High Cholesterol on a Keto Diet
Should You Be Concerned?

High Cholesterol on a Keto Diet - Should You Be Concerned?ShareFollow us 136.9k

As keto and low-carb diets have become increasingly popular, some people who follow this way of eating have noticed a sharp rise in their LDL cholesterol.

Understandably, most have become concerned, since elevated LDL is typically considered a major heart disease risk factor. However, the reason for this response - and whether it poses significant health risks – isn't completely understood or agreed upon by experts. This article takes a balanced look at the issue and its potential implications for cardiovascular disease and overall health.

What is Cholesterol and Why Do We Need It?

Cholesterol is a waxy, fat-like substance that is essential for life. It plays an important role in maintaining the integrity of your body's cells. Cholesterol is used to make hormones like vitamin D, testosterone, and estrogen. Cholesterol is also needed for the production of bile acids that help you digest fat.

Your liver, intestines, and other organs produce most of the cholesterol found in your body. In addition, it can be obtained from eating animal foods like meat, cheese, eggs, and butter.

How Is Blood Cholesterol Connected to Heart Disease?

Historically, elevated blood cholesterol levels have been linked to atherosclerosis, a condition involving deposits of plaque that cause the arterial lining to thicken and potentially impair blood flow to the heart. The process of plaque deposition is complex but involves white blood cells, calcium, cholesterol, and other substances converging at the site of inflamed or damaged arteries.

However, cholesterol doesn't travel on its own in your bloodstream. Instead, it's carried in lipoprotein particles, which contain special proteins called apoproteins, triglycerides, fat-soluble vitamins and other compounds in addition to cholesterol.

Different types of lipoproteins are formed as they move through your bloodstream and drop off or pick up triglycerides and cholesterol.

Low-density lipoprotein (LDL)

Low-density lipoprotein (LDL) particles contain Apolipoprotein B. LDLs are formed from very-low-density lipoproteins (VLDLs), which are made by your liver.

An LDL's primary function is to carry energy and nutrients through your bloodstream and deliver them to cells that need them. LDL particles provide the cells with triglycerides to use as an energy source and cholesterol to use for repair and other functions, as needed.

High Cholesterol on a Keto Diet - Should You Be Concerned?

High-density lipoprotein (HDL)

High-density lipoprotein (HDL) particles contain Apolipoprotein A as their main protein. HDL is synthesized in your intestine and your liver.

One of HDL's main functions is to carry cholesterol back to your liver. HDL contains a higher proportion of protein to lipids than other lipoproteins. This results in a denser molecule, hence the name “high-density lipoprotein.”

High Cholesterol on a Keto Diet - Should You Be Concerned?

LDL Particles and Heart Disease

Many experts believe that the longer LDL particles remain in the bloodstream, the more likely they are to become oxidized, enter the arterial wall, and initiate the process of atherosclerosis.

For this reason, the cholesterol in LDL particles is often referred to as “bad” cholesterol, whereas the cholesterol in HDL particles is considered “good” cholesterol. However, there is really only one type of cholesterol that is transferred among different lipoproteins.

Moreover, the extent to which elevated LDL levels contribute to cardiovascular disease (CVD) risk – particularly in individuals who follow a keto or low-carb diet – remains a topic of debate.

What Are “Normal” Lipid Values?

Traditional Lipid Profile

The following are typical reference ranges for lipid values in those without preexisting heart disease, after a water-only fast of 10-12 hours.

Total Cholesterol < 200 mg/dL (5.2 mmol/L)
LDL Cholesterol < 130 mg/dL (3.4 mmol/L)
VLDL Cholesterol < 40 mg/dL (1.04 mmol/L)
HDL Cholesterol (Men) > 40 mg/dL (1.04 mmol/L)
HDL Cholesterol (Women) > 50 mg/dL (1.3 mmol/L)
Triglycerides < 150 mg/dL (1.7 mmol/L)

Advanced Lipoprotein Values

In recent years, more advanced lipid testing known as the NMR LipoProfile has become available. Below are the values for the reference range indicative of low to moderate risk.

