Many of us have grown up with set ideas about cholesterol, including the impacts of the different types of cholesterol as well as what foods we should eat and what foods we should avoid.
For example, we know to avoid saturated fat and cholesterol in our diet. Anyone with high cholesterol in their blood aims to cut these foods down even further.
In this post, I’m going to show you some of the science behind this perspective on our health – and just how limited that science is.
The problem is, there is this very prevalent cholesterol and heart disease myth.
This is a relationship that is often implied to be fact, but the science behind it isn’t actually that great.
Through this post, I aim to give you the tools to think critically about cholesterol and statins, and to help you be aware of the fact that the science isn’t as simple as health advice suggests.
Much of the current heart health perspective is focused around the concept that cholesterol is a key risk factor in the development of heart disease and that saturated fat contributes to increased cholesterol.
Because of this, people are told to limit the cholesterol in their diet.
Those perspectives have been extremely common recommendations and they have spawned a wide range of health advice. This includes advice like focusing on a low-fat, high-carbohydrate diet, and avoiding fat as much as possible.
But… how realistic is this approach and how much of it is just a cholesterol and heart disease myth?
We live in a society that is suffering from an epidemic of obesity and overall poor health.
Despite the wide range of health recommendations that are made – these issues continue to get worse.
In fact, even heart disease itself continues to be a major issue – despite all the recommendations that are made.
Clearly, something isn’t working.
You might think that people simply aren’t following the health advice they are being given, but it isn’t actually that simple.
The Problem of Heart Disease
Of all the health issues in the United States, heart disease is one of the most significant.
Approximately 610,000 people die from this condition each year, which is roughly a quarter of all deaths in the United States each year. Heart disease is also the most common cause of death for both males and females (1).
Heart disease has been a significant cause of death throughout the history of the United States, but as medical technology and understanding has increased, we have been able to significantly decrease deaths from heart disease.
For example, from 1950 to 2008, the death rate from heart disease decreased by 77%, while the death rate for other diseases only decreased by 15% in the same period (2).
There is still a long way to go, though, because those statistics only look at the deaths from cardiovascular disease, not the prevalence of the disease.
After all, the development of technologies like defibrillators and surgery have played a key role in helping people to survive heart disease but have not had a significant impact on the development of the disease itself.
Despite the significance of heart disease, we don’t actually understand the disease all that well.
This is one of the reasons that it has been so hard to combat.
So, we come back to one really simple question: What causes heart disease?
What Causes Heart Disease?
One of the most common perspectives you will see is that cholesterol builds up in the walls of arteries, causing blockages.
That idea suggests, quite simply, that if you eat less cholesterol, this buildup will be less likely.
But, that isn’t completely accurate.
Instead, heart disease begins with damage to the lining of the arteries. This results in the buildup of plaque.
Plaque does contain cholesterol, but that doesn’t mean that cholesterol is actually the cause.
As the plaque builds up, it narrows the artery, making it more challenging for blood to pass.
If the plaque ruptures it can cause further problems, contributing to the development of blood clots, which can block the artery and cause a heart attack (3).
The truth is, we really don’t know what causes these plaques to build up.
Researchers have some theories, but there still is a lot that we don’t know.
This is the thing that this debate comes back to time and time again. Despite all the claims out there, we really don’t know nearly as much about heart disease as we seem to. Until we truly understand the mechanisms behind the disease, we don’t have the tools we need to fight it.
More than anything, we have a set of factors that can increase the risk of heart disease.
Cholesterol is thought to be one of these, while others include smoking, being physically inactive, having diabetes and having a family history of heart disease (4).
In some cases, we know something increases the risk of heart disease, but it isn’t entirely clear why it does this.
The Heart-Diet Hypothesis
The idea that cholesterol contributes to heart disease and that it can be reduced through dietary measures is often referred to as the heart-diet hypothesis (or the cholesterol and heart disease myth).
This concept has acted as the basis for dietary guidelines in the United States since around 1980 (5), and many other countries have followed suit.
Likewise, the concepts and standard practice around cholesterol and saturated fat have been taught as fact in medical schools for many decades. Because of this, many physicians wholeheartedly agree with this approach, even though they don’t actually understand the science that is behind it.
