Cholesterol, CRP, Fasting Insulin, and HbA1c Update: October 2014

Posted on by BJJ Caveman

Cholesterol October 2014 Update

As you can probably tell with my recent spate of cholesterol focused posts exploring the thoughts of Dr. Dayspring as well as the role of Apo-E and alcohol in high cholesterol… cholesterol has been on my mind of late.

It’s been about 6 months since my last blood test and a lot has happened since then like:

I drew these labs on October 23, 2014.

You can cross reference that date with the entry from the same date in my Carb Nite Redux: Week 1 post to see that on that same day, my AM Blood Ketones measured 0.6 mmol/L and my PM Blood Ketones measured 1.4 mmol/L.

On October 22, 2014, the evening before my blood draw, my PM Blood Ketones were 1.7 mmol/L.

So you can see, at the time my blood was drawn I was well into ketosis for at least a couple days.

Without further ado, here it is:

Cholesterol October 2014

Cholesterol

If you’d like to read about the history of my cholesterol you can feel free to peruse these posts:

Total Cholesterol, LDL-C, LDL-P, and Small LDL-P

My total cholesterol, LDL-C and LDL-P are essentially unchanged… meaning they’re still very very VERY high.

My Small LDL-P is also essentially unchanged, although a small part of me is holding on to the hope that it is slowly coming down, albeit at a glacial pace… though this is probably just wishful thinking since a decrease in 24 points is only a decrease in 2.7% and well within the margin of error.

A man can dream!

HDL and Triglycerides

The consistency of my HDL-C is definitely frustrating.  I think I have to just accept the fact that it’s going to stay in the 50’s no matter what I do.  High carb vs low carb, resistant starch vs no resistant starch, weight training vs cardio… none of it matters.  It, like the famous honey badger, doesn’t give a shit.  It’s gonna keep on doing what it’s doing.

The low triglycerides indicates that I’ve been doing a good job eating low carb (which is confirmed by level of ketosis prior to this blood draw).

It’s the low level of triglycerides that is the saving grace in the calculation of my Triglyceride to HDL ratio, which is 1.11 (the general consensus is that a ratio of less than 2 is ideal).

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C Reactive Protein (CRP)

This is a nonspecific marker for general inflammation, and anything less than 1.0 is good.  I’ve been consistently under 1.0 with the exception of one measurement, and this time it measured 0.8, so I’m confident that whatever I’m doing isn’t leading to underlying inflammation in my body.

Fasting Insulin

I’m just going to plagiarize myself a bit from this post because I also need a quick refresher:

Fasting insulin is perhaps one of the most convenient and practical methods to detect insulin resistance.  Insulin resistance is of course the thing we want to prevent when we avoid the carb heavy standard american diet, since it is associated with such badness as diabetes, obesity, heart disease, high cholesterol, high blood pressure, etc.

…[The normal range is 2.6 – 24.9]

The first question I had is what is the optimal range I should strive for?  Not just the normal, which as you can see is pretty broad, but the ideal range for optimal health.  Here are a few of the best resources that I came across:

According to Stephen Guyenet from the Whole Health Source:

So what’s the ideal fasting insulin level? My current feeling is that we can consider anything between 2 and 6 uIU/mL within our evolutionary template.

These folks think that:

When fasting insulin is over 5 µIU/mL, this indicates a metabolic problem such as pre-diabetes, which sharply increases risk for degenerative diseases.

In a fantastic post by Dr. Mercola he states that:

A normal fasting blood insulin level is below 5, but ideally you’ll want it below 3. If your insulin level is higher than 3 to 5, the most effective way to optimize it is to reduce or eliminate all forms of dietary sugar, particularly fructose.

This time my insulin went even lower to 1.1 uIU/mL which I’m interpreting as a good thing and to be expected since I was eating low carb and in ketosis prior to this test.

HbA1c

Unchanged at 5.7%.  This is another one of those lab values that doesn’t give a crap about what I do.  Usually when you see an HbA1c starting to approach 5.7%, you start getting concerned about insulin resistance… but I know that the fact that my Fasting Insulin, CRP, Triglycerides, and Fasting Blood Sugars are all low indicate that I’m NOT insulin resistant.

(The only things in my life that would lead you to suspect that I’m insulin resistant are my HbA1c and the overall pudginess around my belly).

None of this sways me from the conclusion that my HbA1c is only high because of an increased red blood cell lifespan.

If you’d like to read more about how I arrived at this conclusion you can read:

Given the stability of this number, I think I’ll just limit myself to checking this once a year.

What am I going to do about my LDL?

I’m not sure yet.  At this point, I’m just going to continue to do more research and see…  The more I read the more potential options I encounter.  Once I have an overall sense of what those options are, I’ll probably try to systematically test them out and see what effects they have.

If by some sort of dumb luck I can figure this thing out, I think it’d benefit a lot of low carbbers since Dr. Dayspring said up to 30% of low carbbers present with an increased LDL.

Up Next?

Thyroid numbers… stay tuned!