LDL-P < 1300 nmol/L This value reflects the total number of LDL particles in your bloodstream.
HDL-P > 30.5 umol/L This value reflects the total number of HDL particles in your bloodstream.
Small LDL-P < 527 umol/L This value reflects the number of LDL particles that are small and dense. Elevated levels of small LDL-P are associated with insulin resistance and increased heart disease risk.
LDL Size > 20.5 nm This value reflects the size of your LDL particles. People with large, buoyant LDL are said to have Pattern A, which is typically considered less artherogenic, meaning less likely to cause plaque buildup in the arteries. than Pattern B, which is characterized by higher concentrations of small LDL.

Cholesterol Hyper-responders: A Common Keto Phenomenon?

A person's blood cholesterol levels may increase from previous values for a number of reasons.

Temporary Elevation in LDL Cholesterol

A fairly common one is the temporary elevation in LDL cholesterol that frequently occurs during and after major weight loss (1). Other factors that can raise cholesterol levels include hypothyroidism, age-related hormone changes, injury, and infection.

Significantly Increased LDL Cholesterol

Finally, cholesterol levels may increase dramatically in some people who follow a keto or low-carb diet.

However, this doesn't happen in every case or even most cases. In fact, many people see little to no increase in their LDL cholesterol while experiencing beneficial changes in other markers, such as an increase in HDL cholesterol and a decrease in triglycerides, blood sugar, and insulin levels – all of which are associated with reduced risk of CVD.

By contrast, some people have seen their total, HDL and LDL cholesterol levels increase anywhere from 50% to 200% or more after switching to a low-carb or keto diet. Although a few are overweight or metabolically unhealthy, many of these individuals belong to a group that Dave Feldman at Cholesterol Code calls Lean Mass Hyper-responders (LMHRs): healthy, thin and/or athletic people with LDL cholesterol values of 200 mg/dL (5.2 mmol/L) or higher.

Over the past two years Feldman, a software engineer with a strong interest in science, has performed several dozen experiments on himself and collected data from a number of other keto and low-carb dieters whose cholesterol levels have increased far beyond the “optimal” range. However, whether this is problematic or not isn't entirely clear, especially since their other biomarkers typically improve or remain stable.

Feldman believes that his findings thus far demonstrate that the combination of higher energy demands, lower body fat stores, and lower glycogen stores in LMHRs trigger increased production of LDLs for the purpose of carrying energy (triglycerides) to cells that need them, with cholesterol mainly along for the ride but also used by the cells for repair and other purposes, as needed.

Indeed, Feldman has performed a number of experiments demonstrating that manipulating calorie and fat intake and/or carb and fat intake can dramatically increase or decrease LDL cholesterol levels in just three days.

On the other hand, most lipidologists, including Dr. Thomas Dayspring, believe that extremely high LDL cholesterol and LDL-P increase heart disease risk independently of other risk factors, as discussed in the MESA study that measured risk of coronary artery disease – the most common form of CVD – in more than 5,000 people (2).

What Are the Major Risk Factors for Heart Disease?

Although many experts believe that elevated LDL cholesterol and LDL particles are the main risk factors for developing CVD, recent and older research suggests there are others that contribute equally, if not more.

Hyperinsulinemia

Insulin has a number of important functions in the body, including storing glucose in liver and muscles and stimulating muscle protein synthesis. However, having too much insulin in the bloodstream (hyperinsulinemia) is strongly linked to CAD (3, 4, 5).

In a 1998 study looking at data from more than 2,100 middle-aged and older men, researchers reported that those with the highest fasting insulin levels were found to be at greatest risk for heart disease. What's more, this appeared to be independent of lipid values (3).

A recent 2017 study of over 2,500 adults looked at fasting insulin and high-sensitivity C-reactive protein (hs-CRP), an inflammatory marker considered a strong predictor of heart attack risk. In this study, people with the highest insulin levels were more than four times as likely to have an elevated hs-CRP value compared to those with the lowest insulin levels. By contrast, elevated LDL cholesterol levels showed no association with hs-CRP (4).

High Levels of Small LDL-P

Most lipidologists and cardiologists agree that that high numbers of small, dense LDL particles increase cardiac risk. These particles are also strongly associated with insulin resistance (5).

In a 2017 study looking at data from over 18,00 people, higher concentrations of small LDL particles were linked to increased CVD risk in people with lipid values in the normal range, as well as those already considered at high risk (6).

