There Is Still Something Left to Measure

A public-interest memo to the 9/11 responder community, and a response to recent coverage of the Stony Brook dementia findings.

Why we are writing

Recent coverage in the New York Post brought national attention to a finding that responders and their families have been living with quietly for years: the men and women who worked at Ground Zero are developing dementia far earlier and far more often than they should be.

The underlying research is real and it is careful. Investigators at Stony Brook followed 5,010 World Trade Center responders and found 228 cases of dementia over 15,913 person-years, a crude rate of 14.47 per 1,000 person-years in a group whose median age was just 53. The general population rate for comparable ages is roughly 1.19 per 1,000, as reported by Clouston and colleagues in JAMA Network Open in 2024.

The number that should not be lost in the coverage is this one. Among responders with the least dust exposure, the rate was 2.95 per 1,000 person-years. Among those with the most severe exposure, it was 42.37, more than fourteen times higher.

That gradient is the most hopeful fact in the entire paper, and we want to explain why.

A dose-response relationship that steep means the damage was driven by something that entered the body and could be counted. It was not random. It was not fate. It tracked exposure.

What the study could not do

The investigators were honest about the limit of their own work, and one line in their paper is the reason we are writing at all. They stated that "there is no biomarker that measures exposure severity to neurotoxic substances at the WTC," and went on to say that identifying such a biomarker could improve risk measurement both in this cohort and in the general population.

Exposure in that study was reconstructed from questionnaires: when you arrived, how long you stayed, whether you were in the dust cloud, what you wore. That is careful epidemiology and it is the best that could be done. But it is not a measurement of what actually happened inside a given person's cells.

No one has ever measured that. Not in this cohort, not at scale, not with the biology that matters.

And here is the point we most want to make to responders reading this: unmeasured is not the same as unchangeable. A quarter century on, the internal biology of this exposure remains largely unexamined. That is a gap. It is also an opportunity.

What we believe was actually consumed

The World Trade Center dust was not ordinary dust. It was roughly 80 to 90% pulverized concrete, gypsum and synthetic vitreous fibers, with a pH between 9 and 11 outdoors and above 12 in some interiors. Chemically caustic, not merely gritty. Mixed into it were combustion products from fires that burned for months: polycyclic aromatic hydrocarbons, dioxins, PCBs and metals, as documented in the CDC's account of World Trade Center exposures.

Clearing compounds like these is work, and the body does that work with a molecule called glutathione, the cell's principal internal antioxidant and its main tool for neutralizing and escorting out reactive toxins. Every clearance event spends some.

Our hypothesis, stated plainly, is that the responders who fared worst were carrying the heaviest chemical burden against the smallest antioxidant reserve, and that the reserve itself was never measured because nobody was looking.

There is reason to take this seriously in this specific population. Stony Brook's own investigators have documented brain immune activation on PET imaging in WTC responders, elevated blood markers of neurodegeneration, and a signal involving a superoxide-clearing enzyme variant linking lung injury to brain outcomes. Separately, responders carrying the APOE ε4 variant showed a substantially stronger relationship between exposure and cognitive impairment than non-carriers.

The biology is already pointing in this direction. What is missing is the measurement.

Why individual differences matter enormously, and why past studies missed them

Here is the part of the science that almost never reaches the public, and it changes how the last twenty-five years of disappointing antioxidant research should be read.

People are not equally equipped to handle oxidative damage. The differences are inherited, common, and large.

Take one gene, GSTM1. It makes an enzyme that attaches glutathione to exactly the class of combustion toxins found in the WTC dust so they can be excreted. In roughly half of people of European descent, that gene is deleted outright. Not weakened, absent. The responder cohort in the Stony Brook study was 87.2% White and 91.3% male. Approximately half of those men have no GSTM1 enzyme at all.

Now consider what happens when a study ignores that.

In Mexico City, researchers gave antioxidant supplements to asthmatic children chronically exposed to ozone, an oxidant air pollutant. Analyzed as one group, the effect on small-airway function was essentially zero, a change of −3.3 ml/s, statistically indistinguishable from nothing.

Analyzed by GSTM1 gene copies, using the same children, the same exposure and the same measurement, the picture reversed completely: −36.6 ml/s of harm in children with zero copies, −15.0 with one copy, and +23.7 with two. And the antioxidant benefit was concentrated precisely in the most genetically vulnerable children. The original investigators concluded that such children are more susceptible to ozone's effects on the small airways and "might derive greater benefit from antioxidant supplementation."

The null result was an averaging artifact. A real, graded, dose-dependent effect was hidden inside a group average.

