In my efforts to control my cholesterol I finally decided to seek help from an expert and scheduled a consultation with a board certified lipidologist. Last week I shared my prep work and the questions I wanted to ask when I met her.
This week I’ll share with you the items we discussed during our meeting and her answers to my questions.
A lot of this will be super technical, so if you’d like, you can skip ahead to the bottom of the post where I’ll put together a brief too-long-didn’t-read type of summary, but otherwise read ahead.
Our discussion covered a broad range of topics and was unstructured (like most normal converations), so I did what I could to organize things here.
General Info
- She knows Dr. Attia and Robb Wolf and is familiar with their work (this along with the her being recommended by Dr. Dayspring told me that she was legit)
- She works with Health Diagnostics Labs
- She has taken care of patients following ketogenic diets and has seen a lot of them miraculously improve clinically
- There is a certain percentage though that she’s seen with a dramatic rise in LDL
- Briefly reviewing the physiology of cholesterol metabolism she explained that the vast majority of cholesterol in our system comes from endogenous production and that eating cholesterol from food has minimal effect on blood cholesterol levels
- She likes the Mediterranean low glycemic diet
- Artificial sweeteners and poor quality red meats or pro-inflammatory
- She thinks that eliminating gluten, dairy, soy, and casein can definitely help with gut health, but given my history, doesn’t think that diet is a particularly problematic area for me.
- If I ever get put on antiobiotics, it can really screw up my gut, so it’s important to take probiotics afterwards. Her favorite is Klaire Labs Ther-biotic
- She was impressed by the amount of research that I’ve done (yay, I got a gold star from the expert!)
The Lipidologist’s Thoughts on Cholesterol Tests
NMR Cholesterol Panels – These are her cholesterol study of choice. She only trusts the Liposcience NMR and says that some lab companies are coming up with cockamamie particle tests that are unreliable.
She also explained that the Liposcience machine is a 400 MHz machine, but the NMR machine used at Health Diagnostics Labs is 600 MHz, which may allow for more precision, but this still needs to be studied.
LDL-C – She doesn’t care too much about this. If it goes up and it’s not atherogenic and it’s not oxidized then it doesn’t really concern her. What matters more to her is the particle count.
LDL Particles – A high particle count is correlated with increased cardiovascular disease risk whether it’s primary prevention or secondary prevention.
When she sees a high LDL-P, there can be many potential causes, and it’s important to understand why (this is what I want my doctor thinking, so I was happy when I heard her say this).
Some things that can cause an elevated LDL-P include:
- Familial Hypercholesterolemia (FH) – These typically respond to statins
- Insulin resistance
- Hypothyroidism
- Gut Health – leaky gut can allow proteins into the blood stream that shouldn’t be there and cause inflammation
Regarding my LDL Particle size, on average it’s larger rather than smaller, but it doesn’t matter because particle numbers are what matter to her. The size isn’t as important because large ‘fluffy’ LDL particles are still dangerous! If there are too many and they’re oxidized inflamed, then that’s when we have problems.
Pattern A vs Pattern B is old nomenclature and not really used anymore.
Lp(a) – Despite having a normal level a few years ago, she says that the type of test that was done was the ‘mass test’ which can be less accurate.
Measurements of Lp(a) can be complicated because the molecules are complex. They’re essentially LDL particles but have an extra ‘cringle’ on top, which is individualized, and can affect how their measured.
Health Diagnostic Labs can actually measure the particles themselves, which she feels is more accurate and is independent of the changes caused by the extra cringles. I would only need to have this test done once (I had zero clue into any of this so I was glad I was working with an expert).
Lp(a) particles are extremely atherogenic.
Sterol Testing – Now is a good time for me to test because I’m drug naive. Knowing whether I am a hyper-synthesizer or hyper-absorber will help determine the best course of treatment.