However, other observational studies suggest that higher levels of large LDL particles could potentially also be problematic – although it must be pointed out that presumably few to none of the people studied were following ketogenic or very-low-carb diets. (2, 7).

The MESA study authors concluded:

“Contrary to current opinion, both small and large LDL were significantly associated with subclinical atherosclerosis independent of each other, traditional lipids, and established risk factors, with no association between LDL size and atherosclerosis after accounting for the concentrations of the two subclasses" (2).

Subclinical atherosclerosis is the period when early changes are happening in the arteries but hallmarks of atherosclerosis like calcified plaque haven't developed to the point where the disease can be diagnosed.

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Genetics

Familial hypercholesterolemia (FH) is a condition characterized by extremely elevated total and LDL cholesterol levels, strong family history of heart disease, and fatty deposits under the skin, including the eyelids. People with FH are at very high risk of heart attack. It's a fairly common condition currently estimated to affect one out of every 150 people (8).

Another group at increased CVD risk are those with one or two copies of the apoE4 allele (gene). These individuals tend to have higher VLDL cholesterol but lower HDL cholesterol. In addition to heart disease, they have greater risk for Alzheimer's disease, cancer and other diseases (9). The Apo-E4 forums provide helpful information, guidance and support for those with the apoE4 allele.

In addition to ApoE4, researchers have have identified other genetic mutations that increase CAD risk, although less is known about them at this time (10).

Aging

As people get older, their risk for heart disease increases. This may be due to being less active, having other chronic diseases, and developing arterial stiffness that impairs function.

Menopause

Additionally, research suggests that during menopause, women may experience an increased thickening of the carotid intima and media layers of the arteries, a marker of subclinical atherosclerosis. In a study of 249 middle-aged women, those who were postmenopausal or in the late stages of perimenopause were much more likely to show progression of carotid intima-media thickness (CIMT) than those in early perimenopause (11).

Does Saturated Fat Increase LDL Cholesterol and Raise Heart Disease Risk?

The President of the American Heart Association (AHA) recently issued a statement that lowering saturated fat intake by replacing it with unsaturated fats will lower total and LDL cholesterol and decrease risk of CVD (12).

However, several large reviews haven't been able to establish an association between saturated fat intake and heart disease, including a 2010 meta-analysis looking at 21 studies totalling more than 340,000 people (13).

It's true that certain saturated fatty acids have been reported to raise LDL cholesterol levels, including palmitic, myristic and lauric acid, which make up a large portion of milk fat (14). On the other hand, high-fat dairy has been shown to provide several cardioprotective benefits as well (15).

Therefore, although avoiding all dairy fat may lower LDL cholesterol, it may not be a good strategy for protecting heart health. (You can read more about health benefits of dairy in this post: Dairy on a Ketogenic Diet).

Moreover, it appears that the LDL cholesterol response to saturated fat intake is individualized, with some people experiencing an increase and others seeing little to no change.

Is Elevated LDL Cholesterol a Concern if You Follow a Keto Diet?

Whether extremely high LDL cholesterol and elevated LDL particles increase heart disease risk in people who follow a keto lifestyle isn't known. Dave Feldman isn't entirely convinced that it's a completely benign phenomenon, although his ongoing research suggests that it may be.

The main problem is that there haven't been any long-term formal studies in this population that provide data assuring us that LDL elevations of this magnitude are safe. It's something that just can't be said with absolute certainty at this time.

In addition, although small, dense LDL particles are the type most strongly associated with heart disease risk, as mentioned earlier, there are some observational studies suggesting that high concentrations of large LDL particles may also increase CVD risk. However, the subjects' diets weren't included when risk factors were assessed.

On the other hand, higher HDL cholesterol levels have been linked to less carotid artery intima-media thickness. In a large meta-analysis of data from more than 20,000 people, CIMT tended to decrease as HDL cholesterol increased – regardless of LDL cholesterol values (16). Importantly, although LDL response to carb restriction varies from person to person, HDL virtually always increases.

What's more, insulin-resistant people who follow very-low-carb or ketogenic diets often show more favorable reductions in insulin levels, inflammation, and arterial dysfunction compared to those on “heart-healthy” low-fat diets (17, 18).

