Hard scientific evidence of the effects of diet, pharmaceutical drugs & lifestyle on health from over 1,400 studies from research centers, universities and peer reviewed scientific journals.

Research by David Evans

Sunday, 8 February 2015

Doctor says that statins may be the cause of the current heart failure and atherosclerosis epidemic

This paper was published in Expert Review of Clinical Pharmacology 2015 Feb 6:1-11
 
Study title and authors:
Statins stimulate atherosclerosis and heart failure: pharmacological mechanisms.
Okuyama H, Langsjoen PH, Hamazaki T, Ogushi Y, Hama R, Kobayashi T, Uchino H.
Nagoya City University and Institute for Consumer Science and Human Life, Kinjo Gakuin University, 2-1723 Omori, Moriyama, Nagoya 463-8521, Japan.
 
This paper can be accessed at: http://www.ncbi.nlm.nih.gov/pubmed/25655639

Dr Harumi Okuyama and his team from the Nagoya City University in Japan discuss the mechanisms of how statins may cause atherosclerosis and heart failure.

Dr Okuyama states:
(i) In contrast to the current belief that cholesterol reduction with statins decreases atherosclerosis, we present a perspective that statins may be causative in coronary artery calcification and can function as mitochondrial toxins that impair muscle function in the heart and blood vessels through the depletion of coenzyme Q10 and 'heme A', and thereby ATP generation.
(ii) Statins inhibit the synthesis of vitamin K2. Vitamin K2 protects arteries from calcification.
(iii) Statins inhibit the biosynthesis of selenium containing proteins. An impairment of selenoprotein biosynthesis may be a factor in congestive heart failure.

Dr Okuyama concludes: "The epidemic of heart failure and atherosclerosis that plagues the modern world may paradoxically be aggravated by the pervasive use of statin drugs".

Wednesday, 28 January 2015

Statins unequivocally associated with lower levels of testosterone

This study was published in Endokrynologia Polska 2014;65(6):464-8
 
Study title and authors:
Treatment with statins and testosterone levels in men.
Mędraś M, Kubicka E, Jóźkow P, Słowińska-Lisowska M, Trzmiel-Bira A, Filus A.
Department of Biological Principles of Sport, University School of Physical Education in Wroclaw, Wroclaw, Poland. eliza.kubicka@gmail.com.
 
This study can be accessed at: http://www.ncbi.nlm.nih.gov/pubmed/25554614

The aim of the study was to evaluate whether the use of statins is associated with the concentration of sex hormones. The study included 237 men, average age 58 years.

the study found:
(a) The total testosterone levels of men taking statins was 9% lower than men not taking statins.
(b) The free testosterone levels of men taking statins was 18% lower than men not taking statins.
(c) The calculated free testosterone levels of men taking statins was 11% lower than men not taking statins.
(d) The bioavailable testosterone levels of men taking statins was 19% lower than men not taking statins.

Medras concluded: "Our study unequivocally confirms that the use of statins is associated with lower levels of: total testosterone, free testosterone, calculated free testosterone and bioavailable testosterone".

Thursday, 22 January 2015

High LDL cholesterol helps you live longer

This study was published in Atherosclerosis 2015 Jan 14;239(1):137-142
 
Study title and authors:
Low-density lipoprotein cholesterol was inversely associated with 3-year all-cause mortality among Chinese oldest old: Data from the Chinese Longitudinal Healthy Longevity Survey.
Lv YB, Yin ZX, Chei CL, Qian HZ, Kraus VB, Zhang J, Brasher MS, Shi XM, Matchar DB, Zeng Y.
Division of Non-Communicable Disease Control and Community Health, Chinese Center for Disease Control and Prevention, Beijing, China.
 
This study can be accessed at: http://www.ncbi.nlm.nih.gov/pubmed/25602855

This study examined the relationship between LDL-Cholesterol and all-cause mortality among the elderly. The study included 935 participants, aged 80 and older, who were followed for three years.

The study found:
(a) Each 1 mmol/L (38 mg/dL) increase of LDL-Cholesterol concentration corresponded to a 19% decreased risk of death. 
(b) Those with a LDL-Cholesterol concentration of more than 3.37 mmol/L (130 mg/dL) had a 40% decreased risk of death. 

