the fight into one of prevention vs. reaction and an immediate turn to pharmaceuticals.
Statins Aren’t a Perfect Solution
Statins are the most commonly prescribed medication by healthcare providers looking to lower their patients’ LDL cholesterol and risk of coronary artery disease. The thing is, they don’t directly target or reduce LDL levels. Instead, they block liver enzymes that produce it.
In fact, they don’t just block enzymes and synthesis in the liver. They also block cholesterol synthesis in every cell within the body, particularly in muscles. With cholesterol acting as an essential building block for cellular function, this disruption of synthesis is what causes the production of unwanted side effects from statins.
While studies show statins are linked to a reduced risk of bad cardiovascular outcomes and stroke, this may be due to their modest anti-clotting and endothelial protective effects. (16) Any effects on lower cholesterol don’t address the underlying causes of heart disease, either.
They can also come with unwanted side effects. Some patients on statins report muscle pain or cramping, digestive issues, sleep problems, headaches, fatigue, and dizziness.
Fortunately, there are better options. For better long-term heart health, lifestyle changes should focus on reducing endothelial damage. High blood pressure, smoking, and inflammation are all risk factors for increased heart disease risk due to harm done to your blood vessels.
Smoking cessation, stress management, maintaining a healthy weight, and eating an anti-inflammatory diet are all great tools for vascular health.
Natural solutions like nattokinase, a natural enzyme commonly derived from fermented soybeans, can also support healthy blood flow for a more sustainable heart-healthy strategy.
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Toku Flow is a daily supplement that combines nattokinase with vitamin K2 and beta-glucan to support reduced coronary plaque and balanced cholesterol with fewer side effects.The Takeaway
The majority of people at high risk for heart disease and, as a result, statin use aren’t given the chance to address the underlying causes of their status. We tend to turn to quick fixes without questioning what we can do as preventative measures to keep us from getting to the point of pharmaceuticals in the first place.
Cholesterol is just one piece of the puzzle, and managing your cholesterol shouldn’t be the only thing you do for better heart health.
Sources
The LDL cumulative exposure hypothesis: evidence and practical applications
Carbohydrate Restriction-Induced Elevations in LDL-Cholesterol and Atherosclerosis: The KETO Trial
Cholesterol and Atherosclerotic Cardiovascular Disease: A Lifelong Problem
Is It All About Endothelial Dysfunction and Thrombosis Formation? The Secret of COVID-19
Fibrin clot properties in cardiovascular disease: from basic mechanisms to clinical practice
