Exploring Dietary Cholesterol and Blood Cholesterol: Unveiling the Connection

Cholesterol often rings alarm bells, commonly linked to cardiovascular diseases. For decades, a cloud of concern has hovered over dietary cholesterol, believed to directly impact blood cholesterol levels, paving a perilous path toward heart ailments. However, is this belief rooted in reality or merely a nutritional myth?

This article delves into the longstanding debate surrounding dietary cholesterol and its real influence on blood cholesterol. Unveiling the intricacies of cholesterol, from the foods we eat to the bloodstream, this piece will navigate through scientific insights, demystifying whether the cholesterol on your plate is a friend or foe to your heart’s health.

What Is Cholesterol?

Let’s start at the beginning.  Biochemically, cholesterol is a sterol compound found in most body tissues.  Your body needs some cholesterol to function. 

Cholesterol is a waxy substance that serves as a precursor to various compounds your body needs to survive and thrive.

What Are the Roles of Cholesterol in the Body?

Cholesterol is involved in numerous bodily processes, making it vital for human survival.  For example:

  • Cholesterol is a precursor for synthesising sex hormones like estrogen, progesterone, testosterone, and corticosteroids like cortisol.   
  • Cholesterol is required to produce vitamin D, a prohormone we get from sunlight exposure.
  • Because of its role as a hormone precursor, we need cholesterol for muscle protein synthesis (testosterone), fertility (male and female hormones), regulated menstrual cycles (female hormones), cognition, and energy production (cortisol).  Some studies have even linked higher intakes of cholesterol with increased muscle gain.
  • We require cholesterol to make bile acids, which help you break down and absorb dietary fat.  Bile also serves as a necessary antimicrobial, and it’s the main vessel your body uses to detoxify and eliminate through your poop.
  • Without cholesterol, you would not have cells; cholesterol is required to create oxysterols, which are the building blocks for cell membranes and other fatty human tissues, like the brain and myelin sheath around nerve cells.
  • A healthy immune system also needs cholesterol.  Cholesterol is required for the activation, mobilisation and production of various immune cells and thus plays a role in immunity.  In this sense, it seems to also play a role in wound healing.
  • The most surprising inclusion on cholesterol’s resume is its ability to function as an antioxidant.  We require cholesterol to heal and protect the body from free radicals.  Hence, cholesterol helps keep our bodies safe from oxidative stress.

Is Cholesterol an ‘Essential Nutrient’?

While the cholesterol in your food and the cholesterol in your body have the same molecular structure, we don’t have to consume high-cholesterol foods to get what we need.  Cholesterol is so critical to your body that it makes plenty of it.   Hence, cholesterol is considered a non-essential nutrient

We synthesise around 85-90% of our cholesterol needs, whether we eat foods that contain cholesterol or not.  So, while we get some cholesterol from food, it’s minimal compared to the cholesterol made by your liver.  

Cholesterol in your diet will help your body to get what it needs.  However, cholesterol is one of the many nutrients that you need.  So, there’s no need to go out of your way to consume more of it, especially if you end up sacrificing the other essential nutrients. 

Why Did We Fear Cholesterol?

High blood cholesterol has been a significant concern since Dwight D Eisenhower’s heart attack in 1955.  This prompted researchers to start digging into—what they believed to be—the root cause of heart disease, which at the time was one of the top killers in the western world. 

Experts performed autopsies and examinations of arterial build-up and found a build-up of cholesterol within these sclerotic plaques.  They formed the view that dietary cholesterol influenced blood cholesterol and hence contributed to heart attacks and stroke.

Building on this assumption, subsequent research showed the deleterious effects of cholesterol.  Researchers like Ancel Keys drew attention to his 1958 Seven Countries Study, which showed the correlation between fat intake and deaths from cardiovascular disease in seven countries.

This study has influenced modern nutrition guidelines and public policies for years to come.  This avoidance of cholesterol was eventually incorporated into the 1977 Dietary Goals for Americans that recommended people minimise their intake of saturated fat and cholesterol

As shown in the ship below from the 1977 Dietary Goals for Americans, the recommendation for the next 38 years was to limit cholesterol to less than 350 mg per day.  For reference, in 1977, the average dietary cholesterol intake was 500 mg/day.

However, after further investigation, it was found that Keys had analysed 22 countries.  However, they did not fit the ‘cholesterol is bad’ narrative and were removed from his analysis.  It was too late, though.  Keys had already made a lasting impact on our government and nutrition guidelines.

