A Demonstration of the "Energy Delivery" Nature of Lipid Mechanics
Last Monday, I had my blood drawn and triglycerides measured
at 103 mg/dl. On a Tuesday test they spiked to 241 mg/dl and by Thursday had
once again returned to a baseline of 106 mg/dl.
I didn’t “cheat” on any of these blood draws. They were all
standard, appropriately fasted tests that no clinician would ever take issue
with. So what happened to cause these dramatic changes?
The answer, in short, is that I ate a bit of fruit. Two
bananas and an apple to be exact. But a little fruit obviously doesn’t usually
send a person’s triglycerides skyrocketing, so it’s the context that make this
demonstration so interesting and illustrative.
What I Did
To be clear, this is hardly the world’s most rigorous
experiment. It really wasn’t an experiment at all, just a decision to measure
an effect I knew would occur during a planned real-life event. I had been
eating only meat for the last couple weeks and was now planning to reintroduce a
bit of fruit to my diet. As such, my reliance on stored body fat was going to
decrease and create a prime opportunity to illustrate the energy delivery
nature of lipid mechanics. The conventional wisdom that chronic fat consumption drives
gradual changes in lipid levels is broadly incorrect and insufficient to
explain lipid behavior, and the expected rapid changes during this dietary
transition would serve as a demonstration of this reality.
So anyway….I ate nothing but meat for a while before
reintroducing a small amount of fruit last Monday with my dinner (2 bananas, an apple, some ground beef). I had my blood drawn for
three lipid panels during the transition – Monday (before introducing fruit),
Tuesday, and Thursday. The total fat and carbohydrate consumption in the days
leading into and during the transition are given in the graph below.
The Results
Full lipid panels are given in the following chart. As can
be seen, dramatic changes in triglycerides were observed, with values spiking
significantly on the second day before returning to baseline shortly
thereafter. LDL-C changes are also fairly dramatic, but LDL-C + VLDL-C levels
decrease gradually across the 3 tests. While the triglyceride changes were the
main point of the demonstration, the LDL/VLDL changes also occur in a manner
that can be much better explained by an energy delivery model of lipid behavior
rather than the standard “fat consumption” paradigm. The second graph shows how dramatic an outlier this triglyceride result was compared to my
typical values.
|
Date |
4/8/24 |
4/9/24 |
4/11/24 |
|
LDL-C |
137 |
109 |
120 |
|
HDL-C |
56 |
43 |
49 |
|
Triglycerides |
103 |
241 |
106 |
|
VLDL-C |
18 |
42 |
19 |
|
LDL+VLDL |
155 |
151 |
139 |
What This Shows
What this essentially demonstrates is the degree of reliance
on fatty acids for energy in the complete absence of carbohydrates. In a low
glycemic, low insulin environment stored triglycerides are being broken down
rapidly and returned to the liver to be packaged and distributed to the body
within VLDL particles. The extreme lack of insulin and high reliance on fatty
acids for energy means this is happening at an increased rate – It shows up on
the lipid panel as a moderate increase in LDL-C.
**Quick refresher/explainer on terminology and physiology - fat entering the liver is converted to triglycerides and packaged into lipoproteins called VLDL. VLDL carry cholesterol and triglycerides away from the liver to the muscle and fat cells of the body. VLDL are typically short-lived and are converted to LDL particles after they offload triglycerides either to the cells of the body or back at the liver. LDL particles have a longer lifespan (days instead of hours) and carry primarily cholesterol around the bloodstream. VLDL-C and LDL-C refer to the amount of cholesterol contained within each particle class. LDL-C, but not VLDL-C, typically goes up when larger amount of triglycerides need to be trafficked for energy because the higher number of VLDL particles offload triglycerides quickly and convert to LDL. More background info can be found here**
Why not elevated triglycerides though? Because despite my
body producing more triglyceride containing VLDL particles than the average
person would, blood levels of triglycerides remain unelevated due to their
rapid utilization. In essence, the total fatty acid throughput – first from
body fat to liver, then in VLDL from liver to muscle (and, for some, back to
body fat) – is high, but the levels in the blood at any given time are not.
The introduction of even a small amount of carbohydrates
demonstrates the rate at which triglycerides were moving around. Upon
consumption, they elevate the blood sugar and their removal from the bloodstream prioritizes them as
an energy source over the significant flow of triglycerides. Because it takes
some amount of time for newly liberated fat stores to travel to the liver and
be repackaged in VLDL particles (and perhaps because insulin does not spike
high enough or fast enough after limited carb consumption to immediately “shut
off” fat breakdown), there will for some time be a build-up of triglycerides
leaving the liver waiting to be taken up by the body.
