At first glance the title of this article may seem stunning to you, shocking or jolting even. You have been told all of your life that cholesterol is either “good” or “bad”. You have been told that elevated cholesterol is the cause of heart disease.
These concepts are absolutely 100% false. It may be true that patients with heart disease have high LDL levels (low density lipo-protein) and even high total blood cholesterol values. However a critical distinction must be made between the cholesterol in your blood versus the cholesterol in your tissues. LDL and cholesterol present in your tissues are there to protect your cells from the damaging effects of toxins, inflammatory fatty acids and free radical activity.
For heart disease patients, high levels of LDL may be on the “scene of the crime” but LDL does NOT “pull the heart disease trigger”. Cholesterol and LDL (the so called “bad” cholesterol) are in effect the patsies, the fall guys for the real offenders: ultra pathological conjugated fatty acids such as the leukotrienes and virulent free radicals such as the hydroxyl.
Cholesterol and other sterols are better described as “anti-fatty acids”. Other “anti-fatty acids” include sex hormones and corticosteroids such as cortisol. Anti-fatty acids protect your cells from the potentially harmful and damaging effects of pro-inflammatory fatty acids, which can undergo lipid peroxidation and can generate tremendous amounts of free radicals.
Cholesterol’s anti-free radical activity in fact neutralizes the damaging effects of fatty acids and free radicals in the tissues.
LDL & HDL Deliver Cholesterol
LDL is not cholesterol, and it certainly is NOT “bad” like you have been misled. LDL and HDL are lipo-proteins. They function to transport cholesterol to and from the various parts of the body.
LDL delivers cholesterol. HDL brings it back to your liver.
LDL (the so called “bad” cholesterol) is essential in order for your cells to make steroidal hormones from cholesterol such as: pregnenolone, testosterone, cortisol, progesterone, estrogen and DHEA.
Your body is incapable of functioning without LDL!
Since cholesterol is a primary antioxidant and free radical scavenger, LDL levels will increase when toxins and free radical activity is present and elevated in your tissues.
Cholesterol & Immune Activation
Much recent reseacrch indicates that cholesterol, fatty acids, triglycerides and steroid hormones are major components of the various lipid defense mechanisms. This defense is the response to:
- Free Radicals
- Excessive Conjugated Fatty Acids
- Abnormal Cells
- Damaged Cells
The defense of certain lipids is a mechanism by which the body attempts to stop inflammation and disease processes, illness, allergies, infections and pathogens. Think of how corticosteroids down regulate immune function through their anti-inflammatory effects.
While certain immune fatty acids are released in response to internal stressors, toxins, or inflammation, these fatty acids can also result in dangerous free radical activity themselves. The free radicals and inflammation induced by the 5-LOX pathway is one example. These free radicals are at the root of disease processes, including cardiovascular disease. The purpose of fatty acids such as leukotrienes (released by leukocytes or white blood cells) is to initiate the inflammatory process. They are lipid mediators.
Because of their inflammatory nature, these fatty acids must be controlled and neutralized. Cholesterol and the other anabolic lipids are in many ways responsible for this. Observe that cholesterol levels will elevate naturally, and should elevate when inflammation is present.
Send In The Cholesterol Captain Liver
When inflammation and free radicals (high amounts of fatty acids and the damage they induce when excessive) run rampant through the tissues, the liver should makes more cholesterol, and LDL is its carrier. Out they go to the tissues to do exactly as they’re supposed to do: halt the catabolic disintegration of cells that is taking place at the sites of inflammation.
This is why LDL values will increase after a tooth extraction, surgery and any activity that involves the damage of cells, all of which are inflammatory and catabolic by nature.
If inflammation, toxicity, free radicals and lipid peroxidation are not resolved, cholesterol will continually be sent out to quell the fire. At the sites of inflammation in the body, the virulent free radicals can directly and indirectly cause cholesterol and LDL to become “oxidized”. When free radicals cause cholesterol to oxidize, this decreases the density of the lipo proteins, allows the oxidized particles to pass through the epithelium and irritate blood vessels. Here you have a vicious cycle that takes place.
Studies such as THIS have shown that LDL cholesterol has the capability of reducing pathogens and infectious bacteria. Endotoxins from gram negative bacteria bind to LDL particles. When bound to LDL, they are inactivated. Additionally, when endotoxins are bound to LDL, the toxins are unable to trigger the production of pro-inflammatory cytokines such as TNF-a. Therefore if there is insignificant cholesterol and LDL, a person may be at an increased risk for infection.