Cholesterol and our diet

Cholesterol level is not the result of what we eat!

The biggest factor in cholesterol is not diet but genetics or heredity. Our liver is designed to remove excess cholesterol from our body, but genetics play a large part in our liver's ability to regulate cholesterol to a healthy level.

Take, for instance, people with genetic familial hypercholesterolemia. This is a condition characterized by abnormally high cholesterol, which tends to be resistant to lowering with lifestyle strategies like diet and exercise.

Further, eating nutritious cholesterol-rich foods is not something we should feel guilty about; they're good for us and will not drive up our cholesterol levels as we may have been told.

 

To date, extensive research did not show evidence to support a role of dietary cholesterol in the development of CVD. It is worth noting that most foods that are rich in cholesterol are also high in saturated fatty acids and thus may increase the risk of CVD due to the saturated fatty acid content.

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What is the "Right" Cholesterol Level:

Our body makes cholesterol to make hormones, cell membranes, bile, and vitamin D. Total cholesterol is really high-density lipoprotein (HDL) cholesterol, known as the "good" cholesterol because it helps remove other forms of cholesterol from your bloodstream, LDL stands for low-density lipoproteins (LDL), it is sometimes called the "bad" cholesterol because a high LDL level leads to a buildup of cholesterol in our arteries. 

Total cholesterol level includes HDL, LDL and triglycerides.

Triglycerides are a type of fat (lipid) found in our blood. Our body converts any calories it doesn't need into triglycerides. The triglycerides are stored in our fat cells, to be released Later for energy between meals.

There are two types of LDL - a large buoyant type and a small dense (sdLDL-C) one. The type of cholesterol that can be dangerous is the small dense (sdLDL-C).

This study discusses the influence of the quality of LDL on cardiovascular risk confirming "that subjects in the highest quartile of sdLDL-C (≥43.7 mg/dL), had a 5.4-fold higher risk of CHD than those in the lowest quartile (≤24.4 mg/dL), and that sdLDL-C measurement significantly (p < 0.001) improves net reclassification".

Bottom-line, the best coronary heart disease (CHD) predictor is the sdLDL-C level and not the LDL level in itself. (Watch this short video for a good quality testimonial magnifying the importance of this difference).

"Because of its small size and higher density compared to larger LDL-C particles, sdLDL-C has a greater ability to penetrate the artery wall, in addition to having a longer half-life and greater susceptibility to oxidative modification. Cardiovascular diseases caused by abnormal sdLDL-C are reflected in many clinical cases. SdLDL-C plays a variety of roles in the process of AS, such as affecting lipid metabolism, promoting the release of inflammatory factors leading to inflammatory reaction, releasing excessive ROS and RNS to produce oxidative stress, activating fibrinolytic system to produce thrombus".

 

This comprehensive study on the subject (the importance of sdLDL-C as a predictor to CHD) concludes: "Expression of small LDL has a strong environmental component, and treatment is often the least expensive and includes reduction of excess body fat, avoidance of simple carbohydrates in the diet, exercise, niacin, fibric acid derivatives and omega-3 fish oil. Specific patient subgroups may benefit from sdLDL-C analysis. Studies have indicated that in patients with existing CHD, an abundance of small, dense LDL predicts disease progression, and reduced levels of small LDL portend a better cardiovascular outcome".

 

Insulin Resistance

"Multiple studies have demonstrated that insulin resistance is a strong predictor of atherosclerotic cardiovascular (CV) disease (ASCVD) and have been summarized in a recent meta-analysis by Gast et al".

Insulin Resistance Implications on blood vessels response to sdLDL-C:

1. Impaired endothelial function (the control of blood fluidity, platelet aggregation and vascular tone): Insulin resistance is associated with endothelial dysfunction, which is characterized by reduced production of nitric oxide, increased inflammation, and oxidative stress in the endothelial cells lining blood vessels. Endothelial dysfunction limits the ability of the blood vessels to repair damage caused by sdLDL-C, as it interferes with the normal processes of vasodilation and the recruitment of repair cells to damaged areas.

2. Decreased nitric oxide production: Insulin resistance can lead to decreased production of nitric oxide, a molecule that plays a key role in maintaining the health and function of blood vessels. Nitric oxide helps to regulate vascular tone, inhibit platelet aggregation, and prevent leukocyte adhesion to the endothelium. Reduced nitric oxide levels impair the ability of blood vessels to respond to injury and promote repair processes.

3. Pro-inflammatory state: Insulin resistance is associated with a chronic low-grade inflammatory state characterized by elevated levels of inflammatory cytokines and chemokines. This systemic inflammation can further damage the endothelium and impair repair mechanisms in response to sdLDL-C-induced injury. Additionally, inflammation promotes the development and progression of atherosclerosis, further compromising vascular repair.

