The Functional Medicine Approach to High Cholesterol - RHR

The Functional Medicine Approach to High Cholesterol

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The message that “cholesterol is bad and if you have high cholesterol you should take a statin to lower it” is out of date and not in sync with the most recent scientific evidence. Unfortunately, the latest findings have not trickled down to the average primary care doctor—or even the average cardiologist. Today I discuss the six underlying causes of high cholesterol and how using the Functional Medicine approach to address those issues can often alleviate the need to take statins.

Revolution Health Radio podcast, Chris Kresser

In this episode we cover:

  • The functional approach to high cholesterol
  • Six underlying causes of high cholesterol
  • Conventional markers are not accurate predictors of cardiovascular risk
  • Other important cardiovascular risk markers
  • How I approach familial hypercholesterolemia

Show notes:

Chris Kresser:  Hey, everybody. It’s Chris Kresser. Welcome to another episode of Revolution Health Radio. This week, we’ve got a question from Tyler.

Tyler: Hey, Chris, really enjoy the podcast. I’ve been listening and interested in a Paleo diet ever since I heard you on the Joe Rogan Experience podcast last year. I’m somebody who takes statin medication for familial hypercholesterolemia. I’m wondering if you thought a Paleo diet would still work for somebody like me who’s on that statin medication, and I just wanted to get your thoughts on that. Thank you.

Chris Kresser: Thanks for sending in your question, Tyler. It’s a great one, but unfortunately, it’s difficult to answer in a short time. In a conventional paradigm, this is a really black and white, or binary, issue. You have total cholesterol and LDL cholesterol that are tested regularly, and if they are high, then the doctor will typically prescribe a statin and the patient is instructed to take it for the rest of his or her life and that’s the end of the story, but the reality is actually far more complex. We could do several podcasts on this topic. In fact, we could probably just dedicate a podcast to it and do it over and over again because there’s so much information to cover and there is so much new research that comes out that changes the landscape. Four out of 10 people that die each year die of a heart attack, so this is obviously a really big problem and one that doesn’t lend itself well to pat answers on a 20-minute podcast.

I’ve written a lot about this, and in fact, I got my start in this field writing about the relationship between cholesterol, lipids, and heart disease over 10 years ago now. Some of the earliest writings that I did were on this topic. More recently, I wrote an entire updated series on cholesterol and heart disease which we turned into a free ebook which you can download from chriskresser.com. If you haven’t already done that, then definitely check that out. One of the earliest digital programs that I put together was one called the High Cholesterol Action Plan, and if you Google “high cholesterol action plan” you’ll find it, and we can also put a link in the show notes, but this is a course that goes into much, much more detail than the ebook does because I got so many questions about this topic over the years, especially as I was writing about it early on. I just wanted to have a resource that I could direct people to that went into a lot more detail and provided a lot more assistance than I could ever do in a blog post or an ebook. So, if you haven’t checked all that stuff out, I would definitely do that.

In this show, I’m going to just provide an overview of what I think the key factors are to be thinking about with this particular question.

The Functional Approach to High Cholesterol

The first factor is to understand that a functional approach to dyslipidemia, high cholesterol, and even familial hypercholesterolemia is really different than the conventional approach. For those listeners who aren’t aware with familial hypercholesterolemia (or FH, as we’re going to call it so I don’t have to say that every time), FH is a disease that is—well, I mean, I don’t like the term disease but that’s what it’s referred to as—it’s a condition that is genetically mediated. There are genetic mutations involved that lead to very high cholesterol levels, often higher than 300 mg/dL. Believe it or not, it’s not that easy to test for. Some of the genetic testing that you have to do to completely be certain that you have it is very expensive and not widely available. In many cases, doctors will just—there are certain criteria called Simon Broome criteria that can be used to get a more accurate indication of whether FH is likely to be present. But I’ve seen that many clinicians in practice, if they see a total cholesterol above 300, they’ll often just diagnose the patient with FH on that basis alone, which is not a particularly accurate way of doing it, but there is certainly an argument to be made that FH is likely if total cholesterol is north of 300 mg/dL.

