The Ketogenic Diet and High Cholesterol (The Hyper-Responder’s Ultimate Guide)

Ketogenic Diet High Cholesterol: the Hyper-Responders Ultimate Survival Guide for dealing with super high cholesterol on a LCHF or Keto Diet.

ketogenic diet high cholesterol covers off the most important things you need to know about the ketogenic diet and high cholesterol

20-Jul 2017, by Lee Sandwith

As discussed in my last article, the ketogenic diet may not be for everyone. One of those reasons is cholesterol and, although most people should experience an improved lipid profile whilst following a LCHF diet, it seems to be fairly common for a subset of people to see detrimental results, especially related to LDL.

I am one of those unlucky people and, as a result, I’ve been doing a lot of research on what this is all about. If you’re in the same boat, fear not, things may not be as bad as you think and there are some reassuring things you should understand before you take any further steps.

The rationale behind my desire to write about this stems from a very lengthy, confusing and frustrating experience with various GPs which, until now, has been without conclusion.

To corroborate that my experience is not unique, and to set the tone for the article, please enjoy the words of Dr.Peter Attia, directly ‘borrowed’ from post 1 of 8 in his ‘The Straight Dope On Cholesterol’ series:

“The topic bears an unsettling parallel reality to nutrition science in that virtually all health care providers have no understanding of it and seem to only reiterate conventional wisdom (e.g. “LDL is bad”, “HDL is good”)”.

In summary, whilst the standard approach to cholesterol testing has its place, the science of cholesterol has moved on and, if you have high cholesterol, you must look beyond the pale.

My objective here is to provide a comprehensive guide to support anyone experiencing issues with high cholesterol after adopting a ketogenic or LCHF diet.

Thus, by reading this article you should have a much better idea of what you are dealing with and some tangible leads on how to move forward.

In particular, it is aimed at anyone dealing with super high cholesterol after following a LCHF diet, i.e. the Cholesterol Hyper-Responder. However, anyone dealing with high cholesterol should benefit from the content within.

Some important points before you get started

  1. Firstly, this does not constitute medical advice. I am not a medical doctor and all advice should be taken within the spirit in which it is shared. I am sharing it as a health and fitness enthusiast, a longevity adventurer, blogger and a writer. Please feel free to use this information to support your own personal learning journey and to facilitate any conversations you may have with your medical professional of choice. However, how you interpret the information and whether you choose to implement the advice given is left for you to decide 🙂
  2. The objective of this guide is to bring together the most important points on keto cholesterol so you, the reader, has most of what you need to know in one place. Most of the content has been published previously by a few ‘go to’ resources whom I have grown to trust and greatly respect. I’d like to confess up front that I may have ‘borrowed’ some of their fine words. If you’d like to go straight to the source, the links to many are cited and linked to within the relevant post section and all sources are referenced at the end.
  3. I’m constantly looking for new information so if you come across anything similar I’d love to hear about it. In addition, if you believe that any of the content found within the following sections is incorrect, please let me know in the comments as I would like to keep this as up to date and accurate as possible.
  4. Throughout the article I use the terms ‘ketogenic diet’ and Low Carb High Fat (LCHF) interchangeably as, for all intents and purposes, they are the same thing.
  5. The guide is intentionally comprehensive so I’ve broken it down into sections to make it easier to navigate. It’s written in a way that it flows from beginning to end, however, you should be able to jump between sections seamlessly as required.

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Concerned About Your Results? Start here

The benefits of switching to the Ketogenic Diet are many and the reduction of cholesterol is one which finds its way into many a blog post.

However, whilst the vast majority of people see favourable changes in their numbers, what many of the proponents of the Ketogenic Diet don’t share (or adequately address) is that there is a real risk of elevated cholesterol associated with LCHF diet.

What’s more, it seems that many people experience an extreme elevation in Total Cholesterol (Total-C) and LDL (the bad kind).

In the LCHF sphere, the term Hyper-Responder has been coined to describe anyone who sees such a dramatic rise in their cholesterol levels.

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The Cholesterol Hyper-Responder’s Journey

Super high cholesterol numbers are worrying at the best of times but for the hyper-responder things are taken to the next level.

200 mg/dl of Total Cholesterol (Total-C) is at the top end of the reference range but, for the hyper-responder, results in excess of 300 mg/dl, or even 400 mg/dl are commonplace.

Rest assured, you’re not alone. According to several experts in the field, this anomaly actually affects up to 33% of people who try the diet (1,2).

To provide some context to your results, and hopefully some reassurance, my highest ever score was 455 mg/dl. I don’t want to dwell on this here so if you’re interested, you you can catch my backstory here.

However, high cholesterol is not the hyper-responder’s only worry. The science behind cholesterol is complex and ever evolving.

As a result, it’s likely that your own GP is well behind the curve and unable to provide much support in the way of a tangible, modern intervention.

For the Hyper-Responder, a visit to the GP often meets with disdain. “Why are you trying this crazy diet, so much fat in the diet is dangerous?”.

Dietary disapproval may be disheartening, but for the hyper-responder, the prescription of a ‘healthy’, low fat diet; or even worse, statins is paralysing!

