Excessive Running Doesn't Kill You the Way Some People Seemingly Wish it Did

 

A paper was published recently in the British Journal of Sports Medicine that sought to examine the longevity of extremely serious endurance athletes, motivated largely by the persistent undercurrent of thought that too much extreme exercise may in fact be harmful, especially for one’s heart. The cohort chosen for this study was an interesting one – the first 200 people to ever run a sub-4 minute mile.¹ The idea here is obvious – these men clearly existed on the very edge of human aerobic exertion for some amount of time and did so long enough ago to have now reached advanced age or death.

While this is an interesting study, the results aren’t necessarily what I’m here to talk about. This really just serves as a jumping off point for the broader topic of “excessive” endurance exercise and mortality, something that pops up in the news every year or two as concerns over the potential cardiovascular harm of serious endurance training are regurgitated anew. Its something I’ve been meaning to write about for a while, so…here we go.

Oh right, the results – the researchers found these world-class milers lived an average of 4.7 years beyond their predicted life expectancy. They didn’t catalogue or analyze cause of death, but did note that among the 7 individuals who died young – before the age of 55 – six died of traumatic causes and one of pancreatic cancer. Not a catastrophic heart among them. But like I said, that isn’t the point of this post. There’s a lot we don’t know about these athletes’ lives, or about their exercise habits later in life, and so we can’t really draw sweeping conclusions. We can, at least, be sure that world-class levels of training and performance in early adulthood did not negatively impact the lifespan of these men relative to the general population.

This isn’t an entirely novel exploration either. A similar, larger study of past Tour de France participants also found significant decreases in all-cause and cardiovascular mortality in later life.² While again we can’t “prove” a lot from this, the fact that elite middle distance running and elite endurance cycling both fail to negatively impact lifespan is certainly credible evidence against the notion that such activity is overwhelmingly damaging to health.

Excessively Flimsy Evidence

Ok, so the point isn’t to talk about this one study. The point instead is to push back against the creeping notion that excessive endurance training leads to elevated risk of early cardiovascular death. That claim has percolated for upwards of 15 years or more now, largely thanks to the efforts of two cardiologists – James O’Keefe and Carl Lavie. They’ve worked together on a number of papers that frequently make headlines by claiming that excessive running just might kill you. A selection -

·       “Running too fast, too far, and for too many years may speed one’s progress towards the finish line of life”³

·       “Chronic excessive endurance exercise might adversely impact CV health”⁴

·       “Cardiac overuse injury may be associated with more ominous outcomes, including threatening cardiac arrhythmias, accelerated coronary plaque formation, premature aging of the heart, myocardial fibrosis, plaque rupture and acute coronary thrombosis, and even sudden cardiac death”⁵

·       “It is common, in our experience, that mothers tend to urge their offspring not to do marathons and other extreme endurance events. Just as we would all be better off if we heeded our mothers’ advice to eat fruits and vegetables, we would likely do well to not make a habit out of doing marathons”⁶

 

Their position is clear – running very much or very hard is likely to impact your heart in a negative way, which in turn places you at risk of early death. Which….sounds very scary right? Of course it does – you don’t want to accidently run too much and suddenly drop dead because of it. And these guys don’t really beat around the bush. They tell you, and make national news for telling you, that you are playing with fire and placing your health in danger if you run too much.

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You can probably guess what happens next – I look at some of their papers and tell you that their claims are mostly baseless nonsense.

Lets start with a paper titled “Dose of Jogging and Long-Term Mortality: The Copenhagen City Heart Study,” that divides people by volume and frequency of running and tracks deaths over a decade.⁷ The premise is simple enough – the researchers grabbed about 1,000 people from the larger Copenhagen City Heart Study and surveyed their running habits, ultimately breaking them up into the following groups by running status: Sedentary, Light, Moderate, and Strenuous. After 10 years, when counting up the number of deaths, they found that “strenuous joggers have a mortality rate not statistically different from that of the sedentary group.”

There you have it, apparently – Running far and/or frequently is just as bad as not running at all. If you want to be healthy, jog only a small amount and don’t risk damaging your heart. But, of course, this is all ridiculous bullshit. For at least a couple reasons. Deaths are as follows:

 

  

Notice that the actual death rates differ remarkably. 30 percent of the sedentary group died during the follow up. But it wasn’t (specifically) because they were sedentary, although that surely didn’t help. Its because they were in their 60s, on average, when the study began. Meanwhile, there were only 2 total deaths in the much smaller strenuous running group. And it’s the nature of this group that’s such a major problem, for a couple of reasons.

