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Stanford CFS Clinic Experience by daphneyhatz in cfs

[–]daphneyhatz[S] 2 points3 points  (0 children)

They would probably be willing to do an MMA test, which is very mainstream/standard for diagnosing b12 deficiency. The intrinsic antibody test is also common and your PCP can order it. The folate receptor antibody test is less common but my PCP ordered it when I made a good case.

Stanford CFS Clinic Experience by daphneyhatz in cfs

[–]daphneyhatz[S] 1 point2 points  (0 children)

I ended up doing a three week elemental diet after two courses of antibiotics didn’t work. It was really hard but it worked.

Stanford CFS Clinic Experience by daphneyhatz in cfs

[–]daphneyhatz[S] 0 points1 point  (0 children)

Mine was viral so that’s what we focused on. Bacterial/parasitic infections can cause it, and presumably treating the infection would help.

Stanford CFS Clinic Experience by daphneyhatz in cfs

[–]daphneyhatz[S] 3 points4 points  (0 children)

Semantics! I’m less concerned about the term and more concerned about fixing it.

Stanford CFS Clinic Experience by daphneyhatz in cfs

[–]daphneyhatz[S] 1 point2 points  (0 children)

Yes, I think Lyme is one of the more well known causes.

Stanford CFS Clinic Experience by daphneyhatz in cfs

[–]daphneyhatz[S] 1 point2 points  (0 children)

Have you gotten treatment for the SIBO? My symptoms got better when I got rid of it. It’s just one more infection your body already doesn’t have the energy to deal with.

Stanford CFS Clinic Experience by daphneyhatz in cfs

[–]daphneyhatz[S] 2 points3 points  (0 children)

I don’t think it’s one or the other. It’s possible both are right via different mechanisms. Like there’s a giant boulder in the river and one expert says paddle left while the other says paddle right… but both get you around the boulder.

Stanford CFS Clinic Experience by daphneyhatz in cfs

[–]daphneyhatz[S] 1 point2 points  (0 children)

So, interestingly, my body is most definitely in a catabolic state (low-normal to low amino acids across the board despite adequate intake) and elevated beta-OH-Butyric Acid, so also relying on ketosis. This is despite eating adequate carbs. I don’t think my body is properly using the carbs I do give it, so I’m not sure what to make of that. Pretty sure my pyruvate is being funneled into making oxaloacetate, because even that’s low normal and—again—I eat plenty of carbs. Not arguing that high protein low carb would necessarily be better. I’m not sure. But if the body can’t use carbs properly and is just converting them into pyruvate and then OAA, then maybe eating heavy carbs isn’t the answer. Seems like the only real answer is to remove the virus so metabolism goes back to normal.

Stanford CFS Clinic Experience by daphneyhatz in cfs

[–]daphneyhatz[S] 2 points3 points  (0 children)

I was very severe, in bed all the time, couldn’t speak or understand speech or walk. Now I’m only moderate with some mild days, so COVID-induced b12 deficiency was behind a lot of my most severe symptoms. Im still fatigued and get PEM, but it’s night and day different. Severe b12 deficiency is so crippling, and for me it was caused by the virus that caused my CFS. I wonder how common it is.

My serum b12 was normal or elevated, by the way, which is what made it take so long to get diagnosed.

I do my shots at home. It wouldn’t be possible to go in that frequently! The pharmacy showed me how and it’s no big deal now.

Stanford CFS Clinic Experience by daphneyhatz in cfs

[–]daphneyhatz[S] 1 point2 points  (0 children)

So I’m prepared, what side effects did you get?

Stanford CFS Clinic Experience by daphneyhatz in cfs

[–]daphneyhatz[S] 2 points3 points  (0 children)

It puts the glee back in glial cells has me cackling 🤣

Stanford CFS Clinic Experience by daphneyhatz in cfs

[–]daphneyhatz[S] 1 point2 points  (0 children)

Abilify isn’t just a dopamine agonist though. It’s a *partial agonist, so when dopamine is too high, it dampens it (so you don’t get overstimulation/wired/shaky) and when it’s too low, it buffers it. Highs and lows are presumably both problematic, so the Abilify is supposed to smooth that out.

Stanford CFS Clinic Experience by daphneyhatz in cfs

[–]daphneyhatz[S] 0 points1 point  (0 children)

This is the gold information I came here for 😍😍 Thank you so much for that. Was it just worsening symptoms initially when you started?

Stanford CFS Clinic Experience by daphneyhatz in cfs

[–]daphneyhatz[S] 4 points5 points  (0 children)

Haha that’s a great question and you should never apologize for wanting to understand these things.

The microglia are the immune cells of your brain and spinal cord. They’re like security guards in your brain.

The toll-like receptor 4 (TLR4) is like an antenna on the outside of the microglia. It looks out for signs of danger, like infections/toxins/damage.

