When I was in medical school, my clinical medicine teacher Dr. Lamden used to say that if you want certainty, medicine is not the move. Go into electronics instead, he told us — there is a manual. With humans there is so much diversity, and even more diversity within diversity.

So, if this feels unsettled, that is not a sign that you are a difficult case or that your clinician is failing you. It is the state of the science in this corner of medicine. Roughly one-third to one-half of patients with hEDS also have POTS or MCAS, so the overlap is the norm rather than the exception — and there is still no blood test that settles hEDS, and no single agreed-on definition of MCAS.

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By the end of this you will know where that uncertainty actually sits, and what a complete workup covers — so you can tell when you have gone as far as this process currently goes, and start building the team that gets you there.

There are two sets of diagnostic criteria for MCAS:

1. Consensus-1 (2012, the allergy/immunology framework) — a stricter, lab-anchored approach. It looks for a rise in serum tryptase of “20% + 2” ng/mL during a flare (or elevation of a few other mast cell mediators), and it requires that you improve at least partially on antihistamines or cromolyn before the diagnosis is made.

2. Consensus-2 (2011, updated in 2020 by a larger international group) — a broader, symptom-anchored approach. It relies on chronic multisystem symptoms typical of mast cell activation plus a wider panel of mediator tests, and treats response to treatment as supporting evidence rather than a requirement.

The practical difference is how many patients qualify: Consensus-1 gives more diagnostic certainty but can delay treatment, while Consensus-2 allows earlier treatment with some risk of overdiagnosis. Consensus-2 is the framework most mast cell specialists now use.

How much difference does that actually make?

In one 2025 chart review of 100 young patients with POTS, the same set of records was scored three ways. Two percent met Consensus-1. Thirty-seven percent met a conservative reading of Consensus-2, where lab support is still expected. Eighty-seven percent met clinical criteria alone, with no lab support required. Same patients, same charts — the number moved because the definition moved.

The same thing happened with hypermobility in that cohort. Thirteen percent met the full hEDS criteria; 34% met the broader HSD criteria. And since hEDS and HSD patients appear to carry the same musculoskeletal burden, the label you land on often changes your access and whether you feel believed more than it changes the care you actually need. That is the argument for comprehensive consideration — not for waiting until the definitions settle.

That is the part worth holding onto.

When you are told you do not have MCAS, that is often a statement about which framework the clinician is working from rather than a finding about your body. It is also why nobody can tell you precisely how common this is: no study has ever compared the two criteria sets head-to-head for validity — a point the Consensus-2 authors make about their own field.

So why do these three travel together? It is probably not an accident, and the leading explanation is connective tissue.

Mast cells do not just live in the blood. They sit throughout connective tissue — in the skin, around blood vessels, along the lining of the gut — and the mediators they release act on the very tissues that hEDS involves. Blood vessels are connective tissue too, which is what links all this to the standing problem in POTS: vessels that do not tighten the way they should let blood pool, and the heart rate climbs to compensate.

So you can be masty, potsy, and stretchy all at once, as the patient community puts it. The three interplay rather than simply coexist.

One honest caveat. This is the leading hypothesis, not settled fact. The authors of that 2025 review propose exactly this link — mast cell mediators loosening connective tissue and irritating nerves — but nobody has demonstrated it. It is the best current explanation for a pattern everyone can see.

MCAS and hEDS get tangled together more than the others, and two things about hEDS cause most of the confusion.

First, genetic panels sometimes turn up a variant of uncertain significance related to vascular EDS. Vascular EDS is a separate, genetically defined subtype rather than a form of hEDS, which is why a finding like that belongs with a geneticist rather than being folded into an hEDS diagnosis.

Second, hEDS is challenging in a different way: the criteria are agreed on, but there is no blood test that confirms it, so the diagnosis rests on clinical exam and ruling other things out.

For hEDS, getting to a firm diagnosis takes more discussion.
See this handout: https://www.ehlers-danlos.com/wp-content/uploads/2017/05/hEDS-Dx-Criteria-checklist-1.pdf

And the classification itself is in flux — the International Consortium is releasing a full update to the EDS and HSD criteria in December 2026, and hEDS is expected to be divided into subtypes based on symptom clusters and emerging genetic markers. There is also a growing recognition of the neurological features that travel with EDS, including cranio-cervical instability and small fiber neuropathy, though these are considered associated features rather than a separate subtype.

As you are in this world of MCAS, EDS, and POTS it may never feel certain. You are likely not going to fall into one box perfectly. So, the goal is completeness, not certainty. And completeness is not a reason to wait on treatment. In that same review, 82% of those assessed improved on mast-cell-directed treatment — and that included patients whose labs never confirmed anything (Yao et al., Frontiers in Neurology, 2025: https://doi.org/10.3389/fneur.2025.1513199). The label can stay unsettled while the care moves. A while ago I put together this (developing) checklist to help people on this journey make sure they have the most comprehensive care. Look at it like a navigation guide — the things worth considering on the way toward stability and better care.

If you align or present like MCAS, then start here:

Screening

– Mast Cell Mediator Release Syndrome (MCMRS) questionnaire — Molderings’ 57-item checklist. Above 8 points suggests pathological mast cell activation; 14 or more is treated as clinically verifying a mediator release syndrome. Symptoms alone can reach 37 of the points; the rest come from labs, imaging, and biopsy, so a score you calculate at home is only part of it

– Baseline Tryptase and Symptomatic Tryptase

o If Tryptase is elevated test for Hereditary alpha Tryptasemia (HaT). This involves tryptase gene copy-number testing, to check for hereditary alpha-Tryptasemia — an extra copy raises your baseline tryptase, which can confound the Consensus-1 lab criteria

– Smoldering criteria for other mediators (see my article here)

– Please note this is not a screening for primary mastocytosis specifically

Specialist Visits

– Consult with an MCAS-informed Allergist and/or MCAS-focused hematologist/oncologist.