This is, in our view, the single most important lesson available to anyone trying to help this population. Give the same thing to everyone without knowing who they are, measure everyone together, and you will conclude that nothing works, even when it is working for the people who needed it most.

Can antioxidant reserve actually be raised in a living person?

This is the fair question, and it deserves a straight answer, including where the answer is uncomfortable.

Swallowing glutathione itself does not work. Six months of oral glutathione at 250 or 1,000 mg per day failed to raise glutathione anywhere the investigators looked, not in blood, red cells, plasma, lymphocytes or cheek cells, in a randomized placebo-controlled trial by Allen and Bradley. We want to be blunt about this because responders are being marketed glutathione products right now, and the International Association of Fire Fighters issued a safety advisory in August 2026 warning that glutathione is not an FDA-approved treatment for post-exposure detoxification and that no published evidence supports the claims being made for it.

We agree with that advisory. We do not sell glutathione. We measure it, and we supply the raw materials the body needs to make its own.

And that approach has worked in humans. When researchers gave older adults with documented glutathione deficiency the precursor nutrients their bodies needed, red-cell glutathione deficiency was corrected, and alongside it, oxidative stress fell, mitochondrial function improved, inflammation and insulin resistance improved, genomic damage decreased, and strength, walking speed, exercise capacity and cognition improved. When supplementation stopped, the benefits declined again. A subsequent randomized controlled trial in older adults confirmed that the supplement, and not placebo, improved these measures, and that it was safe and well tolerated over 16 weeks. Both trials are the work of Kumar and colleagues.

Those trials were small, 8 and 24 older adults, and they were not conducted in 9/11 responders, and they did not use our formula. We are not going to overstate them. But they establish the principle that matters: in living human beings, a depleted glutathione reserve can be refilled, and refilling it produces measurable functional improvement across multiple body systems.

That is the foundation the ReBalU protocol is built on.

What the ReBalU protocol is

It is three steps, and the third is the one most programs skip.

Test. Measure the antioxidant system directly: the inherited variants that set a person's capacity, including SOD2, GPX1, GPX4, APOE and GSTM1, together with functional biomarkers of what that system is actually doing now, chief among them total and reduced glutathione measured as a pair.

Treat. Supply the substrates the body uses to rebuild, through the ReBalU Essential Gummie, formulated entirely from ingredients that are Generally Recognized As Safe.

D-tagatose is a rare sugar that largely escapes absorption and is fermented in the colon. In a randomized, double-blind, placebo-controlled five-way crossover study in 30 healthy adults, daily doses of 7.5 or 12.5 g increased butyrate production and lactobacilli counts without serious gastrointestinal complaints, leading the investigators to conclude that tagatose "may be considered a prebiotic substrate."

Fibersol-2, a digestion-resistant maltodextrin, is a soluble, fermentable fiber affirmed as Generally Recognized As Safe in the United States and fermented by colonic bacteria to short-chain fatty acids.

High-methoxyl pectin was chosen deliberately over the low-methoxyl form. In controlled fermentation using pooled human gut microbiota, the high-methoxyl pectins produced the largest cumulative total short-chain fatty acids and the single highest butyrate yield tested, 32.9 mmol, against 21.9 to 28.2 mmol for the low-methoxyl pectins.

European refined microalgae oil for DHA is a direct, non-fish source shown to be bioequivalent to fish oil. In a 14-week randomized double-blind placebo-controlled trial, microalgal oil and fish oil both significantly raised plasma phospholipid DHA and EPA against placebo, and earlier work established algal DHA as producing a linear, dose-dependent, bioequivalent rise in plasma and red-cell DHA.

The design intent is a continuous, endogenous supply of butyrate produced by a person's own microbiome in the colon where it is needed, rather than a swallowed bolus, paired with the omega-3 the brain is built from. Where a person's genetics indicate it, additional targeted components are layered on top.

Retest. Measure the same biomarkers again and find out whether the reserve actually moved in that specific person. Not in a group average. In them.

This third step is the entire point. It is what converts hope into evidence, and it is what will tell us honestly whether we are right.

What we are asking Stony Brook for

It is SOD Sciences Inc.'s intention to formally request that the Stony Brook investigators provide de-identified data from the World Trade Center responder cohort, with no names, no identifying details, and nothing that could expose a single responder's privacy, so that the genetic and biomarker patterns we observe in our own trial can be compared against the outcomes actually recorded in this cohort.

We want to be clear about how we think this should be done. Stony Brook should lead and publish first. The work is theirs, the cohort is theirs, and the credit belongs to them. Our study site would follow. SOD Sciences will be named openly as the funder. Any such request requires institutional review board approval and a data use agreement with the WTC Data Center, and we will follow that process exactly.

