Study says there's no link between cholesterol and heart disease - NHS
Cholesterol contributes to atherosclerosis -- a condition that greatly increases the risk of heart attack and stroke -- by suppressing the activity of. Not only is there a lack of evidence of causal link between LDL and heart disease , the statistical approach statin advocates have used to. When there is too much cholesterol in your blood, it builds up in the walls of your arteries, causing a process called atherosclerosis, a form of heart disease.
There are other factors found in eggs that may influence risk for heart disease by reducing serum lipids, such as phospholipids, and these may also modify the response to dietary cholesterol found in eggs. In this review, we discuss how eggs and dietary cholesterol affect serum cholesterol concentrations, as well as more advanced lipoprotein measures, such as lipoprotein particle profiles and HDL metabolism. Introduction Cardiovascular disease CVD contributes to more than 17 million deaths per year globally, which accounts for nearly half of all deaths from non-communicable diseases [ 1 ].
Cardiovascular disease is primarily caused by atherosclerosis, a chronic inflammatory disease of the arteries in which the deposition of cholesterol and fibrous materials in artery walls forms a plaque or lesion [ 2 ]. Key risk factors that associate with the number of atherosclerotic CVD events include the total concentration of cholesterol found in the blood, as well as the cholesterol found in individual lipoprotein subclasses [ 3 ]. Cholesterol, Eggs, and Heart Disease 2.
This hypothesis was consistent with evidence from animal studies, such as the seminal work by Nikolai N. Anichkov in rabbits inshowing large doses of cholesterol in the diet markedly induced atherosclerotic plaques in aortas [ 8 ].
Does High Cholesterol Cause Heart Disease?
Even with these early studies, it was clear that there were species-specific differences in the atherosclerotic response to large doses of dietary cholesterol, with rats being markedly more resistant than rabbits and guinea pigs [ 8 ].
The average intake of dietary cholesterol in U. Eggs are a major source of dietary cholesterol in the typical Western diet; one large egg yolk contains approximately mg of cholesterol.
The consumption of eggs and egg products contributes about a quarter of the daily cholesterol intake in the U. Saturated fat is known to strongly increase serum cholesterol, and eggs, which are relatively low in saturated fat, only contribute about 2. Early observational studies demonstrated a link between dietary cholesterol and risk for CVD [ 1213 ]; however, these initial studies failed to account for many confounding variables that may limit their findings, such as other dietary and lifestyle factors.
However, there does appear to be a more consistent relationship between egg intake and CVD in diabetics [ 1415 ], however, this is not always found [ 17 ]. Interestingly, this risk in diabetics may be related to the phosphatidylcholine content of eggs [ 18 ], and not the cholesterol since dietary cholesterol is shown to be more poorly absorbed in obese and insulin-resistant populations compared to lean individuals [ 192021 ].
Phosphatidylcholine intake has been linked to the gut microbial-dependent generation of trimethylamine N-oxide TMAOa metabolite shown to promote atherosclerosis in hyperlipidemic mouse models and associated with CVD risk in human cohort studies [ 2223 ]. However, the consumption of 2—3 eggs per day was not associated with increases in fasting TMAO concentrations in healthy, young adults [ 2425 ], while postprandial TMAO concentrations in the plasma of healthy men were found to be markedly lower after egg intake than fish intake, a direct source of dietary TMAO [ 26 ].
Dietary cholesterol intake was not found to be significantly associated with either heart disease, ischemic stroke, or hemorrhagic stroke. Serum Cholesterol Responses and Adaptations to Cholesterol Intake Early dietary recommendations assumed that increasing dietary cholesterol intake would lead to an increase in cholesterol in the blood, which over several decades would promote the development of heart disease.
However, this is an oversimplification since the serum cholesterol response to dietary cholesterol is much more complicated. Humans can produce cholesterol endogenously and most of the cholesterol in the body comes from biosynthesis [ 3031 ]. Cholesterol balance is affected by synthesis rates of cholesterol and bile acids, as well as their excretion from the body.
Sterol balance studies have shown feedback inhibition of cholesterol biosynthesis and increased excretion of bile acids with high cholesterol diets [ 33 ]. Cellular cholesterol biosynthesis is tightly regulated by a transcriptional program coordinated by sterol regulatory element-binding protein-2 SREBP-2 [ 34 ]. When cellular cholesterol is increased, both cholesterol biosynthesis and lipoprotein uptake are reduced via feedback inhibition. It has long been thought that cholesterol is a key cause of the fatty build-up in arteries atherosclerosis that causes heart disease.
However, the researchers say there are contradictions to this view.
Cholesterol and Heart Disease – What’s the Evidence? - Students 4 Best Evidence
Recent research has suggested that total cholesterol becomes less of a risk factor for all-cause or cardiovascular mortality the older people get. Less is known about LDL specifically and that's what this research aimed to look at.
A systematic review is the best way of gathering evidence from cohort studies that have looked at the link between an exposure or risk factor and an outcome. However, the strength of a review's findings is only as good as the studies they include. In cohort studies, it is often difficult to directly attribute an outcome to a specific cause, and there is always the potential that other factors are influencing the outcome.
What did the research involve? The researchers searched one literature database PubMed in December to identify English-language cohort studies that had included a general population sample aged 60 and over.
Studies had to have taken baseline measures of LDL cholesterol and then followed participants up over time, looking at the link with all-cause or cardiovascular mortality. Three authors reviewed potential studies and extracted data. From an initial 2, hits, 19 publications, covering 30 cohorts and including 68, participants, were included.
The majority of studies were excluded outright, as they didn't seem to contain anything relevant in the study title or abstract summary.
The other reasons for exclusion were non-English language, participants not being representative of the general population, not measuring LDL cholesterol at baseline, and not giving separate data for older adults or looking at mortality outcomes.
What were the basic results?
That is, as LDL cholesterol went down, all-cause mortality went up — higher LDL was apparently linked to lower all-cause mortality. In 14 of these 16, this was said to be a statistically significant link. The remaining 12 cohorts found no link with all-cause mortality.
Only nine of the identified cohorts specifically reported cardiovascular mortality. Seven found no link between LDL cholesterol and cardiovascular mortality. The other two found that those in the lowest fourth quartile of LDL levels actually had the highest cardiovascular mortality.
No connection between LDL cholesterol levels and heart disease, according to researchers
How did the researchers interpret the results? The researchers concluded that, "High LDL-C is inversely associated with mortality in most people over 60 years". They said their finding contradicts the cholesterol hypothesis: They consider that as they found older adults with high LDL live just as long as those with low LDL, this "provides the rationale for a re-evaluation of guidelines recommending pharmacological reduction of LDL-C in the elderly".
However, before accepting this as fact, there are many important limitations to consider — both to the review and the included studies — many of which the review authors themselves acknowledge: There is the potential that many studies relevant to this question may have been missed out.
The review searched only a single literature database, excluded studies only available in non-English language, and excluded studies where the title and abstract did not appear to contain information on the link between LDL and mortality in older adults. The study only looked at the link in older adults aged over LDL-cholesterol levels may show different links with long-term mortality in younger adults.