The Light at the End of the Tunnel Isn't Moving Any Closer

Medical Retirement 

For more than a year, I’ve been trying to apply for medical disability through the federal government. If you’re new here, I used to be an air traffic controller in the Washington DC area, until a neuroautoimmune reaction to the Pfizer covid vaccine crippled me with devastating neurological symptoms and widespread brain dysfunction. These impairments often left me unable to hold conversions or safely traverse the stairs, let alone sequence airplanes. For a couple years after, I tried to make it work in an office job, working with new hire training, airline routing, and facility safety issues. That was, unfortunately, not much better.  

As the adverse test results stacked up and the debilitating symptoms persisted, I eventually felt it was time to pursue a medical disability retirement. It was quite the process, to put it lightly. Beginning in November of 2024, I gathered clinical notes, physician testimony, supervisor statements, and more to make the case that working with my condition was impairing both my health and my ability to satisfactorily perform my job. It took until March to finally submit a final application – thanks in part to glacial paper passing in the FAA, and in part due to the difficulty in obtaining concrete physician support. 

To be entirely honest, the quasi-interlude to follow is only partially to illustrate that difficulty, and partially because I’m bitter and angry. The ways in which I was mistreated by a number of physicians remains staggering to me. I already touched on the neurology practice that was the first to voice support for my application, but reneged when my IQ testing showed “only” single digit percentile performances in acute cognitive skills. And special thanks to the neurologist who told me my test results were meaningless because they were “only consistent with serious conditions like Alzheimer’s and Parkinson’s.” Two other doctors accused me, directly and to my face, of faking everything - not only my severe symptoms and pronounced cognitive decline, but apparently also the PET scan demonstrating widespread brain dysfunction and the range of adverse autoimmune symptoms suggestive of neuropsychiatric lupus. It was an uphill battle, even with simple things like scheduling and paperwork, to eventually get multiple medical professionals on board. 

In any event...the application finally submitted in March was initially denied in July - failure to demonstrate that my health was sufficiently impacting my job performance, they said. What had been a ray of hope was, all of a sudden, a massive shot in the gut. I actually feel like I handled this stretch of disappointment fairly well, but was obviously dejected about the prospect of continuing to hurt myself at work every day when it could have already been over. I fell back into my usual routine of suffering and survival (and taking as much time away from work as I could) pretty easily, stacking a week or two of good health and good running before falling apart for days or weeks after. Repeat, ad nauseum.  

The application was resubmitted a few week later and this time, finally, was approved at the beginning of November (in the middle of a government shutdown, no less!). This was, obviously, a moment of great relief and joy. I had viewed this retirement as a clear light at the end of the tunnel, the moment that would change my life for the better. I had locked in so hard for so long, just trying to make it to the other side, and this was the moment that was going to mark a real change. Unfortunately, I still had to make it through quite a bit more work, the reopening of the government, and the HR logistics necessary to finally get me out the door. Ultimately, November 19th was the last day in the office, but I was still missing entire days of work sick in bed as late as the 17th. The excitement and optimism had worn a bit by then, but maybe now things could finally be alright.  

Retirement Hasn't Meant Relief

Well...Here we are, three weeks since my last day of work, and I’m in a pretty bad place. The last couple weeks of the government shutdown were extremely brutal (ironically, I was hoping I’d have less work without a government...), leaving me broken and sick despite only managing to work about half of my hours during that time. Since then I’ve recovered a bit, but haven't actually been able to turn a corner. I’m....OK.  

But what OK means is that trying to clean the basement destroyed my neck, leaving my neck and head numb and “asleep” for days. It means I haven’t had legitimate feeling in my hands or feet for over a week. It means every morning is a crapshoot as to whether my legs will actually move properly or if I’ll need to hold myself up against the wall in order to get to the bathroom. It means I struggle massively with processing information and making decisions, or really even understanding how to make a decision. It means I’ve tried and failed to run several times, simply because I can’t force my legs to move properly or control where they land, while my heart rates tickles threshold levels at 11 minute pace (to be clear, I’ve run a number of times as well with less issue).  

