An average cholesterol blood test is the last thing that you want to rely on when determining your risk for heart disease, stroke, or blood clots. Unlike popular belief, the term “cholesterol” does not simply stand for one particle that floats around in your blood, clogging up arteries as it goes. Instead, “cholesterol” really implies a variety of different lipoproteins that all have their own specific functions and importance. The three major players the blood are VLDLs (very low density lipoproteins), LDLs (low density lipoproteins), and HDLs (high density lipoproteins). These lipoproteins also contain different amounts cholesterol, triglycerides, and minor fats, all of which determine whether it is a harmful or beneficial particle to the body. It is also important to note that when dietary intake of cholesterol is intentionally lowered (as is the case for most trying to avoid cardiovascular disease), the body naturally makes more in attempt to compensate for the loss.
Quality Over Quantity
HDL, usually termed the “good cholesterol,” take up approximately 30% of the total amount in a healthy individual, and has a job of cleaning the bloodstream of any oxidized cholesterol by taking it back to the liver for recycling or excretion. VLDLs, which are made up of 80% triglycerides, produce in the liver and have the job of bring triglyceride and cholesterol to target fat and muscle cells throughout the body. Once this transportation process is completed, VLDLs either become big, “fluffy” LDLs or small, dense LDLs. Big, “fluffy” LDL are for the most part harmless, as they are formed when triglyceride and insulin levels are low (a good sign that overall inflammation is low). Conversely, when these big LDLs are present alongside of systemic inflammation from poor diet and lifestyle, they can become factors in the cause of heart disease. Small, dense LDL on the other hand, are created when the opposite blood counts occur (high triglycerides and insulin), and cause an inflammatory immune response in arteries due to resisting oxidative stress created by the constant oxygen exposure. Because of the differing sizes of these two LDL types, the average blood test accounting for the total value of cholesterol, shows to be useless. The real issue of the matter is not how big you overall LDL numbers are, but rather which types of molecules make up the amount (small and dense or big and fluffy).
Process of Prevention
Risks for heart disease occur when small, dense LDL (full of triglycerides via excess insulin production) are able to cram themselves into the sensitive ECL (endothelial cell layer) of an artery that has been previously damaged from inflammation in the body. Though small, ECL cells are incredibly important in the body, due to the ability of detecting the tiniest chemical changes in the blood from poor external factors. When they sense there is something wrong happening, an urgent response of the “inflammation alarm” is released. In healthy individuals, this pro-inflammatory response is very productive and helpful, as it is able to defend and aid in the healing of any arising problems. However, in a compromised system (which is the case for those with high insulin and triglycerides), this response ends up worsening the issue through the release of macrophages- white blood cells that swallow cellular debris, which in this case is the small, dense LDL lodged in the ECL. In effort to try and "eat up" the large amount of oxidized LDL molecules now stuck in the artery wall, the macrophages transform themselves into foam cells, which then produce a chemical (myeloperoxidase) that only further oxidizes the LDL debris. After all that, foam cells release yet another chemical (cytokines) that attracts more macrophages, making an inevitable and destructive cycle in the artery. When this inflammatory sequence happens, clots form from the accumulation of plaque, which then makes the chance of a rupture highly probable. However, where a rupture occurs does not necessarily determine where it will stay, as they commonly detach from their origin and place themselves anywhere in the bodies circulatory system that they please. Two common examples of this are strokes, where an artery to the brain gets blocked, and a heart attack, where obstruction occurs in the coronary artery.
Bad Cop Good Cop
To say that this process of inflammation and pro-inflammatory responses (via the accumulation of small, compact LDL in an already weakened ECL) was due to cholesterol in animal meat and saturated fat, is very vague and deceiving. Yes, cholesterol is present in the process leading up to a heart attack, however, it is not the one to blame. In hopes to simplify the reasoning behind heart disease, experts have altered the way we view the helpful and essential assignment put on cholesterol in the body. Accusing a helpless particle simply trying to balance inflammation in the body is quite ignorant, as it is clear that the real culprits are unhealthy external factors (excessive carb, sugar, processed food and oil intake, lack of exercise, and (or) too much chronic exercise.), all of which are NOT from actual cholesterol containing foods and saturated fat. 
Instead of focusing on the overall blood count of your cholesterol, there are quite a few alternative routes that can serve as true indicators for any existing health problem that are much more reliable. According to Dr. Cat Shanahan, one of the most important blood metric assessments for heart disease is the triglycerides to HDL count, which is ideally a ratio of 1:1, due to the dangers caused by excess triglycerides, or insufficient HDL. Others include blood pressure (ideally diastolic/systolic of 120/80 or lower), vitamin D (healthy: 50-70 ng/mL, treating disease: 70-100 ng/mL), fasting blood insulin, HbA1C (estimated average glucose test over an extended period), triglycerides (dangerous: +150 mg/dL, optimal: 100 mg/dL), and hs-CRP (“high sensitivity C-reactive protein” normal: 1 mg/L, pregnancy or systemic inflammation: 10-40+ mg/L). Elevated markers that also indicate high risk of heart disease, cardiac mortality, damaged tissue, systemic inflammation, and overall health are Interleukin-6 (secretion of “T” white blood cells and macrophages), homocysteine (amino acid), CPK enzyme (creatine phosphokinase in the brain, heart, lungs, and skeletal muscles), LpA2 enzyme (promotes lipoprotein oxidation), ApoB protein (readings in context to “normal” ranges), LDL particle size & advanced lipid profile testing, and coronary calcium testing (via CT scan). You can also request a separate reading for LDL particle size on your standard cholesterol test.
What About Statins?
The problem with statins is that they lower the overall count of your cholesterol (both LDL and HDL). As discussed previously, not enough of the “good” HDL can lead to plaque build up, even in the presence of of a relatively low amount of small, compact LDL levels. Because this pro-inflammatory suppression of the liver’s cholesterol production stifles overall lipoprotein blood values, simultaneously ever cell membrane is depleting of their energy-producing coenzyme “Q-10,” which then causes fatigue, muscle pain and dysfunction, as well as inability to fight inflammation and free radical damage. All negative side effects aside, statins have never even been proven to address excessive triglycerides or small, dense LDL levels, both of which are the real risks behind heart disease. That being said, there have been a few random cholesterol lowering benefits that did occur for some people in high-risk populations, through incidental blood thinning, plaque-stabilization, and anti-inflammatory effects. However, through various studies, it has been shown that after four years, prescribed multiple cardiac medications have risen their patients risk of mortality by 40%. All in all, statins do not save people's lives, nor do their subsidiary side effects (good or bad) make them a smart choice regarding overall health.
Your Choice Only
Overall, the true causes for heart disease can be summed down to three things; oxidation, inflammation, and coagulation (thickening of the arterial wall). No study, including the extensive Framingham Heart Study, have ever shown a link between dietary fat, cholesterol intake, and heart disease. Instead, poor external practices such as smoking and alcohol consumption, lack of exercise, carb-dependency, PUFA intake, and excess sugar, (all of which ultimately contribute to skyrocketing inflammation in the body) deceivingly turn the true “good guy” (aka cholesterol & saturated fat) into an inflamed internal mess. Instead of depending on a vague and misleading number off an average cholesterol test, take into account the whole picture of your past and present lifestyle. Consider the fact that common vehicles for butter and meat all happen to be be high insulin and inflammatory products, while those naturally full of saturated fats really are the real definition behind super food.
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