Heart Disease
Diet
Omega-6 vegetable oils as a driver of coronary heart disease: the oxidized linoleic acid hypothesis
Summary
The consumption of the omega-6 polyunsaturated fat linoleic acid has dramatically increased in the western world primarily in the form of vegetable oils. OxLDL is thought to play an important role in atherosclerosis formation; however, it is the oxidised linoleic acid contained in LDL that leads to harmful OXLAMs, which induces atherosclerosis and CHD. Thus, reducing the amount of dietary linoleic acid, mainly from industrial vegetable/seed oils, will reduce the amount of linoleic acid in LDL and likely reduce oxLDL as well as the risk for CHDcoronary heart disease.
In summary, numerous lines of evidence show that the omega-6 polyunsaturated fat linoleic acid promotes oxidative stress, oxidised LDL, chronic low-grade inflammation and atherosclerosis, and is likely a major dietary culprit for causing CHD, especially when consumed in the form of industrial seed oils commonly referred to as ‘vegetable oils’.
Mortality Among Patients With Familial Hypercholesterolemia: A Registry‐Based Study in Norway, 1992–2010
In this registry‐based study, 4688 male and female patients from the Unit for Cardiac and Cardiovascular Genetics (UCCG) Registry with verified molecular genetic diagnosis of familial hypercholesterolemia in the period 1992–2010 were linked to the Norwegian Cause of Death Registry. Standardized mortality ratios and 95% CIs were estimated. There were 113 deaths. Mean age of death was 61.1 years. Cardiovascular disease was the most common cause of death (46.0%), followed by cancer (30.1%). Compared with the Norwegian population, cardiovascular disease mortality was significantly higher in the UCCG Registry in all age groups younger than 70 years (standardized mortality ratio 2.29, 95% CI 1.65 to 3.19 in men and women combined; standardized mortality ratio 2.00, 95% CI 1.32 to 3.04 in men; standardized mortality ratio 3.03, 95% CI 1.76 to 5.21 in women). No significant differences were found in all‐cause mortality or cancer mortality.
Statins
Statins stimulate atherosclerosis and heart failure: pharmacological mechanisms
Abstract
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. Statins inhibit the synthesis of vitamin K2, the cofactor for matrix Gla-protein activation, which in turn protects arteries from calcification. Statins inhibit the biosynthesis of selenium containing proteins, one of which is glutathione peroxidase serving to suppress peroxidative stress. An impairment of selenoprotein biosynthesis may be a factor in congestive heart failure, reminiscent of the dilated cardiomyopathies seen with selenium deficiency. Thus, the epidemic of heart failure and atherosclerosis that plagues the modern world may paradoxically be aggravated by the pervasive use of statin drugs. We propose that current statin treatment guidelines be critically reevaluated.
https://www.tandfonline.com/doi/abs/10.1586/17512433.2015.1011125
Statins and telomere length: risk assessment and management for coronary heart disease
Abstract
Cornoary heart disease (CHD) is identified as one of the diseases characterised by biological ageing as one of the important risk factors in several epidemiological studies. Premature biological ageing is distinct from chronological ageing and may predispose the individual to myocardial infarction, atherosclerosis and CHD in particular. The mean telomere length serves as a marker for the biological age at the cellular level, with shorter telomeres defining the increased biological age. Telomere length, therefore, correlates with the risk of CHD and atherosclerosis. Statins serve as the drugs of obvious choice based on their well established efficacy and safety profiles for the treatment of CHD and associated atherosclerosis. A present clinical study states that the treatment with a statin is associated with a reduction in the number of clinical events but only in individuals with increased risk based on their telomere length. This suggests a positive relationship of telomere length with the risk of CHD and, therefore, would help clinicians to categorise the patient populations based on their leucocyte telomere length for treatment with statins.
https://www.tandfonline.com/doi/abs/10.1517/14728222.11.7.979
Statins and mortality: the untold story
Abstract
Statins are first‐line evidence‐based drugs for the management of dyslipidaemias and to reduce the risk of cardiovascular events. However, statin clinical trials have shown marginally significant benefits on mortality, especially in the primary prevention setting. A major limitation of those trials is their relatively short follow‐up. A reduced number of fatal events within a 5‐year follow‐up make mortality benefits unlikely to arise. This is particularly relevant for the primary prevention trials, where the risk of cardiovascular death is low. The short follow‐up is a limitation for safety assessments too. However, extended major statin trials failed to detect any major safety concerns. Safety and efficacy assessments are even more complicated considering the differences of cardiovascular risk status in primary prevention individuals, and also given some potential ethnic and inter‐individual genetic variations in response to statin treatment. Considerable evidence suggests a favourable risk–benefit balance for statin treatment. It can be assumed that statins reduce mortality in the long term by preventing cardiovascular events with complications that reduce lifespan. Unfortunately, this hypothesis cannot be proven as there is no current ethical basis on designing long‐term placebo‐controlled statin trials. Nevertheless, by effectively reducing disabilities related to cardiovascular events, statins have major benefits for public health. Therefore, clinicians should not withhold statin treatment awaiting proof of mortality benefits, as this may remain an ‘untold story’.