Doctor says there is no evidence that statins are safe

This paper was published in the Canadian Medical Association Journal May 6: 2008

Study title and author:
Statins - Safe?
Dr Herbert H. Nehrlich

This paper can be accessed at: http://www.cmaj.ca/content/178/5/576.abstract/reply#content-block

Dr Nehrlich, a doctor from Australia, discusses the effects of statin drugs.

(i) Statins reduce the body's production of mevalonate through the suppression of a liver enzyme called hydroxymethylglutaryl (HMG) coenzyme A reductase.
(ii) This enzyme is crucial in enabling the body to synthesize such substances as cholesterol, Co-enzyme Q-10 etc., substances that are essential for every living cell.
(iii) So, if you reduce the supply of mevalonate, the liver can no longer keep up production of sufficient cholesterol and has to slow the shipping of cholesterol from the depot (liver) to the various areas in need of it via the bloodstream. Hence, blood cholesterol will be lower in lab tests.
(iv) Mevalonate is not just important in this respect but is heavily involved in muscle metabolism as well as in the production of thromboxane. Thromboxane, of course, is the agent responsible for the important stage in healing called clotting and originates in the platelets of our blood.
(v) Mitochondria are energy factories that MUST have coenzyme Q- 10, the very substance that is in short supply when people undergo statin treatment.
(vi) The dismal success record of statin treatment, combined with their sometimes atrocious side effects (identified and hidden) makes the prescription of statins in humans an assault with unknown and likely dire consequences.
(vii) People tend to die with low cholesterol blood levels.
(viii) May I ask for the studies that have shown that lowering cholesterol is reasonable and thus good practice? Statins are safe? Let us look at the PROSPER Trial and the all cause mortality. It is not improved by statins.
(ix) I prefer to see cholesterol as an extremely vital substance, essential for good health and indispensable when it comes to repair and maintenance of the body.
(x) Statins are now Big Pharma's golden goose and the price of gold is rising.
(xi) If we think of rhabdomyolysis, of transient global amnesia and of the propensity of statins to initiate cancer in many animals, if we consider the truly dismal success of statin treatment then we can skip looking at the plausibility of using these drugs altogether.
(xii) Statins are mayhem to Coenzyme Q-10 and it follows that statins may thus weaken the heart. They may cause cancer in humans.

Dr Nehrlich concludes: "There is no evidence that statins are safe".

High cholesterol levels associated with a reduced risk of kidney cancer

This study was published in the International Journal of Cancer 2012 May 1;130(9):2118-28

Study title and authors:
The interplay between lipid profiles, glucose, BMI and risk of kidney cancer in the Swedish AMORIS study.

Van Hemelrijck M, Garmo H, Hammar N, Jungner I, Walldius G, Lambe M, Holmberg L.
King's College London, School of Medicine, Division of Cancer Studies, Cancer Epidemiology Group, London, UK. mieke.vanhemelrijck@kcl.ac.uk

This study can be accessed at: http://www.ncbi.nlm.nih.gov/pubmed/21630265

This study assessed possible links between cholesterol levels and kidney cancer risk. The study included 542,924 subjects, aged 20 years or older, who were followed for 13 years.

The study found:
(a) Those with the highest cholesterol levels (above 6.5 mmol/L or 251 mg/dL) had a 13% decreased risk of kidney cancer compared to those with the lowest cholesterol levels (below 4.9 mmol/L or 189 mg/dL).
(b) Those with the highest levels of low density lipoprotein (LDL) cholesterol (above 4.25 mmol/L or 164 mg/dL) had a 9% decreased risk of kidney cancer compared to those with the lowest cholesterol levels (below 2.82 mmol/L or 109 mg/dL).
(c) Those with the highest levels of high density lipoprotein (HDL) cholesterol (above 1.8 mmol/L or 69 mg/dL) had a 36% decreased risk of kidney cancer compared to those with the lowest cholesterol levels (below 1.25 mmol/L or 48 mg/dL).

The study reveals that high cholesterol levels are associated with a reduced risk of kidney cancer.

Simvastatin has deleterious effects on human first trimester placental cells

This study was published in Human Reproduction 2005 Oct;20(10):2866-72

Study title and authors:
Simvastatin has deleterious effects on human first trimester placental explants.

Kenis I, Tartakover-Matalon S, Cherepnin N, Drucker L, Fishman A, Pomeranz M, Lishner M.
Oncogenetic Laboratory, Department of Internal Medicine A, Sapir Medical Center, Kfar-Saba, Israel.