And the science… well… that’s where the whole problem starts.
First of all, the science surrounding this idea is old.
We base most of our perspectives off research done around 1970. Since then, the outcomes of that research have become popularized and politicized. In contrast, the outcomes of any contradictory research (and there has been a lot of it) has been largely ignored.
In particular, the perspective comes from the research from Ancel Keys, who had a theory that saturated fats resulted in clogged arteries and the development of heart disease.
The most significant study was known as the Seven Countries Study, and it was the first study to consider both diet and lifestyle in relation to cardiovascular disease risk.
That sounds pretty clear cut – and certainly it was convincing. To see that, you just have to look at the heath recommendations that have come out since that time along with the Time Magazine covers that focused on the research and the overall topic.
However, since that point, there has been a lot of controversy about the research.
For one thing, critics have argued that the research and theory greatly oversimplify the problem of heart disease (8).
At the same time, some researchers have argued that the study itself had multiple issues, including some data being misinterpreted or having methodological errors (9).
One factor is that in research, a very strong mantra is the idea that correlation does not equal causation. This means that just because a relationship is observed, doesn’t mean one factor causes another.
For example, if you found a relationship between shoe size and math ability in school students, it would be really bad science to say that one caused the other (it also would make no sense). But, with research you could figure out that that there is a relationship between age and shoe size, and one between age and math ability.
The seven countries study just looked at the relationship between risk factors and cardiovascular disease – offering no evidence that one causes the other.
Another factor is that looking at evidence for just seven countries isn’t all that strong.
The study was able to find a relatively strong trend with the countries considered, but some critics argue that the countries were ‘cherry-picked’. In particular, there was actually data available for 22 countries, but only seven were used in the final study (10).
When all of the data is included, the trend isn’t nearly as strong as the seven countries study implied.
This isn’t actually too surprising.
After all, there are some pretty major differences between countries, especially in their approaches to food.
Taking data from just a handful of countries and using this as evidence that fat and heart disease are linked could never provide particularly strong evidence, yet, that evidence has formed much of the basis of our current beliefs about heart disease.
How Strong Is The Evidence?
If you listen to the rhetoric, you’ll find a lot of people talking about the large amount of evidence into the role of cholesterol (specifically LDL cholesterol) in the development of heart disease.
One problem is that most of the studies that get cited tend to be studies that just make similar claims.
This is actually an issue that can happen sometimes with research.
Different studies will cite relatively recent studies before them. In some cases, people don’t look far enough back to see whether the actual studies underlying it all were solid to start off with.
Even in the official recommendations and discussions about heart disease prevention, talk almost exclusively focuses on risk factors for heart disease, rather than actual causes (e.g. 11).
This really highlights on just how little we know.
Yes, there are a lot of risk factors for heart disease, and cholesterol is probably one of them.
However, calling something a risk factor doesn’t actually mean a whole lot.
After all, everything you do in life is going to be a risk factor for something or another, whether that is getting in a car accident or increasing your disease risk.
A much more relevant piece of information is just how much of a risk factor something is – and even that is going to vary from person to person.
Since the early research into cholesterol, there has been an emphasis on finding out more about the relationship. In many cases, scientists have been focused on proving the presence of the relationship and its potential to reduce cardiovascular disease risk.
Yet, despite the common assumptions that cholesterol causes heart disease, there are many examples of evidence that doesn’t support it. For example, one study highlighted the fact that around three-quarters of heart attack patients already have low levels of LDL cholesterol (12).
This is also a really good indication of the brokenness of the way that we currently think of heart disease and cholesterol.
Another interesting point is dietary changes.
Many people dramatically change their diet to decrease their risk of heart disease, often at their doctor’s recommendation.
Frequently this type of change would involve dramatically decreasing fat and saturated fat in the diet, while increasing the consumption of fruits and vegetables, along with other healthy foods.
Yet, that type of intervention doesn’t seem to have any impact on heart disease risk, even in prolonged studies (17).
In fact, heart disease risk has even increased as the result of people trying to remove saturated fat from their diet (18).
All of this suggests that approaches for lowering cholesterol really aren’t having the expected impacts on heart disease.
