• Siri DeMarche

Everything you know about Cholesterol is (at least) Incomplete & What You Can Do About It

Updated: Jul 23

*As always, scroll to the very bottom for a TLDR synopsis*


Cholesterol has a bad rap, and you've probably bucketed it into two categories; "good" and "bad" cholesterol. You've been told that your cholesterol levels are creeping up, so you watch your saturated fat intake. But like most of society you've been duped, because it's not that simple, and saturated fat is not the root of all evil. In fact, everything that you've been told about saturated fat, cholesterol, and cardiovascular disease is (at best) incomplete. Luckily things are changing and comprehensive tests are becoming more routine (at least in integrative medicine offices). I will include important tests that you may want to discuss with your doctor, if you are concerned about your cardiovascular health.


Research shows that cholesterol is a symptom of heart disease and NOT the cause, as we've been led to believe. In fact, LDL or "bad cholesterol" isn't even cholesterol, its a vessel that carries fat-based energy to your cells. Cholesterol is one of many passengers on this LDL vessel. Cholesterol's job is to fix your cells. YOU NEED IT. Now, why is this so confusing? Well in the world of higher fat diets (& lower overall carbohydrate intake), you will have high LDL and this is actually a good thing. More LDL means more fatty acids to fuel your cells, which means increased energy for you. If you're in good health, your cells don't need constant cellular repair. Your body can use cholesterol for other things, like balancing your hormones. Now, what about with heart disease?


The misconception of LDL cholesterol causing heart disease is a prime example of correlation vs. causation, and one that has catapulted generations into a fat-fearing frenzy while wrecking the health of populations. Your arteries circulate blood throughout your body and when your arterial walls are damaged, cholesterol fixes the damage. Here in lies the misconception. LDL particles are large and they can get stuck in the tears of your arterial walls. Plaque starts to form and BOOM heart disease. Correlation vs. Causation; plaque is the result of something getting stuck that leads to heart disease, not the fact that LDL was present (and trying to fix the damage in the first place). The real question is, what is damaging your arteries in the first place? What is creating the tears in your arterial walls where LDL particles are getting stuck and plaque is forming? Eradicate the underlying cause and you eradicate the actual problem, not a symptom of the problem. The real problem and the cause of these arterial tears is chronic inflammation overload. Inflammation causes the damage to your arterial wall, cholesterol comes in to fix the problem and gets stuck at the damaged site, becoming the scapegoat for heart disease. So now...we've got a population trying to lower their LDL cholesterol levels while not addressing the root issue. Is it any wonder why heart disease is such an issue today? We have chronic inflammation overload tearing up our arterial walls and decreased levels of important molecules needed to patch up these tears.


"The more I reviewed the literature, the more I realized, 'You know what? It seems like everything they teach us in nursing school, in medical school, in pharmacy school about lipids, about LDL, about VLDL, and HDL, the good cholesterol, the bad cholesterol, and how the stuff works--it's probably wrong, or at least incomplete."-Dr. Zubin Damania. Dr. Damania is a primary care clinical director and internal medicine doctor at Stanford. Dr. Damania is helping to shed light on the demonization of cholesterol and is one of too few trying to change the perception of cholesterol's role in heart disease. Especially if you are on a lower carbohydrate and higher fat diet, higher cholesterol levels are not necessarily a bad thing. Fighting inflammation is actually what you need to worry about to achieve ultimate health.



Let's take a closer look at what is really going on. When you follow a higher-carbohydrate intake (respective to other macronutrients), you are getting the majority of your energy from glucose. The carbohydrate that you ingest is digested into glucose, and is sent through your bloodstream to cells with some help from insulin. Because your blood is primarily water, glucose gets dissolved without issue- think stirring sugar into water. If you are following a higher-fat intake (respective to other macronutrients), you are getting most of your energy from fat. Fat is not like glucose. The fat that you eat digests into fatty acids, but fatty acids cannot be sent through your blood like glucose because fats and liquids do not mix (think trying to dissolve oil in water). Instead, fat must be carried through the bloodstream to reach your cells. To do this your body must:


1) package fatty acids into triglycerides (a bundle of three fatty acids) to make it easier for them to be transported through your blood.