Six Underlying Causes of High Cholesterol

Anyways, back to the factors here. As I said, the first factor to consider is that the functional approach to dealing with this issue is very different than the conventional approach because in functional medicine, we view high cholesterol not as a disease but as a symptom. What is it a symptom of? Well, there at least six key underlying processes that can lead to hypercholesterolemia:

  1. One is metabolic dysfunction
  2. Another is chronic infections like H. pylori or even latent viral infections
  3. Another is gut dysbiosis permeability, that’s number three
  4. Number four is poor thyroid function, and this doesn’t have to be frank hypothyroidism, it can even be subclinical hypothyroidism or the thyroid is just—it’s not completely shut but it’s just underfunctioning, it’s not functioning optimally. In fact, back in the ’80s and prior to that, before statins came onto the scene in a big way, doctors used to use low doses of thyroid hormone to treat high cholesterol even when the patient had relatively normal thyroid numbers.
  5. The fifth cause is environmental toxins, especially heavy metals.
  6. And then the sixth cause would be genetic.

There are, of course, others, but those are the six main ones that we look for in functional medicine. We explore all of these causes to determine and address whatever the underlying or root pathology is because if you treat the root, that will often fix the branch. If you think of the disease process like a tree, the roots are those core pathologies or underlying mechanisms that lead to the symptoms, which in this analogy are the branches. You can mess around with the branches and try to deal with things on that level, which is the conventional approach, or you can try to address the roots of the problem, which is what we’re doing in functional medicine.

In a conventional paradigm, it’s really a lot more about symptom suppression. If you have high cholesterol, you take a drug to lower it, a statin drug in this case. If you have high blood pressure, you take a drug to lower that, and it’s the same for many other conditions.

In your case, Tyler, you mentioned that you have FH, which means we know you have at least one of the six underlying factors present—the genetic predisposition, but that doesn’t mean that other factors aren’t also playing a role. In fact, I see this very often in my practice where the patients come in and they already know that they have FH but when we do a full comprehensive workup, we find that they also have poor thyroid function, SIBO and gut dysbiosis, maybe a latent chronic infection and heavy metal toxicity and all of those things are exacerbating the genetic predisposition to high cholesterol.

Conventional Markers Are Not Accurate Predictors of Cardiovascular Risk

The second factor to consider is that conventional lipid markers, which are the ones that we typically have tested for if you go to your doctor for routine blood work, so I’m talking about total cholesterol, LDL cholesterol, and HDL cholesterol, are not accurate predictors of cardiovascular risk. The most recent research has shown that these markers, total and LDL cholesterol, are not strongly associated with heart disease. The ratio of total-to-HDL cholesterol as well as non-HDL cholesterol, which is similar, are better predictors than total cholesterol or LDL cholesterol, but they are nowhere near as predictive as some of the newer markers like LDL particle number, which in turn itself isn’t as predictive as lipoprotein(a), or Lp(a). These markers, they tell us something different than the standard lipid markers.

The standard lipid markers tell us how much cholesterol is inside of the lipoproteins, so if we use an analogy in your bloodstream as like a highway, the passengers inside of a car are equivalent to cholesterol inside the lipoproteins, whereas the cars themselves would be equivalent to the lipoproteins. Extending this analogy, if you have a lot of cars on the road, there is a much greater likelihood that they’ll get into an accident, they’ll be off the road and slam into the side of the road, and the side of the road here would be the fragile lining of the artery, the endothelium. If you have a lot of LDL particles, which is reflected in the LDL particle number measurement, then because atherosclerosis is a gradient-driven process, there’s a much greater likelihood that one of these LDL particles is going to damage the fragile endothelium and initiate the process of plaque formation.