The first is that with a sample size this small, the 2 deaths are essentially “random.” A change of one death in either direction massively changes the outcome. If there had been 3 deaths instead of 2, we might have been subject to headlines about running killing more people than smoking. You simply can’t get any kind of precise number in a tiny population. 

However, this first problem is extremely minor compared to the second – There is no effort made in this study to assess cause of death. They acknowledge as much, somehow blaming that problem on the number of deaths they recorded – “The small number of deaths in each group made it impossible to report different causes of deaths.”

I have no idea why this should make it impossible to report cause of death, but I have no problem whatsoever levying an accusation as to why they’d claim it to be impossible - Its impossible for them to report cause of death because in order to demonstrate that running increases cardiovascular mortality, you need runners to die of cardiac-related causes. And that probably never happened.

Recall that the sedentary group began this study at an average age of 61. The strenuous running group? They were only 38, on average, at the study’s outset (to be clear, they do adjust for the age difference). Which does help explain the low mortality rate, but also helps us make educated guesses about the cause of these 2 deaths (since the researchers won’t tell us). The most common cause of death, by a wide margin, for a person in the 35-44 age group is by accident. In fact, individuals in this age range are some 3.5 times more likely to die by accident, homicide, or suicide than they are by “diseases of the heart,” which account for only about 12% of deaths.⁸ So, knowing literally nothing else about these people except that they died and were most likely in their early 40s, we can estimate that there’s about a 77% chance neither of them died from “diseases of the heart.” 

And that’s why the researchers didn’t attempt to report cause of death. Because the entire point of this paper is only to fabricate “evidence” to support the notion that too much running promotes fatal cardiac consequences. In order to demonstrate that this happens, first you need to demonstrate that running “causes” people to die. And you can only do that by grabbing a very small sample size, hoping at least 2 of them randomly die (again, only random 1 death would have torpedoed their analysis), and then ignoring actual cause of death in order that you may theorize it must be due to cardiac complications. This entire paper pushes the narrative that running is bad for your heart because exactly 2 people (2 people!!) died in what, statistically speaking, was far more likely to be a car crash.

Furthermore, this is the only paper I can find in which O’Keefe or Lavie actually produce data to support their argument, although of course I’m using the term “support” in only the loosest possible sense. They do occasionally reference other pieces of data, but only in ridiculous and hyperbolic ways. For example, the claim that “considerable evidence has established the link between high levels of physical activity and all-cause and cardiovascular disease-specific mortality” is seemingly only supported by findings that higher levels of exercise fail to reduce (but not increase!) cardiovascular deaths in patients that previously suffered a heart attack.^9,10

 

Excessive Bullshitting

We aren’t done. Lets now consider another paper O’Keefe and friends wrote a few years later, in part about how the previous paper helps prove excess exercise to be detrimental to health. This paper begins by claiming the following:

 

“Middle-aged and older individuals engaging in excessive strenuous endurance exercise appear to be at increased risk for a variety of adverse effects—mostly CV in nature”¹¹

Which is a claim indeed. And a claim that is, ostensibly, well-supported – the authors attach 18 unique references to this claim. That’s a lot! That makes the claim seem more credible! That’s probably why they included so many! And listen, I won’t claim to be entirely innocent of the same tactic. I’ve added more references than necessary at times because more studies confirming the same finding add weight to said finding. But the huge, major, overwhelming difference between me and these clowns is that when I cite 18 references, all 18 of them are absolutely going to support the statement I’m making. On the other hand, among our 18 studies cited here, apparently demonstrating that strenuous exercise increases CV risk, is one that reaches the following conclusion:

 

“We observed a benefit threshold at approximately 3 to 5 times the recommended leisure time physical activity minimum and no excess risk at 10 or more times the minimum”¹²

 

And another that found “excessive” vigorous exercisers in fact die the least:

 

“Among people reporting any activity, there was an inverse dose-response relationship between proportion of vigorous activity and mortality. Our findings suggest that vigorous activities should be endorsed in clinical and public health activity guidelines to maximize the population benefits of physical activity.”¹³

 

And another that found that…

 

“In the analyses of change in running behaviors and mortality, persistent runners had the most significant benefits”¹⁴

 

And here’s a fourth!

