(Note: Please consult
with your healthcare provider for any personal health issues)
Now that I have your attention, the question above is
certainly rhetorical and one could easily substitute ApoB or Non-HDL
cholesterol, so I am not singling out LDL-P (or picking on NMR technology).
It has been a several weeks since AHS 2012 occurred and
unfortunately I was unable to attend. From the twittersphere, I read about some
good presentations including Peter Attia’s discussion on cholesterol (if you
have not checked out The Eating Academy, you really should).
I fell down the low carb rabbit hole several years ago and
have never felt better, both physically and mentally. As that rabbit hole goes
deeper (read: greater carb restriction), there have been some inherent
“problems”. There are numerous reports of low carbers having their cholesterol
go thru the roof when they restrict their carbs (for definition let’s say less
than 50 grams a day). Food quality is good, exercise is good, they feel good,
but their lipids look horrible.
I would like to share my story, my n=1 case. I started a
lower carb Paleolithic diet over 2 years ago after I had read Steven Gundry’s Diet Evolution (also see books by Cordain, DeVany, Wolf, Taubes, among others).
I have progressed in my personal views and have progressed to where currently I
eat a form of a cyclic ketogenic diet (CarbNiteSolution (CNS) by Kiefer).
There are many reasons, but I am a fat kid at heart and it allows me some
flexibility with my “re-feeds”.
Last fall I had a NMR LipoProfile done which showed a LDL-P
of 2700 (less than 1000 is optimal). For a physician who focuses on heart attack prevention, this was quite
horrifying. What should I do? My initial thought was to slug down 20 mg of
Crestor daily. The only thing was that I was losing weight (more precisely, fat
via body composition testing) and I felt better than ever. My energy was
amazing. So I continued and eventually started Kiefer’s protocol described in
CNS earlier this year. There was one problem, my LDL-P was not changing and as
of this writing the last value was over 3000.
Well, as I do with my patients, I always want to know if a
patient has disease or not. That really is the question, not how high is the
cholesterol. I know from my practice that risk factor assessment means very
little without actually knowing if disease exists. Using standard risk assessment tools can miss
people who really are at risk (3). By looking at risk assessment models (like Framingham Risk Score) we can over- or
under-estimate risk greatly. My workhorse disease detection is Carotid Intima
Media Thickness (CIMT). This test simply put, measures the “lining” of the
carotid artery via ultrasound. The thicker the lining is, the greater the risk.
It is also a way to assess for plaque (atherosclerosis) of the artery. Having
plaque means you have atherosclerosis. I believe it is a significantly better
way of looking at risk because we are looking for the actual pathology (1,2).
I had my CIMT done in 2006 on the Standard American “heart
healthy diet” eating low fat, higher carb. You know those espoused by the ADA
and AHA. My lipids were “normal” at this time. My thickness was 0.6 mm (about
the 50th percentile). I also had two small “road bumps “ (minimal
plaques) at my left carotid bulb both measuring 1.2 mm. I was not happy. I also
had similar findings on a study in 1/2010.
Flash-forward to June 2012, about 4 months into CNS, my CIMT
showed a thickness of 0.445 mm (13th percentile) and I had the
vascular age of a 16 year old! And oh by the way, the “road bumps” were gone. All
the while carrying an LDL-P of over 2500 consistently for over a year. I have
also had a CT Coronary Calcium score that was zero.
Epidemiology tells us that high LDL-P is associated with
greater CVD risk (4,5). Where is mine?
Lets address the high LDL-P issue on low carb diets first.
Unfortunately, I do not have the complete answer. The literature does not
reveal much. The work of Paul Jaminet/Chris Masterjohn proves interesting (6).
To sum, high cholesterol on a low carb diet could be due to:
1. Thyroid
dysfunction (my TSH, T4, T3, rT3 were normal)
2.
Micronutrient deficiency (none noted via testing)
3.
Toxin/Infectious exposure (no periodontal disease or other sources of
infection)
4. Active
weight loss (check, but does not explain why others with active weight loss
have better/normal lipids)
Let’s take a 50000 ft. view. My hypothesis is that insulin
signaling is playing a huge role. We know that the root cause of
atherosclerosis in 80% of people is due to insulin resistance (7). Insulin is an anabolic hormone (ask
bodybuilders). Unfortunately it is not very discriminatory. Meaning: subcutaneous
areas, the liver and the arteries can be storage depots for fat in the setting of
insulin resistance. I see insulin resistance as “loading the gun” for initial
heart attack risk/event.
Inflammation is the second part. If insulin resistance loads
the gun, then inflammation pulls the trigger. Inflammation has a role in the
development and progression of atherosclerosis AND in the
rupture/destabilization of plaques (8). In addition, to complicate matters, the majority of plaque rupture/erosions do not cause events.
So what does one due to mitigate all of this disease? Well,
that would be to minimize the effects of insulin. That can be done by a
carbohydrate-restricted diet. In the largest extreme that would be a ketogenic diet.
What does a ketogenic diet do? Well simply put, it minimizes
the effect of insulin from the dietary component. This mitigation can be a reason for fat efflux (ala LPL and HSL activity). Could one also hypothesize
that fat is being effluxed not only from the subcutaneous tissue, but also the
liver, hence a potential treatment of nonalcoholic hepatitis (NASH)? By this
same thought process, could this be a mechanism to efflux “fat” out of arteries,
which may be one mechanism of action which may account for disease in patients
with high HDL-C cholesterol in the presence of insulin resistance?
Although not widely studied, Ketogenic diets (which remove
agents of Neolithic disease) can minimize inflammation. I have seen this
clinically in my practice and in myself. My hs-CRP is not detectable (all my
other markers of inflammation are normal as well, Lp-PLA2 and Myeloperoxidase).
Inflammation IS the key component to events (ie plaque rupture) as stated above.
So if LDL-P is high but inflammation is very low and there
is no insulin resistance, does it matter? This, of course, does not preclude
the possibility of atherosclerosis to progress in the setting of insulin
resistance and no/low inflammation (think the 78 yr old that needs a stent but
never had the event). So if one is
eating low carb, one would think these metabolic issues should take care of
themselves.
I definitely think in the Standard American Diet (SAD), high
LDL-P is a huge problem. Primarily due to the significant insulin resistance
associated with the discordance of LDL-C to LDL-P in the setting of
inflammation. It is a recipe for disaster. It also represents nearly 80% of
patients coming thru my door. Yes, 80%,
it is that high! (9,10)
I propose diet DOES matter (shocking, I know). In
particular, those that minimize carbohydrate exposure and thus insulin
signaling; will have difficulty developing atherosclerosis, inflammation and
thus events and potentially reverse it. What are the diets that do this? A
ketogenic diet, low carb/LC Paleo diet AND
as much as it pains me to say, the plant based diet.
This is a very complex issue and one that warrants further
investigation and for now most of my answers are “it depends”. But we must
always remember to treat the patient/disease and not the number.
References:
