By Duane Graveline, MD, MPH
R. Karas and others reported in the Journal of the American College of Cardiology, July 07, of the increased cancer risk associated with the use of high dose statins.
This research team observed higher rates of newly diagnosed cancer among patients with lower cholesterol levels, a consequence of increased statin dosing. In addition, the new cancers were not of any specific type or location.
This observation fits with predictions made years ago by those familiar with the mechanisms of action of the various statin drugs. Regardless of the stated focus of these authors on cholesterol reduction, it is the nuclear factor kappa B (NF-kB) inhibition action of statins that mediate increased cancer risk.
NF-kB is an intracellular transcriptase, mediating much of the action of the immune system. The resulting inhibition of vascular inflammation by statins does improve atherosclerosis, but to inhibit this substance is also to impair our immuno-resistance.
Whether attacked by alien bacteria, viruses or mutated cancer cells. our immune system has evolved mechanisms for early identification and destruction of foreign cancer-causing elements. All of this is dependent upon NF-kB placed there by eons of evolutionary trial and error.
This is the basis of the concerns about cancer risk and the equal concern about increased risk of certain infectious diseases, all of which are mediated by NF-kB. To inhibit this important substance with the use of statins is like opening up Pandora’s box of unexpected consequences. Karas has given us a peek at the consequence of so doing and it is disturbing.
Although those focused on better heart disease control are happy with statin use, those who must deal with the resulting cancers are demanding greater caution, especially with the use of higher and higher doses of statins.
Recent observations from longitudinal studies that link intensive cholesterol lowering with higher incidence of reported health problems, including liver and muscle toxicity and cancer, have introduced major concerns over the safety of such treatments.
A number of studies of the possible adverse reactions of statin drugs have revealed an increase in the risk of breast cancer. A recent review of cancer susceptibility in rodents exposed to statin drugs already had revealed an increase in various types of cancers, including breast cancers, in these experimental mice. In most cases, the exposure level was of the same order of magnitude as for the maximum recommended statin dose for humans.
Ora Shovman in 2001 first published on the anti-inflammatory and immunomodulatory effects of statin drugs. The essence of Shovman’s assessment of statin action was their ability to inhibit nuclear factor kappa B, a transcriptase vital to both inflammatory response and imunmodefense.
To inhibit NF-kB was to lessen the body's immunodefense and for the past decade a small behind the scenes war has been going on between scientists, like myself, believing in the inevitability of increased cancer susceptibility from statin use, against the tempest of studies attempting to prove that statins prevented cancers, not caused them.
Beck's study of statin associated breast cancers in post-menopausal women (http://www.jclinepi.com/article/S0895-4356(02)00614-5/abstract) has been supported by the very recent work of McDougall and others reporting on long-term statin use and risk of ductal and lobular breast cancer among women 55-74 years of age (https://www.ncbi.nlm.nih.gov/pubmed/23833125). They utilized data from a population-based case-control study of breast cancer conducted in the Seattle-Puget Sound region to investigate the relationship between long-term statin use and breast cancer risk.
916 invasive ductal carcinoma (IDC) and 1,068 invasive lobular carcinoma (ILC) cases 55-74 years of age diagnosed between 2000 and 2008 were compared to 902 control women. All participants were interviewed in-person and data on hypercholesterolemia and all episodes of lipid lowering medication use were collected through a structured questionnaire. They assessed the relationship between statin use and IDC and ILC risk using appropriate statistical methodology.
They found that current users of statins for 10 years or longer had a 1.83-fold increased risk of IDC and a 1.97-fold increased risk of ILC compared to never users of statins. Among women diagnosed with hypercholesterolemia, current users of statins for 10 years or longer had more than double the risk of both IDC and ILC compared to those who had never used a statin.
Their conclusion was that in this contemporary population-based case-control study, long-term use of statins was associated with increased risk of invasive ductal and lobular carcinoma.
I have said previously that sensitivity to statins increases susceptibility. This is how that process works:
1) The patient is on a statin drug.
2) The patient starts to experience early symptoms such as cognitive dysfunction, subtle emotional and behavioral disorders, weakness, shortness of breath or mild neuromuscular complaints. The doctor decides to take them off the statin because it might be the source of their troubles.
This would give a cohort of former statin users with demonstrated sensitivity to statin use and along with this sensitivity comes increased susceptibility because of their relative immunodeficiency.
3) The patient then goes on to develop full-blown Parkinsonism, ALS, Alzheimers or various cancers.
4) The patient is counted as one who got Parkinsonism, ALS, Alzheimers or various cancers because of stopping their statin.
This sequence of events helps greatly to explain the remarkably diverse results of recent clinical studies, some of which, for example, support statin causality for many neurodegenerative conditions while others support statin treatment for the same condition.
Duane Graveline MD MPH
Former USAF Flight Surgeon
Former NASA Astronaut
Retired Family Doctor
Updated September 2013.