I’m writing this on a Thursday, having been unable to complete my run yesterday and unable to attempt it today. I couldn’t get through the dog walk this morning, actually. Yesterday afternoon I did maybe an hour of work around the house (ok, 20 minutes of work spread across an hour), babying myself through laundry and dishes. But I could only do a couple minutes at a time, because my spinal cord couldn’t handle looking down. A couple minutes left my spine shooting with pain, my arms and legs fully numb, my brain dizzy and nauseated. Rest for a few minutes on the ground, then repeat.  

I would have been better today had I not done that but the real problem isn’t folding laundry, it’s the inability to provide any meaningful continuous energy to my nervous system. That’s by far the greatest fundamental problem, that my brain and nervous system can’t produce or utilize energy through traditional means. I make constant efforts to mitigate those effects through deliberate ketosis, but that’s been made extremely difficult lately.  

What I’ve found again and again (to be clear, this checks out fairly obviously physiologically as well) is that any great stress response tends to inhibit ketosis. Your body responds to stress by prompting your liver to create glucose, raising blood sugar and inhibiting ketone production. Part of why I’m in my current mess is because I had a cold that had exactly this effect, but the persistent issue is how massively difficult it is to actually recover. When I’m reasonably healthy, a high-fat/zero-carb diet will commonly lead to stable blood sugar in the 70-80s and blood ketones of 2.0 or higher (those values are “below average” and “quite high” respectfully). But when I’m in a bad place and can’t get out from behind it, the same diet will instead produce fasting blood sugars of 100-110 and ketones barely above zero. When this happens, I’m providing extremely limited energy to my nervous system for days at a time. In both cases, the situation is prone to self-propagation. Long-term elevated ketones prevent many or most symptoms and issues, maintaining a fairly healthy state. But low ketones and limited energy availability means things as simple as reading emails or sitting on the wrong chair can exacerbate ongoing issues, further driving the downward spiral.  

Moving Forward

You might read that and wonder how I’m even writing this today, given I just told you how bad today was. If you’re wondering, my blood levels a couple hours after waking were glucose of 102 mg/dl and ketones of 0.3mmol/L. Those are not good numbers, and suggestive of a continuing long-term trap of poor energy availability and debilitating symptoms. So what am I doing? I’m cheating, in a sense. Taking drastic measures, more accurately. I wrote once before about the varying alternative manners by which you can provide energy to the nervous system, and how ketones are by far the healthiest and most stable long-term option. But as just described, its massively difficult to pull out of a spiral and raise ketones high enough without somehow first providing some sort of reprieve.  

So I’m currently or soon to be utilizing every other method I outlined in that previous post. I’ve had many, many carbohydrates (fruit) today. Enough to raise blood sugar high enough and long enough to at least partially overcome my nervous system’s relative inability to properly use carbs for energy. I’ve had some alcohol. Not enough for true intoxication, but enough to provide another stream of energy over the course of a few hours. And I’ve had and will have supplemental ketones as well. This is not healthy, or a good long-term solution, but between the overconsumption of carbs, the alcohol, and the exogenous ketones, I have massive energy availability for at least the time being. Which right now means I can write. I can put together thoughts and sentences in a way I wouldn’t have been able to recently, and can do so without cratering my health. But its a temporary reprieve, that I need to take advantage of while I’m able.  

The result of these efforts should be that my nervous system will recover all day today, and that tomorrow morning I’ll have a relatively easier time getting out the door for a run. Which is the last, best alternative option for energy delivery. Exercise is really the only way to acutely increase glucose metabolism in the brain and nervous system (without binging sugar) and thus has been a reliable tool in my battle for health. But much like the ketone spiral, I can’t take advantage of that pathway when I’m too unwell to get out the door (the days I can't get out the door never get logged, but my Strava is still littered with quasi-failures like these).