– Confirm subtype of MCAS with specialist

o Primary Mastocytosis /Primary Clonal Disease

o Mixed MCAS — primary plus secondary (c-KIT mutation plus allergic-type reactions)

o Secondary MCAS (which is due to allergy, other MCAS trigger)

o or Idiopathic (neither allergy, or genetic)

– see this article for more https://pmc.ncbi.nlm.nih.gov/articles/PMC11212760/

– Coordinate Care with Mast Cell-informed Naturopathic and Functional Medicine Provider

– Coordinate Care with Mast Cell-informed nutritionist

If you align with hypermobility, hEDS or HSD, start here.

Screening

– Screening using Beighton score and five-point questionnaire

– If the Beighton score is negative, screen for HSD instead

Specialist Visits

– Diagnostic confirmation by Rheumatologist that is EDS-aware such as through reference on the Ehlers Danlos Society website.

– Physiatrist referral for pain management

– Hypermobility Physical therapy and personal trainer referral

Additional Testing to Round Out the Diagnosis

– An autoimmune panel to rule out Connective Tissue Disorders as they often overlap

– Genetic panel to rule out Ehlers-Danlos variants which often can be ordered by any licensed EDS-fluent provider or through a referral to a geneticist.

– Consider upright cervical MRI if the clinical picture warrants it — though it is expensive and facilities are hard to find

If you align with POTS and/or neurologic features, start here.

Screening

– Home or in-office modified tilt test using NASA Lean Test Criteria. If positive, then see specialist

Specialist Visits

– Discuss appropriateness of the in-office test with primary care.

– Cardiologist to perform Tilt Table Test. (Please note the wait is often many months) Define if hypovolemic POTS or hyperadrenergic POTS.

– Referral to Autonomic Neurologist or Neurologist with other features such as Neuropathy, Headache, Chronic Neck Pain, Coat Hanger Patterned neck pain

– Coordinate foundational POTS support with Naturopathic and Functional Medicine Provider who is trained in POTS

Common Questions

All my MCAS tests came back normal. Does that mean I don’t have MCAS?

Many providers would say yes. Practitioners working from the Consensus-2 framework do not stop there. They use a standardized symptom checklist — the mast cell mediator release syndrome (MCMRS) score, where more than 8 points suggests pathological mast cell activation and 14 or more is treated as clinically verifying a mediator release syndrome — together with the work of ruling out the other conditions that could explain your picture. That second half matters: it is what makes a therapeutic trial reasonable rather than reflexive. If the symptom pattern holds and nothing else accounts for it, a trial of treatment is a legitimate next step. I have linked the checklist below. Two honest caveats. This questionnaire has never been tested for diagnostic accuracy against any other scheme, and the framework it comes from does not explicitly require ruling out conditions that might better explain your picture — which is why that exclusion step matters so much. And remember what the study above found: people whose labs never confirmed anything still improved.

I don’t have a high enough Beighton score to qualify, but I am convinced I have hEDS. Are there other criteria?

There is more room here than most people are told. If your Beighton score is one point below your age- and sex-specific cutoff, two or more positive answers on the five-point questionnaire — could you contort as a child, could you do the splits — still satisfies that part of the criteria. That matters if your joints have stiffened over the years.

And if you land outside hEDS, the diagnosis is usually hypermobility spectrum disorder. Historical HSD exists for exactly the person whose joints used to move more than they do now. HSD is not a consolation prize: in one clinic series of 2,695 patients, 60% were diagnosed with HSD and 18% with hEDS, and there is no evidence that people meeting hEDS criteria are more severely affected. The management is the same.

The criteria are also being revised. Researchers have argued the Beighton score is too narrow — it leans on the upper limbs and was never designed as a diagnostic tool — and the December 2026 update is expected to widen how hypermobility is assessed.

What this looks like in practice

Here is a composite — not one person, but a pattern I see often.

Someone comes in scoring at the top of the Beighton scale, with years of joint pain and dislocations behind her. We do a modified tilt test. Her heart rate climbs, but not enough to meet the POTS threshold. On the usual way of thinking that is a dead end — hypermobile, but no POTS, so nothing to account for the rest of it.

Because the symptom pattern pointed at mast cells, we tested for them. Her tryptase and a prostaglandin metabolite both came back elevated. That is worth pausing on: the broader framework is often what gets the labs ordered in the first place, and sometimes those labs are positive. Symptom-first does not mean lab-negative.

The connective tissue panel turned up a variant of uncertain significance on a vascular EDS gene. That did not get folded into an hEDS diagnosis. It went to a geneticist, because these are different conditions with different implications, and a maybe on a vascular gene deserves a specialist’s read rather than a guess.

Meanwhile — and this is the part that matters — treatment started. A low-histamine trial. Work on the reflux that was making everything worse. Support for the fatigue. She was getting better while rheumatology, genetics, and allergy were all still pending.

Nothing in her case is settled. She does not have one clean label. What she has is a complete picture, a team assembling around it, and less symptom burden than she came in with. That is what completeness buys you.

Where to start

If you do nothing else with this, do this. Pick the branch above that matches what you are actually dealing with, read down it, and find the first line you have never done. Not all twenty. One. Bring that line to your next appointment and ask for it by name.

