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Three Health Issues Converge on One Bone
How a neurological problem, clogged Eustachian tubes, and a hearing problem all converge on a little bony protuberance behind the ear.
Over the last week I have developed a fascinating insight on how three health issues that had seemed independent all relate to tightness around the little bony protuberance behind the ear known as the mastoid process of the temporal bone.
In laying out this insight, I will also reveal the first glimpse at the metabolic experiments I’ve been conducting on myself for the past three months, all centered around characterizing what I believe to be a mild state of biotin deficiency.
Why I Wrote This Post Tonight
The question was what enzyme and nutrient(s) am I investigating if I show that 30 grams of carbs from white rice increases my ketone levels for 15 minutes? The answer is pyruvate carboxylase and biotin. Zzz Zzz figured out the enzyme and nutrient on Telegram, while Paint the Girl helped Zzz Zzz with the explanation on Twitter. An honorable mention goes to Sergey Andryukhin, who finished the explanation on Telegram just three minutes after Paint the Girl finished it on Twitter.
As covered in Lesson 32 of my Energy Metabolism class, ketogenesis has one and only one proximate cause: a high ratio of acetyl CoA to oxaloacetate. The physiological contributors to ketogenesis, such as a low insulin-to-glucagon ratio, contribute only because they alter the single biochemical cause of ketogenesis: they raise the acetyl CoA-to-oxaloacetate ratio. Oxaloacetate is formed mainly from pyruvate, which is formed mainly from glucose. The formation of oxaloacetate from pyruvate requires the enzyme pyruvate carboxylase. As I described in High Protein? You Need More Biotin, pyruvate carboxylase is one of the five biotin-dependent enzymes. Thus, in a severe genetic deficiency of pyruvate carboxylase or in a severe biotin deficiency, you expect the biochemical abnormality known as paradoxical postprandial ketogenesis.
Ketones should go down when you eat, and should go down the most when you eat carbs. For them to rise in response to a carb load is paradoxical because the carb load should do the opposite.
Toward the end of the summer, I identified what appears to be a mild biotin deficiency in myself despite a diet very rich in biotin. I now believe I inherited a mild genetic deficiency in a biotin transporter from my mother and my maternal grandfather, and that I have spent my entire life in a state of biotin deficiency that was mild when I was eating a diet rich in liver and egg yolks and extreme when I was a vegan.
I have spent the past three months purposefully remaining in this mildly biotin-deficient state to thoroughly characterize my metabolism, so that I can document in exhaustive detail what fixing this deficiency does for me in the new year.
If you find this post useful, please thank Zzz Zzz and Sergey Andryukhin on Telegram, Paint the Girl on Twitter, and everyone else who participated in the pop quiz. This post is the prize they won for you.
And now, for the three health issues that all converge on one bone.
Problem 1: Terbinafine-Induced Neurological Dysfunction
In 2017, I developed a severe, aggressively spreading cutaneous fungal infection. A dermatologist put me on terbinafine, an anti-fungal. The day I started the terbinafine I developed the worst twitching I had ever — and have ever — experienced in my life, with the large muscles of my thighs jerking and going crazy. I tested all the major electrolytes and quickly identified potassium as the only one that stopped the twitching. I soon found that getting 5 grams or more potassium a day reduced the twitching by 80%. I soon after found that the other 20% was eliminated if I stayed away from acidic beverages.
At some point I developed a gait abnormality that seemed like a foot drop. I had been sleeping under an air conditioner that was blowing dust from severely chipping paint on a window sill over me, and I worried the paint had lead in it. I analyzed the elements in hair and urine and measured my blood levels of lead. Everything was normal except my urinary barium was 17 times the upper limit. I ultimately traced the barium to the paint in my apartment and to the makeup I was using to reduce the glare in my videos.
The reason I was sleeping in this way was that my bedroom was too hot to sleep in, but it had a fire escape, making it illegal to install an AC. So I was sleeping on my couch under the living room AC because it was the only room I could cool well enough to fall asleep in without violating the law. In retrospect I should have used a window AC in the living room, a portable AC venting from my bedroom to the living room, and a blackout curtain around the portable AC to keep my room blacked out, but I didn’t think of it at the time.