Cholesterol and the Diet
Discussion on cholesterol often comes back to two things. One is the amount of cholesterol in the blood, and the other is cholesterol in the diet.
This is a pretty big part of the cholesterol and heart disease myth.
Many people blindly accept the idea that eating cholesterol and saturated fat will increase cholesterol in the blood. After all, the idea does seem quite logical.
But, that’s not how the body works.
The things that we consume have many different fates in the body.
One of the things with cholesterol is that we can produce the compound. In fact, that production is specifically what cholesterol-fighting drugs target (19).
That isn’t too surprising – because despite all the negative press surrounding cholesterol, it is actually an important compound in the body and it is needed for human health.
Furthermore, the majority of cholesterol in our bloodstream is produced in our bodies (20).
That pattern is true for most of the population. However, there is a group of hyper-responders, which make up around 25% of the population. In this group of people, consuming cholesterol does increase cholesterol (both LDL and HDL cholesterol). Despite this, the changes in cholesterol don’t contribute to increased heart disease risk (23). We’ll come back to that last point in more detail soon.
Another major challenge comes from actually measuring cholesterol levels.
If scientists are going to research the impact of cholesterol and heart disease – you would think they would be consistent about how they measure it. That’s not the case, not really.
With cholesterol, there are some complex factors to take into account.
One area is HDL and LDL.
In general, research on cholesterol and heart disease tends to focus on LDL levels and total cholesterol levels.
But, there are variations within LDL cholesterol.
In particular, the cholesterol exists in different sizes.
There are two key types of LDL molecules and they differ by size. The small molecules are known as small density LDL (often shortened to sdLDL). The larger molecules are called large density LDL (or ldLDL) (24).
The subtypes are important because they have different impacts. The sdLDL is the type to be concerned about and this subtype is being considered a risk factor for heart disease (25).
The presence of different subtypes of cholesterol is very significant for measuring.
For example, two people could have the same overall level of LDL cholesterol. However, if one of them had a high amount of sdLDL and the other had mostly ldLDL, it’s likely that their risk of heart disease would also be very different.
An interesting thing is that eating cholesterol in the diet can influence the ratio of sdLDL and ldLDL (26). Specifically, eating cholesterol lowers the amount of sdLDL.
By doing this, eating cholesterol may be decreasing heart disease risk – which is the opposite to what is often suggested.
And the thing is, many studies into the topic just looked at LDL. They didn’t consider the different subtypes of LDL. This limits the patterns that research has been able to show.
Here’s another factor.
When measuring cholesterol, the common approach is to measure LDL cholesterol (known as LDL-C). This approach looks at the number of cholesterol molecules within the LDL particles.
There is a second approach to measurement known as LDL particles (LDL-P). This approach looks at the actual number of LDL particles, regardless of whether they are carrying cholesterol or not. Doing that is important because heart disease risk is more strongly linked to the LDL particles rather than the cholesterol in them.
Much of the time LDL-P and LDL-C levels are closely related to one another.
However, that isn’t always true.
By just measuring LDL-C, physicians and researchers may not be getting an accurate picture of heart disease risk.
When people have very different levels of LDL-P and LDL-C, research suggests that LDL-P is a better predictor of heart disease risk. For example, one study found that out of patients with different LDL-P and LDL-C levels, the patients with low LDL-C and high LDL-P were at high risk while those with low LDL-P and high LDL-C were at low risk (27).
These areas highlight just how complex cholesterol is.
Many studies haven’t taken this complexity into account, which limits how much evidence their outcomes actually offer.
The Problem of Statins
One of the outcomes of the cholesterol and heart disease myth has been the development of statins.
Statins are considered to be almost a wonder drug.
They have the ability to dramatically decrease the amount of cholesterol in the body by cutting off a key pathway that generates cholesterol (28).
These drugs are widely recommended as a critical way to keep down blood cholesterol levels.
In fact, they are so popular that there are even some calls for healthy people to be taking statins, including people who don’t even have heart disease.
I can say without hesitation that statins really do lower cholesterol. That much isn’t under debate.
But, statins are only wonderful if they actually decrease cardiovascular disease risk.