With lipoprotein(a), we know this is a different type of lipoprotein. I’m not going to go into a lot of detail here because it’s, I guess, pretty geeky, but it’s known as one of the most atherogenic lipoproteins that have been identified and it’s the single most significant lipid risk marker for heart disease. Of all of the things we could measure in terms of lipid markers, lipoprotein(a), or Lp(a), is the most predictive for future risk of heart disease.

The point of this second factor is that what we measure is important. Usually, doctors are only measuring total and LDL cholesterol, but what we really should be measuring as clinicians are things like LDL particle number, HDL particle number, and lipoprotein(a). These give us a much better idea of overall risk.

Other Important Cardiovascular Risk Markers

Third factor is that lipid markers, even the good ones, are only one part of the puzzle when it comes to quantifying overall risk. We need to look at things like family history, inflammatory markers like C-reactive protein, fibrinogen, Lp-PLA2, oxidized LDL, metabolic markers, so things like fasting insulin, fasting glucose, fasting leptin, post-meal blood sugar, hemoglobin A1c, and a variety of other markers that tell us what’s happening with metabolic function. Hypertension and smoking are two of the strongest risk factors for heart disease, hands down, so those of course should always be looked at. Diet, lifestyle, stress, nutritional status—either not enough of nutrients like vitamin D or too much of a nutrient like iron can increase the risk of heart disease. Status of the gut microbiota, there is an increasing amount of research that shows that this plays a significant role in heart disease pathogenesis.

There are certain calculators out there that are available for free online that use at least a small number of these risk factors. The Reynolds Risk Score, for example, uses C-reactive protein and systolic blood pressure in addition to age, total cholesterol, HDL cholesterol, and family history to determine the 10-year risk of heart disease expressed as a percentage. You enter all of your information in and it turns back up a percentage of what percent of the risk you have for having a heart attack in the next 10 years based on all of these validated criteria. The lowest it could be is 1 percent, and then it goes up from there, and you can put different numbers in there and play around and see what has the biggest impact on risk, and you’ll see that it’s not total cholesterol or even HDL cholesterol, but age actually is the biggest risk factor for heart disease. You’ll see changing the age around has the biggest impact on that risk prediction.

There are other types of testing that look for objective evidence of plaque accumulation, like a calcium score and CIMT, and these are tests that a doctor can do when/if they are warranted, and they provide a different angle. The lipid markers are just looking at blood markers that are typically associated with heart disease, but a calcium score and carotid intima-media thickness test can tell you what’s actually happening in terms of plaque accumulation.

How I Approach Familial Hypercholesterolemia

Those are three factors to consider, and here’s how I would approach someone with FH: I’ve had many patients with FH, so this is what I actually do. I would start with a more advanced testing to determine what their LDL particle number, lipoprotein(a), and other important markers are like—fasting insulin, fasting post-meal glucose, inflammatory markers etc.—and then I do a thorough history and get a thorough family history as well. We do then an entire functional medicine workup to determine if they have other contributing factors like SIBO, dysbiosis, infections, heavy metal toxicity, hypothyroidism, etc. We address all of those factors that we discover in that extensive workup. Then we retest all of these markers, and if they are then normal, great, our work is finished.

If the markers are still elevated, we’ll move onto a more detailed risk quantification. We may refer them out for calcium score, a CIMT, and we may look at some of the other risk factors, lifestyle, stress, etc. Then if we deem that the risk is still significant, we’ll try more advanced diet modification strategies. If they are a hyper-responder to saturated fat and that increases their LDL particle number, we might put them on more of what I call a Mediterranean Paleo approach, which is Paleo that’s lower in fat and higher in Paleo-friendly carbohydrates, whole-food carbohydrates like starchy plants, and even whole fruits, non-starchy vegetables, and then we’ll emphasize monounsaturated fat more than saturated fat. Then, we might use some supplements that have been shown to reduce LDL particle number and address inflammatory processes like delta and tocotrienols, pantethine, curcumin, etc., and these will often lead to a significant reduction in these various biomarkers that are risk factors for heart disease, even lipoprotein(a), which is in the conventional paradigm, thought to be almost entirely genetically mediated and not really amenable to diet and lifestyle change. Furthermore, it’s not typically affected by statins.