However, the average LCHF adventurer is self-educated, well informed and relentless in the quest for optimal health.

The hyper-responder’s n-1 experiments generally leave them with no doubt that the LCHF lifestyle provides the key to unlocking maximum longevity potential. As such, switching back to the standard low fat diet is not an option and the call for statins remains unanswered, unable to win a seat at the table.

As a result, the hyper-responder finds themselves in no man’s land. Consultation with Google only murkies the waters. Yes, there is information, however, it’s technical in nature and sparsely distributed. Finding a solution becomes a frustrating endeavour.

Fortunately, the risks associated with high cholesterol are probably much less of an issue than you have been lead to believe. So, if like most hyper-responders, you’re desire to continue with LCHF is strong, then you should embark on a journey of self-education. As a first step on your journey, relax, don’t freak out and read on.

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Does High Cholesterol Even Matter?

In the medical community, it appears to be fairly well accepted that there is a relationship between elevated cholesterol and the risk of cardiovascular disease (CVD) or stroke (3,4,5,6).

With heart disease and stroke sitting at the top of the table of reasons for premature death in the UK and USA (7), and atherosclerotic coronary artery diseases accounting for >4.5 million deaths annually in developing countries (8), the scale of the issue is quite clearly pandemic.

However, conversely, controversially and rather confusingly, studies have also shown that the cholesterol levels of many patients (up to 75%) hospitalized for a heart attack were well within the clinically accepted ‘reference ranges’ and that there may even be an inverse association between LDL and mortality in some cohorts (9,10).

As a result, there seems to be widely differing opinions on whether high cholesterol is, in fact, a concern in relation to heart disease risk.

So, what should we believe?

The true answer to the exam question on whether high cholesterol matters is that we simply don’t know.

So, whilst it seems that the jury may still be out in the medical arena, for the average Joe interested in longevity, it probably makes sense to at least pay attention to cholesterol levels.

However, as you will soon learn, it’s a very complex subject and you would be foolish to make any long-term lifestyle decisions on the back of a single, standalone cholesterol result.

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It’s No Longer Just About The Numbers

It seems that the clinical recommendations for the treatment of cholesterol have evolved in recent years as the focus is shifting away from a pure cholesterol ‘numbers’ game to a more considered CVD and stroke risk assessment approach (11).

This means that all GPs should be taking a broader look at your CVD risk and shouldn’t be making drug treatment recommendations on cholesterol results alone.

According an article on GP Notebook “Cholesterol measurements must be considered in context of primary and secondary prevention of coronary heart disease (CHD)” and statin treatment should only be considered for individuals who score greater than 10% on 10 year cardiovascular risk assessment using the ASCVD algorithm.

However, it’s apparent that there’s a great deal of confusion out there and there’s a good chance that your GP may be of the old school and, as a result, may prematurely recommend statins.

To illuminate this point, according to formal guidelines from the American Heart Association and the American College of Cardiology, anyone over the age of 21 with LDL-C in excess of 190 mg/dl should be evaluated for secondary causes of hyperlipidemia and treated with statins, regardless of the 10 year ASCVD risk assessment result (12).

As a result of this ambiguity, there are multiple accounts of GPs using the lipid panel results to conclude that statins are required (including mine), however, the best GPs will want to look a bit deeper.

There are plenty of CVD risk score calculators available online – here’s a link to one if you want to run your own number through it – Framington Risk Score calculator.

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High Cholesterol and Atherosclerosis

As you are probably already aware, the widely accepted link between cardiovascular disease (CVD) and high cholesterol is related to an assumed elevated risk of atherosclerosis.

Essentially, the theory is that high LDL causes a buildup of plaque in the artery wall resulting in a blockage and then heart attack or stroke.

This idea has dominated the public domain since 1984 when Nobel Award winners Michael Brown and Joseph Goldstein stated that “The more LDL there is in the blood, the more rapidly atherosclerosis develops” (13).

However, research in this area has moved on and the link between high cholesterol and atherosclerosis, and, therefore the risk between high cholesterol and CVD risk, has been called into question.

Although there are several experts in the field who still subscribe to the idea that there is a relationship between LDL and atherosclerosis, there seems to be a growing number opponents to this theory.

According to an article included in QJM as far back as 2002, “The role of LDLcholesterol for atherosclerosis growth has been exaggerated….” and “elevated LDL-cholesterol should not be the primary target in cardiovascular prevention, researchers should direct more attention to other hypotheses” (14).

As such, in all likelihood, it is no longer as simple as high cholesterol = atherosclerosis, however, given the range of opinions, it would be sensible to keep an open mind.

What is clear, though, is that a cholesterol score outside the normal reference range – even one as high as mine – does not necessarily correlate with cardiovascular disease (CVD) risk.

To demonstrate this, an unbelievable thing which you probably don’t know is that rather than relying on your cholesterol scores you can directly test for atherosclerosis.

This is a very important point which is often overlooked and is something that I have only just learned after stumbling into Dave Feldman’s great website.

The test is called a Cartoid Intima Media Thickness Test, or CIMT for short. The test, described as a “non-invasive technique which uses ultrasound to detect and quantify vascular disease and cardiovascular risk”, is widely available and costs around $250.