For example, one comprehensive study found that 96% of the sample (from a number of meta-analyses) saw no benefit from the statins (31).Likewise, statins don’t seem to play a role in decreasing mortality as a whole (32).
There are, of course, some studies that contradict this idea, such as studies that indicate that statins can be effective at decreasing heart disease and stroke in patients between 50 and 70 years of age (33) and a meta-analysis that found similar outcomes (34).
However, it is important to note that the vast majority of studies that have found positive outcomes for statin use were also funded by drug companies (35).
One of the more challenging and confusing aspects of statins and their impacts on health comes from the way that their effectiveness is measured.
Specifically, this tends to be measured using a hazard ratio approach.
This tends to be the main measure that studies report and in many cases, it is the only measure (36).
Hazard ratios can be a useful tool, but they have their limitations.
In particular, they can actually change over time and they’re subject to selection bias (37).
At the same time, they mask the true magnitude of any observed effect.
For example, a reported a 20% decrease in the risk of heart disease would sound like a great thing on paper. But, if the participants in the study only had a 5% risk of heart disease anyway, reducing that by 20% would be largely meaningless.
To make matters worse…
This is a really concerning idea.
There simply isn’t the evidence to show that statins are beneficial for people who haven’t had heart disease.
For example, statins don’t actually reduce the risk of death overall (40).
Furthermore, if relatively few people with a history of heart disease benefit from statins, it seems likely that even fewer people without a history of heart disease experience any benefit.
Side Effects and Risk
Interestingly, there have been multiple research studies that have found associations between low cholesterol levels and increased risk of death as well as increased risk of dementia (41,42,43). Indeed, there is some concern that statins may have cognitive effects for older adults (44).
At the same time, people on statins frequently experience significant side effects from the medications (45).
To make matters worse, statins have little to no effect on heart disease risk for people who don’t have a history of heart disease (46).
This begs the question – are statins really that great?
For people without a history of heart disease, statins are kind of a tradeoff.
You may decrease your heart disease risk, but if you do, the decrease will probably be relatively minimal. The statins can also increase your risk of other health issues because of some of the impacts observed with low cholesterol levels.
The studies in question were observational, so it isn’t clear whether low cholesterol levels were the cause of the observed issues, like increased risk of dementia.
It does seem likely though.
After all, cholesterol is a key compound in the body and it is needed for the body to function. If you artificially lower your cholesterol levels, then there is the very real chance that you could do significant damage to your body.
For people without a history of heart disease, cholesterol medication doesn’t result in a change in life expectancy (47).
Side effects may well be part of that process.
I mean, if statins slightly decrease the risk of heart disease, but slightly increase the risk of other negative health outcomes, then they aren’t going to have a net benefit for most people.
Yet, research tends to focus almost exclusively on the implications of statins for cholesterol and heart disease.
That leaves a whole lot unexplored and the implications of what we don’t know about statins could be considerable.
For example, part of the action of statins is to shut off the mevalonate pathway.
This pathway plays a critical role in the production of cholesterol. So, it makes sense that blocking of the pathway would dramatically reduce the amount of cholesterol produced.
But… playing around with biological pathways is always a bit risky.
Any pathway is going to have multiple roles and many of them may be significant.
In this case, one of the other roles of the mevalonate pathway is in the production of the co-factor coenzyme Q10 (CoQ10). CoQ10 is a pretty significant compound, and its production is dramatically decreased with the use of statins (48).
Indeed, some people end up supplementing with CoQ10 when they are taking statins medication, to try and mitigate some of the side effects.
That pattern is just one indication of the potential impacts that statins can have on the body.
Another indication is the way that one study suggested that people on statin medication significantly increased their consumption of calories and of fat (49).
The mechanism behind that change isn’t too clear, but it may be connected to something known as the health halo.
This effect is surprisingly common.
With this, people will change their behavior because they are doing something they consider to be healthy.
For example, one study found that smokers who took multivitamins smoked more than those who did not. This happened because the people taking multivitamins convinced themselves that the supplements were negating some of the negative effects of smoking (50).
In the case of statins, people taking statins may feel that they need to watch their diet less carefully.
