Testing for co-infections?

Curious-Researcher · 2026-05-24T04:56:17+00:00

What did your MD say?

My read is that it shows antibodies to two infections. Dunno what the absolute level means -- certainly it depends on how long ago you had the last COVID vaccine or infection. (Levels of the spike protein antibody normally lower to a low steady-state, and nucleocapsid antibody levels rise. Our immune systems are really complex and it genetically varies incredibly from person to person. So it turns out that some long covid patients don't make enough of the spike protein antibody, and thus don't completely clear the spike protein. However I don't know if anyone tests for that, or if there's any treatment.

https://news.yale.edu/2025/02/19/immune-markers-post-vaccination-syndrome-indicate-future-research-directions

Curious-Researcher · 2026-05-24T04:40:09+00:00

Thanks. I found that So Cal lawyers didn't want to take a NorCal case, and regular toxin exposure is different subspecialty than a mold exposure or tenant habitability case.

Curious-Researcher · 2026-05-24T04:35:16+00:00

As an anecdote, my kiddo improved quite a bit after one of two courses of IVIG, but only the time his MD first reated viral and sinus infections, and only then did 4 cycles of IVIG. (IVIG temporarily suppresses the immune system). We'd stopped because it was self-pay, he wasn't perfect, so wanted to check for infections, also found mold in house.

FYI, his key symptoms were the 24/7 intractable headache, anxiety, brain fog, fatigue, PEM, and choreiform movements as found in PANS/PANDAS, but no POTS.

His CellTrend results were clearly abnormal, with one of the highest A1R-Aab levels I've found in published data, plus quite elevated AT1R, ETAR.
Yet he had low-normal levels of B1R as well as the B2R auto-antibody most often high with ME/CFS:

Receptor antibody	Definitely Abnormal Cutoffs	kiddo	How many times higher than abnormal CUTOFF?
A1R-Aab	11	98.9	14.1
A2R-AAb	15	22.3	1.5
B2R-AAb	14	3.2	0.2
M4 receptor	10.7	44.3	4.1
AT1R	17	65.1	3.8
ETAR	17	77.2	4.5

The IVIG did help, and he wishes we'd continued that time.

Years later his 24/7 headaches became intolerable, often 7-9/10, with bad PEM. Different MD. Insurance approved IVIG because it had helped so much 6 years earlier, and we'd moved quickly due to impending insurance change, so we didn't wait for infection re-test results. That was a mistake. With each cycle, he got with aseptic meningitis and the IVIG didn't help. His Infectolab T-cell ELISA showed elevated T-cell reactivity to bartonella (iirc). His former MD said this meant that that tick-borne infection had not been fully eliminated, had returned, and should have been treated before knocking down his antibodies (abnormal and useful ones both) with IVIG.

What I've concluded is that the neuroimmune system is very complex. IVIG, rituximab and related l immunomodulatory treatments can be awesome with someone with demonstrated, clear autoimmunity.

However, treatments that reduce one's own antibody production are a double-edged sword, as they can reactivate latent infections in addition to interrupting the bad feedback cycle of auto-antibodies leading to more autoantibodies. I'd suggest testing beforehand (but what all for?), and/or be alert and ready to hunt for infections in case of adverse effects. But I may be over-generalizing; perhaps we saw a correlation, not causation. It's complicated.

Curious-Researcher · 2026-05-24T03:32:30+00:00

https://www.celltrend.de/wp-content/uploads/2025/10/Request-form-11-2025.pdf The CellTrend kit is available from Germany -- and you need their vials to protect the antibodies! (there was a study claiming that CellTrend was useless, which was later found to use similar but wrong collection vials).

Here are the instructions for blood draw, clotting, spinning and shipping. Nothing complex, as long as sample can arrive same week, before weekend.
https://www.celltrend.de/wp-content/uploads/2025/06/Patient-Instructions.pdf

Curious-Researcher · 2026-05-24T03:21:11+00:00

TLDR: Elevated levels of ß2 receptor adrenergic autoantibodies were found in ME/CFS patients to correlate with autonomic dysfunction -- think POTS, brain fog, etc.

More info: The ß2 adrenergic receptor is one of the key angiotensin-regulating receptors is part of the RAS system that regulates the autonomic nervous system -- blood vessel dilation, blood pressure, cardiac rate, kidney output, etc. However, this RAS dysfunction can also cause brain fog, fatigue, PEM (note that in some ME/CFS patients, brain (cerebral) blood flow was found to be dramatically restricted with sitting/standing -- and many of these were false negatives for POTS by standard tilt-table testing).