Tomorrow I’ll wake up with zero ketones, but should feel far less numb, less dizzy, in better control of my limbs. The trick then will be transitioning from today’s short-term energy availability back to something more lasting. But the transition to ketosis is, generally, when I’m at my worst and most susceptible.  

As an aside – the “transition” to ketosis is where I existed for most of the first year I was dealing with this. In the long-term, that just means sensible but non-zero carbohydrate consumption that results in stable, healthy blood sugar that is too low for my nervous system to utilize but too high to allow ketone production. The same state occurs transiently in the days after high carbohydrate consumption while waiting for meaningful ketone production to return. I don’t typically spend much time in that state anymore, because I can manage it in the way I’ll describe in short order.  

But I have, unfortunately, still been there from time to time. I’ve been flirting with that place a fair bit lately. And that place, those circumstances, are when it’s made clear to me that things aren’t actually getting better. Quite honestly I think they’re getting a little worse. It is glaringly obvious that even without great cognitive stress, normal human function is difficult if not impossible to achieve - the constant numbness, dizziness, stabbing pain, impaired motor control, and so on and so on, the squeezing blackout feeling compressing my spine and brain, all of that – it feels more and more difficult to actually escape.  

And has been made clear on multiple occasions, the addition of cognitive strain – the actual acute stressor placed on an unfueled brain – sends things to a place that simply doesn’t feel survivable. I am, at this “baseline” - the existence that a healthy person would take for granted – too sick to hold my life together. I scored in the single digit percentiles in acute intellectual skills when I was healthy. When I’m not I can’t even hold a conversation, in either direction. I am, in what really is just a “normal” human state, still too sick to fully understand the things people say to me, and too sick to remember words or piece together sentences when trying to go the other way. I am, still, too sick to get up and down the stairs without using all fours for balance, without stopping to take a break.  

What the hell was I talking about? I think my rambling got off track a bit. I know my underlying health hasn’t improved and I suspect if anything it’s a little worse, but I can avoid those catastrophic situations for the most part these days (even if I’m bedridden nonetheless).  

And the way I do it is how I’m going to do it tomorrow. Through constant utilization of some kind of energy source. I’ve utilized several today, in order to write this and in order to get myself out of bed tomorrow morning. More ketone supplements (on which I’ve spent some $800 this year...) will help make sure tomorrow’s run gets started. And then, I’ll run... and run some more. Hopefully all day, more or less.  

Two things should hopefully happen tomorrow – the run itself, for what I hope will be 5, 6, 7+ hours, will provide another fantastic source of energy/brain metabolism to help get through tomorrow. And I swear to you, that if I’m actually well enough to run for 6 hours, my legs will hurt less after than they did after the six-miler I couldn’t complete the other day. Even the generic neuromuscular pain is worse than anything I’ve ever been able to inflict running or racing. I’ll also fuel that run entirely with ketones and fat. Despite eating a lot of carbs today, I hope to reach meaningful levels of ketosis in 24 hours by virtue of simply moving all day, depleting all stored glycogen, and driving insulin down around zero.  

And then we’ll see what happens. If I get the run started, tomorrow will probably be ok. I’ll run for hours and, if that's true, will feel reasonably ok for the next day regardless of what I eat just on the strength of the run alone. But hopefully in concert with high-fat/zero carb fueling and diet, I’ll be back to a meaningful level of ketosis by the following morning. Or at least meaningful enough, while feeling healthy enough, that the next day’s run is enough to finally see big ketone numbers again. 

I’m still waiting to be healthy for the first time since my retirement, and hope this “Hail Mary” of sorts is enough to ultimately get there (Update: Only kinda. I made it just a couple hours into that run, and it took a couple more days to finally start getting over the hump). I remain optimistic, for lack of a choice as much as anything else, that I can reach a long-term stable, healthy state in which I’m able to exercise daily and avoid the kinds of crushing circumstances that used to plague me at work.  

But I also feel like it needs to happen soon. I know these massive binge/alcohol/supplement/long run episodes are not a healthy long-term solution and not something I should be trying to repeat if I can avoid it. Combine that with the sobering research into dementia and other neurodegenerative diseases, the ways in which the inflammatory cascades, neurotransmitter disruptions, and so forth result directly from acute energy deficits while simultaneously causing further long-term damage, and it becomes obviously apparent how important a stable energy source really is.  