A similar effect was found with older men tending to be less engaged in physical activity when they were on statins (51).
Yet, impacts such as these continue to be majorly under-researched and not examined in detail.
This means that there really are risks involved in taking statins and that risk is simply not researched in depth.
Honestly though, those risks aren’t too surprising.
After all, you’re taking a medication that stops your body from producing something that it is supposed to produce. Taking that type of approach is always likely to have dramatic effects and some unintended ones.
At the same time, there are pretty strong interactions between medications and lifestyle.
These links are very hard to research because they are very individual in nature. But, they are certainly there.
Here’s the thing…
For many people, statins dramatically lower their quality of life.
Is it worth it?
Would you take a drug that made everything in your life harder, but also decreased your risk of a heart attack?
Maybe, maybe not.
But if that medication only decreased your risk by 1%? Would you still take it?
Many of us wouldn’t.
In fact, more than 99% of people taking statins don’t benefit from them (52).
The Prevalence of the Heart-Diet Hypothesis
The cholesterol and heart disease myth is everywhere.
It has become an area of major emphasis in just about every health recommendation. In fact, one of the first health decisions that people often make is to try and lower their cholesterol by lowering fat intake.
With how prevalent this theory is, you would honestly expect the support for it to be iron-clad. But, as I’ve already shown, it really isn’t.
Instead, there are a few key factors that play a role in why the emphasis on cholesterol is so strong.
The Role of Industry
One of the key aspects of the heart-diet hypothesis is that we need to significantly lower our levels of cholesterol in order to decrease the risk of heart disease.
This led to cholesterol becoming a key compound of concern.
Because of this, there was a huge emphasis on finding ways to decrease cholesterol – and there has been a strong focus on medications to fill this role.
Statins were a critical outcome of this emphasis and they are some of the most heavily prescribed drugs in the United States. They are also drugs associated with the most money.
For example, in 2010, the $7.2 billion was spent on the statin Lipitor, more than any other drug. A second statin drug, Crestor, was also on the list of top ten best-selling drugs, coming in at $3.8 billion (53).
This means that there is a huge amount of money involved in drugs.
In turn, this means that there is a very powerful industry out there that does not want statin use to decrease.
That industry has the ability to lobby the government and to place pressure in various subtle ways. This includes paying doctors to promote statins – a practice that is already common.
Companies in the industry also have the ability to fund scientific research into the effects of their own drugs.
Indeed, you will often find that studies into cholesterol or statins are frequently funded by companies involved in the industry (such as this one).
That brings me to one final point about the industry (or big pharma, as it is often called).
Scientific research presents the results of research rather than the actual data.
This is the case with all scientific research and it isn’t a problem as such. The issue is that this means that research can be biased – especially when the researchers do have a particular perspective that they want to prove.
Often, there is also a degree of picking and choosing which data is included and which data isn’t. Likewise, researchers have the option of simply not publishing research that differs from what they want to present.
There are other approaches that can be taken too, such as using a sample population that is less likely to have side effects or only including people who aren’t on medications. Both of those are completely unrealistic because the general population that relies on statin drugs will often have multiple health issues and be taking a number of different drugs.
Those patterns don’t tend to be too common among people doing pure scientific research, but pharmaceutical companies are a bit different.
After all, they have a strong financial incentive to make their drugs look as good as possible.
The truth is that unless the research data is subpoenaed from drug companies, no one really knows the risks associated with statins – which is a pretty concerning factor.
So, not only does the industry have every incentive to keep people using statins and to keep the emphasis strongly on lowering cholesterol, they also may be misleading people about the risk profiles of their medications.
Bad Science Meets Politics
Science is an area of continual change and development.
We often find that early research says one thing while later research ends up proving a completely different perspective.
Not only is this common – but it’s actually one of the main purposes of science.
We want to have accurate knowledge and that means constantly challenging old ideas.
When it comes to pure science, bad science tends to get refuted relatively quickly. Sometimes there are cases of egos and people being stubborn, but generally speaking, the bad science just doesn’t stick around.
But we aren’t talking about pure science.
The heart-diet impact has had major impacts in the public arena. The research has defined policy and dietary advice while also forming the basis of a key portion of the education that medical professionals receive.