Dave, also a hyper-responder with Total-C of around 380 mg/dl, regularly gets a CIMT and there is no sign of atherosclerosis.

Dave also provides an example of another hyper-responder, Nicole Recine, who has Total-C over 700 mg/dl who gets tested regularly with no issues found.

This alone should be enough to reassure any hyper-responder. If you are really concerned, get your arteries directly checked.

Note: In addition to the CIMT, there is another test called a Carotid Doppler Exam which is a much more detailed ultrasound study of the neck arteries, generally performed when a blockage is suspected.

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The Evolution of Cholesterol Testing

With the conventional cholesterol test you will typically receive results for your serum levels of Total Cholesterol (Total-C), LDL, HDL and Triglycerides.

However, within the field of lipidology, it is now pretty much ubiquitously accepted that these metrics alone should no longer be considered as accurate predictors for CVD risk.

Firstly, there is much more emphasis on the ratios between certain particles, and secondly, in relation to LDL, the LDL particle number (LDP-P) and LDL particle size are thought to be much more important than overall LDL. (LDL-C).

Whilst the ratios can be calculated using the standard test, LDL subparticles need to be measured using a more advanced test such as an Nuclear Magnetic Reasoning Test (NMR) or VAP panel.

Unfortunately, most GPs don’t offer up these tests proactively so you may have to specifically request them. To boot, your GP, or cardiologist for that matter, may not know how to interpret the results so you will need to do your homework to work out whether you have an issue or not.

We’ll get into all of this in a bit more depth later, but for now, just be reassured that if you’ve had a scary result which was obtained using conventional testing, it’s probably meaningless so relax.

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What’s the Problem with Statins Anyway?

The potential side effects of statins alone should be enough to start the alarm bells ringing: muscle pain and damage, weakness, liver damage, increased risk of blood sugar and type 2 diabetes, neurological side effects, to name a few! (15).

If that’s not enough to put you off, it may be worth taking some time to read Mark Sisson’s excellent ‘definitive guide to cholesterol’ article within which a strong case is put forward for not messing with an evolutionary, honed, self-regulating system.

On the flip side, it seems to be pretty much unanimous in the clinical world that there is an unequivocal application in the prevention of second heart attacks or strokes, and in those cases the benefits of the drug most certainly outweigh the risks (16).

But for someone like me, who’s generally healthy with 4% 10 year CVD risk score, the waters become more murky.

Personally, I have a major issue with big pharma and I strongly believe that most issues can be resolved through adopting a healthy, active lifestyle with a major focus on high quality exercise and nutrition.

So, at this point in time, super high LDL or not, I’m staying clear of the statins, even though, according to the American Heart Association, I’m a clear cut case!

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Cholesterol is in a Constant State of Flux

There’s a good chance that you have been led to believe that the cholesterol in your bloodstream is fairly constant.

However, this is simply not true as cholesterol is in a constant state of flux and is highly dependent on what you ate in the days leading up to your test.

As evidence for this, check out one of my earlier articles where I show how I reduced my Total-C from 455 mg/dl to 329 mg/dl within two weeks by making some very simple dietary changes.  That’s a 28% reduction in only two weeks!

If you need further evidence of this, check out the awesome work of Dave Feldman who has developed his own protocol for manipulating results within a period as short as three days!

Frustratingly, most GPs aren’t aware of this so the chances are you’ll be prescribed a low fat diet, or statins, and scheduled for a follow up in 3-6 months.

That’s the standard protocol, however, the key takeaway from this section should be that a standalone result is a snapshot of the cholesterol within your bloodstream at that particular point in time.

As such, it should not be used form the basis of any long-term lifestyle decisions and should definitely not result in the prescription of statins!!

I do not intend to get super technical here, so if you want to delve further into the lipid system, Dave Feldman has put together an awesome series of articles which cover this off.

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The Role of Dietary Cholesterol

The thinking that there is a causal relationship between the amount of dietary cholesterol you consume and your serum cholesterol levels is simply obsolete.

The lipid system is a self-regulating, ‘closed system’ as the cholesterol in your bloodstream is 85% controlled by the liver, making the amount of cholesterol you consume irrelevant.

There are scores of articles available to back this up so I don’t wish to spend any more time debating it here. If you want further reassurance on this, please check out these articles:

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What is the Ketogenic Diet?

This topic has been discovered extensively and assuming that you’re here to learn about the risk of elevated cholesterol, I will keep this section short and sweet. That said, the article would not be complete without covering the essentials on what the Ketogenic Diet is so here goes:

The Ketogenic Diet is one which promotes ketosis: a state where the body uses fat as the main energy source instead of carbs, essentially by converting fat (dietary or stored) into ketone bodies.

The state of ketosis can be achieved in several ways:

  1. Diet (nutritional ketosis)
  2. Fasting (fasting ketosis)
  3. The consumption of exogenous ketones
  4. Vigorous exercise.