The researchers concluded: "Higher LDL-Cholesterol level was associated with lower risk of all-cause mortality. Our findings suggested the necessity of re-evaluating the optimal level of LDL-Cholesterol among the oldest old".

Monday, 12 January 2015

Statin use increases the risk of multiple colorectal adenomas by 25%

This study was published in Cancer Epidemiology, Biomarkers and Prevention 2005 Apr;14(4):1026-7

Study title and authors:
Reported use of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors was not associated with reduced recurrence of colorectal adenomas.
Wei JT, Mott LA, Baron JA, Sandler RS; Polyp Prevention Study Group.
Division of Gastroenterology and Hepatology, University of North Carolina, Campus Box 7080, Chapel Hill, NC 27599, USA. jwei@med.unc.edu

This study can be accessed at: http://www.ncbi.nlm.nih.gov/pubmed/15824186

This study investigated the association of statins with the risk of recurrent colorectal adenomas. (An adenoma is a benign tumour. Colorectal adenomas are removed because of their tendency to become malignant and to lead to colon cancer). The study analysed data from three randomised trials regarding the recurrence of colorectal adenomas in patients with a history of adenomas. The trials included 2,638 patients.

The analysis revealed:
(a) Statin users had a 3% increased risk of any adenoma compared to statin never-users.
(b) Statin users had a 13% increased risk of any advanced adenoma compared to statin never-users.
(c) Statin users had a 25% increased risk of multiple adenoma compared to statin never-users.

Tuesday, 30 December 2014

Statins increase the risk of liver damage

This study was published in the Medical Journal of Basrah University Vol: 25, No: 1 2007

Study title and authors:
Comparative Effects of Lovastatin and Simvastatin on Liver Function tests in Hyperlipidaemic Patients
Zena Sattam, Hamad Al-Jubori, Isam Hamo Mahmood
This study can be accessed at: http://www.iasj.net/iasj?func=fulltext&aId=48121

Drug-induced liver damage has become an important public health problem, contributing to more than 50% of acute liver failure cases, and there have been observations of a large number of liver failure cases on statin therapy. 

In liver function tests, liver damage is confirmed with increased levels of bilirubin and the liver enzymes; Alanine transaminase, aspartate aminotransferase and alkaline phosphatase.

This study measured the effects of statins on liver function tests. The study included: 

(i) 53 patients, aged 35-60 years, took simvastatin therapy. The simvastatin dose ranged from 10 to 20mg a day. Duration of treatment ranged from one month to four years. (Simvastatin group).
(ii) 42 patients, aged 38-60, took lovastatin therapy. The lovastatin dose ranged from 10 to 20mg a day. Duration of treatment ranged from one month to three years. (Lovastatin group).
(iii) A control group of 50 subjects, aged 35-58 who did not take statins. (No-statin group).

The study found:
(a) The alanine transaminase levels of the lovastatin group were 113% higher than the no-statin group.
(b) The aspartate aminotransferase levels of the lovastatin group were 90% higher than the no-statin group.
(c) The alkaline phosphatase levels of the lovastatin group were 11% higher than the no-statin group.(d) The bilirubin levels of the lovastatin group were 40% higher than the no-statin group.
(e) The alanine transaminase levels of the high dose (20 mg a day) lovastatin group were 181% higher than the no-statin group.
(f) The aspartate aminotransferase levels of the high dose (20 mg a day) lovastatin group were 151% higher than the no-statin group.
(g) The alkaline phosphatase levels of the high dose (20 mg a day) lovastatin group were 20% higher than the no-statin group.
(h) The bilirubin levels of the high dose (20 mg a day) lovastatin group were 72% higher than the no-statin group.
(i) The alanine transaminase levels of the long term usage (over 12 months) lovastatin group were 333% higher than the no-statin group.
(j) The aspartate aminotransferase levels of the long term usage (over 12 months) lovastatin group were 321% higher than the no-statin group.
(k) The alkaline phosphatase levels of the long term usage (over 12 months) lovastatin group were 24% higher than the no-statin group.
(l) The bilirubin levels of the long term usage (over 12 months) lovastatin group were 145% higher than the no-statin group.
(m) The alanine transaminase levels of the simvastatin group were 103% higher than the no-statin group.
(n) The aspartate aminotransferase levels of the simvastatin group were 60% higher than the no-statin group.
(o) The alkaline phosphatase levels of the simvastatin group were 6% higher than the no-statin group.(p) The bilirubin levels of the simvastatin group were 45% higher than the no-statin group.
(q) The alanine transaminase levels of the high dose (20 mg a day) simvastatin group were 150% higher than the no-statin group.
(r) The aspartate aminotransferase levels of the high dose (20 mg a day) simvastatin group were 102% higher than the no-statin group.
(s) The alkaline phosphatase levels of the high dose (20 mg a day) simvastatin group were 3% higher than the no-statin group.
(t) The bilirubin levels of the high dose (20 mg a day) simvastatin group were 55% higher than the no-statin group.
(u) The alanine transaminase levels of the long term usage (over 12 months) simvastatin group were 255% higher than the no-statin group.
(v) The aspartate aminotransferase levels of the long term usage (over 12 months) simvastatin group were 240% higher than the no-statin group.
(w) The alkaline phosphatase levels of the long term usage (over 12 months) simvastatin group were 3% higher than the no-statin group.
(x) The bilirubin levels of the long term usage (over 12 months) simvastatin group were 83% higher than the no-statin group.