Oxidized LDL – This is something we can measure now, but the assay is not perfect. At her lab, they’re still trying to understand what the proper reference ranges should be and there can be a lot of noise to interfere with the results. While she wouldn’t put all her eggs in this one basket, she thinks it’s still helpful to know.
Apo B – Her bias is to do NMR over Apo B to measure LDL particles, but she likes to order both. People who are insulin resistant have small LDL particles which the Apo B assay just might not pick up.
Some people can also have a high Apo B and a normal LDL-P (seen in type 3 dyslipoproteinemia) because they have a lot of remnant particles, so the LDL- looks normal but the remnants cause the Apo B numbers to be high.
LP-IR Score – A proprietary formula taking into account NMR info, created to simplify things for physicians. In my case it’s saying that I’m not insulin resistant, but she doesn’t put a whole lot of weight into what it says. It should also only be used in drug naive patients because drugs will impact the score.
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The Lipidologist’s Thoughts on Other Tests
APO E Genotype – People with E4 alleles are associated with cholesterol hyperabsorption and therefore don’t tend to respond to statins.
E4s have a higher risk of cardiovascular disease and Alzheimer’s risk. She was actually very careful about this part and made sure I was ok with knowing my Alzheimers risk of we decided to get this study because informed consent is very important to her (another sign of a good doctor).
There can be a psychological impact to knowing this information and some patients opt absolutely don’t want to know. I wasn’t one of them, and opted to have the test done.
MTHFR – She thinks it’s very important to know my MTHFR status because this system is involved in methylation pathways that involves B12, folate, homocysteine, and other neurotransmitters.
Mutations in these single nucleotide polymorphisms can mean an increased risk of clotting and determine whether the methylated forms of folate and B12 are better for my body.
23 and Me – I asked if instead of checking genetic markers separately, whether it would just be easier for me to get a 23 and me test done, my main concern was the privacy issues with 23 and Me selling data to big pharma.
She said that she doesn’t recommend her patients get this done because there’s just too much noise and it can be easy to drive yourself nuts.
Homocysteine – A high level is associated with increased clotting risk and cardiovascular disease. It’s not realted to LDL-P but is a separate risk factor for atherogenesis. If this is high, it’s important to understand why.
Genova Diagnostics Gut Test – Stool test to determine if there are is any infection, inflammation, or pathogenic microbiota in the gut.
She’s had patients with atherogenic lipoprotiens resulting from a damaged gut after prolonged antibiotic use. After treatment with probtiotics, there was a significant drop in the lipoprotein particles.
TSH – She likes it under 2.0. If it’s over then she would start thinking about subclinical hypothyroidism.
Insulin Resistance Panel – This includes glucose, HbA1c, Ferritin, alpha hydroxybutyrate (early marker of insulin resistance), insulin, pro-insulin C peptide, and Anti-GAD antibody (antibodies to pancreas).
While I don’t look like someone who is insulin resistant by my physical appearance (I took this as a compliment), she said that you can’t always tell by looking at someone. People who are insulin resistant typically have increased abdominal fat, but then there are plenty of thin people who are also fit that turn out to be insulin resistant.
Post Prandial Glucose Index – This will help determine what my post prandial glucose trends are. If my glucose levels go over 180 consistently, then we should see an increase in PPGI. This will tell us how my body processes sugar, so if I have a normal average glucose, but it spikes high after a meal and plummets down immediately, this can cause inflammation.
Omega 3 Index – This will look at how much omega 3 is being incorporated into RBC membranes. When this is low, this can be associated with increased cardiovascular risk.
We want this value to be over 8%. She recommends eating salmon, herring, and fish oil to get it up. She recommends against Krill Oil because there isn’t a lot of EPA and DHA in it, so it has very little effect on the Omega 3 index.
PCSK9 – This is part of the genetic panel and can be ordered in the future, but she wouldn’t recommend checking it now since it wouldn’t change what we would do.
PCSK9 drugs are coming out now which show an improvement in cholesterol numbers, but there still isn’t enough data on long term outcomes.
