By Duane Graveline MD, MPH
Statins and Mitochondrial Damage Part 3 of 11
In 2007, I managed to acquire a copy of Medwatch raw data for LipitorTM from the period 1998 through 2006, and using the same criteria used by Wagstaff, found 662 reports of TGA or comparable memory dysfunction (4).
On the basis of reported rates of TGA seen throughout the last year I had data (2006), and I could project with reasonable validity that the total number of such reports received at the time (Oct. 2009) would easily exceed 1,000.
Far more important than the numbers, knowing that five more commonly used statins also had contributed their share of cognitive dysfunction during this same time period, not one word of this observation had been officially reported to the medical and scientific communities. The average MD was still completely unaware of the cognitive impact of statins.
We must remember that TGA is only the tip of the iceberg in that for every case of TGA reported, hundreds of cases of statin associated confusion, disorientation and increased forgetfulness have occurred, and many cases are misdiagnosed as Alzheimers.
Additionally, hundreds of short term TGA's measured in minutes rather than hours almost undoubtedly have occurred during this time period, only to be completely missed unless an attentive observer was present to document it. The victim would be completely amnestic for this experience.
The classic definition for transient global amnesia is the abrupt inability to formulate new memory for a time period ranging from 2 to 24 hours. Any duration longer than 24 hours is increasingly likely to have an organic basis. No mention is generally made of the fact that there is no neurophysiologic reason why TGAs measured in minutes can not occur.
A TGA lasting for minutes would be impossible to detect by the victim and quite difficult even for a perceptive observer. When a TGA victim is unobserved, only the passage of time as evident by the position of the sun in the sky or time passage as recorded by a time-piece (if one is available) that might provoke a TGA victim to consider that a serious time loss had occurred. So I had my explanation for cognitive dysfunction and LipitorTM, thief of Memory is still the best book for those with primarily cognitive impairment.
I soon became aware, however, that much more was happening to statin users than cognitive dysfunction. Statin drugs disable a single reductase step along the biochemical path of cholesterol synthesis. What does this really mean?
From the very beginning Merck proudly announced the fact that their statins worked by a mysterious process known as reductase inhibition. Physicians perhaps should have been more perceptive and might even have consulted their biochemistry books, for only a glance at the biochemical pathways would have told us something very worrisome was possible, but we trusted the drug companies.
We were all on the same team, weren't we? We were so pleased with this new statin, lovastatin, with its capacity to drastically lower cholesterol that we simply forgot to ask picky questions of the drug companies. After 40 years of anti-cholesterol brainwashing we all agreed that cholesterol was our enemy and none of the many drugs we had used during that time really had much effect on cholesterol. Any drug that could almost guarantee to lower this biochemical by 40-50 points in a few weeks simply had to be good. Statins were our friend, no questions asked.
It was in this climate that I wrote my second book, Statin Drugs Side Effects (5), for the problems were far more than cognitive and all statins were contributing to the rising tide of adverse reactions, not just LipitorTM. This is when I learned what reductase inhibition really meant.
The reductase step that all biochemists know as very susceptible to blockade was at the very beginning of the mevalonate pathway. Yes, this pathway to cholesterol synthesis is also shared by many extremely important biochemical substances, including Coenzyme Q10, dolichols, selenoproteins, normal phosphorylation and Rho (vital for cognition). These all are extraordinarily vital to human function.
To block this pathway with statins, to reduce cholesterol synthesis, must also inhibit synthesis of these other biochemicals. It is not just possible, it is virtually guaranteed. One cannot reduce cholesterol by the use of statins without simultaneously blocking these other biochemicals sharing the mevalonate pathway. This is much like the girding of a tree trunk - all the branches are inhibited, not just the cholesterol branch. This is the cause of most of the statin side effects.
Neuropathies, myopathies, rhabdomyolysis, emotional and behavioral disorders and even certain neuro-degenerative conditions resembling ALS are side effects based on mevalonate pathway inhibition. Even the one solid good that statins appear to do, the reduction of atherosclerosis in middle aged men, is actually a previously unsuspected side effect from the inhibition of nuclear factor-kappa B, a powerful anti-inflammatory transcriptase present in the cytoplasm of all cells, a substance felt by most biochemists to be dependent upon the mevalonate pathway for synthesis. Cholesterol lowering has nothing to do with it.
4. Graveline D and Cohen J. 2008 spacedoc.net/662_cases_memory_loss
5. Graveline D. Statin Drugs Side Effect. 2005
Duane Graveline MD MPH
Former USAF Flight Surgeon
Former NASA Astronaut
Retired Family Doctor