And three questions worth sitting with:

– Which of these three have you actually been worked up for, and which have only been mentioned in passing?

– When you were told no, do you know which framework that no came from?

– Where does your own workup stop right now — and is that because it is complete, or because it stalled?

None of this is about arriving at certainty. It is about reaching somewhere you can stand: a workup you know is complete, a team that knows what the others are doing, and treatment that is already moving while the labels catch up.

In the world of MCAS, dysautonomia, and EDS we are all in this together. So if you have learned anything else that should be added to this navigation guide, drop me an email or comment.

If you want my full MCAS Treatment Framework go here also enjoy the episodes below that were on the podcast

YouTube

When conventional medicine says ‘there’s nothing else we can do,’

Dr. Marty Ross knows you’re just getting started. This episode explores the overlooked co-infections, mold toxicity, and system dysfunctions behind chronic fatigue and fibromyalgia—and the terrain-based healing approach .

Dr. Ross walks through a s patient case: a young missionary bedridden from what appeared to be Lyme disease received eighteen months of IV antibiotics with minimal improvement. The course changed when he recognized mold toxicity as the missing link—cholestyramine alone brought 90% recovery in weeks.

He reveals why treating the system—not just killing the germ—matters.

He discusses testing recommendations (IgeneX for Borrelia and co-infections; Vibrant Lab or Mosaic for mold biotoxins), then three no-cost starting points: sleep hygiene (7-9 hours nightly), feeding your microbiome with polyphenols and plant-forward foods, and addressing limbic system dysfunction via tools like the Gupta Program or Primal Trust.

For those suffering with Lyme diagnosis or suspect chronic illness which has terrain-based roots, this conversation offers both immediate steps and the framework to reframe your healing—plus Dr. Ross’s resources for personalized guidance.

About Dr. Ross

Dr. Marty Ross is a functional medicine physician based in Seattle and one of the leading clinical voices in chronic Lyme disease, tick-borne infections, and complex chronic illness in the United States. Over 25 years, he has helped thousands of patients across the US and internationally recover from conditions that mainstream medicine often dismisses, including Lyme, mold toxicity, fibromyalgia, and long COVID.

He is the founder of Treat Lyme, one of the largest chronic illness education platforms online, and is the author of Hacking Lyme Disease: An Action Guide to Wellness. He also runs a monthly live Q&A webinar and a curated supplement line in partnership with Femologist. Before opening the practice in Seattle, Marty shaped US public health legislation from the Senate. Today, he is the doctor who shows up for patients when everyone else has stopped looking.

https://www.linkedin.com/in/marty-ross-md/

https://www.instagram.com/martyrossmd/

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In the even the podcast exceeds 300 views in the first week, The One Thing Podcast will donate at least $100 in your honor of Plus One Foundation (https://plusonefoundation.networkforgood.com/projects/194639-everyday-donation-page)

Show notes below for paid members:

I was my usual Friday Trader Joes run.

I looked up and saw an elderly woman walk by.

A sense of calm and peacefulness crept over me when I saw her.

“That will be $110.85” the cheerful checker– who already recommended gorgonzola cheese to go on top of my mixed greens– interrupted my calm moment.

I took the debit card and inserted into the wobbly card swiper.

And went back to my business of loading my cart and headed to the car.

It has been an interesting week

So many patients are using AI to interface with, signing up for online digital programs, using apps, and even signing up for programs to order their own labs.

You can see the temptation.

Taking the charge of ones own health.

Feeling empowered with knowledge data.

Breaking free of the unsupportive health care system.

And AI – wow –you can almost feel like you can figure out all your problems with a deep chat with the machine.

In fact many feel they can come to visits with self-ordered-labwork and a chat-gpt generated diagnosis and direct the care from the jump.

Its such a change from 20 years ago when I first hung my shingle.

That was before EHR .

Information was gathered through reading books, journal articles, attending courses, and taking certifications.

We had paper charts.

Labs were faxed to us or snail mailed.

Patients read health books and magazines for information.

Patients took notes during the visit.

They left the visit with a plan hand written on a sheet.

And the next time you saw or heard from them was at the follow up.

Fast forward to 2026

Between visits patients are scrolling, chatting, ordering their own labs, listening to podcasts, sharing in online forums , seeing multiple providers and at the follow up visits they come with a whole new experience and set of information.

I have friends that tell me that Dr.’s will be replaced by AI soon.

Maybe , who knows.

I grabbed my keys and started thinking about making dinner and maybe getting a quick workout in before Shabbat started.

And then I saw her again.

The same peaceful feeling came over me and my brain started putting it together as I loaded my trunk.

‘The Bank –20 years ago –paper checks –rushing on Fridays to make deposits to keep afloat –the warm teller who always was kind to me and wishing me well –that’s her!’

”Diane?!” I said ,

For a moment she paused and looked at me like she had no idea what I was talking about.

“From the bank?" I said with a bit of a crack in my voice realizing that I might have just misfired.

“Yes! that’s me” she said.

Now in her early 80’s she took a moment to get her bearings straight.

“How are you doing ? You used to be in Kirkland right?”

We started to catch up a bit.

“Glad to see that you are doing so well” She said.

Even though by no means did I imply that I was a success by any regards.

But her complement felt good.

“You know how I remembered you Diane?” I said in my parting words.

“I remembered you because of the way you made me feel; you remember people by the way the make me you feel”.

She smiled and said goodbye.

Earlier in the day , a long-time patient said to me that she wanted to meet with me because “ I know her well and understand her” .

She brought the same line of questions that could easily be fed into chat GPT.

But instead they were fed into “Me-GPT” …wink wink.