 

“Higher levels of physical activity were associated with greater gains in life expectancy”¹⁵

 

So that’s 4 studies that find “excessive” exercise to be at least as, if not more, healthy than moderate levels, yet all 4 are cited as evidence that excess running has the power to kill. There’s a fifth paper I can’t access behind a paywall, and then 13 additional papers authored at least in part by O’Keefe, Lavie, or both, in which they repeatedly cite their own theories as basis for the next paper in a circular logic kind of way. This is a time-honored tradition for these gentleman, who over the course of some 15 years have created a catalogue of essays on the theoretical dangers of running that cite greater and greater numbers of their previous musings, each paper counting as an additional “evidence” about the potential harm of excessive running.

All these papers do, for the most part, is repeat each other and reference themselves back and forth in order to increase the volume of papers that suggest the same thing. They will, of course, throw in scary bits about exactly what it is that’s killing you when you run too much, like sudden cardiac death (SCD). And here’s the thing – SCD is, unfortunately, real. Something like 1 in 100,000 marathon or Ironman participants will simply drop dead. Some people are going to be unlucky. Occasionally, some person with an underlying heart condition may die during great physical exertion. However, the notion that SCD is proof of running’s cardiac destruction is ridiculous, particularly when the risk of SCD during a particular bout of physical activity is as much as 30 times lower in the most physically active individuals vs. their sedentary counterparts.¹⁶

 

Excessive Risks?

Are there any real risks that I’m thus far underselling? Maybe…The most legitimate and most commonly cited as a cause of SCD is probably atrial fibrillation or other arrhythmias developing from extreme endurance training. One of O’Keefe and Lavie’s many papers on the dangers of running includes the following graph:

And such arrhythmias do in fact seem more common among extreme endurance athletes later in life, although (as suggested by those massive uncertainty lines), this isn’t a particularly consistent finding. Beyond that, its difficult to figure out what such an increase would even mean. I can’t find any studies, for example, that show elevated rates of arrythmias among endurance athletes and then also track mortality and CVD data for years to assess potential negative consequences of those arrythmias. It’s possible that arrhythmias could increase while still remaining benign in nature.

Take, for example, a study examining previous finishers of the 90km Vasaloppet ski race. The researchers demonstrated that future arrythmias were more likely in older participants and those who completed more editions of the race, while being lowest among the slowest finishers. They did not, however, “observe higher incidence of sudden cardiac death with higher number of completed races or finishing time,” although this only considered Vasaloppet finishers and not the general population.¹⁷ Meanwhile, a second study on largely the same population of finishers demonstrated significant reductions in death and cardiovascular complications relative to the general populations – With a trend towards greatest reductions among the oldest competitors and those who had finished the greatest number of races. There’s just no good evidence that any increase in arrythmias among endurance athletes translates to tangible mortality risk.¹⁸

 

Conclusion

So…will running a bunch place you at increased risk for future cardiovascular complications or death? Probably not. We can say a couple things with pretty high confidence. One, that the most extreme levels of endurance training and racing inarguably improve cardiovascular health and future health outcomes. Two, that those extreme levels of training probably offer little to no additional health benefit vs. more moderate levels. We can say with somewhat less confidence that you may be placing yourself at increased risk for future arrhythmias by training at high volume and intensities. We can’t really say with any confidence at all if those arrhythmias would translate into any tangible consequence.

So, no, I don’t deny the possibility that sudden cardiac death or arrythmias could result from extreme levels of endurance training. But there is no data whatsoever that suggests this risk translates into negative consequences on a population level. Serious endurance athletes, by and large, are healthier than and live longer than most other people. To any degree that negative cardiac complications occur, they occur only at the margins. They occur only as statistical noise, that does little to limit the greatly increased cardiac/cardiovascular health of persistent life-long endurance athletes.

