We cannot deny the truth that even more than half of all people who suffer heart attacks have “normal” or lower cholesterol levels; or the truth that most elderly people live longer and healthier lives with higher cholesterol levels; or the fact that every cell plasma membrane in our body is made up of cholesterol and that most cholesterol in the body is purposely produced by the liver to help build hormones (including all steroid hormones), vitamin D metabolism, and bile acid production. And we simply cannot deny the truth that much of the human brain is actually made up of cholesterol and that low cholesterol is indicative of depression and memory loss. With all that said though, too much of the “wrong” type of cholesterol, especially when it’s oxidized, is believed to be a major contributor to plaque formation in the arteries, leading to a dreaded condition known as atherosclerosis. This article was a great challenge for me, especially in finding the way to put things in simple terms — but here, I will discuss all the basics of cholesterol in the body, its protein carriers and exactly what we should do to normalize and utilize cholesterol in our body.

Defined as a waxy, whitish-yellow and fat-like substance, cholesterol exists in two forms in the body — and only two: free cholesterol and cholesteryl ester. Free cholesterol is exactly what it sounds like: cholesterol that is in its free state; coming from the fats in our diet, devoid of any enzymatic reaction or protein attached to it. This free cholesterol acts as an antioxidant, fighting cancer, infection and inflammation. Cholesteryl ester — the second form — is what happens to free cholesterol when it is processed in the body from all the enzymatic activities and protein attachments, to make it acclimated and useful to the body’s metabolism. The proteins that carry cholesterol come in many groups. They are officially called lipoproteins because, they contain both lipids (fats) and protein that hold and carry cholesterol. These lipoproteins are classified into: (a) Chylomicrons, (b) Chylomicron remnant, (c) vLDL, (d) IDL, (e) LDL, (f) HDL, (g) Lp(a).

Chylomicrons are unprocessed lipids that come from our diet — the food and fats we eat. They mostly consist of triglycerides. vLDL is the lipoprotein that is produced specifically in the liver, from processed chylomicron remnants. They are still full of triglycerides. LDL is what is produced from enzymatic processes when the triglycerides are removed from IDL and vLDL particles. These LDL mostly contain cholesterol — the same cholesterol that is sometimes oxidized in our arteries, and starting the formation of plaque. HDL — made in the liver and intestine — is the aged-form of LDL, that has been reduced in size and is densely packed mostly with protein. This is the lipoprotein that goes through arteries easily and picks up triglycerides and cholesterol from the various parts of the body and blood, sending them back to the liver to be recycled or excreted out of the body via bile. Lp(a) is a sticky lipoprotein, associated with very atherogenic activity, mostly affects people of African ancestry. All of these lipoproteins can be damaging to our arteries, including the so called “good” cholesterol carried by HDL.

To be clear, lipoproteins like LDL and HDL are not cholesterol! They are what they sound like: lipid/fat attached to proteins. (These are lipid/fat that bind to a special protein called apolipoprotein.) LDL and HDL are lipoprotein particles that hold and transport cholesterol. Calling LDL or HDL  “cholesterol” is like calling an elevator transporting people an, “elevator people”. It is an “elevator transporting people”, just like “LDL cholesterol” is really, “LDL transporting cholesterol”. If there is no cholesterol in the LDL, then it is still an LDL particle regardless, with or without cholesterol — same as an elevator is still an elevator whether or not it is transporting anyone. When you hear of arteries being clogged with LDL cholesterol, oftentimes, these LDL are detached from the cholesterol — forming separate oxidized LDL as well as oxidized cholesterol. LDL and cholesterol only become plaque when they are oxidized. This formation is what leads to what we know as arteriosclerosis or hardening of the arteries.

All lipoproteins can be damaging to the arteries. For example, LDL comes primarily in two patterns: Pattern A — which is large and buoyant; and Pattern B  — which is small, hard and dense. It is this Pattern B that is the “bad cholesterol” associated with plaque formation. MGmin-LDL is another particular form of LDL that is quite sticky, and capable of easily forming plaques in the arteries. HDL comes also in two main forms: A1 — which is considered the desirable form; and A1/A11 — which may serve no discernable purpose in helping the arteries. And further, HDL that carries the apolipoportein C-III is actually quite damaging to the arteries. So HDL type also does matter! (So consider, then, getting the advanced lipid profile, to distinguish these differing patterns of lipoproteins and cholesterol however.)

But what is plaque — and how is it formed. And why is it formed?

When our arteries are damaged by the foods we eat, the toxins we inhale or absorb through our skin, then these toxins damage the inner layers of the blood vessel walls. These toxins bruise the arteries that supply nutrients to the organs because arteries are much more susceptible to injury more so than veins are. When the endothelial layers of these arteries are damaged, then a signal is given, and small oxidized LDL cholesterol comes in to patch up these damages. Then another signal is given for macrophage cells sent by the immune system to engulf these oxidized LDL — the development of what we call foam cells. Then fibrin comes in to clot the area. Then calcium along with other cellular debris byproduct come in to harden and stabilize the region. This is a survival mechanism initiated by the body to prevent a sudden heart attack! But as this progression goes on unimpeded, the arteries begin to narrow, and blood flow becomes jeopardized.