And the texture, granularity, history, and weight of her questions were filtered through a 15 year screen play I have in my mind of our experience together and her life path.

Humans feel.

Humans have emotions.

Humans create space for other Humans.

That makes us remember

That makes us an irreplaceable technology.

Yet, remembering Diane and being chosen over AI made me realize once again that humans will always have a place as long as we are serving each other for the good.

For now, at least.

P.S. this purposely wasn’t edited. Just raw.

After 22 years on antidepressants; escalating from a quarter dose to maximum doses of multiple medication…

Dr. Noushin Hart hit a wall: her psychiatrist said he had nothing else to offer.

Instead of accepting that as an ending, she embarked on a journey revealing the real root of her depression: 30 years of untreated childhood trauma and a nervous system locked in survival mode. This episode explores why the serotonin hypothesis misses the full picture, why repeating trauma stories in talk therapy can re-traumatize you, and how somatic approaches process trauma in the body without requiring you to relive it—leading to genuine healing without medication dependency. You’ll learn the neuroscience behind why your HPA axis and nervous system dysregulation matter more than serotonin levels, hear about alternatives like transcranial magnetic stimulation and plant medicine, and discover how saffron offers natural mood support. Whether you’re stuck on antidepressants, skeptical of talk therapy alone, or searching for integrative solutions, Dr. Hart’s story and practical insights offer both hope and a clear path forward.

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Dr. Noushin Hart shares her 22-year journey from antidepressant dependency to somatic healing, revealing why conventional psychiatry missed the trauma-informed approach her body needed. This conversation examines the limitations of the serotonin model, the re-traumatization trap of repetitive talk therapy, and the nervous-system science behind why body-based modalities create lasting transformation.

Key takeaways:

• Antidepressants work for acute depression but long-term chronic use leads to tolerance, escalating doses, and side effects that mirror original symptoms—making it impossible to distinguish depression from medication effects.

• Depression frequently roots in unprocessed childhood trauma and nervous system dysregulation (HPA axis), not serotonin deficiency alone; the body keeps score for decades.

• Repetitive talk therapy—retelling trauma stories over and over—can re-traumatize the nervous system; somatic approaches that process trauma at the body level without re-narration create safer, faster healing.

• The sympathetic nervous system (fight-or-flight) can remain dominantly activated for 30+ years due to childhood trauma; somatic work restores parasympathetic balance and safety.

• Dependency on practitioners or modalities signals unhealthy treatment; true healing empowers you with self-directed tools so you become your own healer.

• Natural alternatives like saffron show strong evidence for mood support, insomnia, and concentration—offering a gentler starting point or complement to other interventions.

• Being told ‘there’s nothing else to offer you’ reflects a practitioner’s limitation, not your capacity to heal; seek modalities and practitioners that fit your nervous system’s needs.

Resources mentioned:

• MAP (somatic trauma processing modality)

• Plant medicine protocols for trauma and depression

• Transcranial Magnetic Stimulation (TMS)

• Saffron (clinical evidence for mood, insomnia, and concentration)

• Dr. Gabor Maté (trauma framework and nervous system science)

• HPA axis regulation and polyvagal theory

• Somatic and energy-based healing approaches

Links mentioned:

• Heart to Heart Cancer Consultants —https://h2hcc.com/

• Healing by Hart — https://healingbyhart.com/

Share Sound Bites with Dr. Adam Rinde

If you’ve lived with IBS, you know the drill. There’s the cramping that quietly reorganizes your day around bathrooms, and the bloating that turns your own clothes into a negotiation, so that “fit check” takes on a whole new meaning. And there’s the advice: cut this food, add that fiber, try this probiotic, most of it delivered in the last ninety seconds of a seven-minute appointment. (Oh wait, nobody has ever told you to add fiber? I joke.)

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So when a new study lands promising relief, two reflexes tend to fire at once: hope, and the tired suspicion that you’ve heard this one before. Both are appropriate. I want to walk you through a paper I’ve been reading, because it’s a good chance to practice something more durable than any single supplement, which is how to read the evidence itself.

The study is a 2026 systematic review in the Journal of Gastroenterology and Hepatology, looking at postbiotics for IBS. The first thing worth your attention is that word itself: postbiotic.

The strange idea that dead bacteria can help

You already know about probiotics, the live bacteria you swallow in a fermented food or a supplement, hoping they will set up shop. Postbiotics are the odd cousin. They are preparations of bacteria that have been deliberately inactivated, essentially killed, along with the useful molecules they leave behind.

That sounds backwards. Why would dead bacteria do anything? The short answer is that a fragment of a bacterial cell wall can still communicate with your gut’s immune cells, and the metabolites bacteria produce can still feed the cells lining your colon. You do not always need the live strain; sometimes the message is enough.

It helps to hold the three cousins together:

• Prebiotics are the food, the fibers that feed your microbes.

• Probiotics are the live bacteria themselves.

• Postbiotics are the inactivated microbes and their leftover parts, the message without the messenger.

That understanding is worth a lot, because it loosens an anxious idea a lot of my patients carry, the belief that healing requires keeping some fragile colony of bugs perfectly alive inside them. Often it does not.

If you look a little closer, though, that one word, postbiotic, turns out to point at three quite different things, and sorting them out is most of the work.

One word, three different things

1. The ones your own gut makes. When you feed your resident microbes the right fibers, they ferment them into beneficial compounds. This is your body producing its own postbiotics, continuously and for free. You have probably heard of these as the short-chain fatty acids (propionate, butyrate, acetate, and others), which I cover extensively in this article. When a lab report shows someone running low on them, this is the tier that is under-producing, and the fix is not a bottle; it is feeding the garden.