Overall, the many cardiovascular health benefits of very-low-carb diets for metabolically compromised individuals are impressive. In addition, Lean Mass Hyper-responders often report feeling better and having more sustained energy as a result of following a keto lifestyle.

How to Reduce Cardiovascular Risk While Remaining Keto or Low-Carb

If your LDL cholesterol has significantly increased on a keto or low-carb diet, it's completely understandable if you're at least somewhat concerned. However, you might be reluctant to make any changes to your diet given the benefits you've experienced. On the other hand, you may decide that you want to try to lower your LDL values while still following a keto/low-carb lifestyle.

Here are some tips that may help manage cardiovascular risk, including potentially lowering LDL. However, keep in mind that the effects may vary from person to person, and your LDL may not change much.

Eat More Fatty Fish

Although the long-chain omega-3 fatty acids found in fish typically reduce triglycerides more than LDL cholesterol, they're anti-inflammatory and may help protect against heart attacks (19).

Fish highest in omega-3 fats include salmon, sardines, mackerel, herring, and anchovies.

Increase Fiber Intake

Fiber, especially the soluble type, may be beneficial for heart health. It's been shown to help lower cholesterol levels, yet it doesn't seem to interfere with the absorption of fat-soluble vitamins and other nutrients (20).

Excellent keto-friendly sources of soluble fiber include avocado, blackberries, broccoli, brussels sprouts, and flaxseed.

Increase Net Carb Intake

Dave Feldman recently demonstrated that increasing net carb intake from 30 grams to 95 grams per day – (going from 4% of total calories to 13% of total calories) led to a significant drop in his LDL cholesterol level. Obviously, this level of carb intake isn't ketogenic; however, it is still moderately low carb. On the other hand, this will likely increase your blood sugar and insulin levels to some extent.

Eating about 50-60 grams of net carb daily (15-20 grams per meal) may be enough to help lower LDL without jeopardizing blood sugar and insulin stability.

Consume Fat-Soluble Antioxidants

Getting plenty of antioxidants in your diet like vitamin E and the phytochemicals lycopene and beta carotene may help protect your LDL cholesterol from becoming oxidized, thereby reducing CAD risk (21).

Leafy greens, almonds, sunflower seeds, hazelnuts, tomatoes, avocado, and red peppers are good sources that meet keto criteria.

Get a CAC or CIMT test

Having a coronary artery calcium (CAC) scan or CIMT test can provide information about actual heart disease that lab tests can't. Some people with extremely high levels of LDL cholesterol have calcium scores showing no plaque accumulation in the arteries and normal intima-media thickness, whereas others demonstrate mild to moderate atherosclerosis even when LDL cholesterol is within the normal range.

A zero CAC score is typically associated with very low risk of heart attack or other adverse cardiac event within 10 years (22).

However, some experts like Dr. Dayspring believe CAC scores are only meaningful in middle-aged and older adults. On the other hand, CIMT evaluation can identify early signs of heart disease in young to middle-aged people, including those with zero CAC scores (23).

Recommended Reading and Viewing

In addition to Dave Feldman's posts linked to earlier, there are several other articles and videos discussing diet, lipids, and cardiovascular risk. Here are just a few:

Articles and Websites

Videos

My Own Experience with the Cholesterol Drop Protocol

To date, more than 50 people have successfully completed Dave Feldman's Cholesterol Drop Protocol, which consists of 3.5-10.5 days of keto/LCHF eating and 1-4 blood tests. I've done the 6.5-day experiment twice, once in early May and again in mid-September of this year.

Although 86% of people who have undergone the protocol have experienced a decrease in LDL cholesterol after ramping up their calorie and fat intake for three days, my own LDL cholesterol increased, the first time by 47 mg/dL and the second time by 15 mg/dL. At this point, I'm the only one who had both an increase in LDL and a decrease in triglycerides after the high-fat, high-calorie portion of the experiment. All of my other markers, including HDL and small LDL particle counts, were excellent for both the low-calorie and high-calorie days.

For reference, I'm a Lean Mass Hyper-responder and have been following a low-carb diet for more than 6 years. My net carb intake typically ranges from 20-40 grams per day, and I remained at the lower end of this range during the experiment.