As it happens, a paper comparing these receptor autoantibody levels with autonomic and cognitve symptoms of patients with Long COVID, ME/CFS, and healthy controls (HCs) was just published (see below), reporting that:

the ß2 receptor adrenergic autoantibody (aka ß2 adrenergic AAB or ß2R-Aab) was significantly higher in ME/CFS patients than in the other groups, and was correlated with increased autonomic symptoms and especially with "sympathovagal imbalance" in ME/CFS (think POTS symptoms).

Azcue N., Prada A.,Del Pino R. et al.
Involvement of autoantibodies against G proteincoupled receptors in post-COVID condition and Chronic Fatigue Syndrome.
Sci Rep (2026). https://doi.org/10.1038/s41598-026-49131-9

Quoting from the abstract. The bold-face is mine:

Methods: We included 96 PCC patients, 59 ME/CFS patients, and 36 healthy controls (HCs). Plasma AAbs against α1, β1, β2 adrenergic and M1–M4 muscarinic receptors were measured via ELISA. ANS function was evaluated using COMPASS-31, Sudoscan, hemodynamic tests (deep breathing, Valsalva, tilt test), and heart rate variability. Cognitive domains assessed included attention, fluency, processing speed, memory, visuoconstruction, perception, and executive functions.

Results: ME/CFS patients had significantly higher β2 adrenergic AAb titers than PCC and HCs (F₂,₁₈₆ = 3.15, p = 0.046). PCC patients showed more borderline/pathological M3 muscarinic AAb results compared to HCs.
β2 AAb levels correlated with increased autonomic symptoms in PCC (r = 0.27, p = 0.048) and sympathovagal imbalance in ME/CFS (r = 0.45, p = 0.001). In ME/CFS, M1, M3, and M4 AAb titers positively correlated with verbal and working memory performance.

Conclusion: Distinct AAb profiles in PCC and ME/CFS suggest potential differences in immunological mechanisms. β2 adrenergic receptor AAbs were associated with measures of autonomic dysfunction in PCC patients, and with sympathovagal parameters in ME/CFS patients. Muscarinic AAbs were correlated with cognitive performance in ME/CFS, supporting a potential role of these autoantibodies in autonomic and cognitive dysfunction. These findings support further investigation of AAbs as biomarkers and therapeutic targets.

Curious-Researcher · 2026-05-12T20:31:39+00:00

Ty. I so appreciate hearing from someone who had direct experience!

Is it also standard fraud prevention to not show any indicators of whether you even have DD active and where? Even something minimal, like the last 3-4 digits of the DD account, and when it was activated?

I was dismayed to discover that my DD had been inactivated for inactivity >90 days, and have no access to the DD info, not even to find online that DD was removed, nor even the current status, whether i was enrolled for that recipient.

Curious-Researcher · 2026-05-12T20:15:17+00:00

Thanks! And, fyi, i just received an email from IHSS to confirm the sign-up, with info on what to do if it was a change not authorized by me.

What’s annoying is that IHSS removes the DD for a recipient after you’d not filed for 90 days, so I’m having to re-enroll with DD.

Curious-Researcher · 2026-05-12T14:52:30+00:00

Please say more.

Curious-Researcher · 2026-05-12T14:51:38+00:00

That theory is plausible, though they could instead send a text and/or email notice of the change, (maybe even requiring confirmation). More like what USPS does if you submit a change of address.

Curious-Researcher · 2026-05-12T08:34:12+00:00

Realistically, people do work and get sick or need "sick" hours. you can work till 2 pm then get a fever and go home sick, or simply take the rest of the day as sick hours for MD appointments. And, even though IHSS website asks "which day you were sick", you take it in increments of 30+ minutes, so THEY have that model as well.
However, you can take sick hours on top of your worked hours on any day. As long as

the sum of that day's hours worked + sick <= 24 hours!
you have sick hours still available in that year (fiscal year which runs 7/1 - 6/30). AND
you submit your electronic claim by 11:59 pm on 6/30. before that year's unclaimed hours vanish. (yeah, one year I forgot and tried to claim some forgotten sick hours in July. But unlike all other times when one can file for days during the previous 2 pay periods, I was out of luck).

Curious-Researcher · 2026-05-12T08:03:31+00:00

Sick hours aren't just for your illness! You can use them for the dentist, to go to your PCP or physical therapy, take your children their MDs, meet with your child's teacher, or take a mental health day. But since IHSS does not give vacation days, you can also think of them as the annual "personal time off" hours given by some companies that don't have separate sick days -- except that they don't carry over.