Top benefits of the Ketogenic Diet

Interestingly, the ketogenic diet was first developed as treatment for epilepsy, however, many people are turning towards the LCHF approach due to the myriad of other benefits, especially:

  • Better control over appetite and hunger
  • Increased cognitive ability
  • Weight loss
  • Improved lipid profile: Triglycerides and HDL cholesterol
  • Optimisation of blood sugar and insulin
  • Potential treatment and cure for type 1&2 diabetes
  • Potential cancer prevention and treatment
  • Athletic performance
  • To promote longevity

If you want to explore this further here are links to three articles which I believe are good starting points:

For further reading, you could check out my What is the Ketogenic Diet article where I outline some further points including:

  • How’re achieve the state of nutrition ketosis
  • Macronutrient balance
  • What the ketogenic diet is not

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What is Cholesterol?

Cholesterol is a waxy steroid of fat that serves as an essential structural component of cellular membranes and in the production of [among others] steroid hormones, vitamin D and bile acids (17).

HDL and LDL are lipoproteins: spherical fat particles that transport cholesterol around the body.

This means that your lipid panel does not directly measure the amount of cholesterol in your blood, it measures the particles that transport cholesterol around the body.

HDL stands for High Density Lipoprotein and is known as the “good” cholesterol as it transports excess cholesterol back to the liver.

In contrast, LDL, or Low Density Lipoprotein, transports cholesterol to the body’s tissues (and arteries), hence it being an otherwise known as the “bad” cholesterol.

As well as LDL, the standard test normally measures VLDL which is essentially. a “more dense” form of LDL which also falls into the “bad cholesterol” category. Whilst LDL carries mostly cholesterol, some protein and minimal triglycerides, VLDL contains minimal protein and mainly triglycerides (18).

Triglycerides, although different to cholesterol, are other important molecules which will be measured in a standard cholesterol test. Triglyceride molecules are made up of glycerol and three fatty acids which provide energy to cells. Similarly to cholesterol, triglycerides are transported around the bloodstream by LDL (19,20,21).

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Not all LDL Particles are Created Equally

In a standard test you will normally only get the overall LDL estimate. Essentially, this is a measurement of the cholesterol mass within LDL-particles and is, therefore, more accurately defined as LDL-C (Total LDL Cholesterol).

In fact, the standard test uses an algorithm to calculate LDL as it is difficult to measure directly. Most labs will use the The Friedewald formula (22):

LDL = Total cholesterol − HDL − (Triglycerides/5)

Beyond the standard lipid panel, there are two important distinctions which you should be aware of: LDL particle size and LDL particle number.

Regarding LDL particle size, broadly, the smaller, more dense particles are believed to be more dangerous than the larger, fluffier ones which are thought to play little or no role in the role of heart disease.

The results of a lipid panel which measures particle size will look something like this:

cholesterol test ldl particle size

LDL particle number, or LDP-P, is a measure of the number of LDL particles circulating within the bloodstream. You can see an example of how this looks on a report in the next section.

Most cardiologists should be up to speed on LDL particle size and LPD-P and should pay attention to both measures, however, at the forefront of lipidology, more weight seems to be assigned to LDP-P as the driving factor in atherosclerosis.

According to Dr. Peter Attia, “LDL-P is the best predictor of adverse cardiac events, which has been documented repeatedly in every major cardiovascular risk study” (23), hence the importance of understanding what is hiding behind that overall LDL-C number.

To summarise, In terms of assessing heart disease risk, LDL-C may be quite a misleading measure and, as a result, the standard approach to cholesterol testing is most likely obsolete.

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Measuring Cholesterol Sub-categories

Now that we have an understanding of LDL particle size and LDP-P, it’s time to introduce two new other important sub-particles:

  • Apolipoprotein B (ApoB)
  • Apolipoprotein A-1 (ApoA-1)

ApoB is important because it is used as a proxy to measure LDP-P and is analogous with LDL, whereas ApoA-1 is analogous with HDL. As such, measuring these two sub-particles allows us to do two important things:

  1. Measure LDP-P
  2. More accurately measure the ratio between HDL and LDL

There are a number of new tests available which measure all of these sub-categories, the two major players being NMR (Lipid Nuclear Magnetic Resonance Test) and VAP Panel (Vertical Auto Profile).

From what I understand, the NMR is the ‘gold standard’ but, unfortunately, it is not available in all parts of the world just yet.

If an NMR is not available to you, ask your GP to find a lab which can measure LDL particle size, Apo-A1 and ApoB. LPL-P is a ‘nice to have’ as ApoB can be used as the proxy.

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Reference ranges

Standard test

At the highest level possible, your GP will be looking for high HDL (good cholesterol) and low everything else, including Total-C, LDL and Triglycerides.

The reference ranges are summarised as follows (24,25,26):

  • Total-C should be less than 200 mg/dl.
  • In terms of High Density Lipoprotein (HDL), the clinically accepted reference ranges are 40-60 mg/dl and 50-60 mg/dl for men and women respectively with levels above 60 mg/dl considered ideal
  • For Low Density Protein (LDL, bad cholesterol), under 130 mg/dl would be considered desirable, less than 70 mg/dl ideal.
  • Triglycerides should be below 150 mg/dl.

As you will soon learn, the old school assessment on LDL may be very misleading due to discordance (23), but for now, to make it easy on your eyes, here’s a nice chart which summarises the whole picture of the accepted reference ranges (24).