2) create carriers to transport these triglycerides.


These carriers are lipoproteins. Lipoproteins carrying a load of triglycerides are called very-low-density lipoproteins (VLDL) and lipoproteins that have already dropped their triglycerides are called low-density lipoproteins (LDL). Unfortunately, LDL has been deemed "bad cholesterol." LOL. LDL isn't even cholesterol! So...what is cholesterol?


Cholesterol is a passenger in LDL and if you're in good health, it rarely leaves the LDL carrier. LDL carriers really only have cholesterol in them for emergency repair, because a main function of cholesterol is cellular repair. Because LDL carries fat-based compounds to hungry cells, by definition, your LDL levels will go up if you are on a high-fat diet. This is a good thing because it means that you have more fatty acids to transport through your bloodstream to deliver as energy to your cells. If you don't need constant cellular repair, the unused cholesterol can be bundled into high-density lipoprotein (HDL) particles and directed to your liver to create sex hormones- this is one reason why a higher fat diet is good for testosterone production.


If high cholesterol levels do not cause heart disease, what does? The answer is chronic inflammation. Elevated levels of inflammation cause arterial wall damage. LDL transports cholesterol to the damaged site to repair it. Because LDL carriers are large, they can get stuck at the damaged site and consequently plaque begins to build up. Therefore the answer is not to decrease your LDL levels and thus your body's ability to repair itself, but to eradicate whatever is causing the arterial wall damage in the first place. "Elevated levels of cholesterol" are a symptom of a larger issue.


To date the most influential study in determining heart disease risk factors was the Framingham Heart Study. The Framingham Heart Study began in 1940 and followed many generations collecting data on their heart health. While The Framingham Heart Study is incredibly useful for learning about heart disease, there are aspects of the study that can be misinterpreted. According to the study, the main risk factors for heart disease are: high cholesterol (LDL) & arterial plaques, smoking, obesity, lack of exercise, high blood pressure, and psychological stress. Now here's the kicker....every single one of these risk factors except LDL (debunked above) is associated with, or is the cause, of inflammation and inflammation damages arterial walls. Chronic inflammation destroys artery walls, cholesterol carrying LDL shows up to do some damage control, gets stuck in the arterial wall tears, and becomes the scapegoat for being the cause of heart disease.


Fortunately, more and more researchers and doctors like Dr. Damania are questioning preliminary assumptions about the Framingham Study and taking their concerns mainstream. If you are concerned about your cardiovascular health, below are some tests and concerns to ask your doctor about:

  • Oxidized LDL cholesterol: these particles get stuck in your arteries & your immune system mistakes them for invaders, leading to inflammation in your arteries.

Stop eating fried foods, cut your sugar intake, & keep your inflammation down

  • Low HDL (high-density lipoprotein) cholesterol: HDL assists in transporting cholesterol from arteries & tissues for metabolism.

Eat more high-quality saturated fat

  • Small dense LDL (low-density lipoprotein) cholesterol: this is LDL cholesterol that is smaller & heavier than other LDL particles, this type spends more time in the is more likely to oxidize.

High levels are associated with risk of atheroscierosis

  • High triglycerides: fatty acid molecules that are bonded with a glycerol, measured in the bloodstream.

High levels could indicate cardiovascular disease risk or metabolic syndrome

  • High triglycerides/HDL ratio: too much fat in the blood with not enough HDL to transport cholesterol for metabolism increases cardiovascular disease risk.

  • Non-HDL Cholesterol: total cholesterol - HDL. Without HDL to transport cholesterol for metabolism, other forms can start to clog up arteries.

