A never ending stream of media propaganda promotes yet another “statin” drug to lower your “bad LDL cholesterol” that supposedly leads to heart attack, stroke, erectile dysfunction, etc.
It is amazing to watch and listen to this deceptive and misleading information being transmitted to the masses. An estimated six billion dollars were spent on pharmaceutical drug TV ads last year.
Why? Because the ads work by desensitization, in spite of the litany of side-effects (even death!) listed at the end of each ad. “Statin” drugs themselves are hepatotoxic and regular blood testing for elevated liver enzymes must be performed.
So how can you achieve the outcome you’re hoping for –lowering your cholesterol and decreasing your chance of cardiovascular death– without the harmful side effects?
|% of people who experienced this side effect|
|Headache||up to 16.7%|
|Infections||up to 10.3%|
|Joint Pain||up to 5.1%|
|Diarrhea||up to 5.3%|
|Muscle Pain||up to 5.6%|
|Sinus Infections (Sinusitis)||up to 6.4%|
“Statin” drugs are being promoted to reduce LDL cholesterol levels because elevated LDL cholesterol has statistically been associated with a higher rate of cardiovascular deaths. However, a statistical association does not prove “cause and effect”. It makes no more sense to say that the firemen found fighting a fire are, in fact, the cause of the fire.
Within the cell membrane, cholesterol functions in intracellular transport, cell signaling and nerve conduction. Cholesterol is essential for the structure and function of the cell membrane. The role of cholesterol in endocytosis is critical. Recently, cholesterol has also been implicated in cell signaling processes, assisting in the formation of lipid rafts in the plasma membrane. In many neurons a myelin sheath, rich in cholesterol, provides insulation for more efficient conduction of impulses. (2)
Within cells, cholesterol is the precursor molecule in several biochemical pathways. In the liver, cholesterol is converted to bile, which is then stored in the gallbladder. Bile contains bile salts, which solubilize fats in the digestive tract and aid in the intestinal absorption of fat molecules as well as the fat soluble vitamins, Vitamin A, Vitamin D, Vitamin E and Vitamin K. Cholesterol is an important precursor molecule for the synthesis of Vitamin D and the steroid hormones, including the adrenal gland hormones cortisol and aldosterone as well as the sex hormones progesterone, estrogens, and testosterone and their derivatives. (2)
The side effects of statin drugs correlate exactly to their known mechanisms of action. One of the most important side-effects is the interference with the production of Coenzyme Q10 (CoQ10). (6)
CoQ10is the naturally-occurring form of ubiquinone in humans. Ubiquinone is widely recognized as an essential component of energy metabolism in the electron-transfer system in mitochondrial membranes. At physiological concentrations it is also recognized as an effective lipid-soluble antioxidant. It is one of the end products of the mevalonate pathway where dolichol and cholesterol are synthesized. Both ubiqionone and dolichol are released by the liver cells into the blood circulation, but in much lower concentrations than that of cholesterol. (2, 7, 8)
Ghirlanda et al reported in a double-blind, placebo-controlled study a decrease of 50-54% of CoQ10 levels in the statin treatment groups, and similar results were reproduced by Watts et al. (7, 8)
Bliznakov and Wilkins reviewed studies of the effect of statins on the biosynthesis of CoQ10 and the clinical implication of CoQ10 deficiency. The authors report that lovastatin, pravastatin and simvastatin lower the endogenous levels of CoQ10. (9)
Considering that Co Q10 is essential for mitochondrial function and antioxidant activity, and since oxidative mechanisms are important in atherogenesis, it can be assumed that a reduction in CoQ10 level may compromise cardiac function despite optimal reduction in cholesterol levels by the use of “statin” drugs. (10)
Furthermore, the reduction of ubiquinone levels might be associated with myopathy, a rare adverse effect associated with statin drugs. This “metabolic” myopathy is related to ubiquinone deficiency in muscle cell mitochondria, disturbing normal cellular respiration and causing adverse effects such as rhabdomyolysis, exercise intolerance, and recurrent myoglobinuria, and encephalopathies. (11, 12, 13)
Cholesterol Cause and Effect
Elevated LDL cholesterol poses a risk for cardiovascular disease when it invades the endothelium and becomes oxidized, since the oxidized form is more easily retained by the proteoglycans. A complex set of biochemical reactions regulates the oxidation of LDL, chiefly stimulated by the presence of free radicals in the endothelium. The more toxic metals residing in the body, the higher the free radical activity. Heavy metals in the body exponentially increase free radical activity and today everyone has far more heavy metals than ever. Thus, removing toxic metals from the body will greatly reduce the number and activity of free radicals. (5)
Detoxifying the body of toxic heavy metals and reducing free radical exposure may alter the contribution of cholesterol to atherosclerosis. (5)
Selective detoxification by Adsorption
In weighing the advantages and disadvantages of the evidence-based detoxification products available, the mechanism of toxicant binding is of primary consideration. Although profound in application, the binding action of zeolite is simple to understand.