For my own two cents, given the dearth of evidence linking extreme endurance competition to cardiac complications, I’d wager an unfortunate soul is a lot more likely to discover or exacerbate an underlying heart condition during extreme exercise than they are to breed a new one (but, unlike certain others, I’m willing to admit this is largely conjecture on my part). I’d also venture a guess that, to whatever degree future cardiac complications may arise in this population, that they may be just as well linked to the “anything goes” sugar-guzzling mindset that permeates much of both elite and recreational endurance pursuits. If I were offering candid advice, it would be that there are no real downsides to avoiding the underlying dietary drivers of cardiovascular disease – sugar, seed oils, grains – or ensuring easy training is indeed sufficiently easy (we perhaps agree here, as O’Keefe uses the hilariously arbitrary pace of 10 minutes/mile as slow enough to be safe).

I can’t say what will happen to your heart if you train your ass off for the next 15 years. What I can say, unequivocally, is that people who train their ass off for years on end absolutely live longer and suffer fewer cardiovascular complications than the average person. And there’s some important nuance there – people typically don’t train their asses off for health reasons. Even if there were a tangible argument for moderating, maybe half a year of expected lifespan, I don’t think most serious athletes would be interested in making that trade.

And they shouldn’t have to. The claim that “running too fast, too far, and for too many years may speed one’s progress towards the finish line of life” is not only highly irresponsible but is in fact an outright fabrication. When literally zero of the first 200 sub-4 milers die of early cardiovascular complications, when Tour de France cyclists outlive the general population by years, when no evidence has ever, ever, ever demonstrated an increase in early death among highly competitive endurance athletes (and when “great” maximal oxygen consumption is associated much longer lifespan than “good” oxygen consumption¹⁹)…Statements like these exist beyond the realm of conjecture or hypothesis. They, instead, are fantasy.

I won’t claim to know that there is literally no risk when one engages in extreme endurance competition, but I will certainly accuse O’Keefe and Lavie of fabricating evidence to push the narrative that it may kill you. Not only do they use twisted data to support their agenda, they support their narrative with evidence that is entirely contrary to their claims. This is not a mistake, or a misrepresentation, or a small stretching of the truth on their end. It is a lie, an outright fabrication. It is not something fit to be print in an academic journal, and it is not something a respectable journalist should be engaged in promoting. It is a scare tactic, for reasons still not clear to me. But they have a clear agenda, and they have proven time and time again that they will lie to promote it.

While I must, as always, stress that this is not medical advice (you should probably see a doctor if your heart is doing something weird...), it is absolutely a claim that these fearmongers are stoking baseless fear for reasons unknown, and a steadfast opinion that you should probably just go ahead and relax and head out for that run. 

 

 

1.           Foulkes S, Hewitt D, Skow R, et al. Outrunning the grim reaper: longevity of the first 200 sub-4 min mile male runners. Br J Sports Med. Published online May 6, 2024. doi:10.1136/bjsports-2024-108386

2.           Marijon E, Tafflet M, Antero-Jacquemin J, et al. Mortality of French participants in the Tour de France (1947–2012). European Heart Journal. 2013;34(40):3145-3150. doi:10.1093/eurheartj/eht347

3.           O’Keefe JH, Lavie CJ. Run for your life … at a comfortable speed and not too far. Heart. 2013;99(8):516-519. doi:10.1136/heartjnl-2012-302886

4.           O’Keefe EL, Torres-Acosta N, O’Keefe JH, Lavie CJ. Training for Longevity: The Reverse J-Curve for Exercise. Mo Med. 2020;117(4):355-361.

5.           O’Keefe JH, Franklin B, Lavie CJ. Exercising for Health and Longevity vs Peak Performance: Different Regimens for Different Goals. Mayo Clinic Proceedings. 2014;89(9):1171-1175. doi:10.1016/j.mayocp.2014.07.007

6.           Bhatti SK, O’Keefe JH, Hagan JC, Lavie CJ. The Lady Doth Protest Too Much, Methinks. Mo Med. 2013;110(1):17-20.

7.           Schnohr P, O ’Keefe James H., Marott JL, Lange P, Jensen GB. Dose of Jogging and Long-Term Mortality. Journal of the American College of Cardiology. 2015;65(5):411-419. doi:10.1016/j.jacc.2014.11.023

8.           nvsr70-09-tables-508.pdf. Accessed May 28, 2024. https://www.cdc.gov/nchs/data/nvsr/nvsr70/nvsr70-09-tables-508.pdf

9.           Lavie CJ, Lee D chul, Sui X, et al. Effects of Running on Chronic Diseases and Cardiovascular and All-Cause Mortality. Mayo Clinic Proceedings. 2015;90(11):1541-1552. doi:10.1016/j.mayocp.2015.08.001

10.         Williams PT, Thompson PD. Increased Cardiovascular Disease Mortality Associated With Excessive Exercise in Heart Attack Survivors. Mayo Clinic Proceedings. 2014;89(9):1187-1194. doi:10.1016/j.mayocp.2014.05.006

11.         O’Keefe JH, O’Keefe EL, Lavie CJ. The Goldilocks Zone for Exercise: Not Too Little, Not Too Much. Mo Med. 2018;115(2):98-105.