If you follow a keto or low-carb diet, please consider doing the Cholesterol Drop Protocol – especially if your lab results indicate you're a hyper-responder. Be sure to keep detailed food records and share all data back to Dave Feldman on his website at Cholesterol Code.

Take Home Message

The connection between elevated LDL cholesterol and heart disease remains controversial.

It seems fairly clear that those on keto and very-low-carb diets who get most of their energy from fat – including their own fat stores – tend to have more LDL particles circulating in their bloodstream, delivering triglycerides to cells and transferring cholesterol to other lipoproteins. Whether this is harmful remains to be seen.

Until we have more data on very high LDL cholesterol and LDL-P in keto and low-carb dieters, it's up to each person to decide the levels he or she is comfortable with, based on everything we know at this point.

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By Franziska Spritzler, RD, CDE
Registered dietitian, certified diabetes educator and creator of LowCarbDietitian.com

Franziska Spritzler, a registered dietitian and certified diabetes educator, is a strong proponent of carbohydrate restriction for people struggling with diabetes, insulin resistance, obesity, and PCOS.

She follows a very-low-carbohydrate, ketogenic diet for blood sugar control and has experienced many improvements in her health as a result of making this change.

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Comments (24)

Great article! I have been diagnosed with familial hypercholesterolemia, however, I am not concerned at all. I continue to follow a restricted calorie, zero carb ketogenic diet, that I have been doing strictly for the last year and a half. All of my health markers are excellent, except for LDL particle number and total, and it is the large buoyant type. I am middle-aged (46). I did get both a CT scan and tri-vascular scan, and got perfect scores for both. That alleviated any concerns that I might have previously had. Since this diet has improved my gut issues, bodyfat, blood pressure, insulin, blood glucose, mood, energy, A1C, CRP, etc., - basically every single health parameter I have tested, I am sticking with it! Thank you for clearing up the confusion surrounding LDL!

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Thank you, Thank you, Thank you!!!!! Your article couldn't have been timed any better. I got my blood panel back from my "western" doctor two days ago and the numbers had me very worried. After reading your post yesterday I felt so much better and sent the results off to my naturopath knowing that everything should be fine. I printed it out for my own reference and for any others, doctors included, who may have doubts and questions. Again, a big thanks for all your research and putting it out there for the rest of us trying to live a longer, healthier life!!

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Thank you for your kind words, Rhonda! I wish you the best of luck with everything. - Franziska

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What an excellent and helpful article! I had great cholesterol numbers before starting Keto and now my cholesterol is high. My HDL is good and my Triglycerides are low, but my LDL is high. I'm really questioning what I'm doing. I do experience many benefits of Keto, but I have a family history of heart disease and I'm worried and confused. Unfortunately my doctor is no use. She just says follow a Mediteranean Diet. End of story. Or go on Statins, which I would never do. Thanks to your article, I have some new resources to research.
You really provide such a service with your thoughtful, easy to understand, balanced articles. You have my admiration and my gratitude!

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Thank you so much for your kind words! I'm glad you found my article helpful.