Galectin – It’s a marker for fibrosis (scarring) best used in patients with CHF. She doesn’t think it’ll be useful for me.
NT Pro BNP – A screening test to see if the heart is stressed at all. If it comes back in the intermediate range, that can be due to sleep apnea or hypertension.
What does she think about my overall cardiovascular risk?
She would put me at moderately high because of my LDL particle count.
Does she think I’m insulin resistant?
Given my past LDL-P and HbA1c it looks like I am, and it looks like I’ve maximized what I can do with diet, exercise, and lifestyle.
My HbA1c of 5.7 can be interpreted as pre-diabetic based on certain guidelines.
Why am I insulin resistant?
She thinks it’s genetic. Insulin resistance is basically the body not responding to insulin which can either lead to high blood sugars or high insulin. In fact, people can suffer from hypoglycemia from the high insulin in later stages of insulin resistance before becoming diabetic.
There may also be an autoimmune component in my case since my insulin levels are low.
How she likes to approach insulin resistance
She believes in treating insulin resistance aggressively.
When people are insulin resistant, they get small dense LDL, large GLDL, and small HDL particles, and these particles get worse and worse as people progress to diabetes.
Lipoproteins give us information about insulin resistance and diabetes that glucose can’t.
The tools she uses to treat this include diet, exercise, and other lifestyle changes along with pharmacologic agents like Metformin, Actos, and GLP1 agonists.
Her objective is to address insulin resistance before it becomes overt diabetes where there is permanent damage to the pancreas.
Metformin is a very inexpensive drug and has been around a long time. It’s not as good as other drugs at preserving pancreatic beta cell function, but it can help improve insulin sensitivity and decrease abnormal secretion of glucagon in response to blood sugars. It’s especially effective in the insulin resistant pre-diabetic population.
It makes the body more sensitive to insulin and preserves the general function of the body so the pancreas doesn’t have to work too hard, but it doesn’t have a direct effect on the pancreas.
It can also deplete B12 levels, so it will be important to supplement with B12 if using this.
It’s metabolized through the kidneys, so if used, it will be important to follow kidney function closely.
Actos is another drug that is safely used in pre-diabetics and is good at preventing progression to diabetes and preserving pancreatic beta cell function. It does however have side effects like weight gain, aggravation of CHF, and increased risk of bladder cancer.
Byetta is a GLP1 agonist that is also used in treating insulin resistance and also helps in preserving pancreatic beta cell function.
Berberine is a natural supplement that can be helpful for insulin resistance.
Bergamot is another supplement that can be considered.
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Does she think I’m inflammed?
While my CRP levels have always been low, my elevated Lp-PLA2 concerns her (this is pretty much my own feeling too).
Lp-PLA2 is a marker of vascular wall inflammation, but she’s also seen people who are avid athletes with an elevated Lp-PLA2 (this may be the case with me since I’ve been training BJJ so aggressively lately), and therefore the elevation is benign.
The combination of the high LDL particles and Lp-PLA2 is very worrisome to her (to me too!!!), but she thinks that all of it is treatable and that I’m young enough to deal with these things (whew!).
Why does she think my cholesterol numbers are so crazy?
She suspects the root cause of my high LDL-P is insulin resistance.
When I asked her if it could because my body is shunting ketones into a cholesterol synthesis pathway, she says this could be possible, but there’s no way to really measure this right now.
She’s also familiar with the hypercholesterolemia in anorexics but says that they typically normalize quickly, so she doesn’t think it’s the case with me.
Does she think I could have Familial Hypercholesterolemia?
While my LDL-P numbers are in a range to indicate FH, my family history and prior normal LDL doesn’t fit with it.
People with FH have abnormal LDLs as kids because the underlying issue is an LDL receptor problem. It usually responds well to statins, but in people who don’t respond to statins, she uses Niacin, Zetia, and bile acid sequestrants.
Is there any role in CIMT and Coronary Calcium Scans for me?