2. The ones you take as a single, defined product. This is one specific strain of bacteria, grown and then killed, sometimes left intact and sometimes broken into fragments, and put into a capsule. It is the reductionist version, with one known ingredient and one target, and it is what the new study tested.

3. The ones you take as a whole community’s output. Instead of a single dead strain, this is a full-spectrum mixture, closer to bottling the entire metabolic output of a healthy microbiome than to isolating one piece of it. (I explored this approach on my podcast with Dr. Andrea McBeth of Thaena, whose capsule is made, remarkably, from sterilized human stool.) The logic here is closer to herbal medicine: you work with a complex ecosystem rather than one purified compound.

A clean way to hold all three is to ask two questions. First, who made it, you or a manufacturer? Second, how complex is it, a single molecule or a whole ecosystem? Notice that the third tier is almost the mirror image of the first: someone else’s full-spectrum production, handed to you in a capsule. Keep that map in mind, because the new study only speaks for the middle tier.

What the study actually found

Across four randomized trials and about a thousand people, these single-strain postbiotics beat placebo. Participants taking them were roughly two and a half times more likely to get a meaningful reduction in abdominal pain, and overall symptom severity dropped by an amount that patients actually feel. Importantly for anything you put in your body, side effects were no different from placebo. For an intervention, “it helped, and it was about as safe as a sugar pill” is a reassuring result.

If I stopped there, this would read like every other gut-health post you have scrolled past, so I am not going to stop there. Read honestly, the same study also tells you how much to trust it.

How to read a study without getting sold

Here is the part I most want you to keep. When you meet a “new study shows…” headline, it helps to ask three questions.

1. How much evidence is this, really? Four trials and a thousand people sounds like a lot, until you notice that for any single approach it amounts to a handful of studies, run in different countries and using different products. That is promising, but it is not a conclusion.

2. How confident are the authors themselves? Careful researchers grade their own certainty, and these did. In this paper, the authors’ verdict on their own findings was low certainty. That is not me playing skeptic; that is them, in print, telling you to hold the result loosely. When the people who did the work say to be cautious, it is worth believing them. It is a sign of honesty rather than weakness.

3. Compared to what we already know? The same paper notes that a well-run low-FODMAP diet still outperforms postbiotics for most people. The newer thing is not automatically the better thing.

There is one more question specific to this topic. Notice which kind of postbiotic the study actually looked at. It tested the single-strain products, the middle tier. It says nothing about the whole-community products, which are a different animal with their own, much thinner evidence. A study of one cousin does not get to vouch for the others; each has to earn its own.

Run postbiotics through those questions and you land somewhere honest. This is a promising, competently conducted early look at something real, neither a breakthrough nor nothing at all. My own conclusion is to keep watching this space. It shows promise, but it is not yet ready as a top-tier treatment.

So what do you do with this?

Nothing urgent, which is itself the point. Postbiotics are not first-line therapy, and the major GI guidelines do not recommend them yet. What today’s evidence supports is considering them as one adjunct: a possible addition to a real plan rather than a replacement for one, and certainly not a solo fix you self-prescribe from a podcast.

If your gut has been miserable, the highest-yield moves are still the unglamorous ones: figuring out your particular pattern, addressing the loops that keep it running (stress, sleep, and the gut-brain conversation that IBS is built on), and often feeding the microbes you already have before reaching for anything in a bottle. That is the first tier again, your own production line. Sometimes a targeted trial of a product like this belongs in the mix as well, chosen with someone who can see your whole picture. It should be a tool used on purpose, not another bottle on a shelf that is already too crowded. For the IBS story, then, this is useful to know, but it is likely not my first step.

How I am applying this paper

In my own practice, I am particularly interested in lysate and heat-killed postbiotics for gut-skin interactions and for autoimmunity. This interest rests on models that are, so far, mostly preclinical, which I have referenced below.

Microbial components from heat-killed or lysed probiotics, the MAMPs such as peptidoglycan and lipoteichoic acid (TLR2), CpG DNA (TLR9), and muramyl dipeptide (NOD2), are sampled by the dendritic cell (DC) and bind its pattern-recognition receptors. The DC then reads that signal in context. In a barrier-intact, calm terrain, it matures into a tolerogenic DC that steers naive T cells toward Tregs and IL-10, and inflammation settles. When the same signal arrives at a leaky, Th17-primed terrain, the DC matures into an immunogenic phenotype that drives Th17 and Th1 activity, and the result is a flare.

So you can see how these preparations might be helpful for prevention and for promoting remission in stable autoimmune conditions, yet potentially harmful in the flared, inflamed patient. More to come.

Ayad et al., “Efficacy and Safety of Postbiotics in Irritable Bowel Syndrome: A Systematic Review and Meta-Analysis,” Journal of Gastroenterology and Hepatology, 2026;41:1994–2005.

Kaczynska A, Klosinska M, Janeczek K, Zarobkiewicz M, Emeryk A. Promising Immunomodulatory Effects of Bacterial Lysates in Allergic Diseases. Front Immunol. 2022;13:907149. doi:10.3389/fimmu.2022.907149

Bazzi S, Modjtahedi H, Mudan S, Achkar M, Akle C, Bahr GM. Immunomodulatory effects of heat-killed Mycobacterium obuense on human blood dendritic cells. Innate Immun. 2017;23(7):592-605. doi:10.1177/1753425917727838

In this episode, Dr. Jamie Zeitzer and Lucas Tang of Lumos Glasses (https://www.lumosglasses.com) break down how light acts as a conductor, orchestrating every system in your body: your sleep, mood, metabolism, and immune function.