I went to an environmental doctor for help detoxing the barium. She largely ignored my concerns about the barium and told me she thought I had mold toxicity. She recommended a mold inspector. The inspector almost immediately noticed that my shower wall was bulging forward, and that black mold was seeping out from where the wall met the rim of the tub. The shower wall was opposite the living room wall adjacent to my couch, and the inspector said the mycotoxins would seep out the wall and fall on me while I was sleeping. He also found bulging in my bedroom floor suggestive of water damage that was probably harboring another source of black mold.
All of these things happening in a short span of time made me confused about the twitching and gait abnormality. While the twitching had obviously started the same day as the terbinafine, barium toxicity and mold toxicity were both plausible explanations for either of the neurological problems. Moreover, barium’s mechanism of toxicity is to interfere with potassium handling, so the nearly magical responsiveness of the twitching to potassium really seemed to point toward barium.
The environmental doc ran a Genova ION panel for me, as well as a toxicology screen and a mycotoxin screen. The tox screen found nothing. The mycotoxin screen found mycotoxins in my urine that could easily come from food and bore no resemblance at all to the mycotoxins in the dust of my apartment. The one abnormality on the ION panel was an elevated ratio of glutamate to glutamine.
I knew the mold was affecting me when I went outside to look for an apartment. I had been spending all of my time indoors working. I had newly left academia, so was working from home. I was suffering from brain fog, but I didn’t realize it until a couple hours outside my apartment led to a massive improvement in how my brain felt.
From that experience, I have decided that if you want to see if you have a problem with indoor mold, it makes more sense to spend a few thousand dollars on a vacation than on mold testing. The inspector noticing the bulging and black mold in the shower seam was valuable, but leaving my apartment told me a lot more than the mycotoxin testing told me.
I wanted to detox the barium with sodium sulfate, but could not find a trustworthy food-grade source. So, I used EDTA. I never retested it (I will soon, however), and I accidentally gave myself a zinc deficiency with this. I took sulforaphane, charcoal, and bentonite to try to clear the mycotoxins, but never retested them. I moved, which I think was overwhelmingly the most important thing I did for the mold.
The elevated glutamate-to-glutamine ratio told me that acidity was my main problem. Acidity upregulates the kidney’s expression of glutaminase, which breaks down glutamine to form glutamate so that ammonia can be used to mop up the acidity by generating ammonium. Acidity independently hurts potassium handling. Both mishandled potassium and excessive glutamate would cause twitching.
It was at this point that I figured out I could use baking soda to normalize my urine pH. The biggest problem this solved was improving my exercise tolerance. I explained this in How Measuring My Urine pH Got Me to Love Working Out Again.
However, it also helped big-time with the twitching. You have to realize that when I say I had gotten rid of most of the twitching on a high-potassium diet with strong limitations on acidic beverages, I was starting from a place where the large muscles of my thighs were jerking. On a scale of 1 to 10, the twitching the day I started terbinafine was 150. I had brought the twitching down from horrifying to extremely annoying.
It was also rather difficult to always get five grams of potassium. This required rigorous attention to my diet, and if I slipped below the 5-gram threshold, the twitching would get worse. Working out would ignite twitching flares, and generally laid me out on the bed for hours. Until I started bicarbonate, it would take me five days to recover from one workout.
Bicarbonate supplementation, as long as I hit the sweet spot of maintaining my urine pH in the 6.4-6.8 range once I had eaten my first meal, allowed me to relax a little on the potassium, tolerate more acidic drinks, tolerate working out, and get the twitching more consistently at bay.
Much later, I interviewed Chad Macias along with Danny Lennon and Alex Leaf about sports nutrition. Chad told me he found that fibromyalgia patients had elevated extracellular glutamate, and that he was testing whether transdermal carnosine can help. This made a light bulb go off in my head. Carnosine is a pH buffer within muscle cells. If I could boost my muscular carnosine, I could reduce my acid generation and reduce my dependence on bicarbonate. Chad thought carnosine would get more to the root of the problem since it would buffer acidity before it left the muscle cell, whereas bicarbonate was putting a bandaid on the problem since it was buffering acidity after it had left the muscle cell.