But what should our cholesterol numbers be then? When you get a lipid test, you want your LDL to range anywhere between 130 – 150, 139 being the sweet spot least associated with heart disease, for those not on medication. Your HDL should not be below 40, for below 40 is the start of potential heart disease. And if you are female, that HDL should not be below 50. In fact you may want HDL ideally between 55 and 65. Lp(a) level — which currently is hardly ever tested — should normally be less than 10 mg/dL. ApoB (a.k.a. ApoB100) is the main structural protein of LP(a), which in high levels, is associated with a greater risk for strokes and heart attacks. Normal levels range between 50 to 80 mg/dL. You also want your triglycerides to be below 150, and even more preferably below 100.

But what exactly causes our arteries to bruise in the first place that would cause the need for cholesterol and LDL plaque formation? It is the oxidized fats and oil that we consume — oxycholesterol — that is rancid from the beginning, that causes chaos. It is the chronic lack of certain nutrients in our diet. It is the excess sugar and the insulin resistance that builds in our blood. It is the high animal protein diet that we consume that our pancreas and lymphatic system cannot handle, and that creates high homocysteine levels. And it is the heavy metals and other toxins, like glyphosate and fluoride that we put in our system. These are the causes that wreak havoc on our blood vessel walls.

Personally though, my cholesterol levels were very high over a year ago, especially my LDL section of cholesterol. So I went on a quest, to eat healthy, reduce sugar and reduce excess animal protein, and to avoid all the toxic chemicals and heavy metals found in food and drinks, and even in the air. Then one year later, I rechecked my cholesterol numbers. They were almost exactly the same! My cholesterol numbers did not improve even though I was supposedly doing all the right things! What gives!?

Fixing high cholesterol can be very tricky, and involves specific planning and  following a specific protocol. First, you must find the things that remove excess cholesterol. Then you must find the things to heal the wounded blood vessels. Then you must find the things that prevent the blood vessels from wounding in the first place.

Removing high cholesterol from your blood should never be your primary goal — which is actually the only goal of most cholesterol-lowering drugs. That is why those on these drugs never fix their heart disease problem. In fact, lowering cholesterol for these people is like taking a bandaid off of a wound that never heals! If you remove cholesterol from the arteries, then you must replace that cholesterol with what the arteries need to become healthy again. Furthermore, these medications do not remove the undesirable Pattern B LDL and its cholesterol — but they remove the very needed Pattern A LDL and its cholesterol, creating a worse situation.

So, what will remove the bad type of LDL and bad type of any lipoprotein or cholesterol, what will heal the arteries, and what will prevent this cascade from reoccurring again are the real questions!

To stop the body from producing excess bad cholesterol, black garlic, grapefruit pectin and (a limited small amount of) plant sterols will do that! To heal the damaged arteries, an ayurvedic herb called amla will do that, along with an absorbable form of magnesium, like malate, glycinate, taurate or citrate. To prevent excess bad cholesterol from building in the blood, an ayurvedic herb called kutki will do that — opening up the bile ducts, thus preventing cholesterol and bile from getting stuck in the liver, gallbladder and, consequently, the blood.

So fixing high cholesterol is an at least four steps:

1. Removing bad cholesterol through black garlic, grapefruit pectin and a small amount of plant sterols. Black garlic contains compounds that directly impact the well-being of blood vessel walls. I do not recommend regular garlic or raw garlic, which can actually damage the blood vessels even more. Also, plant sterols containing beta-sitosterol, beta-sitostanol, stigmasterol, and avenasterol will also lower cholesterol numbers. But this must be done on a limited basis — safely about twice per week — else plant sterols may have an opposite effect, increasing heart disease symptoms. The best natural source of plant sterols is probably sea buckthorn berry oil, which may be used more frequently.

2. Using amla because it contains natural vitamin C and copper, which are the nutrients needed to fix damaged blood vessels. In fact, an unusual rise in LDL or decrease in HDL is a sure indicator that natural vitamin C and copper needs to be increased in the diet! Acerola may work as well — at doses of about 500 mg per day.

3. Adding an absorbable form of magnesium, such as magnesium taurate, will actually mature LDL into HDL. In other words, magnesium increases the good HDL particles carrying cholesterol back to the liver for excretion!

4. Adding the bitter herb kutki stimulates bile flow. This bile flow frees trapped cholesterol from building up in the blood. It also prevents the liver from over-producing too much cholesterol. Kutki also prevents cholesterol from becoming oxidized. Other herbs that may help include artichoke extract and burdock root.

Update: Recently, I’ve found an ayurvedic herb that shows power in healing many heart ailments. It may even lower oxidized LDL and its cholesterol. That herb is called Arjuna (Terminalia arjuna).

I cannot recommend red yeast rice or niacin for cholesterol problems. Some red yeast rice products contain mycotoxins, such as citrinin, which is damaging to the liver. Niacin in high doses can create a situation of insulin resistance — the very thing someone with high cholesterol is trying to avoid. And though niacin may raise HDL numbers, it may be the ineffective form of HDL that’s being raised!

Even the plant sterols that I do recommend, should be short term — 3 months — twice per week, since plant sterols are poorly understood, and can cause a condition known as sitosterolemia in people with genetic defects.