 

 

Category: Cholesterol, CRP, HbA1c, Insulin, Lab Tests

11 thoughts on “Cholesterol, CRP, Fasting Insulin, and HbA1c Update: October 2014”

  1. Thanks for posting your results.

    Have you by chance tried Paul Jaminet’s Perfect Health Diet? I was following very low carb for several years, and my particle number was around 1,500, with small LDL at 496. When I went on the PHD my particle number dropped to 1,040 and my small LDL was below 100, while A1c and glucose were both good as well. CRP was also crazy low. Plus I believe adding back some high starch/high glucose carb’s helped fix my thyroid (I was always cold, and esp had cold hands and feet. They were like ice cubes).

    Looking at your results it seems when you add carb’s in your numbers get better.

    I realize many VLC guys don’t care for the PHD (Jimmy Moore, Ron Rosdale), but I’ve felt great since I’ve added parboiled rice, white potato’s, sweet potato’s, and plantains and banana’s back into my diet.

    Ken

    1. I’ve read Pauls perfect health diet… and I like it.

      I suspect that will eventually be the model I will adopt in the future. Not quite ready to give up on cyclic keto just yet though.

      Maybe in a few months…. I still want to experiment around a bit.

      1. I’m in the Sky-High LLD-C Low Carb club. On a very comfortable diet with carbs < 100g/day and lots of fat, LDL-C went from a historical levels of < 100 (< 2.5) to 221 (5.7).

        After 6 months of pushing carbs as high as I comfortably could (150-200g/day. I'm very carb sensitive and suffer even at those levels) and dramatically reducing saturated fat (no coconut, low fat dairy, etc. Ack!), virtually everything on my simple blood panel got slightly worse: HDL down, TG up, LDL up (228). My TSH is slightly elevated.

        Although I wasn't really sure what to expect, I am pretty disappointed that cutting my sat fat probably in half and doubling my carbs, did nothing to help my LDL.

        I haven't had an LDL-P/ApoB as my LDL-C is so high, I know the answer, and being in Australia I haven't yet figured out how to get the test. The last doc I saw patiently explained to me how fat is a carbohydrate. No, I'm not joking. Try getting an ApoB test ordered by that guy.

        1. Fat as a carb??? Geeez.. hope you ran out of that office quick!

          Sorry to hear that things didn’t improve after upping your carbs. I’m still trying to get to the bottom of this as well!

          1. I thought my elevated LDL had to be related to low carb or high sat fat or both, but this latest result has me thinking that is maybe not so. I am mildly sub-clinical hypothyroid, but it seems to be a stretch to blame it on that. I also reduced egg intake, so it’s probably not about being a hyper-responder to dietary cholesterol.

            I’ve seen several leaders of the tribe talk about 30% of of LCHF eaters presenting with very elevated LDL-C, and yet it doesn’t get much attention and no one seems to have many answers to all the obvious questions.

            If anyone knows how to get an ApoB Down Under, I’d love to hear.

            With your trigs under 100, you should have mostly large LDL, which, as I understand it, should mean LDL-C over states your LDL load. But your LDL-C is about 2x “optimal”, while your LDL-P is closer to 3x optimal, which seems counter-intuitive.

            And if they used Friedewald for your LDL-C, one would expect your true LDL-C to be even lower. I had one lab test where they measured LDL-C, and my numbers matched the Iranian equation quite closely. Using the Iranian on your latest results, I get 179 for LDL-C.

            Any thoughts on your LDL-C/LDL-P relationship?

  2. It looks like your LDL is calculated target than measured (as it’s cheaper). Add I understand it, this is commonly done using the “Friedewald” formula which is thrown off where your trigs are under 100.

    If you run your figures through the following calculator, you’ll see that your LDL is more likely to be lower than in your test results.

    1. The LDL-C is the calculated portion…

      this test I obtained was an NMR Lipoprofile and provides direct measurements of the lipoprotein particles.

      The direct measurements are reflected in the LDL-P and small LDL-p numbers. There are also direct HDL-P particle measurements too, but that was in the normal range, so I didn’t post it.

  3. Have you considered taking this test?

    http://www.bostonheartdiagnostics.com/science_portfolio_cholesterol_balance_test.php

    The benefits of the Boston Heart Cholesterol Balance Test are:

    Accurate measurement of lathosterol (the best and most precise marker of cholesterol synthesis) and beta-sitosterol and campesterol (the most precise markers of cholesterol absorption);

    Diagnosis of over-production of cholesterol, observed in the most common genetic cause of elevated LDL-C, known as familial combined hyperlipidemia (seen in 15% of families with premature HEART DISEASE);

    Diagnosis of over-absorption of cholesterol, seen in about 25% of the general population and associated with increased risk of CVD, as well as phytosterolemia, a rare disorder associated with marked cholesterol over-absorption and premature CVD

    1. This is a subject I’ve been meaning to write a post on. I feel like I need to learn more… especially in light of Dr. Dayspring’s use of these in the lipidholics case.

      Is this something you’ve explored yourself?

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