Additionally, ‘Blue Zones’, or regions of the world with a high percentage of centenarians, were highlighted to consume very low-cholesterol diets.  Today, we know the blue zone foundation has been influenced by the Seventh Day Adventist (SDA) church, which even includes their Loma Linda community in California.  

The SDAs strongly oppose cholesterol-rich animal products.  So, it’s likely that starting from the belief that plant-based foods are good and animal products are bad has influenced nutrition research, including much of the thinking around cholesterol. 

If you want to learn more about the SDA church’s significant influence on nutrition guidelines, check out The Perils of Belief-Based Nutrition.

The Perils of Avoiding “Bad Things” in Food

The snip from below the 1977 Dietary Goals for Americans shows their understanding at the time of the major contributors to heart disease. 

At the top of the list is eating too much and not exercising enough which leads to being overweight.  In retrospect, it might have been better if they just stopped there and focussed on the properties of food that lead us to eat more and less than we need (i.e. satiety). 

However, at the time, elevated cholesterol was believed to drive a higher risk of heart disease due to:

  • high cholesterol consumption,
  • high saturated fat consumption,
  • high total fat consumption, and
  • a low polyunsaturated fat:saturated fat ratio. 

In line with this advice, saturated fat has decreased while monounsaturated fat and polyunsaturated fat have increased, mainly from industrial seed oil use.   However, despite compliance with the dietary guidelines (or perhaps because of it), obesity rates have powered onward and upwards. 

For more, check out:

Does Dietary Cholesterol Equal High Blood Cholesterol?

In 2019, The Hellenic National Nutrition and Health Survey (HNNHS) wanted to study the effects of egg intake on blood cholesterol levels.  Researchers administered participants a high-cholesterol, egg-rich diet and analysed their blood lipids. 

To their surprise, they not only saw blood cholesterol levels remain unaffected when someone’s consumption of high-cholesterol eggs increased, but they saw it decrease in some instances.  The researchers pointed out that it might’ve been from a well-balanced, nutrient-dense diet that did not provide excess energy.

Again, it’s important to note that we synthesise 85-90% of our cholesterol needs endogenously, whether we consume it from food or not.  High cholesterol is often a result of errors of inborn metabolism from other factors, which we discuss below.

What Does the Body Do with Cholesterol?

It can be hard to understand how something may be bad for us if we don’t know how it functions.  So, let’s dive into how cholesterol is absorbed and synthesised and how plaques form. 

This section is a little dense!  However, it’s necessary to understand what cholesterol is really doing. 

For starters, dietary fat is broken down into long-chain (LCFA), medium-chain (MCFA), and short-chain fatty acids (SCFA) and then absorbed and bound to proteins in the small intestine.  SCFAs and MCFAs go right to the liver.

LCFAs take a different route, as they are too big to fit through your small blood vessels.  Thus, they are reassembled as triglycerides and packaged into chylomicrons, which are absorbed via the lymphatic system. 

Eventually, these chylomicrons make it into circulation.  As they make their way through the body, an enzyme known as lipoprotein lipase (LPL) that sits within your blood vessels begins absorbing fatty acids from these triglycerides so they can be absorbed via tissues. 

As more and more of these fatty acids are taken up, the original triglyceride begins to shrink as they offload the energy to be used by your heart and muscles.  Eventually, all the fatty acids are absorbed, and the remaining chylomicron returns to the liver as what is known as a chylomicron remnant.

At the same time, your body is making cholesterol using acetyl-coenzyme A and an enzyme known as B-Hydroxy B-methylglutaryl-CoA, or HMG-CoA.  Cholesterol-lower drugs like statins work by inhibiting this enzyme.

Those chylomicron remnants we mentioned earlier are then deconstructed and reassembled in the liver as low-density lipoproteins (VLDL), so they can once again be shuttled around to various tissues for use.  Here, the cholesterol your body created also joins in to be distributed.

VLDL is a transport molecule that carries cholesterol, phospholipids, protein, and triglyceride throughout the body.  You can think of it as a delivery truck.  By mass, VLDL is mostly of triglycerides. 

As VLDL circulates throughout the body, the same LPL starts to accept VLDL’s ‘deliveries’ (i.e., triglycerides) by absorbing them.  Thus, its overall triglyceride content decreases, reducing VLDL to intermediate-density lipase (IDL).