Most concerning if triglycerides are also high

  • Fasting insulin/-glucose: measures your insulin sensitivity - how well you metabolize the sugar you consume.

Higher numbers can indicate insulin resistance

  • APO A-1 (Alphalipoprotein A-1): important to cholesterol transport.

Higher levels are associated with lower occurrence of cardiovascular disease

  • APO B (Alphalipoprotein B): the protein component of LDL.

Lower levels are associated with lower occurrence of cardiovascular disease

  • hsCRP (inflammatory marker) High-sensitivity c-reactive protein: the liver makes C-reactive protein when there is inflammation in the body.

Chronic elevation is associated with cardiovascular disease risk

  • Homocysteine: indicates impaired conversion of methionine to cysteine.

Chronic elevation can indicate inflammation and is associated with cardiovascular disease risk

  • Lp-PLA2 (Lipoprotein-Associated Phospholipase A2): Lp-PLA2 is an enzyme that marks inflammation of blood vessels (which is significant to atheroscierosis).

If anything is damaging your arteries, Lp-PLA2 will increase


In addition to understanding that high cholesterol is the symptom of a larger problem, and not the cause of the problem itself, it is important to understand the factors affecting your LDL cholesterol response numbers. These factors include; individual wiring (your body's response to dietary fat is unique), obesity, insulin resistance, diabetes, Hypertriglyceridemia, gender, and recent injury/infection. Unfortunately saturated fat has gotten a terrible rap when it comes to its role in heart disease, cancer, and serum cholesterol levels. It is not so nuanced as this and there are more prominent factors that contribute to heart disease. These factors are; insulin resistance/metabolic syndrome, inflammation, excessive consumption of refined carbohydrates, high-fructose corn syrup, smoking, high blood pressure, obesity, physical inactivity, pre-diabetes, diabetes, unmanaged stress, and family history. Remember that cholesterol is a protective metabolic response to toxin exposure or infection. All these factors are tied to mitochondrial function (read more here).


Cholesterol and saturated fat do not cause heart disease, inflammation does. Here are some things you can do about it (and of course I am happy to help you):


  • Tweak your dietary fat intake & decrease your carbohydrate intake

Avoid hydrogenated fats (think packaged chips, cookies, crackers...) omega-6 oils from low quality sources (corn, safflower, soy, canola...), don't eat fried foods (aka oxidized fat), reduce your intake of refined carbohydrates (focus on non-starchy vegetables instead), and eat moderate amounts of high-quality protein. Refined carbohydrates and sugar is the number one contributor to inflammation, so take them out of your diet.

  • Lose weight if necessary

Losing weight (if you are overweight) can reduce high LDL-P & small dense LDL particles. However, this will not work if you lose weight but are still eating low-quality fats from vegetable oils.

  • Intermittent Fasting

If done correctly, intermittent fasting will increase your natural energy production, help to fix insulin resistance, reduce triglyceride count, and decrease small dense LDL particles in the blood.

  • Consume Polyphenol-rich plants

Polyphenols protect you from inflammatory damage and are found in colorful plants.

  • Exercise

Exercise decreases inflammation in the long-term (even though it causes short-term muscle damage & inflammation).

  • Cold Exposure

Cold exposure triggers cold-shock proteins that decrease inflammation and speed recovery.

  • Stress reduction methods (like meditation)

By decreasing psychological stress, you are also decreasing inflammation & oxidative damage.



References:

Sedentary Behavior and Adiposity-Associated Inflammation The Multi-Ethnic Study of Atherosclerosis

Obesity, Inflammation and Diet

Psychological Stress, Inflammation, and Coronary Heart Disease

Inflammation and hypertension: new understandings and potential therapeutic targets

The role of inflammatory cytokines in endothelial dysfunction.