You'll discover why the contrast between bright days and dark nights matters more than total light exposure, why morning light directly impacts serotonin production and depression risk, and how light therapy works synergistically with SSRIs.

When you listen I want you to think about this. “How can I develop a healthier pattern to light exposure and light de-exposure?”

Whether you have outdoor access or not, they share practical, evidence-backed tools to reclaim your natural rhythm—from outdoor time to Lumos Glasses, a fashionable light-therapy solution for those who can't get consistent daylight. This episode cuts through outdated light-therapy advice and equips you with science-grounded strategies to transform your health from the inside out.

Light exposure is the most overlooked lever in health. Most people spend less than 15 minutes outside daily—yet our bodies expect dramatic contrast between bright days and dark nights. In this episode, circadian researcher

Dr. Jamie Zeitzer and Lumos Glasses (https://www.lumosglasses.com) co-founder Lucas Tang explain how light orchestrates your sleep, mood, metabolism, and immune system, and share practical strategies to realign with your natural rhythm.

Key takeaways from the Episode:

• Modern humans get less then 5 minutes of outdoor light daily despite believing they get 2-3 hours—a critical gap between perception and reality driving circadian misalignment
• Light acts as a 'conductor' orchestrating your body's peripheral clocks (heart, liver, gut, immune cells), synchronizing all systems from your brain's central circadian oscillator
• The contrast between bright days (10,000-100,000 lux outdoors) and dark nights is more critical for health than total light exposure—it's the pendulum swing that matters
• Morning light exposure directly correlates with serotonin production; a landmark UBC study showed light therapy alone outperformed SSRIs at 8 weeks and works synergistically with medication
• Light at the wrong time (bright screens at night, dim offices by day) is as harmful as insufficient light—timing and intensity both matter for circadian synchronization
• Practical tools range from free (outdoor time) to fashionable (Lumos Glasses) for those with limited daylight access due to weather, work schedule, or health constraints
• Circadian misalignment drives depression, metabolic dysfunction, immune suppression, and poor sleep—making light therapy a foundational health intervention, not just a sleep aid

Resources mentioned:
• Dr. Jamie Zeitzer (circadian rhythm researcher)
• Lucas Tang (Lumos Glasses co-founder)
• Lumos Glasses (light-therapy eyewear)
• Happy Light (light therapy lamp)
• NHANES (National Health and Nutrition Examination Survey)
• US Bureau of Labor Statistics Time Use Survey
• OSHA workplace lighting standards
• UBC landmark study (light therapy + fluoxetine for depression)



Giveaways:
Download Free Circadian Rhythm and Light Therapy Guide here:

It is Free for Paid readers below.

Sponsorship Mentioned:
Pulsetto: Listen for special code mentioned in the episode . Visit Pulsetto here


Links mentioned:
Links:
• Lumos Glasses: https://www.lumosglasses.com
• Lumos Glasses on LinkedIn: https://www.linkedin.com/company/lumosglasses/
• Lumos Glasses on Instagram: https://www.instagram.com/lumosglasses
• Lucas Tang on LinkedIn: https://www.linkedin.com/in/lucaswencanada
• Dr. Jamie Zeitzer on LinkedIn: https://www.linkedin.com/in/jamie-zeitzer-7888185/

Video Replay here

Eden came in with a binder.

This was a binder I used to carry through undergrad in the 90’s

You know the one with the three rings, and tabbed dividers?

It had two years of food logs, a stool test annotated in the margins, and a spreadsheet of supplements cross-referenced against symptoms.

She had done the elimination diet twice.

She had done the mindset work, the therapy, and even the breathing app.

Her labs, by any honest reading, were better than when she’d started.

And she still woke at three in the morning with her jaw clenched and still felt her stomach drop when the phone rang in another room.

Also, still had a gut that flared on a quiet Tuesday for no reason she could name and no trigger she could find.

She flashed the binder at me and asked if I want to look at all the labs she has done.

Before I could answer she closed it and looked at me with a face of resignation.

“I’ve done everything,” she said. “Why am I still like this?”

She had, in fact, done nearly everything.

What no one had done and what the binder had no tab for was a section stating.

The Nervous System Needs Help, from the Bottom-to the Top.

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That Vagus Nerve Is Being Mentioned Again

It helps to remember what the vagus nerve actually is.

We tend to picture the gut and the brain as separate departments that occasionally email each other.

They are wired together, continuously, along a bundle of fibers that carries far more traffic up from the gut than down from the brain.

The vagus is that highway.

When someone lives for years in a body braced for danger — and has stored trauma…the body never learned that the trauma was over and in the past.

It is still bracing.

That bracing doesn’t stay politely in the mind.

It shows up as a gut that won’t settle, sleep that won’t deepen, a startle that fires at nothing.

Which means one of the most direct levers we have on a stubborn gut is not another supplement.

It’s the nervous system itself, addressed from the body up.

Neuromodulation

In the world of Neuromodulation. Or, otherwise described as devices that modulation the nervous system using current, sound, or vibration…there are roughly four tools that I use in practice.

They get lumped together in wellness roundups as if they were interchangeable — four flavors of the same thing, pick whichever.

They are not interchangeable.

Each is a different door into the same stuck house, and the entire clinical art is knowing which door a given nervous system will actually open. Get the door wrong and nothing happens, or worse, the system braces harder.

The first two doors are electrical, and they are cousins.