As a result, the particle size shrinks, but its percentage of cholesterol increases.  This continues, and IDL will eventually become low-density lipoprotein (LDL), or the ‘bad cholesterol’ we have come to fear because it’s predominantly cholesterol by mass.  This illustration might help you visualise how the composition of the particles of fat change as they drop off their energy cargo around your body.

Eventually, LDL circulates throughout the body until it’s taken up by LDL Receptors (LDLR) in the cells.  Here, it’s used to synthesise some of the many materials our bodies require cholesterol for.  LDL contains a protein known as apolipoprotein B-100 (ApoB), which is recognised by LDL receptors and tells LDLR to ‘let me into the cell!’.

In a healthy person, LDL works on a negative feedback loop.  So, when blood levels of LDL are low, the body produces more.  In contrast, someone will downregulate their production of LDL when too much LDL is in the bloodstream until receptors on the cells catch up.

Once cholesterol has been used for whatever bodily process it was needed for, the LDL is transported back to the liver.  Here, free cholesterol is converted into bile acids and removed via bile, which is released when you eat a fatty meal.

It’s interesting to know that the small intestine can also efflux cholesterol.  Here, cholesterol enters the enterocyte via the LDL receptor, releasing it into the intestinal lumen.  This account for nearly 45% of faecal cholesterol excretion.  This will be important later on.

How Does Cholesterol Play a Role in Arterial Plaques?

When too much LDL circulates in the bloodstream for too long—you essentially have ‘high’ cholesterol—we can see problems.  However, it is not simply because there is too much cholesterol; cholesterol is often an innocent bystander that’s ‘caught in the crosshairs’ and at the ‘wrong place at the wrong time’.

Your immune system is constantly on the prowl for things that shouldn’t be in the body (i.e., antigens).  If you have high blood cholesterol, excessive amounts of LDL accumulate in places they shouldn’t.  Thus, this extra cholesterol is prone to oxidation if your immune system stumbles upon it.

In this instance, white blood cells see cholesterol as an antigen, which they are programmed to oxidise, kill, and destroy.  White blood cells then engulf this oxidised cholesterol, leading to the formation of foam cells. 

Over time, layers and layers of oxidised cholesterol accumulate into fatty streaks.  These fatty streaks lead to lesions that make up sclerotic plaques, block arteries and contribute to heart attacks.

As time goes on, these immune cells release inflammatory compounds like IL-6, tumour necrosis factor-alpha (TNF-a), and reactive oxidant species (ROS), cumulatively creating even more inflammation within your blood vessels.  It also propagates a steady state of immune activation, which further catalyses the state of your condition.

Dysfunctional blood vessels and circulation (i.e., endothelial dysfunction) from other pre-existing conditions, like chronic inflammation, hypertension, diabetes, or obesity, can create even more oxidative stress.  

The main risk of high blood cholesterol occurs when we simultaneously have high levels of LDL (predominantly cholesterol) and high levels of blood glucose.  This leads to oxidised LDL, which leads to the build-up of plaque in the blood vessels.  To avoid dangerous cholesterol becoming dangerous, you must also keep your blood glucose and blood fats down by maintaining a healthy body weight. 

The fundamental problem is not cholesterol but rather energy toxicity.  The bottom line is that you don’t want to have high levels of energy floating around in your bloodstream, particularly from both fat and glucose at the same time.  For more details on this, see Cholesterol: When to Worry and What to Do About It.

What Causes High Cholesterol?

While many people point to high intakes of dietary cholesterol as the root cause of elevated blood cholesterol, there are many other factors that can cause it to increase as highlighted below.   