I don’t think I will ever be healthy enough to live like a “normal” person and also walk and talk at the same time. The expectation is that I will be significantly impaired for the rest of my life and will need to fight it, forever. So here’s hoping that if I actually posted this on the internet, that it means I finally broke out of miserable couple of months and reestablished a stable, healthy situation again. The hope then would be to string together several weeks or even months of consistent running, but that’s a lesser concern right now. Running has been extremely difficult lately. It is right now nothing more than a tool, a means to an end.  Its the manner by which I’m trying to force myself back to health, which is why I promise a random 30+ mile run isn’t as crazy as it might seem. Its the manner by which I’m trying to move closer to the light at the end of the tunnel. Hopefully I can find out what happens when I get there.  

April 2025 News and Notes

Why is this a news and notes update? Because I’ve tried writing on some topics longform and my health doesn’t support it. I get too dizzy, my arms go too numb, my head hurts too bad. So I’ve pieced together short snippets over weeks until I had enough to post. Big TBD what happens going forward, as I’m less and less willing to hurt myself to write at length on here:

The Fasted 50K and Heavy Cream Cholesterol Experiment Follow-Up –

o   The run went really well. We can start there. 50K, 3000ft vert, in the snow, 9:30/mile, fully fasted, felt good and easy the whole way. Feel I could have run 100k fasted at that pace, but obviously tough to know for sure.

o   This was fairly disappointing, frankly, because one of the main predicted effects was not observed – my LDL-C was not elevated after my fasted run. I had considered writing in the preview about the degree to which your body can use fat “directly” during exercise, as opposed to that fat trafficking through the liver first. It’s the trafficking through the liver that increases LDL-C. I knew a lot of the fatty acids I burned would by that more direct path but I honestly thought enough would pass through the liver first to raise LDL-C a good amount, and that it was fine to skip that nuisance in the preview.

o   My baseline LDL-C on the morning of the run was only 105 mg/dl on an approximately pure carnivore diet. I suspect the two reasons it was lower than expected were 1) higher weight/body fat than most previous measures. This is basically a proxy for less body fat breakdown, and 2) cheese, which has a few carbs, a more "potent" insulinogenic whey protein, and was consumed a bit more liberally the week prior to this test.

o   My LDL-C only increased to 111 mg/dl at the end of the 50k run. It more or less literally did not change. As just mentioned, this was very surprising to me. I thought enough stored body fat would traffic through the liver to cause a noticeable increase.

o   Triglycerides (108 mg/dl) and HDL-C (58 mg/dl) were, in my opinion, not super great at baseline before the run. Triglycerides decreased to only 97 mg/dl during the run but were down all the way to 61 mg/dl the next morning. HDL-C was still 58 mg/dl the next morning.

o   On the other hand, my LDL-C did drop significantly, to 85 mg/dl, by the next morning. This was one of the major predictions of the experiment – that the induced muscle damage of such a lengthy run would demand the increased uptake of LDL particles to aid in cellular repair. Because LDL particles are formed from the exact same phospholipids that also from cell membranes, it follows (and appears to have been demonstrated in this case at least) that these particles would be taken up (and LDL-C thus decreased) as a source of raw materials.

o   LDL-C remained stable below 90 mg/dl during the fat binge phase over the following days. This was also predicted, as the massive intake of dietary fat would negate the breakdown of my stored body fat and slow the trafficking of said fat through the liver, thus decreasing the production.

o   After more than four months of a near zero carb diet, and coming off a three day average of approximately 6300 calories, 500g fat, and 290g saturated fat (more than 20 times the “healthy” recommendation) per day, my lipids were as listed below. These conventionally excellent metrics obviously fly in the face of the traditional paradigm that saturated fat consumption is the primary driver of elevated cholesterol and dyslipidemia (particularly when my personal LDL-C “PR” is over 200 mg/dl)