Not for someone in my age, besides if they find something, it wouldn’t really alter the course of what we do.
Is there any benefit in reducing dietary fat?
She doesn’t think saturated fat in moderation is bad for everyone. Moderation is hard to define. People who have been on very very low carbohydrate diets are consuming loads of saturated fat, sometimes up to 33% of calories. When she sees high particles, then clearly this is not optimal for this patient.
She doesn’t like putting limits in percentile in diet. Sources are important. If sourced from grassfed beef, then it’s probably going to be less problematic. She’s not a dietician, so it’s a matter of making sense with diet, eating things as close to the earth, and with as little processing as possible.
Bad sources of saturated fat can be problematic for inflammation.
Should I continue eating keto?
She says ketosis probably isn’t the best approach for me, given my past experience.
Low carb without going completely ketogenic is probably what would work best for me.
Some people just do amazing in ketosis. She also sees people who do long term ketosis and end up depressed and have other adverse effects on mood, so she has mixed feelings about long term ketosis.
Too Long, Didn’t Read: Summary
She thinks that my elevated LDL particle count is likely due to an underlying genetic predisposition for insulin resistance, and thinks that currently my cardiovascular risk is moderately high. There are many options to treat this, but we will first order a bunch of tests to try to figure things out.
Next up… we go over the labs she ordered.
*Image found here
would you mind me asking how much to consultancy cost and the lab test cost ?
Sure thing… will email you.
Thanks for sharing the whole. I just can’t stop thinking of some of your previous tests where you reduced LDL when you ate more carbs. Why not give it another try?
I’ve tried upping my carbs up to 150-200 gm per day… and it didn’t have any effect… lowest it got my LDL-P was to around 2400. So while I think the lack of carbs may have had some influence… it definitely isn’t the whole story.
Thanks for sharing all this, very informative. I remeber you blogging about your HbA1c not being correlated with your blood glucose. Have you doene any more tests to verify your HbA1c of 5.7?
Yes, the lipidologist ordered another HbA1c, which my next post will be about.
Also I’ve checked my HbA1c pretty regularly in the past 2-3 years, and it was always a solid 5.7
Also, i think it will be pure guessing to diagnose someone with insulin resistance without doing OGTT with insulin measurement over at least 2 hours?
I had the same thought about this, but given my HbA1c and my particle count and my fasting sugars, she seemed pretty convinced. I may not have overt pre-diabetes, but she seemed to think there is probably some underlying insulin resistance there.
I’ve checked my fasting sugars and when I’m not ketotic my sugars bounce up into the mid to high 90s… Given my activity level, it should probably be lower, so this is another data point the tells me that she’s probably right.
Has she considered low dose statin? Say 20mgs QED atorvastatin?
Yes, that was something we discussed, but we both agreed that statins would be a last line therapy if other things don’t work.
Her recommendation was something like 5 mg of crestor every other day.. and to titrate up from there if needed. She really believes in LOW dose statins… and that they should be avoided as much as possible… which is something I definitely appreciated.
http://www.hcplive.com/publications/internal-medicine-world-report/2014/march-2014/New-Cholesterol-Treatment-Guideline-A-QandA-With-Thomas-Dayspring-MD-FACP-FNLA-NCMP
That’s a great interview, thanks for sharing it!
I think your next best point of attack would be to stop listening to paleo gibberish.
Start by adding lots of beans to your diet in some form or another. Then start increasing carbs from other whole food sources.
You’re LDL and particle numbers are terrible. And I doubt they will ever improve unless you cut wayy back on the butter, ghee, coconut oil and other fats and slowly replacing them with healthy fibre rich carbohydrates.
I think you’re onto something… which I’ll be talking about in the next few posts.
Hi, my recent blood work showed that my total cholesterol was double from my last year result and LDL was 2.5 times more than last year. My result is similar to your. I am really worried. Would you mind to email me her name, practice, address , contact and fees as well. Thank you for your time to read this post and your reply.