  • Being overweight and overfed is perhaps one of the biggest factors influencing high cholesterol levels.  Someone who is obese or overfat has more fat tissue in their body, meaning there are more circulating free fatty acids.  The same could be said for high circulating triglycerides and blood sugar.  Again, eating for satiety and being active to keep your body weight in a healthy range is the number one thing you can do to manage your blood glucose and cholesterol levels.   
  • Hypothyroidism can drive high cholesterol as it slows metabolism.  This reduces the rate at which cholesterol is broken down, leading to lots of it floating throughout the body.
  • The health of your microbiome, or your gut health, is also important for cholesterol metabolism.  When your gut microbiome is imbalanced, certain bacteria can inhibit cholesterol elimination via the intestines, meaning you excrete less cholesterol.  Your microbiome and all the bacteria that make it up also play a role in bile acid metabolism.  Many strains of bacteria in the human GI tract can alter bile acid conjugation, which can allow them to be reabsorbed.
  • Someone with gallbladder disease, gallstones, or liver disease may experience imbalanced cholesterol levels, as they impair bile flow.  Bile is the elimination route of cholesterol, meaning any disruption in its function can contribute to high cholesterol levels.
  • Our bodies are incredibly efficient at recycling bile because it is such a labour-intensive material to make.  Thus, irregular elimination can contribute to high cholesterol levels because bile is excreted through the colon and into the toilets.   
  • Furthermore, if you’re consuming inadequate fibre, wastes released in your bile—including cholesterol—do not have a medium to bind to.  Going back to the idea that your body is excellent at recycling bile, it’s once again reabsorbed.  Fibre also gives your stools bulk, which keeps you regular.  Similar to cholesterol, fibre is not an essential nutrient.  However, a nutrient-dense, minimally processed diet tends to contain plenty of fibre.   For more detail, see Dietary Fiber: How Much Do You Need?
  • Chronic exposure to environmental toxins can contribute to dyslipidaemia.  Studies on various chemicals, compounds, constituents, and pollutants have been shown to alter cholesterol metabolism.  A few examples are heavy metals, mould, and plastic metabolites.
  • Methylation, or the addition of a methyl group (CH4) to a molecule, is a bodily process required to detoxify and synthesise many substances.  Hence, poor methylation—which often results from nutrient deficiency—has been linked to abnormal blood lipid levels.  Additionally, inadequate intakes of nutrients that serve as precursors to bile can impair the route by which we eliminate cholesterol.
  • Chronic stress levels also increase cholesterol levels, along with triglycerides, blood pressure, and blood sugar.  It has also been shown to increase the risk of someone developing Type-2 Diabetes, cardiovascular disease, and other lipid disorders.  This may be because stress increases our demand for the cholesterol-derived hormone cortisol.  Hence, your body needs more cholesterol to produce cortisol to respond to stress.   
  • Finally, dietary cholesterol can raise blood cholesterol; about 10-15% of our cholesterol levels come from diet.  But whether it be dietary cholesterol or the cholesterol your body produces, having some of this compound isn’t necessarily mean it’s a bad thing.  We NEED cholesterol for many biological processes, and lower cholesterol levels have been associated with adverse health outcomes.  As shown in the charts below, low cholesterol is likely more of a concern than high cholesterol levels!   

The Fuel You Give Your Body Influences the Energy in Your Blood

Elevated cholesterol is a popular area of interest in people following a lower-carb or keto diet, with many people finding they have cholesterol above the ‘normal’ range.  But it makes sense that the balance of fat and glucose in your blood is significantly influenced by the fuel you give your body.   

Why Was Cholesterol Deemed to No Longer Be a Nutrient of Concern in 2015? 

In 2015, it was concluded from extensive research that dietary cholesterol did not play a role in the development of cardiovascular disease.  Thus, the recommended limit of 300 mg/day of cholesterol was removed from the 2015-2020 Dietary Guidelines for Americans.  Extensive research has shown no evidence to support the role of dietary cholesterol in the development of cardiovascular disease. 

Foods That Contain More Cholesterol

Cholesterol tends to be found in:

  • Meat
  • Dairy
  • Poultry
  • Seafood

There are no plant foods that provide cholesterol.

Could a Low-Cholesterol Diet Do More Harm Than Good?

Because cholesterol is found in higher-protein nutrient-dense foods like meat, poultry products, dairy, and some seafood, actively avoiding cholesterol may hurt your health. 

While this might seem confusing, let me explain.

Protein and the amino acids that makeup protein are the most satiating nutrients.  In other words, we will continue to eat until we get enough protein.  If you’ve followed the Optimising Nutrition blog for some time, you’ve probably heard this before!  If not, check out our article on the Protein Leverage Hypothesis

Our analysis has shown that the recommended daily intake for protein aligns with the highest calorie intake, and eating more of our calories from protein aligned with a substantial fall in energy consumption.  Hence, avoiding high-protein foods because they happen to contain cholesterol might not be the best for satiety.

Aside from protein, nutrient-dense, higher protein foods also contain clusters of other essential nutrients, like niacin, potassium, selenium, B vitamins, calcium, iron, zinc, copper, selenium, and more. 