- LDL-C: 89mg/dl (recommended <100 mg/dl)

- HDL-C: 64 mg/dl (recommended >40 mg/dl)

- Triglycerides 77 mg/dl (recommended <150 mg/dl)

 

Neurocognitive Testing and Medical Fallout

o   I believe strongly that the American physician has failed me immensely. I have been lied to, accused of faking symptoms, accused of lying, denied relevant testing, and been subject to seemingly endless attacks on my character and my knowledge. I have been mistreated and abused by the American physician. This was, however, the most frustrating episode to date.

o   To put it bluntly and maybe arrogantly, I was very intelligent at baseline. The last time I took a standardized test, when I was considering a Ph.D. program, I scored in the ~99^th percentile of the GRE.

o   Working memory (basically retaining and using a range of information in real time), in particular, was a great skill of mine. At one point I could shuffle a standard deck of playing cards, look at it one time through, and accurately repeat the entire deck back in order.

o   One of my physicians, with whom I had previously had a decent relationship, backed off from helping me with me medical/work situation until I did neurocognitive testing to assess possible intellectual impairment.

o   I ultimately decided to go though with it, and did so shortly after the cholesterol experiment. As would be predicted, the physical effects of this nearly 4 hour test were massively debilitating. I was virtually bed-ridden for several days and did not fully (or perhaps “fully”) recover for about two weeks.

o   I scored very highly (95^th-99^th percentile) in all markers of durable (“crystalized”) intelligence related to long-term memory, verbal fluency, etc. Even scoring in the 99^th percentile on mental math was, ironically, only a reflection of long-term memory, as the testing never stressed any operations I didn’t essentially know by heart from years earlier.

o   My fluid intelligence – my actual raw cognitive skills – were extremely poor. The lowest of these was a score in the 3^rd percentile in a test of working memory. Now, these test results came not only with a percentile but also with a description. Any score at or below the 2^nd percentile was tagged as “intellectual disability” while a score in the 3rd percentile was tagged only as “borderline.”

o   This physician interpreted this and other “borderline” and “low average” results to be normal, despite the clinical physiologist who carried out the test explaining that extremely high crystallized intelligence and extremely low fluid intelligence follows an expected pattern of brain damage in somebody whose acute cognitive capacity was significantly impaired.

o   Full stop, from this man’s mouth – he would have helped me. He would have supported my pursuit of medical accommodation at work, had only my working memory been in the 2^nd percentile. To him, the 2^nd percentile was a disability, while a drop from the 99^th to the 3^rd percentile was normal and healthy.

o   Instead of helping, he accused me of faking and embellishing symptoms in an attempt to scam my way into disability accommodation at a job that I literally cannot continue to do.

o   Instead of helping, he admitted to not being educated enough to understand my adverse test results or how the test even worked, and thus couldn’t know if the symptoms I claimed were real.

o   Instead of helping, he used my 3^rd percentile working memory and other cognitive struggles as a weapon to question and discredit everything about me – my adverse autoimmune results, my impaired brain metabolism, my cognitive decline, and the crushing and debilitating neurological symptoms I deal with on a regular basis.

 

Backyard Burn 10 Mile Trail Race – March 16

o   At the end of a week off from work, I felt well enough to jump in an unplanned trail race

o   I ran exactly 70:00 for 10 miles on a pretty tame trail course to finish third

o   I am/was clearly in poor relative shape, but I actually felt pretty good about this result because I’d not run hard in well over a year and maybe never in a very low carbohydrate state

 

Elm Creek Backyard Ultra – April 25

o   This race was not unplanned and was in fact a terrible idea. I had signed up months earlier in a fit of optimism and, after a very poor April, was ~100% certain I was not going to race just a week out

o   Then I forced my way through a walk, and the next day forced my way through a jog, and the next day the jog was a little better, and I decided the race was still a good excuse to take a few days off and go home to MN

o   I don’t really want to talk about it any further than that. I felt bad all week, felt bad the morning of the race, felt bad during, and didn’t run nearly as far as I would have hoped or thought possible

o   Ultimately completed 13 laps (~54.1 miles) to finish like…50^th or so?

o   The good news is that the effort was minor enough to not cause any real damage, and I actually felt better neurologically in the days following

The Fasted 50K and Heavy Cream Cholesterol Experiment - Preview

 

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 20^th. 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 19^th and run the 50k on the 20^th. 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.