I eventually switched my approach from using bicarbonate to using 1/4 teaspoon of beta-alanine once or twice a day and 25 milligrams of vitamin B6 as pyridoxal 5’-phosphate (P5P) once a day. The beta-alanine is used to synthesize carnosine, which would help buffer acidity and reduce the conversion of glutamine to glutamate. The P5P is used to help convert the glutamate to GABA or dispose of it in the citric acid cycle.
This led to a much more stable effect than bicarbonate. Bicarbonate had a risk that I could overdose. If my urine pH went to 8, I would develop a different type of twitching that was only cured with calcium and acidic foods. This is because alkalinity makes calcium ions bind to albumin in the blood and become unavailable. Beta-alanine generates 15 minutes of uncomfortable tingling if I take too much at once, but it doesn’t have a risk of throwing the pH balance too alkaline. Moreover, once the intramuscular stores of carnosine are high and stay high, you have long-term protection from acidity. You don’t need a new dose every few hours. Each new dose of beta-alanine is simply serving to replace what carnosine gets lost each day so the buffering capacity of the muscle stays high round-the-clock.
Over the years, I repeatedly found that if I dropped the beta-alanine and B6, the twitching would come back within a few weeks. However, this year — five years out from the onset — I stopped taking them for good and the twitching has not come back.
Ultimately, the fungal infection required six weeks of terbinafine to knock it down, and then vitamin A and tanning came to the rescue to kick it while it was down and finish it off for good. I will write a separate post about my skin issues soon, as I have developed a remarkably effective sunlight and tanning protocol to keep my skin very healthy.
As my twitching problem started to recede, it settled into a constant paresthesia on my left cheek.
They may not seem obviously connected, but I assure you from experience that the paresthesia on my left cheek was the much less severe manifestation of the same neurological problem that caused the massive twitching of my large thigh muscles on day one of the terbinafine.
As the healing continued, the constant paresthesia on my left cheek settled into an intermittent paresthesia on my left cheek.
Five years later, this paresthesia has become incredibly subtle and intermittent. On a scale of 1 to 10, the twitching on day one of terbinafine was 150 and the left cheek paresthesia is now 0.1.
What had been horrifying became extremely annoying and then became mildly annoying and is now a curiosity.
It happens rarely, usually when I am fasting or otherwise energy depleted, and it feels like something fuzzy is on my cheek. It can affect anywhere from beneath the eye to above the lip on the left side of my face. Sometimes I scratch that part of my face and the feeling of having just scratched it persists longer than it should.
But here is the question, and here is where we seek to find a connection:
Why did this whole-body problem recede until in its least severe form it only affects my left cheek?
Problem 2: Clogged Eustachian Tubes
In the Spring of 2007, I developed a problem with head and neck tension. This did not come with any pain, but felt like I was wearing a hat when I wasn’t, except it was extremely uncomfortable. Early on, I found that wearing a neck brace could help. Otherwise, I would have to hold my neck up with my hands when my attention was on something in front of me.
I tried many things, and the two things that helped most were 45 minutes on a rowing machine a few times a week, and 30 minutes on an elliptical 3-5 times a week. I wrote about this 2.5 years ago in My Head and Neck Tension: 30 Minutes on the Elliptical to the Rescue.
At the Ancestral Health Symposium in 2021, I talked to someone who had very similar symptoms to me and ultimately had a neurosurgeon install bolts in his cervical vertebrae to lock them into proper position. While I had no desire to get bolts installed in my vertebrae, my conversations inspired me to figure out once and for all what was at the core of my head and neck tension.
I got a bunch of X-rays and an MRI. These showed that I had a dramatic loss of curve in my neck, and that my vertebrae were crushing my discs. Two discs were bulging and one of them had two tears.
For the last year, I have been working with an amazing physical therapist. When I started with her, I could not bend my neck forward or backward while using more than the first couple of vertebrae. I had a “hinge point” after which the vertebrae would not participate in the movement. When I would turn my neck, my thoracic vertebrae would not rotate in the opposite direction like they are supposed to, my manubrium and first rib would not descend like they are supposed to, I had poor range of motion, and pushing my range caused pain. I couldn’t even think about side bending properly.