Like protein, if we aren’t getting adequate amounts of these nutrients, we’re likely to eat more and more as our body tries to get us the raw ingredients it needs to function.  For more on this, see:

Keep in mind that animal foods provide us with all the amino acids in one place, so they are not equal to plant proteins.  So, when we avoid dietary cholesterol, not only are we missing out on easy ways to get protein, but we are also limiting the amount of other satiating micronutrients we’re taking in.

Many of these nutrients are also critical for driving metabolic processes like methylation, which we know has a role in regulating cholesterol levels.  Hence, consuming fewer foods that contain them might not be optimal.

Additionally, when we limit cholesterol and, therefore, protein, we are left with carbs and fat.  This diabolical combination is tasty and delicious—thus, low-satiety—making it easy to overconsume.  As shown in the chart below, we tend to consume a lot more energy when our diet is mainly energy from fat and non-fibre carbs with less protein and fibre. 

Altogether, we’re more prone to overeat and increase our chances of winding up with metabolic syndrome, diabetes, or obesity when we avoid cholesterol-containing foods, at least from a satiety and nutrient-density perspective.  For more on this, see Carbs OR Fat vs Carbs AND Fat.

Satiety Response to Cholesterol        

Interestingly, as shown in the following chart, our satiety analysis has also shown that foods containing more cholesterol per calorie tend to be more satiating.  We tend to consume 39% fewer calories when consuming a diet with more cholesterol per calorie.   Towards the left of the chart below, we can see that the previously recommended cholesterol intake of less than 500 mg/day aligns with the highest overall calorie intake.  For reference, the average cholesterol intake of our Optimisers is 650 mg/day, while the 85th percentile intake is 1.1 g/day. 

This next chart, created from data from the USDA Economic Research Service, shows how the cholesterol has declined in our food system since the 1950s when we started to ramp up industrial agriculture, powered by the increasing use of chemical fertilisers.  This change started two decades before the 1977 Dietary Goals admonished us to reduce cholesterol and conveniently reinforced this trend. 

Interestingly, the decrease in cholesterol in our food system, along with other nutrients like sodium, calcium, potassium and vitamin A, is highly correlated with the increase in obesity rates over the past half-century.  For more details, see How the Biggest Trends in Nutrition Influence How We Currently Eat

Multivariate Analysis of Cholesterol and Satiety

While it’s interesting to consider single nutrients, it’s more useful to consider how nutrients behave as part of the complete food matrix. 

Multivariate regression analysis enables us to understand which nutrients have the most statistically significant effect on how much we eat when all the nutrients are considered together. 

The table below shows the results of our multivariate regression analysis of 136,514 days of data from more than forty thousand people who have used Nutrient Optimiser when we don’t consider cholesterol. 

We see that protein has the most dominant impact on satiety, and moving from low (19%) to high (44%) protein aligns with a 30% reduction in calories.  However, other nutrients like fibre, calcium, potassium and sodium also factor into the satiety equation. 

 nutrient 15th85thcalories%
protein (%)19%44%-452-30%
fibre (g/2000 cal)1144-87-5.7%
calcium (mg/2000 cal)4701909-68-4.5%
potassium (mg/2000 cal)18916043-57-3.7%
sodium (mg/2000 cal)14885179-47-3.1%
total-46.7%

Things get more interesting when we consider cholesterol, which appears to have a large independent impact on satiety.  People who consume 1.1 g/2000 calories of cholesterol tend to consume 12% fewer calories than those who consume 0.24 g/2000 calories of cholesterol!   

nutrient 15th 85th Calories%
protein (%)19%44%-364-20.5%
cholesterol2411137-214-12.1%
fibre1144-153-8.6%
potassium19315915-97-5.5%
sodium14805076-95-5.4%
calcium4691869-67-3.8%
total   -55.8%

It’s also worth noting that the satiety impact of protein falls from 30% to 20% when we also consider cholesterol, suggesting that a large part of the ‘protein leverage’ is actually due to cholesterol (as well as some other essential nutrients).   It appears that we may crave dietary cholesterol independent of protein. 

The multivariate regression analysis also enables us to estimate the total calories that would be consumed from various foods if that’s all we had to eat.  The chart below compares the estimated calorie intake with and without cholesterol.  You can click here to dive into the interactive Tableau version of this chart

Overall, there is a similar trend with and without cholesterol.  However, high-cholesterol foods like sausage, calamari, eggs, pate and butter (on the upper side of the trend line) tend to be viewed more favourably and would lead to a lower calorie intake.