At the same time, there is a lot of industry and business that has stakes in this particular piece of science.
All of these factors mean that suddenly there is a lot of time and money invested into the idea that cholesterol and saturated fats are harmful.
In fact, many modern dietary recommendations are based around this idea.
So, you can see why there is a lot of resistance to any change.
Can you imagine the government coming out and saying it was wrong? What about the media?
A lot of the argument for keeping to the concepts of cholesterol and heart disease comes from the fact that we can’t conclusively prove that the theory isn’t true.
For example, there are so many different factors to consider and try to control for in any health and diet research. This does make it extremely difficult to figure out what impact cholesterol and saturated fat is having and isn’t having.
At the same time, the cholesterol idea is so heavily ingrained in our society that some people would consider an experimental study to be unethical, based on the idea that it would be putting people at unnecessary risk for heart disease.
Yes, it really is difficult to do that kind of research – but it is possible.
Here’s the thing though… science is supposed to work the other way around.
The aim should be to prove that cholesterol does affect heart disease risk, rather than disprove it.
The Inflammatory Hypothesis
Science is all about theories.
With all the complexities in the human body, there is so much that we don’t know about the reactions that occur and how they relate to one another.
Even when we create effective medications, we often don’t fully understand how those work in the body or the precise mechanisms that they are involved in.
This means that over time hypotheses continued to get refined and tweaked – and in some cases discarded altogether – as more research comes in.
As I mentioned before, this process has been pretty strongly subverted in the case of cholesterol, but there are still some people who do research alternative theories. Perhaps the most powerful alternative hypothesis about the potential causes of heart disease is the inflammatory perspective.
Inflammation is a biological response to injury and is a very important process for ensuring that a person remains healthy.
In the short-term, inflammation really can perform an important function and performs it well.
However, when inflammation starts to become chronic and long-term, it can cause some serious issues in the body. For example, health issues like cancer (54), metabolic disease (55), chronic lung disease (56) and Alzheimer’s disease (57) have all been associated with inflammation, and there are many others that I haven’t mentioned here.
This is an area that has considerable potential, even though it has not been researched anywhere near as extensively as cholesterol.
Statins and Inflammation
Now here’s something interesting.
The general purpose of statins is to lower heart disease risk by lowering LDL cholesterol.
This has the interesting effect of meaning that any success with statins is used as evidence that the original heart-diet hypothesis was correct.
That might be true if lowering cholesterol was the only impact that statins have in the body.
However, medication doesn’t work like that.
Instead, there tend to be all sorts of flow on effects and unrelated effects because of a medication.
This means that any positive effects of statins could be because of that anti-inflammatory action, rather than because of cholesterol at all.
Things like this make research even more challenging.
Anyone who supports the heart-diet hypothesis is going to take any positive outcomes of statins as evidence that the hypothesis is correct.
That isn’t accurate though.
It is certainly possible for statins to have some positive impacts even if cholesterol doesn’t have much of an impact on heart disease risk.
Other Risk Factors
The whole point of recommendations against cholesterol and saturated fat is about heart disease, even though current research suggests that there is not enough evidence for many of the recommendations that are made (63).
As I’ve shown, the evidence for cholesterol increasing heart disease risk isn’t all that great and even statins don’t seem to do a whole lot of good.
Here’s the other thing.
By focusing on cholesterol, we almost completely ignore other risk factors for heart disease, including risk factors that are much more significant.
For example, one major study looked at heart disease across 52 different countries and 15,152 cases. The authors of the study found the following nine factors to be highly significant for contributing to the development of heart disease (64).
- Abnormal lipids ratio (specifically ApoB/apoA1)
- History of hypertension (high blood pressure)
- Abdominal obesity
- Psychosocial factors
- Drinking alcohol regularly
- Not eating fruit and vegetables daily
- Not engaging in regular activity
Collectively, those nine risk factors accounted for 90% of the risk for males and 94% for females (65).
That’s most of the risk right there.
You’ll notice that cholesterol isn’t even on the list.
Regardless of whether or not cholesterol contributes to heart disease – it’s very clear that we are overemphasizing cholesterol and ignoring many other risk factors for heart disease.