2024 In Review Part 3 - Impaired Brain Metabolism and How to Deal with It

 

Part 1 Here, Part 2 Here

As I outlined in the previous section, the major long-term issue I’m dealing with at this point is widespread impaired brain metabolism - Most areas of my brain are deficient in their capacity to produce energy through traditional means. What I’m going to do here is expand a bit on what that means and how that works.

In a standard, simplified framework the brain is considered to run entirely or nearly entirely on glucose. This makes the cells of your brain and nervous system distinct from nearly every other cell in your body, which can seamlessly blend glucose and fatty acids as fuel sources in various proportions. Your muscle cells, for example, can freely convert fatty acids to energy through a process called beta-oxidation, essentially the “burning” of pure fatty acids.

But beta-oxidation doesn’t occur in the brain or nervous system. Thus, the typical understanding (which is indeed true in a general sense) is that the brain must use glucose for its required energy production. What happens in a range of neurodegenerative and other neurological conditions, however, is that your brain simply doesn’t take up and utilize glucose to a degree sufficient to meet energy demands. I would contend that the reason this usually happens, typically in an aging, metabolically unhealthy population, is related to chronic hyperglycemia, hyperinsulinemia, and insulin resistance. The same insulin resistance and chronically elevated insulin that characterize diabetes and other chronic metabolic conditions manifest in the brain as well (you may have heard Alzheimer’s referred to as “type 3 diabetes” at some point) and usher in a gradual, years-long degradation of metabolic function.

That situation, obviously, does not apply to me. My metabolic health is fantastic, and there was no gradual onset over the course of years or decades. My onset was acute, the result of whatever exact autoimmune reaction was triggered in response to the Pfizer Covid-19 vaccine. While my onset was clearly sudden, its hard to establish exactly how sudden. It may have been nearly instantaneous with the initial autoimmune manifestation, or it may have been exacerbated over months of severe autoimmune symptoms. Regardless, it was not the typical insidious onset you’d see in chronic neurodegenerative disease.

PET Scan Results

So what does my testing show? Unfortunately, there aren’t a ton of clues. The way a PET scan works is by essentially administering an IV of radioactive glucose and observing the reactive signature “light up” as those radioactive molecules are utilized in the brain. The more glucose each part of the brain uses, the brighter and redder that area will show up on a scan. A localized red spot, for example, might indicate a tumor greedily gobbling up glucose at an increased rate. Conversely, areas that take up less glucose than you might expect are a blue-green color. This is what you might see a dementia patient slowly losing functional capacity as their ability to convert glucose to energy wanes.

My brain had a lot of blue and green areas, indicating widespread failure to take up and/or utilize glucose at a level consistent with my brain’s energy needs. But there isn’t much more to it than that. The PET scan doesn’t tell us exactly what is damaged, or how and why that damage prevents proper function (although I do have ideas). I also don’t have a neat and tidy number attached to the result - There’s no highly quantitative assessment that lets me tell you how deficient my brain function is. I also don’t know anything about the rest of my nervous system, which may very well be suffering from the same defects. The only thing I really know for sure is that my brain doesn’t produce energy properly and that attempts to force it to through basically any level of mental effort result in a range of neurological complications as it ultimately fails to meet the demand, instead propagating whatever inflammatory damage drives symptoms for hours, days, or even weeks after the effort.