Because cholesterol is still controversial and data is not always available for the cholesterol content of foods, we’ve elected not to include cholesterol in our default satiety calculations.  However, this analysis shows that we should not avoid nutrient dense that happens to cholesterol. 

How Can I Reduce My Cholesterol?

Aside from cholesterol-lowering drugs, reducing dietary cholesterol is one of the most common approaches to lowering blood lipids.  However, it may do the opposite. 

Recent studies have shown an inverse correlation between eating less cholesterol and blood cholesterol levels.  In other words, blood lipids increased when dietary cholesterol decreased!

The likely explanation for this is that avoiding cholesterol leads us to increase our intake of processed foods (that are usually some combination of starch, sugar and industrial seed oils).  This leads to obesity, energy toxicity and increased cholesterol in the blood.

Remember that dietary cholesterol only accounts for 10-15% of our blood cholesterol levels.  Thus, we must look at some of the other factors that could be contributing to higher levels.  These are summarised below.

  1. Begin reducing your body weight.  Excess body fat can contribute to high cholesterol levels, as more energy is circulating throughout the body than it needs.  However, while most people try to eat less of the same foods, it’s critical to change what you eat to ensure you get the nutrients your body is craving so it will be satisfied with less energy. 
  2. Avoid low-satiety processed foods that quickly overfill your carb and fat fuel tanks and make you gain weight quickly.
  3. Eat a nutrient-dense diet full of high-protein foods, even if they contain cholesterol.  Protein provides you with satiety, and a lot of nutrients tend to accompany protein when it’s found in whole foods like meat, eggs, fish, and dairy.  Additionally, nutrients in food drive your metabolism, which can help your body efficiently process and eliminate things like cholesterol.
  4. Consume lots of fibre from whole foods like low-energy-density, nutrient-rich vegetables.  Fibre will help keep you regular.  It also binds to the bile acids released during digestion so they can make their way out of the body.
  5. Build muscle mass through resistance and strength training, as it improves energy utilisation via increased metabolism.
  6. Eat when you’re hungry, not when you’re bored!

What are Normal Ranges of Dietary Cholesterol?

Since it was removed as a nutrient of concern in the 2015-2020 Dietary Guidelines for Americans, there is no target intake for cholesterol.   

Because our analysis has shown that consuming more cholesterol tends to coincide with a lower calorie intake, we wanted to look at cholesterol consumption among our Optimisers. 

Although we haven’t set an Optimal Nutrient Intake target for cholesterol, the table below shows intake ranges of this inessential nutrient for different daily calorie intakes based on our Optimiser data.  Here, ‘low’ intakes are considered the 15th percentile intake, ‘medium’ intakes are the average, and ‘high’ refers to the 85th percentile intake.

CaloriesLow (mg)Medium (mg)High (mg)
1000120350570
1500170520860
20002306901140
25002908701430
300035010401720

As we explained above and in our Nutrient Cluster Theory Analysis, cholesterol may influence satiety on its own.  However, it is likely that the satiating effects we see from cholesterol may also be in part from the high-satiety nutrients that tend to accompany it in healthy whole foods, like protein, zinc, b vitamins, selenium, and copper.

What Is the Quickest Way to Lower Cholesterol?

Unfortunately, there are no overnight fixes to long-term problems.  There is no kill that will fix the root cause of high cholesterol: energy toxicity.

Simply avoiding high-cholesterol foods might not be the best long-term option, especially from a nutrient-density perspective.  Many foods that contain cholesterol also contain a lot of other high-priority nutrients we need for satiety.

While cholesterol-lowering drugs might be helpful to get your numbers down, they’re often not ideal over the long term as they can impair cholesterol production, which we do need for many bodily processes.  Additionally, they don’t exactly work on the root cause.

Transitioning to a high-satiety, nutrient-dense diet will have you feeling full on fewer meals and fewer calories so you can balance your body weight.  It will also give your body the nutrients to handle cholesterol properly.

Action Steps

If all of this seems overwhelming, you may be interested in our four-week Macros Masterclass, which walks you through dialling up your protein and fibre while dialling back your carbs and fat until you find the right ratio that starts getting you results.  Increasing satiety and nutrient density will help to reduce the excess energy throughout your body, including in your blood. 