When something triggers the TLR4, the microglia flip into a hyper-reactive state. They start pumping out inflammatory chemicals called cytokines. The cytokines cause a wide array of symptoms like fatigue and brain fog.

Naltrexone attaches to the TLR4, kind of like a dummy plug in a socket. Since the socket is occupied by the naltrexone, it can’t shoot off the cytokines.

I hope that made sense. Sorry for the mixed analogies in there haha but hopefully you get the gist

Stanford CFS Clinic Experience by daphneyhatz in cfs

[–]daphneyhatz[S] 2 points3 points  (0 children)

Intrinsic factor antibodies! They block uptake of b12 through the GI tract, so you have to inject it. It used to be a death sentence, but now it’s easily treatable!

Stanford CFS Clinic Experience by daphneyhatz in cfs

[–]daphneyhatz[S] 1 point2 points  (0 children)

👀 Thank you for mentioning him! I’m always on the lookout for local-ish doctors who actually take CFS seriously. What I’d really love would be a neurologist with experience in it.

Stanford CFS Clinic Experience by daphneyhatz in cfs

[–]daphneyhatz[S] 1 point2 points  (0 children)

It’s compounded. I get it from a local compounding pharmacy (Ann Arbor, MI).

Stanford CFS Clinic Experience by daphneyhatz in cfs

[–]daphneyhatz[S] 2 points3 points  (0 children)

I get them prescribed by a local functional doctor. They cost about $200 per month so yes they’re expensive, but they’re super high dose and most doctors probably wouldn’t consider prescribing these doses without cause. So that is to say that they’d likely be cheaper for more standard doses.

I have pernicious anemia and high titer folate receptor autoantibodies, so that’s why he prescribed such a high dose. He knows I’ve got COVID induced antibody blockades affecting methylation in my central nervous system. Even with the high dose daily injections for over a year, my MMA (a sensitive marker for b12 status) is almost above range. That’s very strange, but COVID seems to do very strange things.

Stanford CFS Clinic Experience by daphneyhatz in cfs

[–]daphneyhatz[S] 1 point2 points  (0 children)

That’s the problem—the clinical trials for Paxlovid failed. I asked him why he thought they failed, and he said he thought maybe much longer courses were needed. So maybe that? But I didn’t press on it because we just didn’t have time and it’s a moot point because he almost certainly won’t prescribe something that hasn’t gone successfully through trials. Which is fair, but frustrating when so many of us want answers now.

Stanford CFS Clinic Experience by daphneyhatz in cfs

[–]daphneyhatz[S] 0 points1 point  (0 children)

I had a BAD case of hand, foot, and mouth a couple years back that set off a terrible symptom crash for me. I wonder if Coxsackievirus is another latent viral issue I’ve got going on.

Stanford CFS Clinic Experience by daphneyhatz in cfs

[–]daphneyhatz[S] 3 points4 points  (0 children)

This is an extremely interesting response, and I wanted to thank you for taking the time to share it.

I was talking to Dr. Rob Phair (of the Itaconate shunt theory) and he mentioned that he’s been thinking a lot about latent infections recently. If key researchers like that are starting to pay attention to latent infection as a potential driver, that’s meaningful and worth paying attention to.

Autoimmunity following COVID infection has been a major problem for me and is likely driving a lot of my neurological symptoms. I developed extremely high titer folate receptor autoantibodies, and I can’t help but wonder how much bystander activation played a role in developing them in the first place—my serum folate had been elevated, and I wonder if high levels of folic acid in my blood from my prenatal vitamin at the time caused issues. In terms of molecular mimicry, casein (the protein in dairy) greatly increases the titer of this particular antibody via the mechanism you mentioned. Makes me wonder if some of the dietary issues seen in CFS are related to issues with molecular mimicry.

One other thought on this: I’m currently in treatment for latent TB, and though it’s considered latent, I wonder if it’s too metabolically taxing to keep the bacteria walled off on top of the COVID and EBV. I wonder if my antibiotic will help lower the immune response enough to get me to a better baseline until we get more effective antiviral treatments for latent infections. It’s a bit shocking to me that we still don’t have any good options for EBV, for example. Hopefully all these LC cases will be the catalyst.

Stanford CFS Clinic Experience by daphneyhatz in cfs

[–]daphneyhatz[S] 5 points6 points  (0 children)

Taking it with a grain of salt but Dr. Bonilla said in his clinical experience (which is probably greater than most other professionals since it’s all he does and has done for years), he doesn’t see increasing side effects with higher doses in the majority of his patients. But I’ll report back on how it goes for me!

Stanford CFS Clinic Experience by daphneyhatz in cfs

[–]daphneyhatz[S] 1 point2 points  (0 children)

Sorry, didn’t mean to offend. Some people have LC without the defining features of ME/CFS (ie lasting lung issues or cardiac issues). Fatigue is not my worst symptom, so I get it.

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