If the numbers are still high after all of that, which is a lot, that process takes typically several months if not longer because of all of the testing and all of the dietary intervention and the retesting, exploring, and investigating all of those various underlying causes, then if the numbers are still high and the patient is in a very high risk group, only then would I, especially if it were me, consider statins and other medications. Statins are not effective, as I mentioned, for reducing lipoprotein(a) in many patients, and so if that’s the primary marker that’s still elevated after all of this workup and treatment, those patients may need new drugs called antisense nucleotides, or ASOs, that specifically target lipoprotein(a). That’s just one example of how even the pharmaceutical aspect of the treatment, if it’s determined that it’s needed, can be more individually tailored based on the patient’s unique circumstances and based on the most recent evidence rather than just using a one-size-fits-all, black-and-white approach, which is the typical way that it’s done in the conventional paradigm.

Tyler, I realize this may have raised more questions than an answer perhaps. Unfortunately, that’s what happens when you dig into some of these topics. And this is, as I said at the outset of the show, certainly one of the most complex and nuanced areas of medicine and treatment. There are so many different things to consider and I think the big public health campaign during the latter part of the 20th century was oriented around making this message as simple as possible, so that people would comply with the diet and lifestyle recommendations that were being made. This really oversimplified the message of “cholesterol is bad and if you have high cholesterol you need to bring it down and you should take a statin to do that” is really out of date and not in sync with the most recent scientific evidence, and the lipidologists, the folks out there like Dr. Tom Dayspring and others, are way, way ahead of how they approach cardiovascular disease and have been for many many years but that has not trickled down into the mainstream understanding at lexicon and to the average primary care doctor’s office. The training for primary care doctors is really out of date unless someone is really taking an initiative to stay on top of all of this stuff or if they are lipidologists themselves. Even a lot of cardiologists are not current with this information and so it’s a problem for patients who are trying to get help. It is really difficult to do that from your local doctor unless they are really staying abreast of all of these more recent developments. At least this podcast can give you some food for thought and places to look for further information and discussion with your practitioner.

We’ll put some links to all of the resources that I mentioned here in the show notes, and for everybody else, keep sending in your questions. Tyler, thanks again for sending your question in, and that’s it for today. I’ll see you next time. Take care everybody.

  1. Can you comment on the controversy surrounding the use of niacin for reducing triglycerides and Lp(a) and raising HDL? Thanks.

    • I would love to hear advice I have very high lpa 135 nmol and high ldl at 123 but luckily the large particles and I have high HDL and low trigs. I take 3000 mg once every am for lpa I’ve seen some drop not significant. Don’t mind the flush which is very minor but am considering upping it to 4000 mg but not sure if that crosses that liver Safe threshold. I’m very fit but small 102 lbs
      Lpa seems to be the only thing that lowers lpa

      • High Cholesterol could be from a copper Deficiency. Copper is essential for liver health. If the liver lacks copper for proper function, the symptom could be elevated cholesterol. A functional medicine doctor might request an RBC Copper Test. My mom’s Cholesterol was over 300. After a copper test revealed a severe Deficiency, she was given a copper supplement with some dietary changes. After 6 months her total cholesterol dropped to 202 and HDL increased by 10%.

        • originally i actuall had high copper along with mercury and aluminum and vit d 3 i have mthfr and do not clear toxins or heavy metals well. i did take zinc carnosine and picolonate, which reduced copper to normal now but i think i just have that genetic high cholesterol due to apoe 3/4 which means i am a hyperesponder to fats and cholesterol for my high ldl and high lpa, i take 3 grams niacin, pycogenol, magnesium, methyl b complex, l reuteri probiotic and am adding citrus bergamot as i hear it is actually very effective in lowering lpa which is the biggest issue i have . i also take boulouke (lumbrokinease, to keep fibrin levels in check)

          • Policosanol has been shown to be more effective than stations without the side effects. It increased the hdl and lowered the ldl. Whereas Lipitor lowered both lol and hdl. After 8 weeks Policosanol reduced total cholesterol almost as much as the Lipitor. 20 mg of the policosanol crom a sugar cane extract was recommended once a day. The key is no side effects.

