Despite 3 years of struggling with a markedly elevated LDL cholesterol particle count I’ve finally managed to make substantial progress in bringing it down over the past 4 weeks, but before I go into the results and the exact methods I used, I want to give you a detailed description of everything leading up to it.

After experimenting with different macronutrient ratios and various supplements without much success, I finally decided that I took things as far as I could take them on my own and needed help, so I arranged to meet with a lipidologist.

I contacted Dr. Dayspring via Twitter and was disappointed to discover that he wasn’t taking any patients at the moment, so he referred me to a colleague located about 90 miles away from me.  I reached out to her and scheduled an appointment.

These next few posts will be about my experience with the lipidologist.

This post itself is meant to be a sort of prologue.

Before meeting with the doctor I organized a list of questions I wanted to address to ensure that I didn’t forget anything and to make the most of the visit.

A lot of the research that I used for preparation came from Dr. Dayspring’s lecture series on Sterol Testing which I took notes on here.

I thought it might be helpful to give you a window into how I approached this by showing you my list of questions.

Here they are:

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Cholesterol Questions for Lipidologist

What is my cardiovascular risk?  Is it high or low?

Why did my body all of a sudden develop/acquire hypercholesterolemia?  

• Change in gut bacteria?
  • L reuteri can deconjugate bile acids which can lead to decreased FXR stimulation, and subsequent increased bile acid formation (cholesterol excretion)
  • Less of the gut bacteria that metabolize cholesterol into coprostanol/cholestanol
• Increased conversion of ketones into LDL?
  • This should regress with increased carb consumption and not being in ketosis correct?
• Weight loss?
  • Increased mobilization of endogenous fatty acids
  • Recent change in body composition
• Changes in CETP activity?
  • Seen more with binge and purging anorexics
    • Studies (here, here, here, here, here, here)
  • Is there any way to measure this?
• Change in LDL receptor expression or activity?
  • Can this be measured?
  • Thyroid related – but my numbers are normal now
  • Insulin related -?
    • Insulin effect on PCSK9 (PCSK9 destroys LDL receptors)?
  • Fasting -> decreased IGF-1 -> high cholesterol?
  • Late expression of familial hypercholesterolemia
    • Is this possible?
  • Acquired change in genetic expression of NPC1L1 and ABCG5/8?
    • Is this possible?

High ApoB and LDL-P Numbers – What does this mean?

• When these are elevated does it automatically mean overproduction?
• What about in the absence of elevated TGs?

LDL hypersynthesis vs decreased clearance – How can we differentiate these?

Can we review my NMR results in detail?

Am I insulin resistant?

• We have many LP-IR scores to go on.
• HbA1C – Steadily at 5.7% which is high
• Recent fasting blood sugars in 100s despite weight loss.
• Consistently low fasting Insulin.

What tests should we order?

• Apo E Genotype
  • E4s have cholesterol hyperabsorption
• Sterol synthesis/absorption markers
  • Desmosterol, Lathosterol
  • Cholestanol, Campesterol, Sitosterol
  • Absolute values are necessary instead of ratios correct?
    • When investigating synthesis and absorption differences among two groups, one would like to be certain that these effects are independent of the cholesterol concentration and therefore values should be expressed relative to cholesterol (as a ratio).
    • However, investigating the relationship between absorption markers, synthesis markers, and cholesterol levels, the absolute sterol concentrations should be used due to the fact that normalizing or adjusting for total cholesterol would mean that you are masking the outcome variable you are interested in assessing.
  • Omega 3
  • MTHFR
  • Galectin??
  • PCSK9 – is this worth measuring?

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Am I inflamed?

• Lp-PLA2 – Why is it elevated?
  • Periodontal disease?
    • I recently obtained a Myperiopath test
  • What else can cause this to be high?
• CRP – Normal
• Ferritin – Why is it elevated?

What benefit is there in reducing dietary saturated fat?

• “Neither dietary cholesterol nor dietary fat significantly altered % absorption of cholesterol. Regardless of diet type, the individuals within the group differed markedly in the percentage dietary cholesterol absorption.”
• Dayspring said that this will reduce substrate for formation of LDL, but if I’m mobilizing endogenous fat, isn’t that providing the needed substrate?

Will these be my main treatment options?

Hypersynthesis

• Statin
  • Decrease cholesterol production
  • Increase LDL receptor expression
  • Why do patients with high level of synthesis AND LOW level of absorption respond poorly to statin monotherapy?

Hyperabsorption

• Ezetimibe (inhibits NPC1L1)
  • Decrease cholesterol absorption
  • Increase LDL receptor expression
• Bile Acid Sequestrant – Colesevelam, Cholestipol, Cholestyramine
  • Excrete more bile -> increased LDL receptor activity
• Fibrates – Clofibrate, Fenofibrate, Gemfibrozil
  • PPAR alpha agonist, decrease NPC1L1 expression
• Sterol and Stanol Therapy – Benecol
  • Saturate NPC1L1
• Probiotics
  • reuteri deconjugates bile acid, leading to decreased absorption.

Next up… the lipidologist’s answers to these questions.

*Image found here