The carbs delay these triglycerides and, combined with the triglycerides being provided by the rest of my dinner, cause the high throughput to come to an abrupt halt. The next morning, a full 13 hours fasted, the backlog still fails to fully clear, resulting in high measured triglyceride (and VLDL-C) levels. Given a bit more time, however, this backlog does indeed clear as fewer VLDL particles are produced.
Just two days after the spike, triglycerides levels return to Monday’s baseline level. Carbohydrate consumption remains but, overall, things have now changed. The small carbohydrate contribution to energy is no longer additional to the heavy reliance on stored body fat, but instead replaces a portion of it as the breakdown of stored body fat is throttled back a degree. Fewer triglycerides are mobilized from the body’s stores and so the brief excess of energy supply no longer exists.
This same effect can be observed in my LDL-C and VLDL-C
levels as well. Remember, reliance on these lipoproteins for energy transport
is a prime driver of LDL/VLDL cholesterol. As such, those combined values are
highest during my first blood draw but decrease gradually over the next two as
less fat is mobilized from my body’s stored reserves. With less stored fat
being liberated, less fat is necessarily trafficked to the liver to be packaged
and distributed in VLDL particles. The “build-up” effect can be clearly seen on
the second blood draw, where VLDL-C spikes as the VLDL particles fail to
offload triglycerides and convert to LDL particles. The failure of these VLDL
particles to appropriately (ie. quickly) convert to LDL causes the sharp
decrease in LDL-C as old LDL particles are removed from circulation without
being replaced. LDL-C rebounds to a degree on the final draw despite lower VLDL
production because these previously long-lived VLDL particles have now finally
converted to LDL.
What This Implies for Chronic Health
This particular demonstration is a unique sort of one-off
that won’t apply to most people in most situations, but it is nonetheless
relevant to chronic metabolic health as well. While my demonstration succeeds
in creating an “energy back-up” in the short term, it is that same backlogged
delivery of triglycerides that serves as a hallmark of chronic metabolic
dysfunction. In short, it is the precisely the same mechanisms – prolonged VLDL
residence times and increased triglyceride levels due to delayed or failed
triglyceride uptake at the periphery – in each case. The underlying reasons,
however, differ.
In my case, as has been covered, the backlog is very brief
and is caused by essentially dropping some carbohydrates into a fast-moving
river of fatty acid energy. But in chronic cases, the build-up is more gradual
and subject to progressive long-term forces. When a person chronically
overconsumes carbohydrates, becomes insulin resistant, increases fat stores,
and so forth, triglycerides are in certain ways both more prone to enter the
bloodstream and more resistant to leaving.
They fail to leave the bloodstream in an appropriately quick
manner for largely the same reason as in my experiment – chronically elevated
blood sugar forces a prioritized reliance on carbohydrates for energy. This
isn’t a major issue in any acute sense, but becomes one when carbohydrates are
chronically consumed in excess. Many of these carbohydrates, in the form of
fructose, are in fact converted to triglycerides in the liver and join the flow
of VLDL particles to the periphery. Additionally, an overweight, insulin
resistant individual will become dulled to insulin’s fat-storage effects. While
typically the consumption of carbohydrates and corresponding increase in
insulin makes it very difficult to liberate body fat, this effect is
progressively reduced in cases of insulin resistance. Now, triglycerides in the
body’s fat stores are inappropriately broken down and trafficked to the liver
for packing in VLDL particles.
When this person chronically consumes carbohydrates, increasing
insulin levels and extending VLDL residence time, they contribute to a backlog
of these additional sources of VLDL/triglycerides. When the VLDL are unable to
offload triglycerides properly, they must be returned to the liver and be
offloaded there instead. This is in fact the most critical source of excess
triglycerides entering and exiting the liver. When excess triglycerides are
returned to the liver, they join the aforementioned additional sources of
triglycerides in being packaged again into VLDL particles and leaving the liver
to join the triglyceride backlog. For as long as carbohydrate consumption
remains high and insulin levels remain elevated, this risks becoming a
progressively more serious issue, as triglycerides are increasing unable to be
offloaded to the cells of the body and instead returned to the liver to join
the ever-growing backlog once more.
The end result, in this case, is chronically elevated
triglyceride levels that can’t likely snap back to healthy levels in a day or
two. Increasing triglycerides directly lowers HDL-C and increases VLDL
production, ultimately leading to the increase in LDL particles and LDL-C
commonly assumed to be the cause of chronic cardiovascular disease. In fact,
the increased presence of triglyceride-rich lipoproteins is (through the action of
CETP) among the actual instrumental drivers of such disease, as the presence
of excess triglycerides also generate smaller damage-prone LDL (and HDL)
particles. As these effects are secondary to excess carbohydrate consumption,
they will necessarily be accompanied by a trend towards increased development
of advanced glycation end-products, depressed nitric oxide availability,
increased free radical production, and other hyperglycemia-induced facets of
compromised vascular health.