Here’s a nice table which makes it all very easy in the eyes:

image of the standard cholesterol test reference ranges

NMR: Apolipoprotein and LDL Sub-particles

The below image shows the results of a NMR test and the optimal reference ranges (27):

NMR (Lipid Nuclear Magnetic Resonance Test) cholesterol test results

In summary, you’re looking for the following:

  • LDL-p              <1000 moll/l
  • ApoB                <80 mg/dl (28)*
  • ApoA-1             >131 mg/dl

*Interestingly, the NMR and various sources seem to suggest less that 80 mg/dl is ideal, however, Dr.Peter Attia quotes less than 109 mg/dl being ideal. Unfortunately I don’t have a reference for this but will add one as soon as I find the source material again.

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Ratios

To supplement the reference ranges, the ratios between certain particles are important in determining CVD risk.

To boot, if like me, you’re living in a part of the world where a NMR is not yet available, the ratios may be the most important measure available to you.

From my understanding, the following 3 ratios seem to be the most important, in order of priority:

  1. ApoB to ApoA1
  2. Triglycerides to HDL
  3. HDL to total-C

According to several experts, the ratio between Triglycerides and HDL is the most important marker in making a CVD risk assessment (29). The good thing about this is that you should be able to calculate this through the standard test alone.

To provide some context, several studies have shown that those with the highest Triglycerides:HDL ratios have a greater heart disease risk (up to 16x) compared to those with the lowest ratios (30,31).

However, given the weight of the argument for looking at ApoB, or LDL-p, I have given this the highest priority.

  • For ApoB : ApoA1, a ratio under 0.92, below 1 is considered excellent (32).
  • For Triglycerides : HDL, you’re looking for a ratio of less than 2, above 4 is considered too high and above 6 is much too high (33).
  • For Total-C : HDL, Target of under 5.0 is desirable, less that 3.5 ideal (34,35).

Given that the LCHF diet typically promotes high HDL and low Triglycerides, chances are your ratios will be pretty good and this should be enough to eliminate some of your concerns.

However, regardless of all this, there will always be a percentage of people who still want to see their numbers come down to within the reference ranges, and if you’re a hyper-responder with off the charts Total-C and LDL, that is entirely understandable.

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Discordance

Discordance is where there is variability between LPL-C and LDP-P (36). This variability is an important factor as several studies have shown that there is correlation between discordance and CVD risk.

There are 3 possible variability scenarios:

  1. LDL-P > LDL-C (Discordance)
  2. LPL-P = LPL-C (Concordance)
  3. LDL-P < LDL-C (Discordance)

Studies show that the groups with the highest risk factor are the first two, i.e. where LDL-P is greater or equal to LDL-C.

This means that it is possible to have high LDL-C but have a low CVD risk, or, more ominously, you could have a very low LDL-C but, if your LPL-P count is high, your CVD risk factor could be high.

The issue here is that you could return from the GP with a glowing LDL-C report and a pat on the back, where, in fact, you have a higher CVD risk than thought.

According to Dr.Peter Attia: “The real world tragedy: 90-95% of physicians, including cardiologists, would bet their own lives that persons with an LDL-C < 70 mg/dl have no atherosclerotic risk” (37).

In terms of applying this to your own result, you will either need an NMR which shows LDL-P or a measure of ApoB (which as you will recall is analogous to LPL-P.

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Analysis: My Results

cholesterol results including ApoB and ApoA1

  1. At 309 mg/dl and 216 mg/dl respectively, Total-C and LDL-C are both way outside the reference ranges.
  2. ApoB as a standalone measure (LDP-P) is classed as ‘high risk’.
  3. The ApoB to ApoA1 ratio is 0.71 (130/182) which is considered excellent (i.e. HDL is higher than LDL)
  4. The Triglycerides to HDL ratio is 0.57 (48/83.9) which is considered excellent (i.e. HDL is higher than Triglycerides)
  5. The Total-C HDL ratio is 3.68 (309/83.9) which is only slightly outside the ‘desirable’ band.
  6. From a discordance standpoint, my LDL-P (ApoB) is much lower than LDL-C which puts me into the low risk discordant group.

In summary, my only real concern from these results is the high ApoB count which is well above the reference range.

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Causal factors

High cholesterol is not a causal factor, it’s a symptom of downstream issue. This is why statins are such a bad choice for anyone who has not previously suffered a heart attack or stroke as you’re treating the symptoms, not the cause (38).

As such, to support your decision on whether the ketogenic diet is right for you there are a bunch of other important factors which need to be brought into play, measured and analysed.

The Role of Inflammation

Inflammation, whilst not technically a causal factor, should fall very high on the priority list. Not only is inflammation important in the context of high cholesterol, it is one of the most important bio markers in the assessment of overall health and it is thought to be one of the main players in terms of longevity assessment (39).

One of the key functions of LDL is to respond to inflammation whereby the body uses cholesterol as a ‘band-aid’ to temporarily cover any lesions in the artery wall.

Once the inflammation issue is resolved, the ‘band-aid’ goes away and repair takes place, however, in most cases the inflammation proceeds, and the cholesterol ‘plaque’ builds.