We are asking for data, not endorsement. We have no arrangement with Stony Brook, and nothing in this memo should be read as implying that they have agreed to anything or that they support our hypothesis.

Where the study will run

The ReBalU test, treat and retest protocol has been reviewed and approved by the institutional review board of a world-class academic medical institution based in South Florida.

Enrollment is not open yet. This section is a notice of intent, not an invitation to enroll, and nothing here should be read as an offer of treatment.

We are not naming the institution in this memo, and the reason matters. An institutional review board approves a protocol as scientifically coherent and ethically acceptable to conduct. It does not endorse the hypothesis being tested, and no institution has told us that we are right. Printing a hospital's name beside an unproven idea borrows its reputation for our argument, and we are not willing to do that to a partner. We will name the site when enrollment opens and the institution's own research and communications offices have cleared it.

To responders in South Florida

A significant number of 9/11 responders retired to Florida. The state now ranks third in the World Trade Center Health Program, behind New York and New Jersey, with 9,507 enrolled members as of March 2025, and the heaviest concentrations sit in Broward and Palm Beach counties. There is no Clinical Center of Excellence anywhere in Florida. Every one of them is in New York or New Jersey, because the statute built them that way, which means the responders who moved south are among the least closely followed in the entire program. That gap is what this site is meant to address. When enrollment opens, the study is intended for people who are already living with serious chronic illness rather than for healthy volunteers.

The clinical standard we are using to define that is the one the Centers for Medicare and Medicaid Services applies to chronic care management: chronic conditions expected to last at least twelve months, or until death, that place the patient at significant risk of death, acute exacerbation or decompensation, or functional decline.

Two clarifications on that, because they matter to responders reading this.

You do not need to be a Medicare beneficiary. We are borrowing the CMS clinical definition of a serious chronic condition because it is precise and widely understood. We are not requiring Medicare enrollment. The median age in the Stony Brook responder cohort was 53, which means most responders are not yet Medicare-eligible, and it would make no sense to exclude them.

A physician diagnosis in your existing medical record is what establishes eligibility, assessed against the approved protocol's criteria. Final inclusion and exclusion criteria are those stated in the approved protocol, and they govern over any summary in this memo.

If you are a responder who would like to be notified when enrollment opens, we will maintain a simple expression-of-interest list. Write to either of us at joe@sodsciences.com or dan@sodsciences.com and ask to be added. Being on that list commits you to nothing, costs nothing, is not enrollment, and does not create a physician-patient relationship. You can ask to be removed at any time. Please do not send medical details in that email. Your name and a way to reach you is all we need, and we would rather not hold health information we have no approved reason to hold yet.

Three things we will not do. We will not ask a 9/11 responder to pay to participate in research. We will not sell you a product on the strength of this memo. And we will not tell you this works before we know whether it does.

What we are not claiming

We think we owe this community precision more than we owe it enthusiasm, so here is the honest boundary of what we are saying.

Generally Recognized As Safe describes safety as food. It is not a claim of medical benefit, and it is not FDA approval to treat any disease. It means these ingredients are recognized as safe to eat.

We are not claiming to prevent, treat, cure or reverse dementia, or any other disease. We are testing whether a measurable biological reserve can be raised. Whether raising it changes the course of illness is an open question. A real one, worth answering, and not yet answered.

We cannot undo damage already done. Structural loss of brain tissue is not something an antioxidant reserve rebuilds. Any responder who has been told otherwise by anyone selling anything should be extremely skeptical.

The most effective protection in the Stony Brook data was a respirator, at 2.95 versus 42.37 cases per 1,000 person-years between the least and most exposed. Most responders were never given adequate protection, and that is not their failing. Our work is directed at people who were already exposed. It is not a substitute for protection, and we will not pretend it is equivalent.

Our own hypothesis may be wrong. We have built a falsification arm into the protocol specifically so that we find out if it is.

The reason we think this is worth doing anyway

Twenty-five years after the towers came down, the people who ran toward them are getting sick in a pattern that follows how much dust they breathed. The scientists who documented that pattern said plainly that the biological measurement is missing.

It is still missing. It does not have to be.

Every responder in that cohort has an antioxidant system that can be measured today, with existing laboratory assays, for a fraction of what a single PET scan costs. Some will have inherited a robust one. Roughly half are missing GSTM1 entirely. Some are carrying a depleted reserve that nobody has ever looked at, that may be modifiable, and that may be relevant to what happens to them over the next twenty years.