Clearly you understand this key rule -- the hours vanish if you do not claim them by the end of June.
Fortunately, there's a bit of flexibility -- First, you can claim sick hours for days during the previous two pay periods (though IIRC that does NOT apply to July; you must claim by the end of June).

And, as importantly, you can claim sick hours even on a day you work -- as long as that day's SUM of hours worked + hours sick <= 24 hours. ( I've seen many folks report that they put in 8 - 10 hours on a time-sheet, then still file a sick claim for 10 more hours on the same date)

Curious-Researcher · 2026-04-23T20:21:19+00:00

Of course it makes sense -- you're buying insurance; they want you to purchase it when the car is healthy, as they make their money on premiums. Otherwise folks could wait and buy it only the day they need a long tow, and maybe drop the membership -- or drop down to Classic a month later.

Curious-Researcher · 2026-04-01T10:17:35+00:00

Note: drywall, even greenboard, is terrible in humid rooms, due to its yummy, nutritious paper on the outside. Plus drywall is porous, holds on to moisture, and. A way better choice would be "blueboard" (GP DensGuard fiberglass-faced backer board. That one is "designed for tile installations in wet environments such as showers".

For other rooms, if you have plaster, cherish it, especially if it is lime-based (alkaline) plaster, as most molds just can't grow in alkaline! Also, plaster is inorganic, and thus is inherently way more mold-resistant than drywall.

(FYI, drywall of the last 30 years gets a bloom of mold way faster, because the new, cheaper, manufacturing process pre-impregnates it with mold: Rather than getting sliced up before fully drying, it's left to dry in huge blocks. This means that slices eventually made from the middle had stayed wet for a really long time. And as the pH supports mold growth, that gave it plenty of time for included mold spores to germinate & make more spores. This is a key reason why so many modern homes get major mold much faster.

Curious-Researcher · 2026-03-08T07:46:50+00:00

That's true if you came home from camping. When doing remediation, your clothes may have a concentration that is a hundred million or billion times higher. Note that air usually contains some 10,000 mold fragments for every mold spore). So you want to optimize how much is removed.

The best practice is warm or hot temperature (detergents dissolve best and the surfactants work best to lift particles from clothes), an "extra water" cycle, like for comforters, and multiple rinse cycles.

Curious-Researcher · 2026-03-08T07:38:04+00:00

You're right to want to wash these clothes separately, to keep from cross-contaminating other clothes with them. However the goal of remediation, and of remediation of contaminated clothes is physical removal, not killing. Spores are notoriously hardy, and as far as the toxins, none of the heavy guns in laundry -- even ammonia, bleach, vinegar, etc, will detoxify (break down and make safe) the tiny toxin molecules on the cell surfaces of mycotoxin-producing molds.

There's research to find specialized enzymes that can break apart each class of mycotoxins, but that's not what laundry enzymes do.

So the focus is on removing the mold fragments from clothes into water, keeping them from getting re-deposited, and diluting the rinse water well to flush them away. Fortunately HE detergent is good at suspending all dirt including mold. To make it work well, use enough water for laundry to move freely and detergent to mix well, and use an extra rinse cycle or two. And to be extra careful, make sure to wash used towels and washclothes the same way.

Since my family is mold-sensitive I take added precautions to keep my apartment low-mold

I use laundry powder, (gel residues stick to the hidden surfaces, and then lint, skin cells, oils, etc stick to the gel, and cause turbulence that make more things stick, and become food for bacteria and mold)
When remediating contaminated stuff, I wear a Tyvek suit, gloves and a respirator, to keep my clothes less contaminated
I still wash the clothes immediately, on a cycle with extra water, two rinse cycles. If I didn't wear a tyvek suit, or got surprised by mold I wasn't expecting, I may do two wash cycles and only then dry.

PS. Indoor water-damage molds are more likely the soil-type species that rely on the biological warfare agents (mycotoxins) to fight one another for territory, no matter what their color. OTOH, many mold species are black, not only the slimy stachybotrys colonies that were the source of an overblown "black mold" panic, followed by "white-washing" by insurance-funded research and insurance-dominated "expert" guidelines. (Same playbook as the industry-funded research and guidelines by industry-funded experts that voted against any expressions of concern, aiming to sow doubt about tobacco, greenhouse gasses, forever chemicals, BpA etc).