  2. I remember when I first got “sick” with chronic fatigue syndrome around 2009 one of the first doctors I saw tried to put me on statins and say that high cholesterol was causing my brain fog and fatigue.

    Another endocrinologist backed him up too. I’m trying to see if some of this stuff will maybe help my dad though as he is getting up there age wise and is on statins which I don’t think are a good idea except as a last resort.

    • If the ratio of HDL and LDL is more important then the actual amounts, then is the problem the physical properties more important.

      Ted

  3. Chris, have you studied the effect of the ApoE genotypes? I am E2/E4 (“normal” being E3/E3) and have been told that this might cause my HDL to “act” like LDL instead of being a protector of it. Any thoughts on that?

  4. You mentioned latent viral infections as a cause for high blood pressure. But how do you treat viral infections? Particularly infections of the vagus nerve? I believe my vagus is infected and there’s no treatment available for me.

  5. What do I do if I don’t have a healthcare provider who will do all of this? I have very high particle number as well as cholesterol over 300. I’m 52. What do I do?

  6. Great post and good information. I am 67 years old. Recently my lab results show the following: cholesterol is 253 mg/dl; LDL Cholesterol (Calculated) is 150 mg/dl; TG is 47mg/dl; HDL Cholesterol is 101 and my Cholesterol/HDL ratio is 2.57. One year ago I was told that my LP(a) was high, hs-CRP was 0.8 and LDL-p was 1593 and none of these were measured this time. The doctor said that I have E3/E4 genotype. Saturated FA index was borderline and monounsaturated FA index was high. My physician recommends taking niacin if I do not want to take statin. CYP2C19 is (*1/*17). DO I have FA?

    If I understood you well, I really have to worry about lowering my LP (a) as well as my cholesterol? If so what would you suggest that I do. I eat healthy – mostly organic, lots of vegetables and some fruits. Protein from grass fed cattle and free ranch chickens and from beans. My physician also recommended Methyl CpG , metabolic B complex phosporylated and Ubiquinol. Not sure where to begin. I am confused after reading your post and I sure need some guidance. Thank you.

    • How does the Reynolds Risk Score account for the fact that one can have a normal blood pressure due to fact that he is on anti hypertensive medication?

    • Hello your profile sounds almost identical in numbers/levels as me i am an avid athlete, eat very well but still struggle with high LDL and very high lpa(135 nmol) what is your level. i am taking 3 grams of niacin every day but its not helping as much as i expected it to. (niacin apparently works better on those with small lpa vx large lpa isoforms..so im thinking i have more large lpas (i do know i have the large ldl particles) i have recently read a lot of citrus bergamot being very effective in lowering lpa; most drs wont treat lpa they just want to lower ldl as much as possible, i will avoid statins , lowering ldl too much raises risks of cancer and infections, and also raise lpa I agree with a methyl b complex and co q 10, in addition to niacin i would all bergamot and magnesium as well as vit k 2 in mk 7 form, it shuttles calcium from arteries to bones ..

  7. Thanks, Chris, for illuminating this confusing issue!
    Luckily, I don’t have any of the problems you discuss, but from the many comments I see that many people do.

  8. Hi Chris,
    Thanks for your consistently high quality work on cholesterol.
    Would blastocytis hominis(??), be an example of the infections you describe as contributing to cholesterol problems? Any treatment suggestions?

  9. The study below explains why LDL P is a better indicator than LDL C

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3070150/

    As stated above LDL C (the usual measure given by your doc) is the number of passengers on the highway. LDL P is the number of cars. Looking solely at people who have LDL C that does not marry with their LDL P, for example high LDL C but low LDL P, then LDL P was the better predictor. This suggests that the number of cars is more important than the number of passengers. We are better served by having a low number of cars LDL P

    Have I got this right ?