We are almost finished establishing 100% pain-free range of motion for cervical flexion, extension, rotation, and side bending.
The most game-changing adjustment has been on my coccyx, which is the tailbone.
A few months into our work, my PT asked me if I had ever damaged my tailbone. She said that she has seen head tension issues similar to mine in the past in patients with tailbone injuries.
I remembered the feeling of a severe injury to my tailbone, but I couldn’t remember the event. I tried offering suggestions, such as falling on my butt snowboarding, but I knew these suggestions were not that event. The one I knew happened, the one I remembered feeling, but which I just couldn’t bring to the front of my brain.
I spent months trying to think of this event. Over and over, I knew it happened, but I couldn’t remember what it was.
Eventually she gave me an external coccyx adjustment. She was surprised that my coccyx had much less dysfunction than she expected.
Months later, we were stalling on certain issues, and she suggested we do an internal examination of the coccyx. I agreed.
It turned out that my coccyx was hyperflexed to the point of being pressed flat against the back of my sacrum, was rotated counter-clockwise, and was bent to the left.
She said that it was tucked so far inside that when she did the external adjustment she thought she was touching a completely different part of the bone than she actually was. That is, it was so dysfunctional that it appeared normal upon external examination. Only an internal examination could reveal the problem.
There were two immediate effects of the adjustment. The first was that my range of motion in extending my neck went from 45% to 95%. The other was that my anterior pelvic tilt dropped and it was immediately far more comfortable to sit in a chair. I could maintain better posture while sitting without feeling like my core was on fire.
I went home and went to sleep at the end of the day.
In the morning, I woke up, left the apartment to grab a coffee, and was halfway down my block when suddenly I remembered exactly what happened to injure my tailbone:
When I was 14, I was making mischief with my friends in the middle of the night. We ran to hide in the woods, right next to a bridge. Unbeknownst to me, we were running off a ledge. I felt like Wily E. Coyote running off a cliff. Run, run, run… wait, what? Boom! I landed on my tailbone on the concrete.
It was as if that memory was squashed between my coccyx and my sacrum. Once my PT bent my coccyx back into its normal position, the memory fell out and became available to me.
The fact that I immediately nearly doubled my range of motion in my cervical extension and gained a massive improvement in my pelvic tilt suggests that my coccyx had been tugging on the soft tissues that run vertically along my spine and removing an inch or two of slack from the entire stretch.
However, the fact that it was bent to the left and rotated counter-clockwise suggests that it took that slack out asymmetrically.
I now suspect that this may have created the asymmetry that later led me to fall four times and slam my left shoulder into the ground, dislocating it. I never fell on my right shoulder. But I smashed my left into the ground over and over again.
Now I have staples in my left shoulder, and, no doubt, scar tissue. I am sure that this has caused further asymmetry. But it might all be driven by spending 26 years with a bent and twisted coccyx.
Among those asymmetries are the bones of my face.
Over the course of our appointments, my PT did some exploring in my mouth, face, and scalp to try to address the head tension. This led her to ask how my Eustachian tubes functioned. The truth was that they always felt clogged as long as I could remember and that I accepted this as normal.
The Eustachian tubes, also known as the auditory tubes, connect the middle ear with the upper throat. They allow air to flow to balance pressure, normally release when we yawn or swallow, and are what are clogged up when we feel our ears “popping.” The middle ear is in the temporal bone, which is the bone of the skull on each side of our head. In front of the temporal bone is the sphenoid bone, most of which is not accessible on the outside of the head because it runs through the middle of the skull above the mouth.
In trying to address my Eustachian tubes, my PT palpated the sphenoid bone from the roof of my mouth and found that it was twisted, with the left side pushed forward and the right side protruding more into the roof of my mouth. Over the course of several appointments she moved it into proper position, working on it through the roof of my. mouth. The temporal bone has a “zygomatic arch” that passes in front of the sphenoid on the side of the face and connects to the zygomatic bone, which is the one of the main bones of the cheek. These were all pushed forward on the left side of the face, and my PT worked to bring them back into position.