Damage Control: Cellular Mechanisms of Plasma Membrane Repair

The Framingham Study and the Constitution of a Restrictive Concept of Risk Factor

Smoking and Inflammation

Meta-analysis of prospective cohort studies evaluating the associate of saturated with cardiovascular disease

Small, Dense Low-Density Lipoprotein Particles as a Predictor of Risk of Ischemic Heart Disease in Men

Saturated Fatty Acids and Risk Coronary Heart Disease: Modulation by Replacement Nutrients

Do cholesterol Numbers Really Assess Cardiovascular Risk? Lipoprotein Particle Numbers Tell the Story

Saturated fat, carbohydrate, and cardiovascular disease

Very-low-carbohydrate ketogenic diet v. low-fat diet for long-term weight loss: a meta-analysis of randomized controlled trials

Ketogenic Diet for Obesity: Friend or Foe?

Improvements in LDL particle size and distribution by short-term alternate day modified fasting in obese adults

Time-restricted feeding and risk of metabolic disease: a review of human and animal studies

Short-term modified alternate-day fasting: a novel dietary strategy for weight loss and cardioprotection in obese adults

Time-restricted feeding and risk of metabolic disease: a review of human and animal studies

Beyond weight loss: a review of therapeutic uses of very-low carbohydrate (ketogenic) diets

Modification of lipoproteins by very low-carbohydrate diets.

Alternate day calorie restriction improves clinical findings and reduces markers of oxidative stress and inflammation in overweight adults with moderate asthma

Time-restricted feeding and risk of metabolic disease: a review of human and animal studies

Comparison of effects of diet versus exercise weight loss regimens on LDL and HDL particle size in obese adults


TLDR

Research shows that cholesterol is a symptom of heart disease and NOT the cause, as we've been led to believe. In fact, LDL or "bad cholesterol" isn't even cholesterol, its a vessel that carries fat-based energy to your cells. Cholesterol is one of many passengers on this LDL vessel. Cholesterol's job is to fix your cells. In the world of higher fat diets (& lower overall carbohydrate intake), you will have high LDL and this is actually a good thing. More LDL means more fatty acids to fuel your cells, which means increased energy for you. If you're in good health, your cells don't need constant cellular repair. Your body can use cholesterol for other things, like balancing your hormones. The misconception of LDL cholesterol causing heart disease is a prime example of correlation vs. causation, and one that has catapulted generations into a fat-fearing frenzy while wrecking the health of populations. Your arteries circulate blood throughout your body and when your arterial walls are damaged, cholesterol fixes the the damage. LDL particles are large and they can get stuck in the tears of your arterial walls. Plaque starts to form and BOOM heart disease. Correlation vs. Causation; plaque is the result of something getting stuck that leads to heart disease, not the fact that LDL was present (and trying to fix the damage in the first place). The real question is, what is damaging your arteries in the first place? What is creating the tears in your arterial walls where LDL particles are getting stuck and plaque is forming? Eradicate the underlying cause and you eradicate the actual problem, not a symptom of the problem. The real problem and the cause of these arterial tears is chronic inflammation overload. Inflammation causes the damage to your arterial wall, cholesterol comes in to fix the problem and gets stuck at the damaged site, becoming the scapegoat for heart disease. So now...we've got a population trying to lower their LDL cholesterol levels while not addressing the root issue. Is it any wonder why heart disease is such an issue today? We have chronic inflammation overload tearing up our arterial walls and decreased levels important molecules to patch up these tears.


Here are some things you can do:

  • Tweak your dietary fat intake & decrease your carbohydrate intake

  • Lose weight if necessary

  • Intermittent Fasting

  • Consume Polyphenol-rich plants

  • Exercise

  • Cold Exposure

  • Stress reduction methods (like meditation)









Statements made on this website have not been evaluated by the U.S. Food and Drug Administration or any other medical body. I do not aim to diagnose, treat, cure, or prevent any illness or disease. Information is shared for educational purposes only. You must consult your doctor before acting on any content on this website, especially if you are pregnant, nursing, taking medication, or have a medical condition.

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