NEW YORK (Reuters Health) Jul 26 - Patients with asymptomatic neuromuscular disorders may have their condition precipitated by statin use, according to investigators from the University of Athens Medical School.

Dr. Panagiota Manta and colleagues describe four such cases in the July 24th issue of the Archives of Internal Medicine.

Case 1 was a 46-year-old man with a history of hypertension and diabetes mellitus who was prescribed pravastatin for hypercholesterolemia. Three months later, he complained of fatigue, muscle pain and stiffness. Serum creatine kinase levels were persistently elevated. After stopping the drug, creatine kinase levels fell somewhat and there was mild symptom improvement. Mild myopathy was seen on needle electromyography and muscle biopsy showed numerous internal nuclei, nuclear clumps and variations in fiber size. Genetic testing revealed myotonic dystrophy.

Case 2 was a 62-year-old man with a history of MI and diabetes. Hypercholesterolemia was treated with simvastatin. Creatine kinase levels became persistently elevated and did not return to normal after drug discontinuation. Biopsy was positive for muscle enzyme activity. He was eventually diagnosed with McArdle disease.

Case 3 was a 51-year-old man with hypertension and hypercholesterolemia who was hospitalized with acute rhabdomyolytis after taking atorvastatin for 18 months. Exercise intolerance and muscle pain persisted for months after discontinuation of statin therapy. Some time later, he was diagnosed with mitochondrial myopathy.

The last case was a 58-year-old man with a history of hypertension, hyperuricemia and coronary artery disease. He began treatment with pravastatin. Shortly after a dose increase, he developed muscle twitching, muscle cramps and difficulty walking. Like the other cases, there was only mild symptom improvement and a modest decline in creatine kinase levels after the statin was discontinued. He was eventually diagnosed with Kennedy disease.

Statin-induced neuropathy is well recognized and reported more and more often, Dr. Manta's group notes. These four cases show that statins can also trigger underlying neuromuscular conditions.

The investigators suggest that if neuromuscular symptoms persist after discontinuation of statin therapy, clinicians should "pursue further diagnostic evaluations for the detection of underlying neuromuscular disease."

Arch Intern Med 2006;166:1519-1524.

Public release date: 5-Jul-2006
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Contact: Elizabeth Crown
e-crown@northwestern.edu
312-503-8928
Northwestern University

Variations in detoxifying genes linked to Lou Gehrig's disease


Genetic variations in three enzymes that detoxify insecticides and nerve gas

agents as well as metabolize cholesterol-lowering statin drugs may be a risk

factor for developing sporadic amyotrophic lateral sclerosis (ALS, or Lou Gehrig's disease), and possibly responsible for a reported twofold increased risk of ALS in Gulf War veterans.
These findings, from a study led Teepu Siddique, M.D., and colleagues at Northwestern University, open the door to investigating gene-environment interactions as a cause of ALS and other illnesses and to the development of molecular targets for specific treatments. The study was published in the August 22 online issue (available now) of the journal Neurology.

Siddique is Les Turner ALS Foundation/Herbert C. Wenske Professor, Davee Department of Neurology and Clinical Neurosciences, professor of cell and molecular biology and director of the Neuromuscular Disorders Program at Northwestern University Feinberg School of Medicine.

ALS is a complex neurodegenerative disorder of the motor neurons that results in muscle weakness, difficulty speaking, swallowing and breathing and eventual total paralysis and death generally within five years.

In 1993 Siddique and collaborators determined that mutations in a gene known as SOD1 account for 20 percent of familial, or inherited, ALS (2 percent of all cases of ALS). However, the cause of sporadic ALS is still unknown.

In earlier research Siddique and other researchers hypothesized that sporadic ALS is modulated by variations in multiple genes interacting with each other and environmental exposures.

The genes for human paraoxanases (PON 1, PON 2 and PON 3), which are located on chromosome 7q21.3, code for the production of detoxifying enzymes involved in the metabolism of a variety of drugs, organophosphate insecticides, such as parathion, diazinon and chlorpyrifos, and nerve gas agents such as sarin.

Previous research described a possible twofold increased risk for developing ALS in veterans of the Gulf War, indicating a war-related environmental exposure to organophosphates and sarin in genetically susceptible individuals as a possible cause.