  10. Thanks for this nice update, Chris. I’m trying to institute some of these investigations in my traditional hospital neurology practice at a major stroke center. Can you share what lab you’re using for the Lp(a) study, and if you know whether most insurance plans would cover that? Turn-around time has been a problem with getting oxidized LDL or particle number study results back before the patient has been discharged. The physician doing the follow-up visits may not know how to interpret or react to those results.

  11. Hey Chris, I have been working on an article to help the general public (non-health nerds like me) to understand the key markers we can rely on to determine heart disease risk and also, practical ways we can reduce our chance of heart disease. So this podcast is very timely!

    I know you and Dr. Attia run in the same circles and are friends so I’m curious about your thoughts on this. Pete seems to think LDL-P is the best marker for heart disease, but you’re saying Lpa is a better market. Just curious as to why?

    A topic for another episode I guess but wanted to ask the question.

    I’ll be pulling together your thoughts about Heart Disease on this article (http://www.renegadedad.net/what-is-the-best-indicator-of-heart-disease-risk) as well so I’m really looking forward to any additional info on this topic such as:

    1. What are the ideal ranges for the various markers you check like LDL-P, Lpa etc.

    2. What can we do to get these markers into the ideal range – nutritional, exercise, sleep and mental/emotional changes/strategies?

    I know this is a LOT so any feedback is greatly appreciated!

    As always thanks for all you do to help change lives Chris!

  12. I’m 66, do weekly sprints and super-slow weight training, am in the best shape of my life, eat a lot of high cholesterol foods and have a total cholesterol of 516. I don’t have familial hypercholesterolemia. My HDL is high, triglycerides and CRP are low. The total cholesterol only went up after I started eating more high cholesterol foods. I had a heart scan done and my coronary arteries are completely clear. In my experience diet does affect cholesterol levels and it’s irrelevant.

    • Chris Masterjohn reckons 20% of people are sensitive to dietary cholesterol and I reckon he could be right. I had a week on Liver and eggs and my LDL went up from 3.0 mmol to 4.1 mmol

      • yes hyper responders to fat has a lot to do with apoe type apoe 3/3 normal, apoe 3/4 more hyper responsive, apoe 4/4 most hyper responsive to fat wheres apoe 3/2 and 2/2 do well on higher fat, lower carb meal plan also apoe 4s have a tendency to ALSO over absorb plant sterols where in most . plant sterols lower cholesterol, with those who over abosorb plant sterols, good fat like olive oil, nuts etc can turn into a form of cholesterol worse that cholesterol from sat fats (in these people) its frustrating as i am apoe 3/4 which means eating higher carb, low fat, low sat fat BUT also over absorb plant sterols so on other hand told to not eat as much plant foods and more saturated fats! same hold true with lpa and ldl. lpa calls for sat fats whereas ldl calls for plant fats/

  13. I would like to be a patient.
    What do I need to do??

    Also, what blood tests do I need to create a fact based plan. I have an excellent clinician to take blood.

    So thankful for your work!!

  14. Chris, I am on a daily regime of Letrozole which I believe raises cholesterol. Throughout my adult life my doctors have told me that I am genetically pre-disposed for high cholesterol and up until three years ago I was on Lipitor. At that time I stopped to hear negative reports a long-term Lipitor use so I stopped taking it and have been trying to control my cholesterol levels with diet and excersize. Last week my blood profile came back at a combined cholesterol of 340, with a high HDL score of 85. I tend to stick to a Paleo/FTD diet with no gluten grains very little dairy and no processed sugar. I am going for a calcification score on my heart on Monday. Four years ago I had the same test done and the calcium accumulation in my heart was zero. I have recently decided to go Mediterranean Paleo, in other words a pescatarian diet, if my calcium score is again at zero is this necessary?
    I am happy to call and pay for a consultation with you or one of your associates as I live in Ohio and I believe you are in California.