Dietary Approach to Impaired Brain Metabolism

 

Thankfully, the other thing I know for sure is how best to handle this situation to hold myself together as well as I’m able. That notion that your brain only uses glucose for energy? That’s highly simplified, and alternative sources can be leveraged to provide various degrees of relief. Unfortunately, this is a topic on which most physicians appear to have stunningly little education or understanding, which has led to more than a couple dead-end conversations with neurologists who frankly have no understanding of brain metabolism (more on that at a later date, but it includes one doctor trying to tell me that because she didn’t know what they meant, that the test results may be unrelated to my symptoms and that I was probably just depressed. She then tried to prove her point by googling impaired brain metabolism and showing me the first result…which listed only epilepsy, Parkinson’s, and Alzheimer’s as typical manifestations of such brain dysfunction).

I’m going to try to keep it pretty basic, but I do want to at least touch on the three main alternative sources your brain can use to produce energy – alcohol, lactate, and ketones. There’s also a fourth “alternative” – the increased consumption and utilization of glucose itself that occurs in response to exercise.

I mentioned previously that alcohol consumption was fairly pivotal in cementing my understanding of my current situation. The fact that alcohol very clearly improves my symptoms and aids recovery from acute severe episodes drastically limits the number of problems I could be dealing with. But alcohol is an easily available source of brain energy, and in fact its one that healthy people prioritize to a degree when they consume it. This isn’t really for “good” reasons – alcohol can’t be stored in the body and is acutely toxic, so your body will make efforts to use it as an energy source in order to clear it from the bloodstream. In a healthy person, this manifests in part as a downregulation of glucose consumption in the brain and a partial replacement of that energy flow with alcohol instead. For me, glucose consumption is chronically decreased anyway, so alcohol just serves to fill in the gap and make me “whole” for a certain period of time.

As I discussed previously, I was strategically using alcohol this year more often than I would have liked from an overall health perspective. I wasn’t drinking for or to any real level of intoxication, just consuming a deliberately gentle flow of a few drinks maybe two to three times a week. It was, very literally, strategic, and often necessary to keep myself semi-functional for another day. This is something I’ve felt the need to do far less frequently in a ketogenic state.

The next alternative fuel source is lactate, which is tough to separate from the increase in glucose utilization during exercise, so we’ll discuss them together. Lactate (or the very closely related lactic acid) is often viewed somewhat negatively or as a “waste” product because it increases in the bloodstream during strenuous exercise. However, in reality its just a byproduct of typical metabolism and only increases in the blood when the ability to clear it can’t match production. Its production increases even at lower levels of exercise intensity, and one of the manors by which it can be cleared is to be taken up by cells (including those in the brain) and converted to pyruvate for direct energy production. Thus, the increase in lactate metabolism during exercise provides an additional partial source of brain energy.

The degree to which that helps me is unclear, however, because it generally happens in concert with increased glucose uptake. A variety of glucose transporters become more active and efficient during exercise (for good reason – to readily provide you with fuel). Its extremely apparent that this effect still occurs for me as well, despite the general impairment of glucose utilization. Its really quite a weird phenomenon – If I’m just barely well enough to get out the door to exercise, I can begin a slow walk/jog/hike and eventually my neurological health will improve. How long that takes seems to depend on how poor I feel – at functional baseline, its 15-20 minutes before function and feeling both start improving. When I’m worse, it can take closer to an hour – and when I’m in that poor of a state, I can continue to noticeably improve for hours if I continue to exercise. To that end, some of my best stretches of health have actually occurred as a result of hiking trips in the mountains. Not only do I completely avoid cognitive strain, but several hours a day (plus some lasting effect after the fact) of increased glucose and lactate metabolism provides sufficient energy availability for basically an entire day.

Now the most important one, in my opinion – ketones. In a low-carbohydrate, low-insulin environment your liver converts some fatty acids to ketone bodies, which can serve various functions including as a fuel source. Ketones are functionally unique from their parent fatty acids in a number of ways, but the most important for the purpose of this discussion is their ability to be directly taken up by the brain and nervous system as an energy source. Thus, a person in a consistent low-carb/low-insulin state can expect to have access to a consistent stream of ketones for energy.