Our suite of NutriBooster Recipes is also a great way to start.  These recipes were designed with nutrient density and satiety as a priority so you can get more nutrients for fewer calories.

You might also enjoy our Data-Driven Fasting challenge, which teaches you how to use your glucose as a fuel gauge to guide what you eat and when you eat.  Over time, you will drain the energy you’ve stored on board, which may give you lower blood glucose, triglycerides, and cholesterol levels.

Often, focusing on the most nutrient-dense foods will help you feel satiated and regulate your calorie intake and energy balance over time.  If you’re still in need of some improvement, you might try the following:

  • Investigating your gut health and making interventions when needed.  Because of the role of the entire GI tract in cholesterol absorption and elimination, any imbalance anywhere along this tube could impair cholesterol elimination.
  • Fine-tuning your micronutrient intake to ensure you’re giving your body a balanced amount of ALL the nutrients it needs.  You might check out our Micros Masterclass for some help.

Ultimately, if you look after your body composition by staying as strong, fit and lead as you can manage via satiety and nutrient density, the rest will look after themselves. 

Summary

Cholesterol is, unfortunately, a complex topic and carries a lot of baggage.  But to summarise: 

  • Your body requires some cholesterol.  Most of the cholesterol in your body is made in your liver.
  • While dietary cholesterol has been feared over the years, it has now been removed as a nutrient of concern due to a lack of association with heart disease. 
  • Foods that contain more cholesterol also tend to come with protein and other nutrients your body needs and create greater satiety. 
  • In the end, most of our modern health issues stem back to energy toxicity and being overfat.  If you eat for satiety to get the nutrients your body needs from food and maintain healthy body composition, cholesterol and the other minutia will look after themselves. 

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7 thoughts on “Exploring Dietary Cholesterol and Blood Cholesterol: Unveiling the Connection”

  1. Great stuff again Marty, which is to the greatest extent in line with how i see it all. What you may bring in as an extra argument for not using statins is that they also block the cellular synthesis of proteins involved in the cellular reduction of stress (i.e. ROS). this wel thus increase cellular stress, which is why users develop muscle aching when doing sport.

    • Thanks Peter. Trying to stay in my lane a little wrt offering thoughts on statins – there are so many people with passionate and divergent views. I’m definitely aware they are not without their side effects. Body composition/weight loss/satiety/blood sugar control definitely needs to be a the primary focus rather than managing a marker or symptom of the underlying problem.

  2. A good summary writeup. Thanks!
    I make no claim to expertise on the Lipid Energy Model, but it does seem that the main role of lipids is for energy transport, so cholesterol is more or less along for the ride. Cholesterol appears to have a structural/barrier role and within the framework of that concept I struggle to see an aggressive intent around cholesteroal. To me it make more sense to see cholesterol a bandaid agent trying to patch over the damage done by other reactive agents. So cholesterol could be building up on the artery walls to protect the artery. Like firemen, they go to the scenes of fires. If cholesterol were super volitale then it would not make sense for the body to invest so many processes around this compound.

    • Agreed. Energy toxicity due to a low satiety, nutrient poor diet seems to be the fundamental root cause issue.

  3. Hi Marty, enjoyed your fundamental article as always.

    There was one detail, which you might want to reconsider.
    “LCFAs take a different route, as they are too big to fit through your small blood vessels. Thus, they are reassembled as triglycerides”

    hmnn, you did not mention Free fatty acids FFA, which travel together with albumin. This should be the main fatty fuel made available to cells. So we have a 18 carbon fatty acid molecule (LCFA) and the protein together -still a fraction of nm.

    Not to mention, that if HDL dia is say 10 nm, chylomicron dia is roughly 100nm, including tons of triglycerides. In systemic circulation, it must fit everywhere, doesn’t it?

    What is a fascinating fact, that the cells can utilize both (chylo&VLDL / FFA). Lipase activity is enhanced at adiposity after meal, and elsewhere in-between. There must be an excess of energy available, all the time, and liver picks up the extra somehow, to recycle it in VLDL. And we think that energy excess is only glucose excess…

    Like your point of energy toxicity. Extra glucose is like the last red flag, in a long march towards metabolic imbalance and eventually T2D. Why not try to focus on something else like trigs and FFAs, if Kraft like insulin response is too difficult to measure? I remember your earlier opinion into this.

    JR

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