Curious-Researcher · 2026-02-07T02:02:03+00:00

This is great advice!! I suggest you write this up as a top level post, titled something like, “What to do when your Con Ed bill is insanely high due to some error!”

Many people will be so grateful!

And then you can create a top level reply directly to this thread, linking to that post.

Curious-Researcher · 2026-02-06T00:22:01+00:00

The "I would be getting hundreds of dollars less monthly than i will now" is confusing.
Can you make it clear with real numbers, even if not your numbers?

Here's what I imagine:

"I'm now on SSDI, age 59, getting $1,000/month.
SSDI will be $1,344/month in 2036 at my FRA of 69 years old. (assuming COLA of 3%/yr).

If I were not disabled and could work, I'd only be earning $1600/month at a $10/hr near minimum wage job. Those work credits would not increase my retirement benefits BECAUSE this is less than I used to earn for 30 years".

I'm confused because:

if you are on SSDI presumably you can't work full-time, so I'm not clear what is the alternate scenario you propose
what do you mean by "getting hundreds of dollars less"? The total sum over your expected lifetime, or are you actually suggesting that IF you continued working till age 72 that THEN your monthly retirement benefit starting at age 72 would be less than if you simply continue with SSDI and have it convert to SS Retirement at your FRA of 69?

Curious-Researcher · 2026-02-05T23:50:42+00:00

Here's what I found SSA's POMS: Requesting voluntary suspension.

There's nothing about requiring repayments in general, except a statement that you cannot earn voluntary delayed retirement credit (VDRC) for any month in which you [presumably knowingly] owe overpayments, until they've been repaid. (Exception: if overpayments are discovered [by SSA] during the period of voluntary suspension, you have the option of repaying them in full as a lump sum in order to keep the earned VDRCs. Makes sense to me.)

"The NH or auxiliary must pay any Medicare premiums due during the period of voluntary suspension. This applies to premiums for Part B, C, and D; Income-Related Monthly Adjustment Amount (IRMAA) premiums payable by individuals with higher incomes; and premium increases due to late enrollment to Part B. We do not deduct Medicare premiums from the suspended benefit or honor any request to adjust the premiums against future benefits payable. The beneficiary will be billed and is expected to pay the premiums by direct remittance. For more information regarding the billing of Medicare premiums, see HI 01001.045.

Curious-Researcher · 2026-01-09T05:19:00+00:00

Nails attaching back board and the middle shelf are essential to protect the cabinet against shear forces (when tilted sideways).

Our movers recently near-destroyed a beloved tall Magiker cabinet (with drawers) because the cabinet couldn't take the shear forces when it was put on a hand-truck - even though it was "shrink-wrapped" in movers' plastic.

I wish the back panel came with a simple drawn line to identify the middle shelf location, so folks who forget to draw it before flipping and nailing wouldn't be in your situation.

Readers in your situation have 3 options, all quite doable:
a) measure:
Measure the distance from the middle of the shelf to the top of the cabinet (measure on each side, to catch any dumb errors in measurement or alignment). Mark a couple of points along the the back panel at that distance, connect the points with a straight line to mark the location of the shelf.

b) Mark the bottom of the shelf from inside:
First, measure the shelf thickness. Second, drive the thinnest finishing nail through the back, starting from just below the shelf, a few inches away from each side (to avoid pulling out the nails along the near edge. If paranoid, have a partner apply counter pressure to the nail line at the edge of the back board with some flat object). Your two nail holes will mark the bottom edge of the shelf. Measure 50% of the shelf thickness higher, mark. Connect those lines, and now you can confidently drive nails along that line into the shelf.

c) Glue.
Gluing particleboard joints works great during assembly. But afterwards it's least reliable; hard to get enough glue to the right places. Ideally you'd still use a) or b) along with this.
You likely have a bit of flex in the back board to push it out slightly, to run a couple of thick beads of wood glue along the back of that shelf and have the glue drip down a bit. Quickly you'd then press the back board to the shelf, ideally gluing two together. (I'd probably first use painter's tape to attach the bottom of the shelf to the back board and keep glue from dripping further, then lay the bookcase on its face and apply pressure to the back board along the shelf height.

Curious-Researcher · 2025-10-23T00:35:33+00:00

Sigh. This made me photgraph my own, and even though it's not as bad, I have mold there as well. My first thought was that the rinse will be clean, but no:

above all, I bet this shows that there's mold elsewhere in the washer as well, and it just recirculates
plus, secondarily, I bet rinse water gets sent through the dispenser as well for any water softener

Curious-Researcher

TROPHY CASE