The results from this study revealed significant increases of alanine transaminase, aspartate aminotransferase and bilirubin levels in the lovastatin group compared with the control group and significant increases of alanine transaminase and bilirubin in the simvastatin group when compared with the control group.

The study also revealed that the higher the dose of the statin or the longer the dose of the statin generally correlated with increased levels of the liver enzymes.

Wednesday, 17 December 2014

Atorvastatin linked to abnormally high calcium levels

This paper was published in the Archives of the Turkish Society of Cardiology 2014 Oct;42(7):662-6
 
Study title and authors:
Can atorvastatin calcium cause asymptomatic hypercalcemia?
Ipekçi SH, Baldane S, Sözen M, Kebapçılar L
Department of Internal Medicine, Division of Endocrinology and Metabolism, Selcuk University Faculty of Medicine, Konya, Turkey.
 
This paper can be accessed at: http://www.ncbi.nlm.nih.gov/pubmed/25490303

Hypercalcemia is a condition in which the calcium level in your blood is above normal. Too much calcium in your blood can weaken your bones, create kidney stones, and interfere with the way your heart and brain works.

This paper reports the case of a woman who developed hypercalcemia after starting atorvastatin.

(i) A 52-year-old female was referred to hospital for hypercalcemia.
(ii) She had been taking atorvastatin for 1.5 years.
(iii) Atorvastatin induced hypercalcemia was suspected.
(iii) Exhaustive tests were conducted that ruled out all other causes of hypercalcemia.
(iv) She stopped taking atorvastatin and her calcium levels returned to normal.
(v) She restarted atorvastatin and again her hypercalcemia returned.
(vi) She again stopped taking atorvastatin and her calcium levels returned to normal.

Wednesday, 10 December 2014

Long-term exposure to statins may be associated with drug-induced lupus erythematosus and other autoimmune disorders

This study was published in the Journal of the European Academy of Dermatology and Venereology 2007 Jan;21(1):17-24
 
Study title and author:
Lupus erythematosus and other autoimmune diseases related to statin therapy: a systematic review.
Noël B.
Department of Dermatology, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland. bernard.noel@chuv.hospvd.ch
 
This paper can be accessed at: http://www.ncbi.nlm.nih.gov/pubmed/17207162

This paper reviewed the scientific literature concerning statin-induced autoimmune diseases including lupus erythematosus.

The review found:
(a) Statins were associated with various autoimmune diseases such as systemic lupus erythematosus, subacute cutaneous lupus erythematosus, dermatomyositis, polymyositis and lichen planus pemphigoides.
(b) Autoimmune hepatitis was observed in some patients with systemic lupus erythematosus.
(c) The average time of exposure before disease onset was 12 months, with a range from one month to six years.
(d) Aggressive immunosuppressive therapy was required in the majority of cases to aid clinical recovery.
(e) Some patients died despite the immunosuppressive therapy.

Noel concludes: "Long-term exposure to statins may be associated with drug-induced lupus erythematosus and other autoimmune disorders. Fatal cases have been reported despite early drug discontinuation and aggressive systemic immunosuppressive therapy".