4. Dyslipidemia: Insulin resistance is often accompanied by dyslipidemia, characterized by elevated levels of triglycerides, decreased levels of high-density lipoprotein (HDL) cholesterol, and an increase in small, dense LDL particles. This lipid profile contributes to the formation and progression of atherosclerotic plaques and can hinder the repair of damage caused by sdLDL-C by promoting lipid accumulation and inflammation in the vessel wall.

5. Hyperglycemia-induced damage: Insulin resistance is often associated with hyperglycemia (high blood sugar levels), which can lead to the formation of advanced glycation end products (AGEs). AGEs contribute to endothelial dysfunction, oxidative stress, and inflammation, all of which impair the ability of the cardiovascular system to repair damage caused by sdLDL-C.

Overall, insulin resistance contributes to a pro-atherogenic environment characterized by endothelial dysfunction, inflammation, dyslipidemia, and hyperglycemia, which collectively limit the ability of the cardiovascular system to repair damage caused by sdLDL-C and promote the progression of atherosclerosis and cardiovascular disease.

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"The molecular etiology (etiology = attribution of the cause or reason for something) of the insulin resistance directly contributes to the development of atherosclerotic cardiovascular disease by inhibiting nitric oxide production (endothelial dysfunction) and stimulating the MAPK pathway". Rephrasing this statement - insulin resistance impairs the repair process of damages caused by the sdLDL-C cholesterol to blood vasculars.

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In conclusion of the above section, lowering sdLDL-C cholesterol and insulin resistance is the most important action to reduce CHD risk! Our recommended diet, that includes intermittent fasting and physical exercises is most likely to provide the desired results.

 

STATINS

"Of note despite the ability of statins to lower LDL-C, non-HDL-C, and apolipoprotein B levels, statins do not lower Lp(a) levels and may even increase levels (10,11). Finally, statins modestly increase HDL-C levels (8,12,13). In most studies HDL-C levels increase between 5-10% with statin therapy".

 

Statins May Make Heart Health Worse

• There is evidence showing that statins may worsen heart health, and only appear effective due to statistical deception. One scientific study concludes: "Statins stimulate atherosclerosis and heart failure: pharmacological mechanisms".  Another study brings this conclusion: "How statistical deception created the appearance that statins are safe and effective in primary and secondary prevention of cardiovascular disease"

• This study shows that "Use of the statin medications routinely result in lower coenzyme Q10 (CoQ10) levels in the serum. Some studies have also shown reduction of coenzyme Q10 in muscle tissue. Such coenzyme Q10 deficiency may be one mechanism for statin-induced myopathies." "Myopathies are a heterogeneous group of disorders primarily affecting the skeletal muscle structure, metabolism, or channel function. They usually present with muscle weakness interfering in daily life activities. Muscle pain is also a common finding and some myopathies are associated with rhabdomyolysis".

CoQ10 is crucial for efficiently transferring electrons within the mitochondrial oxidative respiratory chain and producing adenosine triphosphate (ATP).  ATP is a coenzyme used as an energy carrier in every cell of our body. When we consider that our heart is the most energy-demanding organ in our body, we can surmise how potentially devastating it can be to deplete our body's main source of cellular energy.

So while one of statins' claims to fame is warding off heart disease, scientific studies show that they actually increase our risk of depleting our body of CoQ10.

The depletion of CoQ10 caused by the drug is why statins can increase our risk of acute heart failure.

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Statins Proliferation Implications

Cholesterol is one out of a few other major contributing factors to heart disease: "Leading risk factors for heart disease and stroke are high blood pressure, high low-density lipoprotein (LDL) cholesterol, diabetes, smoking and secondhand smoke exposure, obesity, unhealthy diet, and physical inactivity".

Still, following the publication of the 2013 ACC/AHA guidelines in the US, "The annual number of statins prescriptions increased from 461 million to 818 million (77%; p = 0.000) between 2008 and 2019".

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Statins, Cholesterol Reduction and Myelin

Given the discussion in this section about the importance of cholesterol for the production of myelin, and the importance of myelin to cognitive functioning, it is not surprising that dementia and altzheimer disease rapidly increased with the expansion of statins usage as shown by these numbers from QuickStats: "Age-Adjusted Death Rates for Alzheimer Disease Among Adults Aged ≥65 Years, by Sex — National Vital Statistics System, United States, 1999–2019. The age-adjusted death rate for Alzheimer disease increased from 128.8 per 100,000 in 1999 to 233.8 in 2019.23 (Apr 2021)"

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Anyone who takes a statin drug, MUST take Coenzyme Q10 as a supplement. For those who are over 40, it is strongly recommend to take ubiquinol (CoQ10's reduced form) instead of CoQ10, as it's far more effectively absorbed by our body.