We do not know yet whether raising that reserve helps. We think there is a serious, mechanistically grounded, testable reason to believe it might. And we think this community has waited long enough for someone to actually run the measurement instead of estimating from a questionnaire.

That is what we intend to do, in the open, with the results published whether they favor us or not.

Joseph M. Salvani Chief Executive Officer, SOD Sciences Inc.

Daniel J. Walsh Chief Operating Officer, SOD Sciences Inc.

For further information

Anyone wanting further information can contact us directly.

Joseph M. Salvani, Chief Executive Officer, joe@sodsciences.com Daniel J. Walsh, Chief Operating Officer, dan@sodsciences.com

We read our own email. If you are a responder, a family member, a clinician or a reporter, you will get a reply from one of us rather than from a form.

For responders: two things worth doing regardless of us

One. Enroll in the World Trade Center Health Program if you have not. It is federally funded, it is free to eligible responders and survivors, and it provides monitoring and treatment for covered conditions through a nationwide provider network, including outside New York. The list of covered conditions changes over time, so check the current list directly rather than relying on what you were told years ago.

Two. Ask for cognitive screening by name if you are having symptoms, and ask that your dust exposure history be recorded in your chart. The Stony Brook findings exist because exposure was written down. Yours should be too.

Sources

1. Clouston SAP, Mann FD, Meliker J, et al. Incidence of dementia before age 65 years among World Trade Center attack responders. JAMA Network Open. 2024;7(6):e2416504.
2. Lioy PJ, Georgopoulos P, et al. Characterization of the World Trade Center dust and its health implications.
3. CDC. World Trade Center Health Program, Exposures.
4. Deri Y, et al. Neuroinflammation in World Trade Center responders assessed by TSPO PET imaging.
5. Kritikos M, et al. Plasma biomarkers of neurodegeneration in World Trade Center responders.
6. Kritikos M, et al. Superoxide dismutase variant, lung injury and brain outcomes in WTC responders.
7. Huang C, et al. APOE ε4 and exposure-related cognitive impairment in WTC responders. Mol Neurobiol.
8. Garte S, et al. Population distributions of GSTM1 and GSTT1 null genotypes. Asian Pac J Cancer Prev.
9. Glutathione S-transferase, Mu-1; GSTM1. OMIM 138350.
10. Moreno-Macías H, et al. Ozone exposure, antioxidant genes and lung function in asthmatic children. Environ Health Perspect. 2013.
11. Romieu I, et al. GSTM1 polymorphism and antioxidant supplementation influence lung function in relation to ozone exposure in asthmatic children in Mexico City. Thorax. 2004.
12. Allen J, Bradley RD. Effects of oral glutathione supplementation on systemic oxidative stress biomarkers in human volunteers.
13. International Association of Fire Fighters. Safety Advisory: Glutathione. August 2026.
14. Kumar P, et al. Glycine and N-acetylcysteine supplementation in older adults improves glutathione deficiency, oxidative stress, mitochondrial dysfunction, inflammation, insulin resistance, endothelial dysfunction, genotoxicity, muscle strength and cognition: results of a pilot clinical trial.
15. Kumar P, et al. Supplementing glycine and N-acetylcysteine in older adults improves glutathione deficiency, oxidative stress, mitochondrial dysfunction, inflammation, physical function and aging hallmarks: a randomized clinical trial.
16. Venema K, et al. D-Tagatose increases butyrate production by the colonic microbiota in healthy men and women. TNO.
17. Tumor suppression by resistant maltodextrin, Fibersol-2. Cancer Prev Res.
18. Larsen N, et al. Potential of pectins to beneficially modulate the gut microbiota depends on their structural properties. Front Microbiol.
19. Comparative bioavailability of DHA and EPA from microalgal and fish oil. Nutrients. 2025.
20. Arterburn LM, et al. Bioequivalence of docosahexaenoic acid from different algal oils in capsules and in a DHA-fortified food.
21. WTC data access requirements: IRB approval and WTC Data Center data use agreement.
22. CDC. WTC Health Program Nationwide Provider Network.
23. Centers for Medicare and Medicaid Services. Chronic Care Management Services, MLN909188.
24. FDA. Recruiting Study Subjects, Information Sheet Guidance.

The ReBalU protocol is investigational. Statements in this memo have not been evaluated by the Food and Drug Administration. The ReBalU Essential Gummie is formulated from ingredients Generally Recognized As Safe as food and is not intended to diagnose, treat, cure or prevent any disease.

Nothing in this memo is medical advice. If you are a responder with symptoms or concerns, seek evaluation from your own physician or through the World Trade Center Health Program, and nothing here is a reason to delay or decline care you have been offered.