The Challenges of Research
Research into health conditions is always a difficult task.
One of the key ideas is to figure out what is causing health issues in the human body and then work out approaches for resolving those issues. Often this will involve designing drugs, like statins, to combat the issue.
In many cases, we don’t know the mechanism behind the health issue.
For heart disease, we know that plaques form, but the mechanism behind this is less clear. Both the cholesterol and heart disease myth and the inflammation hypothesis suggest different types of mechanisms.
Not knowing the exact mechanism is one factor that makes research into heart disease difficult.
Another factor is that designing effective research can be challenging and expensive.
For example, a good study needs to have a large enough sample size to make its results relevant to the population. This is why many studies into cholesterol and heart disease are observational in nature.
Observational studies are a cost-effective way of looking at trends in a large number of people. In many cases, the researcher doesn’t even have to obtain the data themselves, as the dataset may have been gathered for another purpose.
While these studies are a wealth of information, they can’t actually show whether one thing causes another.
That’s where experimental studies come in.
Large-scale studies have been carried out in relation to statins and heart disease and in relation to cholesterol and heart disease. These studies face their own challenges.
One major issue is the difficulty in filtering out all the different variables. There are just so many different things that can influence the observed outcome, even in an experimental study.
This is especially true for statins because there is such a strong connection between medication and lifestyle.
That pattern means that statins may indirectly compromise the health of people taking them.
The complexity of research into this field can also be seen in dietary interventions.
One approach for looking at the significance of cholesterol and fat in the diet on heart disease risk is an intervention that dramatically decreases their prevalence.
But, diets don’t really work like that.
You can’t just cut down a type of nutrient and see what impact that has.
Cutting down (or cutting out) any type of nutrient results in a shift of the person’s entire diet.
So, if you decreased saturated fats, you would probably increase consumption of unsaturated fats – that sort of thing.
That makes it impossible to tell what caused any observed impacts.
This makes it that much more difficult to work out what patterns are occurring and what really influences heart disease risk.
There is one more challenge with research.
If everything else was equal, you would expect scientific research to focus on the areas that showed the most promise. For example, the Mediterranean diet has been associated with significant reductions in the risk of heart disease (68,69).
It would be interesting to find out what it is about this diet that is so powerful and whether there are other diets with similar impacts. After all, research does suggest that dietary patterns can play a role in heart disease risk (70).
The catch is that research costs.
Companies that produce drugs often have a lot of money to throw at research to make sure their topic is studied in depth. That isn’t true for areas like diet or supplements.
Instead, you find that there are some studies, but many of these may be lacking in size and in scope. This makes it that much harder to find evidence about alternative causes of heart disease.
Additionally, research into statins tends to fall into two main types.
One type is the research conducted by drug companies. These companies do have a lot of funding and financial backing, but at the same point, they also have a pretty strong reason for wanting the results to be positive. As I mentioned earlier, that can lead to pretty substantial bias.
The other key type of research is research done outside of the large drug companies.
There can be many forms of this research, but it is often constricted to some degree or another by a limited amount of finances.
Additionally, these researchers don’t have access to the data that the drug companies found, only their outcomes (71).
That’s another pretty major limitation and it makes it difficult to find accurate results about statins and their overall impacts.
The rhetoric surrounding cholesterol simply isn’t supported by science – even though it tends to be presented as fact.
There is some good news though.
While slow, political changes do happen, and that’s what is occurring with this whole cholesterol discussion.
Every five years, a new set of dietary guidelines is released, based on modern research.
The next set of guidelines is due to be released this year.
These guidelines are huge because they influence much of the advice that people receive.
For example, the food pyramid (and the modern MyPlate) is based directly on the guidelines.
The guidelines also have implications for the ways that companies can advertise and what children receive as parts of school lunches (72).
While the guidelines themselves have not been released yet, there is information available on the discussions surrounding these guidelines. One particularly interesting piece of information is this here:
That quote comes from the most recent meeting on the developing guidelines (73).
Until the guidelines actually come out, there is no way to know for certain.
Regardless, the quote is a strong indication that opinion is slowly starting to change about cholesterol.