Transcutaneous auricular vagus nerve stimulation ( taVNS) — sends a mild current to a branch of the vagus that surfaces at the outer ear. You feel a comfortable tingle. It nudges autonomic tone directly, and it tends to help the person whose trauma has settled into the body: the physical tension, the bone-tiredness, the sleep that never reaches its deep floor. The evidence is real but modest, the protocols not yet standardized. It is a nudge, not a switch. (We talked alot about this in the podcast I did Dr. Groysman here).

Cranial electrotherapy stimulation ( CES) — clips a barely-perceptible micro-current to the earlobes and is associated with a shift in brainwave activity toward the calmer alpha band. Where taVNS is for the braced body, CES is for the racing mind — the patient whose barrier to sleep isn’t tension but a brain that will not stop narrating. The devices are FDA-cleared; the trial base behind them is thinner and more mixed than the marketing suggests. I personally prescribe and use the Alpha-stim in this category . (We covered the Alpha Stim in the episode on CES with Kimberly Eller, EAMP, ND, LaC here)

The second two doors are acoustic, and here is where most summaries get it wrong.

The Safe and Sound Protocol (SSP)— is filtered music, engineered to coax the middle ear toward the frequency band of a safe human voice. The idea, drawn from Stephen Porges’s work, is that safety is something the nervous system hears before it thinks. Meaning we tune in for sounds of safety and sounds of danger. In chronic trauma state we are wired for danger sounds. SSP aims to retrain the nervous system for safety.

SSP is aimed at the ventral branch of the system — the circuitry of social engagement, of being safely with another person. It is often the tool for the patient in functional freeze, the one who goes flat and shuts down, because it works by bringing the “safe and connected” state back online. This is based on Polyvagal Theory.

Here is a lecture I gave on the topic.

The Rest and Restore Protocol (RRP) — is also filtered sound, but it is doing something quietly different, and the difference matters. RRP isn’t the “passive” version of SSP. It targets the other branch ; known as the dorsal vagal branch. This is , the deep restorative circuitry . RRP works by entrainment, offering the nervous system steady rhythmic cues to settle at its own pace. Porges calls it stealth meditation. Where SSP restores connection to others, RRP restores connection to self (aka. interoception), the felt sense of one’s own insides. It is the door for the patient who is simply too depleted, too fragile, too burned to the ground for any active trauma work at all.

So the cleaner way to hold the two is not active versus passive.

It’s connection to others versus connection to self.

Word of Caution

A caution, because it’s the part that separates careful practice from enthusiasm.

The ventral-and-dorsal language is a map. It’s a genuinely useful one for making decisions, but its underlying neuroanatomy is still argued over, and it should be worn as a working model, not sold as settled fact.

The evidence under all four of these tools is modest.

They are adjuncts to comprehensive care such as medication and therapy. And in my practice I also support with plant medicine , nutrition, and hormone balance.

They are things you layer onto real trauma-informed care, never substitutes for it.

And there is one rule that matters more than any device selection: with a fragile system, the dose goes down, not up.

The instinct is that if a little helps that more helps faster.

But….

With a nervous system this raw, more is how you set off the alarm you were trying to quiet. Titration isn’t a footnote to these protocols. It is the protocol. You start with minutes and work your way up

Eden with the binder didn’t need a fifth supplement or a stricter diet.

She’d have told you as much, if the framework had existed to ask the right question.

She was doing everything — and everything she was doing spoke to the parts of her that could already hear.

The part that was still braced, still three-in-the-morning awake, still flaring on quiet Tuesdays, had never been addressed in a language it understood.

She hadn’t failed. She’d been knocking, patiently and for years, on the wrong door.

That’s the reframe I keep coming back to with complex cases: often the missing piece isn’t more effort.

It’s a different door.

On a personal note; those who know me should know that I use these devices .

I toggle between vagal stim (this is almost daily) for my nervous system and CES (when I have insomnia-which is about once every 3 months or so).

And use RRP and SSP as practice during certain times of the year that are connected to traumatic memories or seasons.

They have changed my life and frankly make me feel like I have authorship in my nervous system that serves as a companion to my spiritual foundation and practice.

PS. message me if you want to chat more about this.

You fell for it. One of these social-media-stalking labs hooked you in.

Test 100 food sensitivities with a stick of your finger, at home, and you’ll finally figure out what’s making you bloated, constipated, tired, and more.

What a tempting offer, right? Convenient. Promises to erase all the ambiguity in your diet. What is there to lose?

Then the results come back and you are reacting to everything. IgG levels high, medium, and low, a rainbow of red flags next to foods you eat every single day. What the heck are you supposed to eat now? Air?

So you take the results to your PCP, and they laugh and roll their eyes.

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Then you stumble onto a shiny new functional health provider, the kind who got their certification over a weekend, “online,” and they salivate. They tell you to eliminate all 40 foods you reacted to, and they promise to text you every single day to check in.

You run to the hills.

Eventually you find a common-sense naturopathic physician who’s been in this rodeo for years. And they actually explain it to you. They lay out a reasonable plan. The higher reactions might mean something, sure. But the lower reactions? Those might actually mean tolerance.

That makes sense. So you set out, you do the plan, and you feel better.

Then you retest.

And lo and behold, the big reactions came down, just like they said. But now there are more low-level IgG’s on the report than before.

You panic. You did everything right. How are there more reactions?

So he explains.

IgG isn’t a damage report. It’s a guest list.

Your body makes IgG antibodies to things it has seen, not necessarily things that are hurting you. It’s a memory marker, not an alarm bell. Back when you were scared of food and eating the same six “safe” things on repeat, your immune system had almost nothing to write down. Now that you’ve calmed down, widened your plate, and started eating like a human being again (the chicken, the walnuts, that egg you were terrified of), your immune system is doing exactly what it’s designed to do. It’s taking attendance.