This consistency is a major differentiating factor when compared to other alternatives like alcohol, carbohydrate binges, or exercise. Alcohol and massive carb spikes are of course temporary, acutely unhealthy manners by which a person can increase energy availability. And despite my desire to run and hike all day, exercise is ultimately temporary as well. Ketones, however, are not. Ketones are forever. Provided, that is, that you maintain an environment conducive to their production.

An important note on ketones is that their contribution to the brain’s energy requirements is not demand-driven, but supply-driven – the uptake and utilization of ketones is proportional to their concentration in the bloodstream. Thus, a “standard” ketogenic diet that you or a family member or a friend have probably tried won’t actually help me all that much. The traditional advice to remain under 20 grams of carbs per day will typically only elicit low levels of ketone production, and thus low levels of ketone-based energy. This is basically irrelevant for a person who only endeavors to manage blood sugar and curb sugar cravings, but makes a great deal of difference for me.

Not only is my focus on limiting carbohydrates to something like 5 grams per day, but I also moderate protein intake (as it has a mild insulinogenic effect) and maximize the fat percentage of my diet. This “therapeutic” ketogenic approach focuses on maximizing the concentration of ketones in the bloodstream, and thus the degree to which ketones can provide relief in the face of impaired glucose metabolism.

Unfortunately, the ketone levels I’ve found are necessary to truly prevent the onset of symptoms haven’t really been obtainable in the context of “normal” food consumption. For me, for now, it seems only extended fasting or a heavily fat/oil-based diet that even further minimizes protein and incidental carbs can raise my ketones to the levels necessary to approach true non-symptomatic function (For context – a person on a standard mixed diet usually has ketone levels of 0-0.1mmol/L, a “standard” keto dieter might hang out at 0.5, I bounce around between about 1 and 2, and need something more like 3+ to ward off symptom onset).

There are other methods of temporarily elevating ketones above my standard baseline. One is exogenous ketones, suddenly widely available in the last couple years. These work great, raising ketone levels by 1-2mmol/L for a couple hours. However, they are quite expensive and only temporary. That said, I do keep them on hand and use them sometimes to escape potentially calamitous situations. Another shortcut, so to speak, is to drink MCT oil. Medium chain triglycerides are essentially too short to be efficiently burned or stored the way longer chain fatty acids would be. Instead, they are preferentially converted to ketones, even if the person drinking them isn’t consuming a ketogenic diet. This is less effective than exogenous ketones, in additional to being kind of tedious and slightly gross. But its very cheap when purchased in bulk, so I do consume several servings a day at strategic times (ie. During work) in an effort to support ketone levels and minimize symptom onset.

Conclusion 

So that’s basically it. My brain doesn’t properly produce energy through traditional means. If I don’t diligently care for the situation, it quickly becomes dire and I’m relatively easily knocked on my ass by simple mental and cognitive tasks. I am, at baseline, still made bedridden by the job I’m trying to work every day. The reason I make it to work more days than not, the reason I can mostly hide my symptoms while I’m there, and the reason I’m able to even go for a brisk walk (let along run multiple hours at a time), is because I approach each day in a deliberate, evidence-based fashion that leaves little wiggle room if I hope to remain functional. The combination of a therapeutic ketogenic diet, ketone-raising supplements, and as much exercise as I can manage keep my brain functioning far above where it otherwise would be. At all hours of the day, I am, often through multiple avenues, closing the substantial gap between the energy demand of my brain and nervous system and the critical shortage of supply that otherwise exists.

The hope in 2025 is not that I will magically get better, because I think at this point it would be naïve to assume that’ll ever happen at all, let alone soon. The hope is simply that I can manage things at a high enough level so as to continue showing up to work while cobbling together enough exercise that I feel like I can, indeed, exercise. The hope is to string together days and weeks away from work that allow for real adventure, be it running or otherwise. And the hope is, at least temporarily, to be fit and healthy enough to accomplish something cool by the end of the year, whatever that may be – and to prove that my life can be completely ripped apart, left broken by autoimmune disease and brain damage, but that I can still exist fully on the other side.