Another indication is Time Magazine.
Time played a large role in the original cholesterol myth, based on their early articles on cholesterol and heart disease. However, Time has actually retracted that perspective and is instead saying that it is time to end the war on fat (74).
The perspective of that issue is on fat, not cholesterol itself, but it is still a step in the right direction.
At the same time though, not everyone agrees.
Instead, some reports and articles suggest one perspective, while others suggest another. This is pretty confusing for members of society, who are likely to be confused by all the different pieces of advice.
There is Still a Long Way to Go
The cholesterol and heart disease myth has become a significant part of political discourse, media reporting and public consciousness.
Even though there is a growing recognition that these are not the enemy that we have assumed, many of the old points of view remain.
The proposed change in dietary guidelines is a good example of this.
Even if cholesterol is removed as a nutrient of concern, it is clear that other elements of this perspective are going to remain in place.
This includes the presence of high levels of LDL cholesterol in the blood and having too many servings of food containing high amounts of saturated fats (75).
At the same time, a lot of the rhetoric is probably still going to focus on cholesterol.
After all, most physicians were taught extensively about cholesterol as part of their medical training. Likewise, the media has a bad habit of picking and choosing which information to emphasize. It’s easy to imagine that the focus on changes in the perspectives of cholesterol will be minimal.
If you want an example of this, just consider that Time issue on how fat is not the enemy. That issue came out in June 2014 – yet most people probably never even heard about it.
Like anything that is ingrained in public consciousness, perspectives on cholesterol and saturated fat are going to take a long time to change.
Where to From Here?
When it comes down to it, research is controversial and contradictory on most topics, especially when it comes to nutrition.
The simple truth of the matter is that our human bodies are complex systems and they are influenced by a large number of things. We are not aware of all of those factors and we certainly can’t control for all of them.
Heart disease is a complex health issue, and many different factors contribute to its development. Regardless of how much research is done – there is a good chance that we will never fully understand the disease.
I’ve covered a lot of ground in this discussion, but to be honest, the topic is so in-depth that it would be hard to cover entirely in a book.
Modern society has placed this huge emphasis on cholesterol, even though there isn’t all that much research to suggest that decreasing cholesterol will decrease heart disease risk. At the same time, so many people are taking statins regularly to lower their cholesterol even further – often without knowing the risks of the medication.
Cholesterol may well be a risk factor for heart disease (particularly sdLDL), but we still really don’t know. Research is still going on, and much of the early research didn’t focus on the different cholesterol types or the implications of how LDL levels were measured.
Nevertheless – there certainly isn’t the evidence to support the modern demonization of cholesterol and saturated fat.
For most of the population, lowering cholesterol may not be the answer for protecting against heart disease.
Instead, it may be that a more integrative approach is needed.
After all, factors like exercising regularly, staying at a healthy weight, eating fruits and vegetables and being healthy overall are all important. These factors may end up having a much stronger impact on heart disease risk than cholesterol ever could.
Even so, cholesterol and statins will probably be promoted for quite some time. Statins are a major money making drug and any change in rhetoric about cholesterol is going to take time.
At the same time, we simply do not know the best ways to reduce heart disease risk.
Clearly, there is much more research needed.
But what we do know is that cholesterol and saturated fat is not the villain that we thought it was.
We also know that there are many financial interests at play with the current recommendations about limiting cholesterol. This is a major issue, and it is something that we should be aware of and concerned about.
Those financial interests can result in bias during research and also in the way that results are shared and promoted.
The debate around cholesterol, statins and heart disease is huge. In this post I’ve outlined the controversy and the science behind it – showing that the evidence for statins is nowhere near as strong as you or I have been led to believe.
There are many more studies about this topic, both for and against the role of cholesterol in heart disease as well as the use of statins themselves.
With more coming out regularly, it isn’t possible to cover all of these studies in a single discussion.
But if you have to take home a single message from this discussion, remember this: Take the time to be critical about what doctors and the media tell you. They don’t always pay all that much attention to the science.
After all, the evidence that cholesterol has anything at all to do with heart disease is incredibly slim. And that’s the opposite of what we have been taught for so long.