It is the smaller particles which are believed to be most involved in the inflammatory response process which, essentially, begins the atherosclerosis cascade (38).

Ultimately, this means that, whilst cholesterol is clearly involved in the atherosclerosis process, it is being sent in response to deal with the route cause of the issue: inflammation.

Your GP can directly measure your inflammation status by testing CRP, or C-Reactive Protein. You’re looking for the lowest possible CRP score with < 0.1 mg/dl being considered optimal (40)

Other Potential Route Causes, Biomarkers and Things to Test

  • Familial Hypercholesterolemia (FH). FH is a genetic disorder which causes issues with cholesterol metabolism resulting in extremely high LDL. Affecting around 1 in 250, unless treated, FH usually results in early death with men having a 50% greater chance of heart attack by age 50, at 30% risk for women by age 60. FH is ruled out if you have had results anywhere near the normal range, however, it is thought that up to 90% of people with FH have not been properly diagnosed (41).
  • ApoE4. Carriers of the ApoE4 gene polymorphism are at a higher risk of elevated cholesterol with carriers of two copies of the gene at even higher risk. You can find out whether you’re a carrier through a genetic test through a company like 23andMe (2).
  • Hypersynthesis. Typically where insulin resistance causes an abnormally high production of cholesterol (2).
  • Hypothyroidism. If the thyroid is not functioning correctly, it can slow down the efficiency of LDL receptors resulting in high cholesterol. Thyroid function can be tested through your GP and should be something to get checked at the time as a scheduled cholesterol test (2).
  • Untreated diabetes or pre-diabetes. Diabetes tends to lower HDL and raise Triglycerides and LDL. Your GP should be able to schedule with a fasted blood glucose test to assess whether this may be a factor (41).
  • Pregnancy and Lactation. Increased cholesterol during pregnancy is essential and is thought to perform a role in the development of cell membranes, some hormones and vitamin D (42,43).
  • Stress. Studies have shown that increased stress can drive high cholesterol, and in particular LDL. Cortisol, DHEA, adrenaline, noradrenaline, dopamine and aldosterone are some of the commonly used neuroendocrine biomarkers (44,45).
  • Liver conditions. Given that the cholesterol system is largely controlled by the liver, it’s not surprising that issues with liver function may cause something to be out of whack with your lipid profile. Conversely, high cholesterol has been associated with non-alcoholic fatty liver disease making it all the more important that you get your liver function checked. A liver function test will help determine the health of your liver by measuring the levels of proteins, liver enzymes, or bilirubin in your blood (46,47,48).
  • Coffee. In the past few years, increasing evidence suggests that more coffee can increase cholesterol levels. The increase in cholesterol is believed to be caused by oils called terpenes that are found in coffee, not the high caffeine content (49).

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Actionable next steps and experimentation

According to some, high cholesterol settles down for most people after a period of months, however, the evidence for this seems to be anecdotal and I haven’t yet found anything tangible to hang my hat on.

To boot, if your results have been off the charts, like mine, then you may not feel comfortable with the prospect of just playing the ‘wait and see’ game and you may wish to prioritise finding a solution.

Step 1 – Analyse your ratios

If you have the standard test results only, you can analyse the ratios between Triglycerides and HDL, and Total-C and HDL as this alone may be enough to put your mind at ease and allow you to continue with the ketogenic diet.

Step 2 – Work with your GP

Firstly, if your GP is not sympathetic to your desire to continue with the diet, then it’s time to find a new GP. The benefits are of a low carb, LCHF or ketogenic diet, unequivocal and anyone who is unaware of this is not keeping up with the latest research.

Schedule a fresh blood test with your GP and ask for the following tests:

  1. Measure of ApoA-1 and ApoB (NMR or VAP panel)
  2. CRP (C Reactive Protein)
  3. Thyroid function
  4. Fasted Blood Glucose

Note, if you’re in the UK or the USA, you should be able to find a practise which can perform an NMR.

Step 3 – Research potential interventions and start testing

Information on how to improve your lipid profile is comprehensive so I don’t want to unnecessarily duplicate content here.  To summarise, though, you could look at the following interventions:

  • Dave Feldman Protocol
  • Switch out saturated fat for monounsaturated
  • Niacin (Vitamin B3)
  • Increased exercise
  • Red wine, in moderation (resveratrol)
  • Dietary changes, such as increasing fibre intake, replacing saturated fats with ‘healthy’ fats
  • Circadian rhythm
  • Coffee

Please note that this is far from an exhaustive list and my plan is to update the post as and when I learn more through my own personal research and experiments.

If you’re up for experimenting, you should try to isolate one factor and track as many biomarkers as possible, including everything you consume, dietary and supplementary.

I’m planning on doing some further self-experimentation shortly so will update this post as and when things get moving. However, if you’re champing at the bit, the best resources I’ve found in relation to self-experimentation are Dave Feldman and BJJ Caveman.