This study can be accessed at: http://www.ncbi.nlm.nih.gov/pubmed/15958395

A group led by Dr Irina Kenis explored the effects of statins on the placenta. The study compared cultured human first trimester placental cells exposed to small doses of simvastatin with cells not exposed to simvastatin.

The study found:
(a) Compared with unexposed cells, simvastatin sharply inhibited the migration of extravillous trophoblast cells. (The migration of extravillous trophoblast cells into the uterus is a vital stage in the establishment of pregnancy).
(b) Compared with unexposed cells, simvastatin inhibited the formation of trophoblast cells.
(c) Compared with unexposed cells, simvastatin led to more cell death in the trophoblast cells.
(d) Progesterone levels were significantly reduced in the simvastatin-treated cells in comparison with unexposed cells. (Progesterone keeps the placenta functioning properly and the uterine lining healthy and thick).
(e) Human chorionic gonadotropin levels were reduced in the simvastatin-treated cells in comparison with unexposed cells. (Human chorionic gonadotropin is a hormone produced during pregnancy and should almost double every 48 hours in the beginning of a pregnancy. Human chorionic gonadotropin levels that do not rise appropriately may indicate a problem with the pregnancy).

Dr Kenis concludes: "Simvastatin adversely affects human first trimester trophoblast. These effects may contribute to failure of the implantation process and be deleterious to the growth potential of the placenta".

High cholesterol levels decrease the risk of spinal fractures

This study was published in Rheumatology International 2009 Jun;29(8):885-90

 

Study title and authors:

Serum lipid profile: its relationship with osteoporotic vertebrae fractures and bone mineral density in Turkish postmenopausal women.

Sivas F, Alemdaroğlu E, Elverici E, Kuluğ T, Ozoran K.

Physical Medicine and Rehabilitation Department, Ankara Numune Training and Research Hospital, Ankara, Turkey.

 

This study can be accessed at: http://www.ncbi.nlm.nih.gov/pubmed/19043717

One of the aims of the study was to investigate the effect of cholesterol levels on the risk of fractures in the spine. The study included 107 postmenopausal women aged 45-79.

The study found:
(a) Woman without spinal fractures had 10.6% higher cholesterol levels compared to women with spinal fractures.
(b) Woman without spinal fractures had 14.2% higher levels of low density lipoprtein (LDL)cholesterol compared to women with spinal fractures.
(c) Every increase of 1 mg/dL in cholesterol levels decreased the risk of spinal fracture by 2.2%.

How statins cause muscle damage

This study was published in the Journal of Clinical Investigation 2007 Dec;117(12):3940-51

Study title and authors:
The muscle-specific ubiquitin ligase atrogin-1/MAFbx mediates statin-induced muscle toxicity.

Hanai J, Cao P, Tanksale P, Imamura S, Koshimizu E, Zhao J, Kishi S, Yamashita M, Phillips PS, Sukhatme VP, Lecker SH.
Renal Division, Department of Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts 02215, USA.

This study can be accessed at: http://www.ncbi.nlm.nih.gov/pubmed/17992259

In 2001, scientists from the Harvard Medical School discovered the atrogin-1 gene, which plays a major role in muscle atrophy. (Muscle atrophy is the wasting or loss of muscle tissue).

Hanai notes that statins can lead to a number of side effects in muscle, including muscle fibre breakdown. This study sought to find the mechanisms of how statins may induce muscle injury. Since atrogin-1 plays a key role in the development of wasting in skeletal muscle, the study investigated if statins might “turn on” this gene.

They study comprised of three separate experiments to test this hypothesis.

(i) The first experiment examined the expression of the atrogin-1 gene in biopsies of 19 human patients (eight of the patients had muscle pain/damage while using statins). The results showed that atrogin-1 expression was significantly higher among the statin users.
(ii) The second experiment studied statins’ effects on cultured muscle cells treated with various concentrations of lovastatin. Compared with control samples, the lovastatin-treated cells became progressively thinner and more damaged. However, the cells lacking the atrogin-1 gene were resistant to statins’ deleterious effects.
(iii) Thirdly statins were tested on zebra fish. These tests also found that lovastatin led to muscle damage and as the lovastatin levels increased, so too was the damage. Again, (as in the cultured muscle cells) fish lacking the atrogin-1 gene were resistant to statin-induced damage.