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Hi Franziska,
thanks for summing up this debate. I have a couple of ideas about mechanisms;
firstly, the LMHR profile also applies to long-term fasting studies - this is perhaps where it can be observed in its natural, unconfounded state - LDL rises in lean healthy individuals during a fast, but drops or stays stable in those with obesity or atherosclerosis (period varies from 3-21 days). This is consistent with the keto pattern; this evidence clearly shows that LDL divergence is related to burning a high % of fat, and not to eating it, which is to some extent a confounder with keto (as shown by the cholesterol drop protocol and the possible different effects of different fat types and amounts).
No-one I hope thinks fasting causes atherosclerosis.
Secondly, the Scandinavian Simvastatin Survival Study (4S) determined that elevated LDL was associated with 2 phenotypes. One type featured high rates of cholesterol (re)absorption with low rates of cellular cholesterol synthesis. This was associated with high HDL, low event rates, and little or no added benefit from statin treatment.
The other type featured low rates of cholesterol (re)absorption and high rates of intracellular cholesterol synthesis, associated with low HDL, high event rates, and a significant benefit of statin treatment, which lowered event rates to those of the first group on or off statin.
Needless to say the second group was hyperinsulinaemic and IR; insulin stimulates cholesterol synthesis and inhibits (re)absorption, while glucagon has the opposite effect; enterohepatic bile cycling is increased by glucagon.
The second group will, I think, tend to see LDL drop if fasting because intracellular cholesterol synthesis will drop faster than cholesterol (re)absorption will increase. The first group will see it rise because (re)absorption can only increase, and synthesis is not excessive so has nowhere to fall to.
Hyperinsulinaemia also promotes macrophage cholesterol retention, so the risk in the IR group is also elevated for this and very numerous other reasons not seen in the naturally euinsulinaemic.
I don't think this difference explains the whole LMHR phenomenon yet, but it does I think help to characterise divergence in the responses to keto, and I think it possible that keto will eventually shift the phenotype in a low (re)absorber.
Residual risk of CHD also comes from factors such as smoking, pollution, autoimmune diseases (e.g. lupus, psoriasis, RA), infections, and nutritional deficiencies which may not make much impact on a basic lipid panel. Psoriasis for one is usually improved significantly by keto and weight loss.

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George, thanks so much for commenting. As usual, you provide exceptional  insight into the complex mechanisms on this topic (and others as well). I will ask Dave Feldman to take a look at your comments, as he will no doubt find them as intriguing as I do. Thank you again!

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You're welcome!
I'd also like to suggest that this has to relate to the extreme divergence in gallstone risk on a low fat vs high fat calorie restricted weight loss diet.
Increased enterohepatic circulation on high fat means that cholesterol is kept "in play" - bounced back into the bloodstream in ApoB particles - while low enterohepatic circulation, in people with with higher synthesis rates, during weight loss - when cholesterol is being dumped by shrinking cells - means that cholesterol can pile up in the gall bladder faster than it can be conjugated to bile salts and bile acids and faster than it can be extracted by the weak stimulus of low fat food.

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Thanks so much for sharing this additional information, George! I've worked with many women who developed gallstones during previous weight loss experiences on low-fat diets. Great to know the mechanism behind LCHF's protective effect.

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I was surprised that there was no discussion on the two primary risk factor markers which are total cholesterol / HDL and triglycerides / HDL. My HDL and LDL-P both increased with a decrease in triglycerides. As a result both Total / HDL and Trig / HDL decreased while on a ketogenic diet so overall the risk factors decreased.
There is also no need to measure LDL if triglycerides have decreased since there will be a decrease in apoB because triglycerides are the transporter.
Having said that. Given the significantly increased risk of heart disease as a result of hyperinsulinimea and cigarette smoking which far eclipses all other risk factors, if one were to reduce or eliminate both there would be no need to worry about the others.
While I can appreciate Mr. Feldman's efforts and I am also a hyper responder, I have no doubt that cholesterol levels are merely an artifact / symptom of the real cause of CVD which is hyperinsulinemia which for type 2 diebetics or pre-diabetics (which are simply undiagnosed diabetics) is due to high carbohydrate diets causing high blood glucose levels as well as other known causes of infllammation such as trans fat and high omega 6 to omega 3 ratios. In other words, there is no need to try and cure the symptom which is controlling lipoprotein levels directly.  
Given that the consumption of a high carbohydrate diet promotes inflammation and in turn causes CVD, is it any wonder then that our bodies would produce LDL particles which work to repair vascular damage, as they are needed to patch up the damage? Unfortunately LDL can only do so much under the constant onslaught of inflammation but had it not been there in the first place the person would not have survived as long as they did.
Again, I am surprised that there was no discussion regarding these obviously key aspects.  

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Hi Don, Thanks for your comments. I actually did discuss keto's benefits on the markers you mentioned, although I didn't go into the ratios:
"In fact, many people see little to no increase in their LDL cholesterol while experiencing beneficial changes in other markers, such as an increase in HDL cholesterol and a decrease in triglycerides, blood sugar, and insulin levels – all of which are associated with reduced risk of CVD."
On the other hand, there are LMHRs like myself who started off with high HDL, low TG, and low inflammatory markers; those values didn't change, while LDL increased to >200 mg/dL and LDL-P well outside of normal range.

