Saturday, March 26, 2011

6. Long-term Statin Therapy Leads to Damage Everywhere

Statins, then, slowly erode the muscle cells over time. After several years have passed, the muscles reach a point where they can no longer keep up with essentially running a marathon day in and day out. The muscles start literally falling apart, and the debris ends up in the kidney, where it can lead to the rare disorder, rhabdomyolysis, which is often fatal. In fact, 31 of our statin reviews contained references to "rhabdomyolysis" as opposed to none in the comparison set. Kidney failure, a frequent consequence of rhabdomyolysis, showed up 26 times among the statin reviews, as opposed to only four times in the control set.

The dying muscles ultimately expose the nerves that innervate them to toxic substances, which then leads to nerve damage such as neuropathy, and, ultimately Amyloid Lateral Sclerosis (ALS), also known as Lou Gehrig's disease, a very rare, debilitating, and ultimately fatal disease which is now on the rise due (I believe) to statin drugs. People diagnosed with ALS rarely live beyond five years. Seventy-seven of our statin reviews contained references to ALS, as against only 7 in the comparison set.

As ion leaks become untenable, cells will begin to replace the potassium/sodium system with a calcium/magnesium based system. These two ions are in the same rows of the periodic table as sodium/potassium, but advanced by one column, which means that they are substantially larger, and therefore it's much harder for them to accidentally leak out. But this results in extensive calcification of artery walls, heart valves, and the heart muscle itself. Calcified heart valves can no longer function properly to prevent backflow, and diastolic heart failure results from increased left ventricular stiffness. Research has shown that statin therapy leads to increased risk to diastolic heart failure (Silver et al., 2004, Weant and Smith, 2005). Heart failure shows up 36 times in our statin drug data as against only 8 times in the comparison group.

Once the muscles can no longer keep up with lactate supply, the liver and heart will be further imperilled. They're now worse off than they were before statins, because the lactate is no longer available, and the LDL, which would have provided fats as a fuel source, is greatly reduced. So they're stuck processing sugar as fuel, something that is now much more perilous than it used to be, because they are depleted in membrane cholesterol. Glucose entry into muscle cells, including the heart muscle, mediated by insulin, is orchestrated to occur at lipid rafts, where cholesterol is highly concentrated. Less membrane cholesterol results in fewer lipid rafts, and this leads to impaired glucose uptake. Indeed, it has been proposed that statins increase the risk to diabetes (Goldstein and Mascitelli, 2010, Hagedorn and Arora, 2010). Our data bear out this notion, with the probability of the observed distributions of diabetes references happening by chance being only 0.006.

10 comments:

Dave said...

These posts are fascinating.

So far, you seem to be preaching to the choir. I'd like to see you invite a literate expert with an opposite opinion, say a cardiologist who prescribers statins.

Personally, I'm off statins.

Karen said...

Stephanie, I'm a new follower and a statin patient, but a reluctant one. I have found your posts and articles to be fascinating and informative. Now if I could only find an MD who believes any of this, I would be happy. I have experienced the side effects of muscle and joint pain and also unexplained weight gain over the last ten months of being on Simvastatin.

I agree wholeheartedly with what you have written about the 'cure' being worse than the 'disease' of high cholesterol. I wonder when the medication will finally come under the scrutiny it so fully deserves. Thank you for your efforts at educating a brain-washed society; those with medical degrees seem to be the most in need of enlightening.

Meeting with a new doctor tomorrow. I hope for a good outcome, but fear when she hears I am wanting to stop statin 'therapy' what her answer to that will be. Hopefully not as hostile as the last MD's were.

dov baer said...

Dear Dr. Seneff,
I applaud your work. I had been on statins for 20 years. The first 13 years never taking Co-Q10, nor d-ribose nor L-Carnitine. Genetically - i am prone to high cholestrol numbers: LDL 290 HDL 60.
I am totally off the statins - but my muscle pain has grown worse as time as passed.
Can you now explore ways to repair the damage done by the statins?
Many thanks.

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Alexander V. said...

Hi, Stephanie.

I am not a chemist, so i might not understand everything, but data suggests that ion radii of Ca2+ (114 pm) and Mg2+ (86 pm) are smaller than Na+ (116 pm) and K+ (152 pm).

How do you think this fits into the theory?

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Patrick Ryan said...

You deserve a Nobel prize for this work Stephanie. It's beautiful and elegant. Why else would the body put plaque so close to the heart but to guarantee its supply of this nutrient. Brilliant! Light-years ahead of the "cholesterol causes heart-disease flat-earthers". Your theory also explains sudden adult death syndrome; young super-fit athletes dropping dead because their hearts don't have enough cholesterol-sulphate and are over-worked to the point of failure before their bodies have the chance to establish the life-saving plaque. Kudos to you for thinking outside the box. It'll probably be years though before people start eating egg yolks and raw onions and ditching the sunscreen but you've explained the science and without that, understanding and change can't happen. Well done!