Hanai concluded: "Collectively, our human, animal, and in vitro findings shed light on the molecular mechanism of statin-induced myopathy (muscle damage) and suggest that atrogin-1 may be a critical mediator of the muscle damage induced by statins.

High saturated fat and meat consumption lowers the risk of prostate cancer

This study was published in the International Journal of Cancer 1997 Nov 27;73(5):634-8

 

Study title and authors:

Dietary fat intake and risk of prostate cancer: a prospective study of 25,708 Norwegian men.

Veierød MB, Laake P, Thelle DS.

Section of Medical Statistics, University of Oslo, Norway. marit.veierod@basalmed.uio.no

 

This study can be accessed at: http://www.ncbi.nlm.nih.gov/pubmed/9398038

This study investigated the relationship between diet and prostate cancer. The study included 25,708 men aged 16-56 years who were followed for up to 15 years.

The study found:
(a) Men who consumed the most saturated fat had a 30% reduced risk of prostate cancer compared to men who consumed the least saturated fat.
(b) Men who consumed the most meat had a 60% reduced risk of prostate cancer compared to men who consumed the least meat.
(c) Men who drank whole milk had a 120% reduced risk of prostate cancer compared to men who drank skimmed milk.
(d) Men who consumed the most polyunsaturated fat had a 40% increased risk of prostate cancer compared to men who consumed the least polyunsaturated fat.
(e) Men who drank skimmed milk had a significantly higher body mass index compared to men who drank whole milk.

The study suggests that a high saturated fat and meat consumption lowers the risk of prostate cancer.

Statins and the risk of bone fracture in postmenopausal women

This study was published in the Annals of Internal Medicine 2003 Jul 15;139(2):97-104

 

Study title and authors:

Statin use, clinical fracture, and bone density in postmenopausal women: results from the Women's Health Initiative Observational Study.

LaCroix AZ, Cauley JA, Pettinger M, Hsia J, Bauer DC, McGowan J, Chen Z, Lewis CE, McNeeley SG, Passaro MD, Jackson RD.

Women's Health Initiative Clinical Coordinating Center, Fred Hutchinson Cancer Research Center, 1100 Fairview Avenue North, MP-1002, PO Box 19024, Seattle, Washington 98109-1024, USA.

 

This study can be accessed at: http://www.ncbi.nlm.nih.gov/pubmed/12859159

The objective of the study was to examine the association of statin use with the incidence of hip, lower arm or wrist, and other fractures. The study included 93,716 postmenopausal women, aged 50 to 79 years who were followed for an average of 3.9 years.

The study found:
(a) Women using statins had a 22% increased risk of hip fracture compared to women not using statins.
(b) Women using statins had a 4% increased risk of lower arm or wrist fracture compared to women not using statins.
(c) Women using statins had an 11% increased risk of other fractures compared to women not using statins.

Doctor says vegetarians develop vitamin B12 deficiency regardless of wealth, age, where they live or type of vegetarian diet

This paper was published in Nutrition Reviews 2013 Feb;71(2):110-7

 

Study title and authors:

How prevalent is vitamin B(12) deficiency among vegetarians?

Pawlak R, Parrott SJ, Raj S, Cullum-Dugan D, Lucus D.

Department of Nutrition Science, East Carolina University, Greenville, NC 27858, USA. pawlakr@ecu.edu

 

This study can be accessed at: http://www.ncbi.nlm.nih.gov/pubmed/23356638

The aim of this paper, headed by Dr Roman Pawlak from the Department of Nutrition Science at East Carolina University, was to review the scientific literature to assess the rate of vitamin B12 deficiency among vegetarians and vegans. The review found 18 studies that assessed vitamin B12 deficiency rates.

The review found:
(a) 62% of vegetarian pregnant women were vitamin B12 deficient.
(b) Between 25-86% of vegetarian children were vitamin B12 deficient.
(c) Between 21-41% of vegetarian adolescents were vitamin B12 deficient.
(d) Between 11-90% of elderly vegetarians were vitamin B12 deficient.
(e) Higher rates of deficiency were reported among vegans compared with vegetarians.
(f) Higher rates of deficiency were reported among individuals who had adhered to a vegetarian diet since birth compared with those who had adopted such a diet later in life.

Dr Pawlak concluded: "The main finding of this review is that vegetarians develop B12 depletion or deficiency regardless of demographic characteristics, place of residency, age, or type of vegetarian diet".