If you are like most people you instinctively classify foods high in saturated fats as indulgences to avoid in order to keep your heart healthy. The obsession with low-fat food that started in the 1980s persists until today even though some of the science behind the claims against saturated fats has been increasingly called into question.
So how then did saturated fat get a bad rap? The first suggestion that we found about cholesterol being a causative agent in atherosclerosis is a paper published in 1913 by Nikolai N. Anitschkow. Apparently, he was the first to establish a link between elevated cholesterol levels and atherosclerosis in rabbits.
However, it wasn’t until the 1950s that the “diet-heart” hypothesis really took hold. A number of famous studies, including the ongoing Framingham Heart Study and the Seven Countries Study, showed correlations between high levels of total cholesterol and development of heart disease and overall mortality.
Scientists in these and other similar studies observed that diets high in saturated fats increase Low-density lipoprotein (LDL) levels and that high LDL levels were associated with adverse health outcomes like heart attacks and strokes. LDL is one of five classes of fat transport proteins found in the blood. When we eat dietary fats in a meal, they’re metabolized by our digestive organs and shuttled off using LDL and other transport proteins. Some of these LDL particles can permeate the arterial wall and create damage inside the artery over time.
These findings naturally led to a focus on reducing LDL levels by limiting saturated fat intake. By the 1970s the result of the scientific research started to permeate public health policies and beginning in 1980 the US nutritional guidelines started recommending that saturated fatty acid (SFA) intake be limited to <10% of total calories as a means of reducing risk for cardiovascular disease (CVD)
The shunning of fats then went one step further, to a large extent fueled by the marketing of countless new low-fat products. As a nutrient class, fats are energy dense, contributing 9kcal/g in contrast to carbs and proteins which only contribute 4kcal/g. As our obsession with cutting calories to stay slim took hold, diet advice told the public to ditch all fats or switch to low-fat alternatives in order to keep their weight down.
That’s the cliff note version of how the narrative that saturated fats clog your arteries and cause heart disease took hold. More recently, however, a number of meta-analyses and reviews have found no correlation between the consumption of saturated fats and a higher incidence of CVD.
As is always the case when it comes to nutrition, the presence of “contradictory” evidence has been the source of much debate
Introducing Some Nuance
One thing that is clear in the heart-health debate is that there is plenty of evidence supporting a causal role of high levels of LDL in atherosclerosis and CVD progression. What is now becoming clearer is the mechanism by which this damage to the arterial walls is triggered. And it is not all determined by the presence of saturated fats in your diet.
In fact, in this review published in the Journal of the American College of Cardiology, researchers found that “most recent meta-analyses of randomized trials and observational studies found no beneficial effects of reducing [Saturated Fatty Acid] intake on cardiovascular disease (CVD) and total mortality, and instead found protective effects against stroke.”
The review lists a number of recent studies that consitently found no significant correlation between intake of saturated fats and CVD. These include:
- PURE (Prospective Urban Rural Epidemiological) study in 135,000 people mostly without CVD from 18 countries on 5 continents (80% low- and middle-income countries), increased consumption of all types of fat (saturated, monounsaturated, and polyunsaturated) was associated with lower risk of death and had a neutral association with CVD
- A newly published study of 195,658 participants from the UK Biobank who were followed up for 10.6 years, there was no evidence that saturated fat intake was associated with incident CVD.
- Women’s Health Initiative trial in nearly 49,000 women, which demonstrated that risk for heart attack and stroke was unaffected after 8 years on a low-fat diet in which saturated fat provided 9.5% of total daily energy intake
- PREDIMED (Prevención con Dieta Mediterránea) trial compared a standard low-fat diet with a Mediterranean diet supplemented with nuts or olive oil. Despite an increase in total fat intake by 4.5% of total energy (including slightly higher saturated fat consumption), major cardiovascular events and death were significantly reduced compared with the control group (despite not lowering LDL).
The interesting nuisance we learned from this review is that ‘although SFAs increase low-density lipoprotein (LDL) cholesterol, in most individuals, this is not due to increasing levels of small, dense LDL particles, but rather larger LDL particles, which are much less strongly related to CVD risk.
Once thought to be a single protein type, current research suggests that LDL occurs in two sizes—large “pattern A” LDL and small dense “pattern B” LDL. Furthermore, the two proteins don’t behave the same in the bloodstream. Small dense LDL is associated with an increased risk of heart disease and fits more easily into the artery walls, increasing the likelihood of plaque formation. It stands to reason then that increasing saturated fat consumption increases the amount of both types of LDL in the blood and may therefore increase the risk of CVD.
If the lining of the artery is a street, large LDL moves along like a buoyant semi-truck; it has the potential to do damage but for the most part glides along without incident. On the other hand, small dense LDL is like a piece of heavy machinery that chews up the asphalt as it moves along, causing damage and the potential for further issues down the line.
All this seems to suggest “the perceived benefit of dietary restriction of saturated fat could be overstated by reliance on the change in LDL cholesterol levels alone.”