Table of Contents

References

  1. Kris Gunnars. What to do if a Low-Carb Diet Raises Your Cholesterol. Authority Nutrition.
  2. Dave Feldman. Hyper-Responder FAQ. Cholesterol Code
  3. American Heart Association. (2016). What Do My Cholesterol Levels Mean?.
  4. Cholesterol 101. American Heart Association.
  5. Stamler J, Daviglus ML, Garside DB, Dyer AR, Greenland P, Neaton JD. (2000). Relationship of baseline serum cholesterol levels in 3 large cohorts of younger men to long-term coronary, cardiovascular, and all-cause mortality and to longevity. PubMed.
  6. Amanda McMillan. (2017). 7 Ways to Lower Cholesterol. Time health.
  7. USA vs United Kingdom Top 10 Causes of Death. World Life Expectancy.
  8. Okrainec K, Banerjee DK, Eisenberg MJ. (2004). Coronary Artery Disease in the Developing World. PubMed.
  9. Rachel Champeau. (2009). Most heart attack patients’ cholesterol levels did not indicate cardiac risk. UCLA Newsroom.
  10. David M Diamond et.al. (2016). Lack of an association or an inverse association between low-density-lipoprotein cholesterol and mortality in the elderly: a systematic review. British Medical Journal Open.
  11. Reena Pande, M.D. (2013). Cholesterol and statins: it’s no longer just about the numbers. Harvard Health Publications.
  12. Neil J Stone et.al. (2013). Guideline on the Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in Adults. Circulation.
  13. Brown MS, Goldstein JL. (1984). How LDL receptors influence cholesterol and atherosclerosis. Scientific American.
  14. U. Ravnskov. (2002). Is atherosclerosis caused by high cholesterol? QJM, Vol. 95, Issue 5, pp.397-403.
  15. Statin side effects: Weigh the benefits and risks. Mayo Clinic.
  16. Brenda Goodman. More Docs Wonder If Statins Are Worth the Risks. WebMD.
  17. Mark Sisson. (2011). How to Interpret Cholesterol Test Results. Mark’s Daily Apple.
  18. Lisa Nelson. (2008). What is the difference between LDL and VLDL? Health Central.
  19. Yolanda Smith. (2015). What are Triglycerides? News Medical
  20. Dr.Stephen Sinatra. (2014). What Are Triglycerides? Heart MD Institute.
  21. Dave Feldman. (2016). A Simple Guide to Cholesterol on Low Carb – Part I. Cholesterol Code.
  22. Fazia Mir. (2014). LDL Cholesterol. MedScape.
  23. Dr.Peter Attia. (2012). The Straight Dope on Cholesterol – Part VII. Eating Academy.
  24. A Comprehensive Guide On Idea Cholesterol levels. Cholesterol Menu.
  25. Cholesterol Test. Mayo Clinic.
  26. Cholesterol Levels: What You Need to Know. NIH Medicine Plus.
  27. Dr.Peter Attia (2012). The Straight Dope on Cholesterol – Part III. Eating Academy.
  28. Apolipoprotein B (apoB). Doc’s opinion.
  29. Dr.Stephen Sinatra. The Most Important Cholesterol Ratio to Watch.
  30. Ronald Grisanti. Prevent a Heart Attack: Know Your Ratio? Functional Medicine University.
  31. Protasio Lemos da Luz et.al. (2008). High Ratio of Triglycerides to HDL-Cholesterol Predicts Extensive Coronary Disease. PubMed.
  32. Dr.Peter Attia .(2012). How a Low Carb Diet Reduced my Risk of Heart Disease (Part 3). Eating Academy.
  33. Axel F. Sigurdsson. (2014). The Triglyceride/HDL Cholesterol Ratio. Doc’s Opinion.
  34. Francisco Lopez-Jimenez. (2015). Cholesterol Ratio: Is it Important? Mayo Clinic.
  35. Lori Mosca. (2007). Total Cholesterol to HDL Ratio. Everyday Health.
  36. Otvos JD et.al. (2011). Clinical implications of discordance between low-density lipoprotein cholesterol and particle number. PubMed.
  37. Dr.Peter Attia. (2012). The Straight Dope on Cholesterol – Part VI. Eating Academy.
  38. Mark Sisson. (2008). The Definitive Guide to Cholesterol. Mark’s Daily Apple.
  39. Ridker PM. (2007). Inflammatory biomarkers and risks of myocardial infarction, stroke, diabetes, and total mortality: implications for longevity. PubMed.
  40. C-Reactive Protein (CRP). Web MD.
  41. What is FH? The FH Foundation.
  42. Is High Cholesterol During Pregnancy Normal? Parenting.com
  43. Cholesterol levels in pregnancy and feeding. Made for Mums.
  44. How Does Stress Contribute to Cholesterol? Everyday Health.
  45. Konduru, Laalithya. (2012). Biomarkers Of Chronic Stress. Master’s Thesis, University of Pittsburgh.
  46. Non-alcoholic Fatty Liver Disease. Patient.
  47. Sarah Terry. (2013). Liver Function and Cholesterol Levels. Livestrong.
  48. Liver Function Tests. Healthline.
  49. Merritt McKinney. (2013). Coffee and Cholesterol. NBC News.

Table of Contents

Top Resources

Articles

Websites

Podcasts

Video

I have compiled YouTube playlist of some of the best videos – if you find any more worth adding please let me know in the comments section.

