Understanding Your Cholesterol: Diet, Genetics and what you can do about it.

Well, it was only a matter of time before the doctor becomes the patient. After years of watching my cholesterol gradually creep up due to my superb genetic inheritance it finally happened. That bad cholesterol finally climbed high enough for me to head to the pharmacy. So I figured I use my new obsession with cholesterol as a means to the next blog. If you are a genetically gifted person, you can stop reading and go do something better with your life, but if you are genetically or environmentally challenegd, then read on.

Cholesterol metabolism:

We get our cholesterol from two major sources:

1) Liver: 70-80% of our cholesterol is actually made by the liver. Liver uses dietary fat and then creates its own cholesterol. This is the main source of fat in our body. And since cholesterol is not water solube, it has to be packaged into solube particles so it can travel in the blood. Proteins are water solube. So the liver makes large proteins that function as taxi cabs for the cholesterol. These are called lipoproteins (Lp).. We have three types of these Lp:

Low Density Lipoproteins (LDL): Their main job is to take the cholesterol from the liver into the blood and deliver it to tissues like brain, muscle and fat tissue. These organs absorb the cholesterol they need from the the LDL taxi, but the taxi itself (LDL) remains in the blood and goes back to home base (liver) to fill up again. Once in the liver, LDL-receptors on liver cells gobel up the LDL in blood and take them inside for processing and repackaging.

High Density lipoproteins (HDL): Their main job is to bring cholesterol the tissues have in excess back to the liver.

Very Low Density Lipoproteins (VLDL): these transport triglycerides from the liver to the fat and muscle tissues where the triglyceride is absorbed and stored for later use as a source of energy. Once the tyglyceride is stripped off, VLDL acually becomes an LDL. This goes back to the liver to pick up more triglycerides.

Triglycerides: The main form of energy storage, this is how we store fat in our fat cells. It is transported to the fat cells via VLDLs.

2.Diet: the remaining 20-30% of cholesterol comes from diet. This cholesterol is digested in the small intestine and is absorbed into the blood stream. The proteins that transport the dietary cholesterol are called Chylomicrons.. Chylomicrons transport the dietary fat to the liver where it is processed. This is done through a specialized direct connection called the hepato-portal loop between the liver and small intestine. Our liver actually uses cholesterol to make Bile. Bile is stored in the gallbladder and then released into the small intestine after each meal. Bile helps absorb dietary cholestrol via the hepato-portal loop. So, we actually use our own cholesterol (Bile) to absorb dietary cholesteraol.

Types of Clinical Cholesterol

The bad guy: LDL — Low-Density Lipoprotein

The primary carrier of cholesterol from the liver to the body's tissues. When LDL levels are elevated, LDL particles can accumulate in artery walls and contribute to plaque formation, making it the main target of cardiovascular risk reduction. Optimal level: below 100 mg/dL (below 70 mg/dL for high-risk patients)

The good guy: HDL — High-Density Lipoprotein

HDL carries cholesterol away from artery walls back to the liver for disposal. Higher HDL levels are generally associated with lower cardiovascular risk. These tend not to deposit on arterial walls and over all reduce the amount of cholesterol in the circulation. Optimal level: above 60 mg/dL

Triglycerides

The most common form of fat in the body, triglycerides are stored as energy. Elevated levels — especially alongside low HDL — independently raise cardiovascular risk and are strongly influenced by refined carbohydrates, sugar, and alcohol. Normal level: below 150 mg/dL.

VLDL — Very Low-Density Lipoprotein

Produced in the liver, VLDL primarily transports triglycerides. As it offloads triglycerides to tissues, it shrinks and eventually becomes LDL. High VLDL is often a sign of elevated triglycerides. Normal level: 2–30 mg/dL

Total Cholesterol:

The combined measure of LDL, HDL, VLDL, and other lipoproteins. While useful as a screening number, it tells an incomplete story — a high HDL can inflate the total without raising your risk. Total cholesterol is actually calculated as LDL + HDL + (Tryglycerides x 0.2). So unless your Triglycerides are really high, total cholese is mostly LDL + HDL. You can see how if you have a high HDL ( a good thing), your total cholesterol can be elevated.

A note on LDL subtypes: Not all LDL is identical. Small, dense LDL particles are more prone to oxidation and arterial penetration than larger, "fluffy" LDL. Advanced lipid panels can measure particle size and number, which may provide a more precise cardiovascular risk estimate than standard LDL-C alone. So, if you have a LDL above 170, its high regardldess of subtype and you should make lifestyle or medical interventions. But if your LDL is borderline between 100-170, it may help to measure your LDL subtypes. This is a relatively new trend and I persoanlly have started offering it to certain patients. The two most common small high risk LDLs we check are Lipoprotein-A and Apoprotein-B. Unfortunately, Lipoportein A seems to be purely genetic whereas Apoprotein B can be improved with diet and medication.

