By Duane Graveline, MD, MPH
Due to the expanding use of statin drugs, type 2 diabetes mellitus and associated chronic kidney disease (CKD) are rapidly becoming major public health problems. In a misguided effort to limit cardiovascular events, higher and higher statin doses are being utilized in diabetics and those with mild kidney disease with the only benefit being a slight reduction of heart attacks and strokes at a cost most clinicians would consider unacceptable.
It is now becoming realized that myopathy, the most common adverse reaction of statin drug use, is a major cause of kidney tubular blockade. Even a localized myopathic process can be associated with sufficient inflammatory response to trigger muscle cell wall breakdown releasing minute cellular fragments to lodge in kidney tubules causing progressive kidney damage. With the myopathy incidence now estimated at 20 percent, there is reason to believe that myopathy is a major contributor to CKD.
In the past 6 years, 9,111 cases of statin associated rhabdomyolysis have been reported to FDA's Medwatch for an estimated 911 deaths. We are now in the midst of a rapidly growing epidemic of statin associated rhabdomyolysis.
There is reason to believe as well that many myopathy cases are associated with subclinical muscle cell breakdown with progressive renal tubule occlusion from cellular breakdown products that have silently entered the circulation to slowly contribute to this CKD epidemic. Additionally, with increasing use of higher statin dosing, type 2 diabetes mellitus also is reaching epidemic proportions and is contributing to CKD cases.
Statins are reductase inhibitors. The doctors writing the statin prescriptions do not seem to understand what reductase inhibition really means to the mevalonate pathway present in each of our cells.
For a brief statin 101 course: Statin drugs are specifically designed to block cholesterol by blocking the reductase step in the mevalonate pathway. The mevalonate pathway provides for the synthesis of many other critical biochemicals as well so when cholesterol is blocked it is inevitable that these other biochemicals such as CoQ10 and dolichols must also be blocked.
CoQ10 is an anti-oxidant that is also critical for cell wall integrity and for the production of adenosine triphosphate (ATP), our cellular fuel. CoQ10 inhibition will contribute to mitochondrial DNA mutation and ATP insufficiency. It was known that the present epidemic of congestive heart failure would inevitably follow the use of statins for coronary artery disease control. When the CoQ10, vital for heart cell function, is inhibited by statins, it is not difficult to predict heart failure as a result.
Dolichols are critical for glycoprotein synthesis. Dolichol lack contributes to insulin deficiency and diabetes, cell identification and communication problems and errors in neuropeptide formation. All of this becomes inevitable with statin use.
Yes it's complicated. Life is complicated and statin drugs mess with some very sensitive biochemistry but this present epidemic of type 2 diabetes mellitus should have been no surprise.
Duane Graveline MD MPH
Former USAF Flight Surgeon
Former NASA Astronaut
Retired Family Doctor