In the first of these appointments, where she worked on the sphenoid bone from the roof of my mouth, I felt like I had a brand new mouth, surgically installed. I simply felt like I had much more room in my mouth.
I started to yawn during the appointment. When I left her office, I began yawning violently, like I was a roaring lion voraciously consuming air, finding it abundantly all around me for the very first time. This lasted for 45 minutes.
In each successive “mouth-and-face” appointment, I had another yawning attack, but each one was less intense and of less duration than the one before it. Eventually as my bones fell largely into their proper positions, my Eustachian tubes functioned better and the yawning attacks became tame.
It was easy to restore the function of the right Eustachian tube, but clearing the left one has been far more elusive.
At first, we could get the right one to clear normally and just nothing on the left.
Then, we could get some movement of air within the left side, but it would never exit the ear like on the right side. It would just move around.
Then, we could get a weak clearing on the left some of the time.
Eventually, we got it so that if I held my nose and mouth shut and exhaled, the right would immediately clear, while the left one would get a smaller clearance only after I swallowed.
This wasn’t perfect, but we took it as a win.
Over time, it became apparent that I needed a mouth-and-face maintenance appointment about once every three weeks to retain these gains. However, once we had squeezed every last drop my insurance was willing to pay for, I had to cut our appointments from two a week to one a week, and this led us to focus more exclusively on the core issue of the neck.
Since my neck is now almost at perfect function, last week we revisited the Eustachian tubes.
Since we had already done so much work inside the mouth and on the front the face for this purpose and still not reached full function, my PT began working on the back of my skull.
One thing that quickly became apparent: the tissues around the bony protuberance behind and beneath my left ear, which is the mastoid process of the temporal bone, were vastly more tight than the same tissues on the right side.
We started talking about the area we were working on, and my PT noted that the trigeminal nerve passes through this area, which includes the main sensory nerves of the face.
The portion of the trigeminal nerve that controls the area where I experience paresthesia is the maxillary nerve. This nerve has a root on the inner surface of the temporal bone and then runs through the formaen rotunda, which is a hole in the sphenoid bone, very close to the portions of that bone that press against the roof of the mouth!
Thus, everything we had been working on to unclog my Eustachian tubes, all of which involved an asymmetric forward push of the left side, and all of which was harder to resolve on the left side, is all very closely related to the nerve whose post-terbinafine dysfunction has been hardest to resolve!
Problem 3: Noise-Induced Hearing Loss
Although I was not aware of any hearing loss, and no one has ever suggested to me that I have hearing loss, I wanted to investigate the state of my hearing because biotin deficiency causes hearing loss. Thus, testing my hearing before I start supplementing biotin would allow me to see if biotin was improving my hearing.
Additionally, I was having acute attacks of tinnitus that were increasing in frequency this year. I stopped using airpods and earpods and now I do not put any sound or radiation directly in my ear, and those attacks have decreased in frequency by about 95%.
In my recent metabolic experiments, I have found that when I do get an acute tinnitus attack, which usually lasts several seconds, it is five times more likely to occur on days where I fast until 4 PM than when I eat regularly spaced meals, and it is five times more likely to occur in my left ear than my right ear.
I went to an audiologist this week and the results were rather stunning:
I have moderate noise-induced hearing loss only in my left ear.
While she was doing the hearing test, she placed a device on the mastoid process of my left temporal bone — the exact place my PT had been working on last week — to test whether tones could be perceived when broadcast directly through the bone.
It turns out that the transmission through the bone is normal and the loss is with tones entering my ear in the normal way. However, the fact that she had pinpointed this very spot led us to talk about the significance of that spot. The middle ear and internal ear, wherein all the hearing machinery is contained, are located in the temporal bone.
The audiologist asked me if I have asymmetrical exposure to sound.
No. Definitely not.
She pressed the issue. “Are you sure you don’t answer your phone on the left side?”
No. I don’t ever talk on my phone except in speaker phone, and I usually use video chat on my laptop.
Prior to cutting out airpods and earbuds earlier this year, my radiation and sound exposure was symmetrical, using these devices.
When I went to loud concerts or clubs or was around loud machinery in my teens and 20s, it was symmetrical.