Pushback From Within
We found plenty of evidence that the view on saturated fats is coming full circle, and this has led to calls for a paradigm shift within the medical and public health establishments. Many folks seem to agree that trying to control CVD through dietary restriction has not worked and that the focus needs to be on other, more effective forms of prevention.
One voice supporting a change in direction is the outspoken British doctor Aseem Malhotra who has made an open call to think about heart disease as the result of chronic inflammation that happens in the presence of LDL and not the result of saturated fats clogging arteries. So instead of reducing the amount of cholesterol in the arteries, he argues that the focus should be on the inflammatory processes that contribute to cholesterol deposition within the artery wall in the first palace.
He points out that where the “cholesterol clogs arteries” argument falls short is in that most cardiac events occur at sites with less than 70% coronary artery obstruction, and these do not generate ischaemia on stress testing. Instead, Malhotra attributes heart attacks to the rupture of plaques. He compares a plaque rupture to a pimple bursting because the clots formed in response to ruptures are what actually cause heart attacks or strokes.
He also points to another systematic review for which researchers analyzed 41 prospective cohort studies on the association between saturated fats and health outcomes as well as 6 prospective studies on the association between intake of saturated fats and all-cause mortality. After assessing study confidence, potential for bias, and cumulative statistics, the authors concluded that saturated fats were not associated with all-cause mortality, CVD, CHD, ischemic stroke, or type 2 diabetes and that replacement of saturated fats with polyunsaturated fats increased CVD risk.
One thing of note about this review is that while the samples included in the studies were robust, the data used in analysis is self-reported observational information. It doesn’t come from fully controlled dietary studiets.
De Malhotra’s position is that artery plaque is not the root cause of CVD. It’s more like a fire that’s being fueled by underlying systemic inflammation and/or insulin resistance. And the way to address these root causes is through lifestyle interventions such as the adoption the High Fat Mediterranean Diet used in the PREDIMED study, brisk daily walking and better stress management.
Source: Malhotra A, Redberg RF, Meier P. Saturated fat does not clog the arteries: coronary heart disease is a chronic inflammatory condition, the risk of which can be effectively reduced from healthy lifestyle interventions. British Journal of Sports Medicine 2017;51:1111-1112.
Broadly speaking, Malhotra’s hypothesis makes sense. Systemic inflammation and insulin resistance are known to cause damage to the body and lifestyle intervention through diet and exercise has been shown to curb both. It stands to reason that treatment and prevention strategies should hinge on those building blocks.
Not surprisingly, Dr. Lahotra’s call for a paradigm shift has invited strong criticism from fellow clinicians and nutritionists. One comment that jumped out at us included this criticism:
“The Mediterranean diet and daily exercise can help reduce heart disease risk, but I’m afraid the claims about saturated fat made in this opinion piece are unhelpful and misleading. Decades of research have proved that a diet rich in saturated fat increases ‘bad’ LDL cholesterol in your blood, which puts you at greater risk of a heart attack or stroke. When it comes to reducing your risk of heart disease, the lower your cholesterol is the better.” --Dr. Mike Knapton
The reality is that all the studies present methodological differences and structural limitations that make black and white statements based on their results to often be fraught with imprecisions. Nevertheless, Dr Malhotra’s position is certainly worth considering.
A Possible Third View?
We came across a study that predates some of the other news we’ve already cited but which stood out because it proposes a third, even more nuanced view. According to this paper, It is understood that LDL oxidation is an early event in atherosclerosis and that oxidized LDL contributes to the formation of plaques. However, it has been unclear whether oxidative events are a cause rather than an injurious response to atherogenesis. This paper proposes a two-stage model where inflammation needs to be considered as a primary process of atherosclerosis, and oxidative stress as a secondary event. This “oxidative response to inflammation” model presents an interesting way of reconciling the response-to-injury and and oxidative modification hypothesis of atherosclerosis.
Go Deeper: check out this short video for an awesome primer on the latest understanding of heart pathology of arterial plaque formations.
Get Started: use this tool from the American College of Cardiology to calculate your 10-year cardiac risk.
Go Further:ask your doctor about the CardioIQ lab test to gain more information about Saturated fat reduction is a viable treatment and prevention method for heart disease
It’s certain that the debate on saturated fats will continue into the future. Call it a mix of inertia of diet dogma and our continuously evolving understanding of how nutrition affects our metabolism. Bulletproof diet studies are notoriously expensive and difficult to conduct. Instead we see our understanding advance in fits and spurts and oftentimes take opposite directions. As in any field, one must keep an open mind and be willing to consider new ideas as our understanding of the underlying mechanisms of disease improves.
Our best advice is this: test for yourself. We know that high LDL levels are to be avoided. To optimize your diet, try different levels of saturated fat intake and track the impact they have on your overall LDL levels. We all process fats differently and the only way to optimize is to test, measure and learn.
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