 

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image credits: Paleo Magazine

  • Real NIKEBOY 1977

    Hi Lee – much of your story resonates with me. I am 58 and I have been in ketosis for a year, and just became aware that my LDL is quite high at 8.3 mmol/L. I have a requisition to get the particle size testing done. I have been eating saturated fats with reckless abandon (grassfed butter, high fat dairy, MCT oil/caprylic acid, etc…approx 50mg per day) so I will make some substitutions. All my other markers are really good…blood sugar, blood pressure, inflamation, triglycerides, insulin…low stress and lots of exercise.

    So what happens if a person in Ketosis goes on a statin? I would expect that all my lipids will go down…including my HDL, and I wonder if it knocks down my ketones as well? I don’t have any historical data, but my doc says I have had high LDL for a long time…he’s been talking about statins for a few years but it became an issue this year when I could not get covered by life insurance.

    Thanks for the good info you have compiled…all the best!

    • Hi,

      Really sorry for the late reply on this, for some reason I missed it! Thank you for taking the time to comment, it means a lot as it took a long time to put this article together 🙂

      The statins question is a difficult one. I would recommend that you try to find a way to get a Cartoid Intima Media Thickness Test (CIMT) done first and foremost to see whether there is actually any plaque build up which you should be worried about. Your LDL seems to be very high so it’s likely that your ApoB is high too and that there’ll be a high count of small LDL particles. Of course, all of that is meaningless unless there’s any plaque build up so the CIMT may your next step.

      I’ve had similar LDL result and at one point I had a result even higher than yours but managed to bring it down within two weeks by making some small changes – check out this article. There are a few people commenting on these articles and everyone in the community is very helpful so please get involved in the discussions 🙂

      Finally, I haven’t posted on this yet but I’m in the middle of a self-experiment pertaining to coffee! I cut it out completely, went back to a high carb diet and got all of my cholesterol numbers within the normal ranges (Total-C was 198 mg/dl, lowest ever score!). I used the high carb diet as a baseline and had a second blood draw after a week on a strict keto diet and it only went up to 230 mg/dl (my highest was 455 mg/dl). I’ve since been inhaling coffee and go for my next blood draw in about an hour so it will be interesting to see what happens.

      I’ll post my results tomorrow but if it turns out that coffee is the major factor causing high LDL I’ll be delighted as it means I can stick to a ketogenic diet without any major concerns about cholesterol.

      What about you, are you much of a coffee drinker? Best, Lee

    • Hi,

      Really sorry for the late reply on this, for some reason I missed it! Thank you for taking the time to comment, it means a lot as it took a long time to put this article together 🙂

      The statins question is a difficult one. I would recommend that you try to find a way to get a Cartoid Intima Media Thickness Test (CIMT) done first and foremost to see whether there is actually any plaque build up which you should be worried about. Your LDL seems to be very high so it’s likely that your ApoB is high too and that there’ll be a high count of small LDL particles. Of course, all of that is meaningless unless there’s any plaque build up so the CIMT may your next step.

      I’ve had similar LDL results and at one point I had a result even higher than yours but managed to bring it down within two weeks by making some small changes – check out this article

      There’s a few people commenting on these articles and everyone in the community is very helpful so please get involved in the discussions 🙂

      Finally, I haven’t posted on this yet but I’m in the middle of a self-experiment pertaining to coffee! I cut it out completely, went back to a high carb diet and got all of my cholesterol numbers within the normal ranges (Total-C was 198 mg/dl, lowest ever score!). I used the high carb diet as a baseline and had a second blood draw after a week on a strict keto diet and it only went up to 230 mg/dl (my highest was 455 mg/dl). I’ve since been inhaling coffee and go for my next blood draw in about an hour so it will be interesting to see what happens.

      I’ll post my results tomorrow but if it turns out that coffee is the major factor causing high LDL I’ll be delighted as it means I can stick to a ketogenic diet without any major concerns about cholesterol.

      What about you, are you much of a coffee drinker? Best, Lee

      • Real NIKEBOY 1977

        Hi Lee – I really appreciate your thoughts…yes, I am drinking tons of coffee…probably 3-4 per day. I use it for appetite suppression and for energy, especially pre-workout. I actually just re-read your articles yesterday and did more exploring in the links – I had spent the last couple of days reading everything by Dave Feldman. They have helped to calm me down about my high LDL numbers, but I’m still trying to pull my strategy together going forward to address my LDL number.

        I am pushing my GP for the particle number/size test…it is a 6 week turnaround. I’m trying to figure out if I can get a CIMT in Canada…I just called the heart institute here in Ottawa and they had never heard of it.

        So at this point I am thinking that I should cut down on saturated fats (aim at 30g per day or less). I’m not clear on the changes to make on carbs/exercise/coffee and whether to go for a Feldman protocol just before my next LDL testing…it sure is a lot of info to take in!

        …all the best!

        • No problem. My advice, for what it’s worth, would be to not panic and spend some time on the research. Chances are that you already know more than your GP now but spend a bit more time and go back with some really specific requests (ApoB, particle size etc is a good place to start). Then if you’re up for doing a bit of self-experimentation, build yourself a good quality meal plan and try tweaking one thing at a time. Best of luck and keep me posted 🙂

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