12.         Arem H, Moore SC, Patel A, et al. Leisure Time Physical Activity and Mortality: A Detailed Pooled Analysis of the Dose-Response Relationship. JAMA Internal Medicine. 2015;175(6):959-967. doi:10.1001/jamainternmed.2015.0533

13.         Gebel K, Ding D, Chey T, Stamatakis E, Brown WJ, Bauman AE. Effect of Moderate to Vigorous Physical Activity on All-Cause Mortality in Middle-aged and Older Australians. JAMA Internal Medicine. 2015;175(6):970-977. doi:10.1001/jamainternmed.2015.0541

14.         Lee D chul, Pate RR, Lavie CJ, Sui X, Church TS, Blair SN. Leisure-Time Running Reduces All-Cause and Cardiovascular Mortality Risk. Journal of the American College of Cardiology. 2014;64(5):472-481. doi:10.1016/j.jacc.2014.04.058

15.         Moore SC, Patel AV, Matthews CE, et al. Leisure Time Physical Activity of Moderate to Vigorous Intensity and Mortality: A Large Pooled Cohort Analysis. PLOS Medicine. 2012;9(11):e1001335. doi:10.1371/journal.pmed.1001335

16.         Out of Hospital Sudden Cardiac Death Among Physically Active and Inactive Married Persons Younger than 65 Years in Slovenia Out of Hospital Sudden Cardiac Death Among Physically Active and Inactive Married Persons Younger than 65 Years in Slovenia. Accessed May 28, 2024. https://www.researchgate.net/publication/265532052_Out_of_Hospital_Sudden_Cardiac_Death_Among_Physically_Active_and_Inactive_Married_Persons_Younger_than_65_Years_in_Slovenia_Out_of_Hospital_Sudden_Cardiac_Death_Among_Physically_Active_and_Inactive_Ma

17.         Andersen K, Farahmand B, Ahlbom A, et al. Risk of arrhythmias in 52 755 long-distance cross-country skiers: a cohort study. European Heart Journal. 2013;34(47):3624-3631. doi:10.1093/eurheartj/eht188

18.         Farahmand BY, Ahlbom A, Ekblom Ö, et al. Mortality amongst participants in Vasaloppet: a classical long-distance ski race in Sweden. Journal of Internal Medicine. 2003;253(3):276-283. doi:10.1046/j.1365-2796.2003.01122.x

19.         Mandsager K, Harb S, Cremer P, Phelan D, Nissen SE, Jaber W. Association of Cardiorespiratory Fitness With Long-term Mortality Among Adults Undergoing Exercise Treadmill Testing. JAMA Network Open. 2018;1(6):e183605. doi:10.1001/jamanetworkopen.2018.3605

 

 

 

 

 

 

 

 

Why a Couple Pieces of Fruit Sent My Triglycerides Through the Roof, and How it Relates to Chronic Health

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. 

  

Conclusion

In short, I was able to briefly replicate a very unhealthy state that those suffering from metabolic dysfunction experience on a chronic basis. Importantly, the lipid changes observed during this demonstration can only be explained by the demand for energy transport, not by fat consumption. While my failed triglyceride metabolism was effectively a mirage caused only by the unique, acute introduction of carbohydrates, the chronic state is reached by millions and millions who overconsume carbohydrates habitually. This triglyceride backlog and failure of fatty acid metabolism is an instrumental component of cardiovascular disease progression that can be largely moderated or reversed by a shift away from traditional, carbohydrate-based dietary guidelines. 

Further reading on the topics addressed above can be found here - 

• Terminology and Overview of Lipid Classes
• Triglyceride Mechanics - General, Dysfunctional, Efficient/Low-carb Dynamics
• Consequences of Poor Triglyceride Uptake
• Other Factors Influencing Atherosclerosis