The Role of Diet in LDL Levels

Remember that we make most of our own cholesterol, so why do we harp so much on diet? Well, it turns out that diet influences LDL through multiple mechanisms — altering lipoprotein composition, modulating LDL receptor activity, and affecting the balance between production and clearance. Some of this is genetic, hence why yours truly has a elevated cholesterol while the big boss, Mrs. Moini, has a fantastically low cholesterol despite eating from the same pot. But like everything else in life, diet also plays a role.

Dietary Fats That Raise LDL

Saturated fatty acids (found in red meat, butter, full-fat dairy, coconut oil, palm oil) Saturated fats downregulate LDL receptor expression in the liver, meaning fewer receptors are available to clear LDL from the blood. For most people, replacing saturated fat with unsaturated fat is the single most impactful dietary change for LDL.

Trans fatty acids (industrially produced, found in partially hydrogenated oils, some processed snacks) Trans fats are uniquely damaging: they both raise LDL and lower HDL simultaneously. Most artificial trans fats have been removed from the U.S. food supply, but small amounts remain in some processed foods.

Dietary Fats and Foods That Lower LDL

Monounsaturated fats (olive oil, avocados, almonds, cashews) Replacing saturated fats with monounsaturated fats consistently reduces LDL without lowering HDL.

Polyunsaturated fats (vegetable oils, walnuts, fatty fish, flaxseed) Both omega-6 and omega-3 polyunsaturated fats lower LDL when substituted for saturated fats. Omega-3s also significantly reduce triglycerides.

Soluble fiber (oats, barley, beans, lentils, apples, psyllium) Soluble fiber binds bile acids in the gut, interrupting the enterohepatic circulation and forcing the liver to use more cholesterol to make new bile acids. Even 5–10 grams of soluble fiber per day can reduce LDL by 5–10%.

Plant sterols and stanols (found naturally in grains, nuts, and vegetables; added to some fortified foods) These compounds structurally resemble cholesterol and compete with it for intestinal absorption. About 2 grams per day can lower LDL by 8–10%. Unofortunately, most American diets only provide a fraction of this amount. You can increase your intake by consuming each of these food categories on a daily basis:

• Vegetable oils: Olive, canola, corn, and sunflower oils.

• Nuts and seeds: Almonds, peanuts, sesame seeds, and pumpkin seeds.

• Whole grains: Wheat germ, bran, and whole-grain breads/cereals.

• Legumes: Beans, lentils, and peas. 

There are also supplements available, but as always, I recommend natural sources spread out through the day than one big dose of a pill.

What About Dietary Cholesterol?

For decades, patients were told to strictly limit egg yolks and shellfish because of their cholesterol content. Current evidence has substantially revised this view. Dietary cholesterol has a modest effect on blood LDL for most people, because the liver compensates by reducing its own cholesterol synthesis when more arrives from food. How you make the egg has a more meaningful impact on your bad cholesterol: using healthy cooking oil like Olive or Avocado oil versus butter.

The Portfolio Diet: Research has shown that combining multiple LDL-lowering dietary strategies simultaneously — soluble fiber, plant sterols, soy protein, and nuts — can reduce LDL by 20–30%, approaching the effectiveness of a low-dose statin in some individuals.

Part 4: The Role of Genetics in LDL Levels

Here is the part you may not like to hear, or like to hear, depending on your genetics: elevated LDL is not simply a lifestyle problem. Genetics account for a substantial proportion of the variation in LDL levels between individuals — estimates range from 40–60% heritability. Some people eat carefully and exercise regularly yet still have high LDL, while others eat poorly and maintain low levels. Some people, like yours truly again, have a family history of elevated cholesterl and heart disease, but their levels are not atsonomically elevated. This ususally shows up in 30-40s with LDL gradually going up to mid 100s. A typical pattern is LDL of 100s that gradualy peaks at 150-170s. I have seen patients lowering their number back to low 100s with strict diets, but most, including myself, will not be able to reach an optimal level without medication.

There are also known genetic mutations that cause very elevated LDLs at a much younger age. These patients typically have LDLs in the 200 range. Unfortuantely no amount of diet can lower this. Meciation is the only option.

Key Takeaways

• Your lipid panel measures multiple distinct particles — LDL is the primary therapeutic target for cardiovascular risk.

• About 70–80% of your cholesterol is made by your liver; only 20–30% comes from food.

• Replacing saturated and trans fats with unsaturated fats, and adding soluble fiber, are the highest-impact dietary changes for lowering LDL.

• Genetics account for up to 40–60% of LDL variation — elevated cholesterol despite a healthy diet is often genetic, so don't be too disappointed on your efforts.

• Familial Hypercholesterolemia affects 1 in 250 people, and requires medication in addition to dietary changes.