While I cannot remember exactly how I talked on a handheld phone decades ago, I am almost positive I would have answered it with my right hand since I am right-handed, and would have switched it to my left only when my hand, arm, or neck got tired on the right side.
I told her what I’d been working on with my PT, and she did find it plausible that structural misalignment could put more pressure on the left ear and drive greater vulnerability to noise-induced hearing loss.
She told me that some people are musicians around loud music constantly and have perfect hearing, while other people go to one concert and get hearing loss from it. Some ears are just more sensitive.
I told her that, similarly, my left ear went to the same concerts that might right ear went to, and my left ear was the one getting hurt.
Bringing It All Together
Here is my hypothesis:
The vulnerability to neurological problems, ranging from my experience with a vegan diet to the terbinafine-induced dysfunction described above, is a result of an entire lifetime spent in a biotin-deficient state that has been mild when eating lots of liver and egg yolks and severe when vegan.
In fact, the gait abnormality that emerged with terbinafine disappeared in rather short time without me being able to put my finger on what did it. Maybe it was just discontinuing the terbinafine after six weeks.
Yet, years later, it reemerged long after all the other problems were long into resolution. Until recently, my memory was that I cured myself with high doses of all the B vitamins, and then when I ran a bunch of tests with a neurologist, she couldn’t find anything because I had already cured myself.
However, I recently went back into some notes I had drafted for a specialist in inborn errors of metabolism who I never wound up seeing as a result of COVID flipping the world upside down. In those notes, I found that the gait abnormality actually started after I had began supplementing with high doses of pantothenic acid. I started this because my research for my long-form podcast on vitamin B5 (Part 1, Part 2) led me to discover pantothenate kinase deficiency, which is a genetic defect in the ability to activate vitamin B5. I thought this might have been my holy grail, my long sought-after explanation for why a vegan diet wrecked me so badly and why I remain vulnerable to neurological dysfunction whenever the right insult, like terbinafine, comes along.
Yet pantothenic acid will inhibit biotin absorption! Pantothenic acid, biotin, and lipoic acid all share a common transporter. (Although there is controversy over this, since there is evidence that biotin has its own transporter, which might be a splicing variant of the common transporter).
What actually cured the gait abnormality was that I started taking the pantothenic acid with breakfast, and then added lipoic acid at lunch and biotin at dinner. This was to ensure none of them caused a deficiency of the other.
The heart of the problem is a deficiency in ATP production. Terbinafine would cause mitochondrial damage, worsening the deficit in ATP, and this would cause mishandling of electrolytes and acid-base balance. Barium would make the problem much more specific to potassium, and the mycotoxins were likely an aggravating factor in the background.
Since biotin deficiency causes hearing loss, and severe biotin deficiency causes deafness, my suspicion is that mild biotin deficiency makes someone more vulnerable to standard, run-of-the-mill, noise-induced hearing loss.
Nevertheless, why did my neurological problems improve 1000-fold and go from whole-body twitching and a foot-drop to a subtle infrequent paresthesia that only touches my left cheek?
Why is my noise-induced hearing loss only in my left ear?
Why is only my left Eustachian recalcitrantly clogged?
Every single one of these points converges on the temporal bone, which houses the middle and internal ear where the hearing machinery is located, which forms one end of the Eustachian tube, and which contains the root of the maxillary nerve.
Why my left temporal bone and the bones around it, such as the sphenoid and zygomatic bones, are all so forward shifted on the left, is probably owing to the same reason why I slammed my left shoulder into the ground four times and never did that to my right shoulder. I suspect it is the 26 years I spent with my cocccyx hyperflexed, rotated counter-clockwise, and bent leftward, taking vertical slack out of all the soft tissues along my spine and taking that slack out asymmetrically, driving an asymmetric forward drift of many of the bones of my upper body.
What I find fascinating about this is that an injury to my tailbone from mischief-making when I was 14 might be the critical event that has shaped the ultimate manifestation of insults such as biotin deficiency, barium, terbinafine, and excessive noise.
Will that be the case going forward?
No, I believe now that I am finally taking the time and initiative to get to the bottom of the things that have shaped my health history over the past 40 years, and moving forward I will be the one in the driver’s seat rather than the things that have happened to me.
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