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So Don-the fact that I have both high cholesterol (213 overall) and high fasting blood sugar (100) while on a Keto diet means...what????? I've been following a LCHF/Keto diet for the last 2-3 year. I just found this out in the last day or so. Now I'm getting confused and worried.  

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Hi Rhonda,
Neither I nor anyone else reading this can provide personal medical advice, so I am glad you are discussing your results with your naturopath, as you mentioned above. However, the values you shared don't sound high and are in fact quite normal on a keto diet, so I wouldn't be concerned.
Best, Franziska

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Good to know. I see my naturopath next week!

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I saw that the American Heart Association recently added coconut oil to its "Avoid" list. As you know, us keto-heads eat a lot of coconut oil, coconut butter, and other coconut derivatives. What's your take on the AHA's stance on coconut oil and what would you recommend for die-hard ketoers?

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Hello Rai,  I disagree with the AHA. I believe coconut products can definitely be included on a keto or low-carb diet, aside from those with an allergy or sensitivity. In fact, virgin coconut oil is one of my favorite fat sources, along with olive oil and butter  Smile

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Thank you so much for this article.  I just got the news that I have elevated cholesterol (263) and LDL's (142).  I appear to be a Lean Mass Hyper Responder as I have been on a high fat/low carb diet for 4 years and am a recently retired professional Ultra Distance Runner.  I continue to train at a high level.
Since my numbers were high my doc ordered a calcium scoring test which shows some mild calcium increase in my lower depending artery which is not normal for a female of my age and health.  Initially he wanted me to abandon the diet and follow a Mediterranean low fat diet.  I suggested I eat more monounsaturated fats but stay on the low carb diet and he agreed. I have seen a great deal of benefit from the low carb diet and am unwilling to give it up at this time.
I'm hoping my LDL's will go down and my HDL's and Triglycerides will stay where they are.

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Thank you for your comments and for sharing your story, Amanda. I agree with your plan to incorporate more MUFAs into your diet and wish you the best of luck going forward.

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The only time you should make a dietsry change if there is a progression in calcification. Your doctor is only assuming it is from the LCHF diet whereas it could have been developing for several years before and then the progression arrested by going on a LCHF diet (which is more likely in my opinion).

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Indeed, it is possible (indeed seems completely likely to me) that the calcification resulted from injury sustained over your running career, which is why it was unusual - was he comparing you with other ultra marathon runners?
That said, there's nothing wrong with MUFA in a low carb diet.

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Amanda, I'm in a similar boat, I think. Back in July, after 4 months on LCHF, my total cholesterol rose by ~50% to 296 and my LDL rose to 217. My HDL increased to 62 and my triglycerides decreased to 86.
I haven't yet had labwork to look at the important inflammation markers (I plan to ask for these to be included in my next bloodwork), but my doctor was a bit alarmed at the cholesterol increase and wanted me to abandon the LCHF. I was unwilling to do this, but I agreed to limit my intake of saturated fat and dietary cholesterol.
I cut eggs completely out of my diet (completely for a short time; more recently I've allowed myself a single egg every two days) and limited myself to ~15g of saturated fat a day, while increasing MUFA and PUFA. Luckily, I love olive oil and almond butter, or I would have found meeting my fat macro very difficult.
I can report that after a short time on this regimen that my total cholesterol and LDL returned to pre-LCHF levels. I lost part of my gain in HDL, but my triglycerides decreased even further to 79.
I should note that about a month before my most recent labs, my daughter and I took a trip to Italy. Suffice it to say that pizza and pasta was involved, so I can't say how much my most recent results were affected by the temporary high-carb sojourn.

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You mention in the table that “ this value reflects the size of your LDL particles. People with large, buoyant LDL are said to have pattern A, which is typically considered less artherogenic (LIKELY to cause plaque buildup in the arteries).” I think you mean to LESS LIKELY.
Other than that very simple and easy to understand. Maybe some day we will know the answer !

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Hi  Saleem,
Thanks so much for your comments.  I"m sorry if it appeared unclear -- I was actually defining the word "atherogenic" in the parentheses. I will have it arranged in a way that makes that clear Smile

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Wish I had this explanation when I went to nursing school! Excellent points. Thank you for posting!

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