The purpose of this piece is to preview a bit of an
experiment I’m intending to perform in the near future. I’m calling it the “50k
and Heavy Cream Cholesterol Experiment” because, well…I’m going to run 50
kilometers and drink a lot of heavy cream and sample lipid levels a number of
times. Read on for details, reasoning, and predictions.
The Plan
The plan, broadly speaking, is to asses the effects of both
an excessive dose of running and excessive saturated fat consumption on my lipid
levels (LDL-C, HDL-C, triglycerides). These two interventions won’t be
concurrent, but stacked immediately on top of one another over the course of a
handful of days. Ideally, the plan is to begin this next Monday, January 20th.
I say ideally because a major factor in the timing is finding a day when I’m
healthy enough to even run the 50k. As I’ve described recently, I still commonly
miss days of exercise (and work) due to neurological complications. And of the
days I’m healthy enough to get out the door to run, on exceedingly few could I reasonably
hope to run a reliably strong 50k. This makes finding a good opportunity to
carry out this experiment in the course of normal day to day life difficult at
best. But as luck would have it, I’m on vacation this week and have a
reasonable expectation of feeling pretty good when I return.
So, fly home on Sunday the 19th and run the 50k
on the 20th. Beginning that evening and continuing for 3 full days after,
I will consume a purely carnivore diet with as much saturated fat and dietary
cholesterol as I can tolerate. The aim will be to consume several thousand
calories per day above baseline, but exact numbers will depend on how exactly
it feels to so greatly overindulge multiple days in a row (Despite the name I
used in the title, I will not be consuming only heavy cream. Massive quantities
of it, yes, but also meat, cheese, and butter). Baseline diet, for the record, is
an animal-based ketogenic diet averaging about 80% calories from fat and fewer
than 10g of carbohydrate per day.
The planned schedule is as follows:
Monday AM: Lipid Panel #1/Baseline
Monday AM: 50 kilometer run
Monday PM: Lipid Panel #2
Monday PM – Thursday PM: Heavy saturated fat consumption
Tuesday AM: Lipid Panel #3
Tuesday PM: Lipid Panel #4 (non-fasted)
Wednesday AM: Lipid Panel #5
Thursday AM: Lipid Panel #6
Friday AM: Lipid Panel #7/Final
What I’m Hoping to Measure
As you almost certainly know, the traditional paradigms surrounding
diet and cholesterol suggest that consuming too much saturated fat and dietary cholesterol
drives an increase in serum LDL cholesterol levels (in turn considered to be
the prime driver of atherosclerotic cardiovascular disease). I, however, object
to that paradigm, believing instead that the greatest factor influencing LDL-C
levels is the body’s reliance on lipoproteins as an important delivery system.
Probably the most important cargo that lipoproteins carry are
triglycerides, to be either stored as body fat or used as an energy source by
the body. Which brings me to an important caveat that I’ve yet to mention – the
50 kilometer run will be carried out entirely in the fasted state. I will be
consuming exactly zero calories before or during the run, not eating anything
on the day until after my post-run blood draw.
This is a fairly extreme measure of course. Exceedingly few
people ever run that far in a fasted state, and ever fewer (possibly zero?)
have ever measured the effect of that effort on lipid levels. The American
Heart Association and others suggest that saturated fat consumption is the
greatest factor in raising cholesterol levels, with a lack of exercise a strong
contender for number two. Conventual wisdom also tends to suggest that LDL-C
levels don’t change rapidly, but instead over weeks or even months. It would
stand to reason, then, that LDL-C should probably be largely unchanged between
my first and second blood draws. Perhaps they might even tick down a fraction,
as the intervening hours between the first and second blood draws will maximize
typical guidelines for lowering cholesterol (plenty of exercise, zero fat consumption).
If instead LDL-C increased during the run, it might require an update, or at
least a caveat attached, to the typical paradigm.
Lets skip now to the final blood draw. This is, clearly, the
extreme opposite end of the spectrum with respect to traditional cholesterol
risk factors. I won’t exercise the three days between the 50k and the final
blood draw, but I will eat so, so much saturated fat. And its flipping so aggressively
from one extreme to the other that makes this fun. Again, a traditional medical
mindset would suggest that LDL-C should clearly increase throughout the week as
I binge saturated fat and dietary cholesterol. It may not increase a lot, as
its only for a few days, but one would certainly expect it to start trending up
in the face of such prodigious fat consumption (Just for fun – the AHA
recommends capping saturated fat intake at ~13 grams per day. I intend to consume
25-30 times more than that each day. Essentially a month’s “worth” of saturated
fat per day). So again, if the so-called expected outcome is not observed, it
may suggest a shortcoming of the current conventional wisdom.
I’ll further expand on the day 2 blood draws momentarily,
but the intervening lipid panels are largely to track trends throughout the week.
I intended to skip the middle three blood draws at first, as its really the
first and last days that will capture the full effect, but decided it would be
more interesting to have a more complete dataset.
Predictions
Baseline/LP1 – I will have, by conventional standards,
elevated LDL-C at baseline. I don’t know how elevated necessarily, but
certainly it will be a number that would concern your average physician. On the
contrary, I expect reasonably high HDL-C and low triglycerides that would be quite
good by conventional standards. All of these values derive from the fact that I
am a metabolically healthy individual consuming an exceedingly low-carbohydrate
diet and thus relying on fatty acids for energy.