PON GENE CLUSTER VARIANTS HAVE PREVIOUSLY BEEN ASSOCIATED WITH OTHER NEURODEGENERATIVE DISORDERS, INCLUDING ALZHEIMER'S DISEASE, PARKINSON'S DISEASE, CORONARY ARTERY DISEASE AND STROKE.

Although the Northwestern DNA study samples were not analyzed for inclusion of Gulf War veterans, Siddique and co-researchers found significant evidence that gene variations (polymorphisms) on the chromosome region encompassing PON2-PON3 were strongly associated with sporadic ALS.

"Thus, single nucleotide polymorphism genotyping in the intergenic regions of the PON gene cluster, and replication, gene expression, gene-gene interaction and PON serum/enzymatic studies may help elucidate the complexity of PON cluster association with ALS," Siddique said.

Siddique hopes to study DNA samples from Gulf War veterans with increased incidence of sporadic ALS and has applied for their DNA from the Veterans Administration collection.


###
Collaborating with Siddique on this research were Mohammad Saeed, M.D.; Nailah Siddique; Wu-Yen Hung; Elena Usacheva; Erdong Liu, M.D.; Robert L. Sufit, M.D.; Scott L. Heller, M.D., Northwestern University Feinberg School of Medicine; Jonathan L. Haines, Vanderbilt University Medical Center; and Margaret Pericak-Vance, Duke University Medical Center.

Dangers of Statin Drugs: What You Haven’t Been Told About Popular Cholesterol-Lowering Medicines
By Sally Fallon and Mary G. Enig, PhD
http://www.westonaprice.org/moderndiseases/statin.html

Hypercholesterolemia is the health issue of the 21st century. It is actually an invented disease, a "problem" that emerged when health professionals learned how to measure cholesterol levels in the blood. High cholesterol exhibits no outward signs--unlike other conditions of the blood, such as diabetes or anemia, diseases that manifest telltale symptoms like thirst or weakness--hypercholesterolemia requires the services of a physician to detect its presence. Many people who feel perfectly healthy suffer from high cholesterol--in fact, feeling good is actually a symptom of high cholesterol!

Doctors who treat this new disease must first convince their patients that they are sick and need to take one or more expensive drugs for the rest of their lives, drugs that require regular checkups and blood tests. But such doctors do not work in a vacuum--their efforts to convert healthy people into patients are bolstered by the full weight of the US government, the media and the medical establishment, agencies that have worked in concert to disseminate the cholesterol dogma and convince the population that high cholesterol is the forerunner of heart disease and possibly other diseases as well.

Who suffers from hypercholesterolemia? Peruse the medical literature of 25 or 30 years ago and you’ll get the following answer: any middle-aged man whose cholesterol is over 240 with other risk factors, such as smoking or overweight. After the Cholesterol Consensus Conference in 1984, the parameters changed; anyone (male or female) with cholesterol over 200 could receive the dreaded diagnosis and a prescription for pills. Recently that number has been moved down to 180. If you have had a heart attack, you get to take cholesterol-lowering medicines even if your cholesterol is already very low--after all, you have committed the sin of having a heart attack so your cholesterol must therefore be too high. The penance is a lifetime of cholesterol-lowering medications along with a boring lowfat diet. But why wait until you have a heart attack? Since we all labor under the stigma of original sin, we are all candidates for treatment. Current edicts stipulate cholesterol testing and treatment for young adults and even children.

The drugs that doctors use to treat the new disease are called statins--sold under a variety of names including Lipitor (atorvastatin), Zocor (simvastatin), Mevacor (lovastatin) and Pravachol (pravastatin).

How Statins Work
The diagram below illustrates the pathways involved in cholesterol production. The process begins with acetyl-CoA, a two-carbon molecule sometimes referred to as the "building block of life." Three acetyl-CoA molecules combine to form six-carbon hydroxymethyl glutaric acid (HMG). The step from HMG to mevalonate requires an enzyme, HMG-CoA reductase. Statin drugs work by inhibiting this enzyme--hence the formal name of HMG-CoA reductase inhibitors. Herein lies the potential for numerous side effects, because statin drugs inhibit not just the production of cholesterol, but a whole family of intermediary substances, many if not all of which have important biochemical functions in their own right.

Consider the findings of pediatricians at the University of California, San Diego who published a description of a child with an hereditary defect of mevalonic kinase, the enzyme that facilitates the next step beyond HMG-CoA reductase.1 The child was mentally retarded, microcephalic (very small head), small for his age, profoundly anemic, acidotic and febrile. He also had cataracts. Predictably, his cholesterol was consistently low--70-79 mg/dl. He died at the age of 24 months. The child represents an extreme example of cholesterol inhibition, but his case illuminates the possible consequences of taking statins in strong doses or for a lengthy period of time--depression of mental acuity, anemia, acidosis, frequent fevers and cataracts.

Cholesterol is one of three end products in the mevalonate chain. The two others are ubiquinone and dilochol. Ubiquinone or Co-Enzyme Q10 is a critical cellular nutrient biosynthesized in the mitochondria. It plays a role in ATP production in the cells and functions as an electron carrier to cytochrome oxidase, our main respiratory enzyme. The heart requires high levels of Co-Q10. A form of Co-Q10 called ubiquinone is found in all cell membranes where it plays a role in maintaining membrane integrity so critical to nerve conduction and muscle integrity. Co-Q10 is also vital to the formation of elastin and collagen. Side effects of Co-Q10 deficiency include muscle wasting leading to weakness and severe back pain, heart failure (the heart is a muscle!), neuropathy and inflammation of the tendons and ligaments, often leading to rupture.

Dolichols also play a role of immense importance. In the cells they direct various proteins manufactured in response to DNA directives to their proper targets, ensuring that the cells respond correctly to genetically programmed instruction. Thus statin drugs can lead to unpredictable chaos on the cellular level, much like a computer virus that wipes out certain pathways or files.

Squalene, the immediate precursor to cholesterol, has anti-cancer effects, according to research.

The fact that some studies have shown that statins can prevent heart disease, at least in the short term, is most likely explained not by the inhibition of cholesterol production but because they block the creation of mevalonate. Reduced amounts of mevalonate seem to make smooth muscle cells less active, and platelets less able to produce thromboxane. Atherosclerosis begins with the growth of smooth muscle cells in side artery walls and thromboxane is necessary for blood clotting.

Cholesterol
Of course, statins inhibit the production of cholesterol--they do this very well. Nowhere is the failing of our medical system more evident than in the wholesale acceptance of cholesterol reduction as a way to prevent disease--have all these doctors forgotten what they learned in biochemistry 101 about the many roles of cholesterol in the human biochemistry? Every cell membrane in our body contains cholesterol because cholesterol is what makes our cells waterproof--without cholesterol we could not have a different biochemistry on the inside and the outside of the cell. When cholesterol levels are not adequate, the cell membrane becomes leaky or porous, a situation the body interprets as an emergency, releasing a flood of corticoid hormones that work by sequestering cholesterol from one part of the body and transporting it to areas where it is lacking. Cholesterol is the body’s repair substance: scar tissue contains high levels of cholesterol, including scar tissue in the arteries.

Cholesterol is the precursor to vitamin D, necessary for numerous biochemical processes including mineral metabolism. The bile salts, required for the digestion of fat, are made of cholesterol. Those who suffer from low cholesterol often have trouble digesting fats. Cholesterol also functions as a powerful antioxidant, thus protecting us against cancer and aging.

Cholesterol is vital to proper neurological function. It plays a key role in the formation of memory and the uptake of hormones in the brain, including serotonin, the body’s feel-good chemical. When cholesterol levels drop too low, the serotonin receptors cannot work. Cholesterol is the main organic molecule in the brain, constituting over half the dry weight of the cerebral cortex.

Finally, cholesterol is the precursor to all the hormones produced in the adrenal cortex including glucocorticoids, which regulate blood sugar levels, and mineralocorticoids, which regulate mineral balance. Corticoids are the cholesterol-based adrenal hormones that the body uses in response to stress of various types; it promotes healing and balances the tendency to inflammation. The adrenal cortex also produces sex hormones, including testosterone, estrogen and progesterone, out of cholesterol. Thus, low cholesterol--whether due to an innate error of metabolism or induced by cholesterol-lowering diets and drugs--can be expected to disrupt the production of adrenal hormones and lead to blood sugar problems, edema, mineral deficiencies, chronic inflammation, difficulty in healing, allergies, asthma, reduced libido, infertility and various reproductive problems.
to read entire article follow the link -

http://www.westonaprice.org/moderndiseases/statin.html

Does anyone know what to call the disease we get? Or is each case very different? I can sent photos and videos of what happened to me almost immediately. Also,I'd be happy to volunteer for any studies that might help me or others.