  15. As my cholesterol numbers go up so does my bilirubin. Cholesterol numbers go down, so does bilirubin. Both markers are always high, meaning above the high mark in the normal range. There got to be some connection. I am 103lb female.
    Example. Bilirubin-2.7, TC-272; LDL-179; HDL-73; TRIG -167
    I do chronic HPylori.

    • interesting as i have actually read higher bilirubin means you have better cholesterol Bilirubin is known to be negatively associated with serum parameters related to atherosclerosis.

    • Treat H pylori with metula tea from Africa. Drink 2 per day for 30 days. 1 at morning & 2 at night. My fm dr has s success rate of 95%.

  16. I have had some of these tests last month. I return to see the functional medical doctor that ordered them in a few weeks.
    I dont quite understand all the ins and outs of the testing, seeing im a patient, not a practitioner.
    I did understand I do have small particles B type. Few other things were elevated as well. My question is,
    Could these tests be pointing toward greater risk for heart attack or stroke because of a problem with my liver?
    I have NASH and Im trying very hard to turn it around. Evidently my liver is just making fat, in turn i have high cholesterol and triglyceride levels, gallbladder was removed , stones made of cholesterol. I had Sibo its now cured after 2 years. I’m sure i have leaky gut now because I tested positive for hoshimototes. Things seem to be snowballing. I had my doctor refer me to a hepatologist and had a liver biopsy that diagnosed NASH because of elevated enzymes in my blood.
    My Gut is telling me my root cause is Liver disease not sibo.
    Is this possible?
    The functional medical doctor I see, is actually a Gym biodenticle hormone doctor. Im looking for a whole body functional doctor. Im on biodenticle hormones, im on levoxyl which in fact is not working at all. Another reason I think its my liver not converting T4 to T3. Im only a person that advocates for her own health. Ive done some deep researching while sick. I would love to hear your input.
    Thanks!

    • Maybe your thyroid is under medicated. Cholesterol levels normalise when thyroid is optimal ….

      • thyroid can have an affect i struggle with high LDL and high lpa nad actually always am hoping that thyroid tests come back low, but always normal! which is great in one sense but how easy would it be if i could just take thyroid hormone and solve everything i think another factor to mention is estrogen that can profoudly affect chol levels. i have always had low estrogen and believe that is definitely a cause of my levels im 46 now and trying to find a doc who will prescribe bio estrogen and progesterone complex

  17. I have a number of issues arising that are all currently labeled “idiopathic” (neuropathy, osteoporosis, high cholesterol), and I’m not sure they aren’t all connected somehow. Slowly but surely I’m checking off tests in search for resolutions (I feel like I”m on my own in this search- conventional doctors are sympathetic but not too helpful in out-of-the-box tests.) I have had serum tests for heavy metals and all looks well. Is this sufficient? Word is I might need to dig a bit deeper, and am not sure how to find a reputable lab/method? May you make some suggestions on what to look for? Thanks in advance.

    • Serum tests for heavy metals are not enough. I am a practitioner in Australia and use an Oligoscan to test for heavy metals. More reliable.

        • I would look into supplementing with mk 7 form of vit k it can help with cholesterol and bone health and is vital in keeping calcium out of arteries and into bones. also, get a test for the mthfr gene (boston heart dignostics) if you are mthfr, supplementing with a methyl b complex is vital. you could so heavy metal hair test but i would first get the other mthfr test first/

  18. Hey did you see Dr Oz yesterday? First talking about how great statins are and then the amazing benefits of corn oil!!! He said Mazola was one of their sponsors and sent everyone hone with a bottle of corn oil. Said it should be one of the main oils for cooking and will help reduce cholesterol.

  19. Great post and I see this in practice as well. We run a very specific panel as well to test the patients and their overall heart health. Thanks for sharing Chris.

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