LP2 – I expect LDL-C to rise fairly noticeably during the
course of the fasted 50 kilometer run. Reliance on stored body fat for energy
(or really, the hormonal effects of fasted exercise) will drive a significant
increase in the breakdown of stored body fat, which should be largely
trafficked through the liver and packaged in VLDL particles. The triglycerides
in these VLDL particles will be taken up extremely rapidly by working muscles,
causing the VLDL to convert to longer-lived LDL particles. This continuous effect
will cause there to be an acute increase in cholesterol containing LDL
particles, and thus an increase in measured LDL-C. In addition, I expect
measured triglycerides to be extremely low for the same reason (most likely below
my “personal best” of 66 mg/dl) as my working muscles rapidly take them up for
energy.
Final/LP7 – The expectation here is that this result will
also defy conventional wisdom. Not only will the extreme consumption of fatty
animal products fail to raise my LDL-C, it will acutely lower levels to below
baseline. Rather than relying heavily on stored body fat for energy, I’ll be
doing the exact opposite. I’ll be creating a hormonal environment that more heavily
emphasizes the storage of fat rather than its breakdown, thereby reducing the production
of VLDL particles that would typically move my stored triglycerides around my
body. Fewer VLDL particles means fewer LDL particles and thus lower LDL-C. Its
worth noting, however, that this effect won’t be as great as it could be due to
the compressed timeframe of this experiment. The average lifespan on an LDL
particle is in the three and a half day range, and three and a half days before
my final blood draw I’ll be producing huge number of VLDL/LDL particles during
and immediately after my fasted run. A couple more days of binging would ensure
these excess particles would be completely recycled, but frankly I don’t want
to do this for that long, so…
Day 2/LP3 – Saving the best for last. This is, to me, the
real meat of my experiment. I have strong preconceived assumptions about how
the fasted exercise and the fat binge will effect lipids, but the blood draw on
Tuesday morning is for me the one that ventures into the great unknown. And frankly,
in a lot of ways, it ventures into the collective scientific unknown, as I don’t
think anybody has ever documented the effects of such an extreme scenario on
lipid levels.
Let’s first asses what this blood draw might look like if we
only consider the energy deliver nature of lipids. Remember again that LDL
particles have a typical lifespan of 3+ days. This blood draw, maybe 17 hours
after the second, will represent only ~20 percent of the lifespan of a typical LDL
particle. And while the massive effort between the first two blood draws should
generate a significant acute increase in LDL particles, nothing about the rest
and recovery after lipid panel 2 should differ greatly from what I’d be doing
three to four days earlier. That is to say, there shouldn’t be much reason for
the number of particles produced to differ greatly from the number being recycled.
It may even be the case that energy demand remains so high in the immediate
aftermath of the run and the second blood draw that LDL-C could fractionally
increase if I don’t eat enough or quickly enough to fully blunt that effect.
So, from a purely energy driven perspective, LDL-C levels at or just above those
in lipid panel 2 might be reasonably expected (with triglycerides returning closer
to baseline as well).
But…what if energy (and cholesterol) weren’t the only important
components being trafficked by lipoproteins? What if another effect were
present that could also drive a noticeable change in LDL-C levels? This, essentially,
is what I’m hoping to test.
It may be that a very important and underappreciated element
that LDL particles transport…is just themselves. After all, lipoproteins are
made largely of the same phospholipids that comprise cell membranes throughout the
human body. And it could very well be the case that an acute insult to enough of
those cell membranes – for example, the damage caused by running 50 kilometers –
could cause many LDL particles to be taken up by the cells as raw materials for
the repair of these damaged membranes (and/or the creation of new ones).
If this were the case, a reasonable proportion of the existing
LDL particles in circulation might leave the bloodstream earlier than expected,
thus decreasing LDL-C from the energy driven expectation outlined just above.
To be clear, I don’t have a reasonable guess for what my
LDL-C will look like on Tuesday morning. Something wildly different than
expected on the post-run or post-binge panels would require some reevaluation
of the energy delivery paradigm. However, I’m not making any particular prediction
for this lipid panel. I do strongly believe, however, that a decrease in LDL-C from
lipid panel 2 to panel 3 would be indicative only of this proposed effect – the
endocytosis of LDL particles for the repair of cellular damage. And I think
demonstrating this effect would, in theory, go a long ways towards further understanding
a transport model of lipoprotein function and even the underlying causes of
atherosclerotic cardiovascular disease. If that decrease is in fact observed, I’ll
of course have plenty to say about it after the fact.
Summary
So, there you have, in two thousand words – a weeklong experiment
to test the extremes of lipid mechanics and assess the ways in which a lipid
transport system may best explain lipid behavior. To the best of my knowledge, this
is a novel demonstration, at least at this extreme. Studies have demonstrated that
a great energy deficit raises LDL-C, and numerous individuals (myself included)
have lowered LDL-C while binging on fat. But the extreme, hyper-condensed
nature of this N=1 experiment is, I think, without parallel. In particular, the
second day’s blood draw, on the back of a such a significant physiological event,
has the potential to demonstrate a possible underappreciated characteristic of
lipid behavior in the human body. Whether this ultimately demonstrates
something significantly novel, or only highlights the importance of lipids in
energy deliver, or goes up in flames entirely, remains to be seen. But,
regardless, results and summaries should come soon after. To be continued.
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