Since the amazing revelation of Ora Shovman on the powerful anti-inflammation action of statin drugs, published in Immunological Research in 2002, it has been purely a matter of time until an event like the Jupiter trial results of 10 Nov 2008 focused international media attention on this subject.
Neither the FDA nor the drug companies commented on this article at the time. The entire medical community had been focused on cholesterol as the cause of cardiovascular disease and has remained so until now.
When Ancel Keyes started the anti-cholesterol bandwagon in motion back in the fifties the general mood was joyous. The drug companies had a target to shoot at that promised them billions. The food industry too stood to profit from imaginative design of low cholesterol products and fat substitutes and doctors had a new disease with a numerical easily measured level, that could be lowered by conscious attention to your doctor's advice and the taking of expensive medicine.
For every 2% knocked off your cholesterol you were promised another functional year to enjoy life. Truly a win/win for everyone and gradually a multibillion dollar industry was created, directed at cholesterol reduction.
I was an intern at Walter Reed Army Hospital during this time. Ike was there then. We were on a roll with millions of federal dollars going into heart disease, cancer and stroke - cholesterol control quickly became a big part of it.
I talked at service clubs of the evils of whole milk, eggs and butter, the very foodstuffs my grandmother had raised me on. I raised my growing family on no eggs, powdered skim milk and margarine. There was no more staunch advocate of cholesterol causation than me, writing out thousands of prescriptions for cholesterol busters of one kind or another.
Then came statins. Finally we had a real weapon. With the statins we could lower cholesterol 40 to 50 points. At Johnson Space Center my 270 became 145 in just six weeks with 10 mg of Lipitor. I was overjoyed. Then came my transient global amnesia when for 6 hours I no longer knew my wife or new home.
Meanwhile hundreds of reports of myopathies, neuropathies and strange neurodegenerative conditions were being reported all associated with the use of statins and none meaningfully reported to the medical community.
I soon deduced that statin drugs in their officially reported capacity as reductase inhibitors were capable of blockading the critical mevalonate pathway, the biochemical channel for the production of not only cholesterol but CoQ10, dolichols, selenoprotein, Rho and altered phosphorylation.
And now it seems that the benefit of statin drugs has been based upon their anti-inflammatory effects alluded to by Shoveman 7 years previously. Astonishingly, it appears cholesterol reduction had nothing to do with it. Cholesterol was not our biggest enemy, it was our greatest friend.
We simply cannot not live without ample supplies of cholesterol. It is perhaps the most important biochemical in our bodies, mistakenly turned into a monster by a terribly confused Doctor now known to have altered his data and a nation ready to welcome a new disease to show what the Federal government could do.
No questions were asked. We only now are learning what the real effects of statins are in our bodies and it is far more that CoQ10 and dolichol inhibition, though that is quite sufficient. Recently we have seen that the primary mechanism of action of statins, the reason so many of the side effects are permanent, is because they are based on mitochondrial mutations.
With this sad tale behind us we now recognize belatedly that C-reactive protein (CRP) has value as a marker for inflammation. Yes it is a non-specific marker in that an elevated value may just as easily be due to infected teeth, gall bladder or prostate.
This is not a new test. As I recall Ike's CRP was elevated on at least one occasion and in my case it went sky high during a flare-up of diverticulitis 20 years ago that happened to coincide with my astronaut physical as Johnson Space Center. So CRP by itself does not necessarily point to heart disease. Recently it has been refined to help with heart specificity, the hs-CRP (high-sensitivity CRP) test.
C-reactive protein was originally discovered by Tillett and Francis in 1930 as a substance in the serum of patients with acute inflammation that reacted with the C polysaccharide of pneumococcus.
From the very beginning it was known to be associated with a variety of different inflammatory states and as such soon was recognized as a non-specific test for inflammation anywhere in the body.
CRP has no relationship with cholesterol. A person with an elevated CRP can easily be screened for infection in prostate, sinus, teeth, bladder, ovaries or tubes and if found negative becomes suspect for a possible cardiovascular origin and a candidate for use of a low dose statin.
The four elements of inflammation control: platelet activation, monocyte adhesion, lymphyocyte attraction and smooth muscle migration respond very well to the anti-inflammatory impact of any statin, as Shoveman predicted.
Most researchers on this subject believe that certain triggers of inflammation, like homocysteine, cigarette smoking, inherited coagulation defects, inherited platelet defects, transfats, oxycholesterol exposure, etc trigger subendothelial zones of inflammation which if unchecked grow to atheroma.
The use of such markers as the hs-CRP test will allow more judicious selection of candidates for the use of anti-inflammatory drugs. I am confident that both inflammatory markers and anti-inflammatory drugs will drastically improve in time. In the meantime a low dose statin remains an option as do the dietary supplements that are capable of lowering CRP both safely and cost effectively.
Duane Graveline MD MPH
Former USAF Flight Surgeon
Former NASA Astronaut
Retired Family Doctor