The uptake of toxic heavy metals, chemical toxins or other free radicals in zeolites is called adsorption. Adsorption (not to be confused with absorption) is the accumulation of atoms or molecules on the surface of an adsorbent solid, such as zeolite. The driving force behind adsorption is the highly polar surface within the pores of the zeolite structure. This unique characteristic distinguishes zeolites enabling an extremely high adsorption capacity for water and other polar components even at very low concentrations. Advanced Cellular Zeolite (ACZ) nano crystals are characterized by a three-dimensional pore system, with pores of precisely defined diameter. Pores of precisely uniform openings within these nano, crystalline structures allow for molecules smaller than its pore diameter, such as Mercury, to be adsorbed while excluding larger molecules, such as Calcium and Potassium, hence the name “molecular sieve”.
Depicted in the diagram, smaller Mercuric ions are pulled deeply into the nano zeolite cage structure and held securely for safe elimination, while Calcium and Potassium are “sieved”.
ACZ nano Extra Strength: Antioxidant
ACZ nano Extra Strength has powerful antioxidant properties. Its structure not only traps toxins such as toxic heavy metals, but also free radical molecules. However, unlike classic antioxidants, nano zeolite crystals do not neutralize free radicals by donating an electron to stabilize them. Instead, the structure of the zeolite is such that it captures the free radical and locks it safely away so that it cannot harm the body. Once trapped in the zeolite, the inactivated free radical can then safely be eliminated from the body.
A safe and proven detoxification agent, ACZ nano Extra Strength selectively and irreversibly binds toxic substances, without binding or removing nutrient elements. ACZ nano Extra Strength safely removes Mercury, Lead, Aluminum, Antimony, Arsenic, Barium, Bismuth, Cadmium, Cesium, Gadolinium, Gallium, Nickel, Niobium, Platinum, Rubidium, Thallium, Thorium, Tin, Tungsten, Uranium and more.
Patient Case Studies
The following four patients had heavy metal urine challenge testing done and tested positive for a wide range of toxic heavy metals including Mercury, Lead, Aluminum, Arsenic and Tin. As their toxic heavy metal levels were reduced by ACZ nano Extra Strength, their lipid levels shifted to a more favorable profile in a surprisingly short amount of time. There was no toxicity or side effects. Compare these favorable results to the significant life threatening side effects caused by the use of “statin” pharmaceutical drugs.
1. Olson RE (February 1998). “Discovery of the lipoproteins, their role in fat transport and their significance as risk factors”. J. Nutr. 128 (2 Suppl): 439S–443S. PMID 9478044. http://jn.nutrition.org/cgi/pmidlookup?view=long&pmid=9478044.
2. ^ Pawlina, Wojciech; Ross, Michael W. (2006). Histology: a text and atlas: with correlated cell and molecular biology. Philadelphia: Lippincott Wiliams & Wilkins. pp. 230. ISBN 0-7817-5056-3.
3. ^ Smith LL (1991). “Another cholesterol hypothesis: cholesterol as antioxidant”. Free Radic. Biol. Med. 11 (1): 47–61. doi:10.1016/0891-5849(91)90187-8. PMID 1937129.
4. ^ Christie, William (2003). Lipid analysis: isolation, separation, identification, and structural analysis of lipids. Ayr, Scotland: Oily Press. ISBN 0-9531949-5-7.
5. Levy, Thomas (2001). Optimal Nutrition for Optimal Health. Keats Publishing
6. Pelton, La Valle, et al. Drug-Induced Nutrient Depletion Handbook. Lexi-Comp Clinical Reference Library. 1999-2000.
7. Ghirlanda G, Oradei A, Manto A, Lippa S, Uccioli L, Caputo S, Greco AV, Littarru GP. Evidence of plasma CoQ10-lowering effect by HMG-CoA reductase inhibitors: a double-blind, placebo-controlled study. J Clin Pharmacol. 1993.Mar;33(3):226-229.
8. Watts GF, Castelluccio C, Rice-Evans C, Taub NA, Baum H, Quinn PJ. Plasma coenzyme Q (ubiquinone) concentrations in patients treated with simvastatin. J Clin Pathol. Nov 1993;46(11):1055-1057.
9. Bliznakov EG, Wilkins DJ. Biochemical and clinical consequences of inhibiting coenzyme Q10 biosynthesis by lipid-lowering HMG-CoA reductase inhibitors (Statins): a critical overview. Adv Ther. Jul/Aug 1998;15(4):218-228.
10. DiMauro S., Exercise intolerance and the mitochondrial respiratory chain. Ital J Neurol Sci. Dec 1999;20(6):387-393.
11. Artuch R, Colome C, Vilaseca MA, Pineda M, Campistol J. Ubiquinone: metabolism and functions, ubiquinone deficiency, and its implication in mitochondrial encephalopathies. Treatment with ubiquinone. Rev Neurol. Jul 1999;29(1):59-63.
12. Bargossi AM. Exogenous CoQ10 preserves plasma ubiquinone levels in patients treated with 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors. Int J Clin Lab Res. 1994;24(3):171-176
13. Wollschlaeger, Bernd.J.Am.Nutraceutical Assoc. Statin Drugs and CoenzymeQ10: A Potential for Drug Induced Nutrient Deplention. May 2001.