More foods in, more little tick marks on the guest list.

That’s not your body breaking down. That’s your body tolerating.

“But I’m reacting to more things now,” you say.

No. You’re eating more things now. Big difference.

Here’s the part the weekend-certified texter will never tell you, because they only know how to read one column. IgG on its own is a single instrument in the orchestra. Judging the whole song by it is exactly how people end up eating air.

If you want the full picture, not just a guest list, look for a panel that goes beyond IgG alone. For a more comprehensive approach to food sensitivity testing, search for tests that also offer IgE, IgG4, and Complement C3a/b. Those are different arms of the immune system, and read together they can tell you whether a food is truly lighting you up versus simply being remembered. One number can scare you into a cage. Several, read wisely, can set you free.

So don’t treat the number. Treat the person.

The goal was never a clean lab. Nobody feels the inside of their IgG panel. The goal was you, able to sit down to a meal without a spreadsheet, without dread, without cutting yet another food. You got that. The rising IgG’s aren’t a step backward. They’re the receipt for your freedom.

That’s the paradox. The test looks worse because you got better.

So many great episodes to listen from the last 6 months. I have hand selected some for your listening pleasure. Enjoy catching up! If you are fan of our podcast please leave us a review on Apple or Spotify.

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Episode 137 |The Menopause Gut| The Hidden System Medicine Overlooked| Cynthia Thurlow

Cynthia Thurlow shares how a life-threatening medical crisis transformed her understanding of menopause, gut health, and longevity. She explains why the microbiome changes during perimenopause, why so many women experience weight-loss resistance, the role of stress and immunity, and how hormone replacement therapy, strength training, protein, and fiber can help women age with resilience. In this episode: Cynthia’s near-death health crisis. The gut-hormone connection. Immune system aging. Weight loss research and more.

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Episode 136|Beyond the Plate: A Holistic Path to Peaceful Mealtimes with Lena Livinsky

Is picky eating really “just a phase”? Feeding specialist and mom Lena Livinsky says no — and this conversation may completely change the way you see mealtime struggles. In this episode, Lena explains why picky eating is often a biological and nervous system response rather than a simple behavior problem. Drawing from both her clinical expertise and her personal journey with her son, she shares how underlying sensory, mechanical, gut health, and environmental factors can shape a child’s relationship with food. We dive into the hidden causes behind food aversions, how to recognize red flags, and practical ways parents can create calmer, more connected mealtimes.

Guest: Paulina Livinsky, M.A., CCC-SLP

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Episode 135| Your Brain Isn’t Broken with Dr. Steve Rondeau

Episode 134: The Hidden Energy Crisis Behind Brain Fog, Autism & Chronic Illness with Dr. Kurt Woeller

What if the root cause of brain fog, chronic illness—and even autism—wasn’t just neurological… but a metabolic problem at the cellular level?In this episode, Dr. Adam Rinde sits down with Dr. Kurt Woeller, Chief Medical Officer at Mosaic Diagnostics, to break down the critical role of mitochondria in complex chronic conditions. From fatigue and gut dysfunction to regressive autism, this conversation explores how mitochondrial dysfunction may be a hidden driver behind it all.You’ll learn how the Organic Acids Test (OAT) provides a powerful window into metabolic health, revealing patterns that can guide targeted treatment—and why markers like succinic acid can signal deeper dysfunction.Dr. Woeller also shares how advanced tools like the MitoSwab can uncover issues within the electron transport chain, and why healing isn’t something you can force—but something you must support.

Guest: Kurt Woeller

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Episode 133 : The Science of Skin Aging: What Actually Works (and What Doesn’t) With Lily Shapiro, PharmD

Most skincare advice is focused on fixing what you can see—wrinkles, texture, tone. But by the time those changes appear, the underlying biology has already been shifting for years.In this episode of The One Thing Podcast, Dr. Rinde sits down with pharmacist and founder of Atika Wellness , Lily Shapiro, PharmD – to explore a more accurate way to think about skin health—one that moves beyond “anti-aging” and toward what she calls skin span.Lily breaks down the science behind how skin actually ages and why many popular solutions fall short. From the truth about collagen and biotin to the limitations of topical products, this conversation challenges some of the most common assumptions in the skincare world.You’ll also learn the four core drivers of skin longevity—collagen integrity, antioxidant balance, lipid barrier function, and mitochondrial health—and how a systems-based approach can support your skin from the inside out.If you’re looking for a clearer, more science-b…

Guest: Lily Shapiro

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Episode 132 : When Medicine Isn’t Enough: Exploring Energy, Emotional Trauma & Chronic Illness with Eva Müller

Why Some Patients Do Everything Right — and Still Don’t Fully Heal Some patients do everything right — and still don’t fully heal. They follow the plan. Change their diet. Take the supplements. Commit to lifestyle shifts. Show up consistently. And yet something deeper remains unresolved. After more than twenty years in clinical practice, Dr. Adam Rinde has seen this pattern repeatedly. At some point, the question shifts from “What are we missing physically?” to “Is there another layer of healing...

Guest: Eva Müller

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Episode 131: What If Inflammation Could Be Removed? Therapeutic Plasma Exchange with Dr. Pamela Smith

What if inflammation isn’t just something to manage… but something you could actually remove?
For decades, chronic inflammation has been treated with suppression — steroids, biologics, immune blockers. But what if there were a way to physically remove inflammatory burden from the bloodstream? In this episode, we sit down with Dr. Pamela Smith — ER physician, toxicologist, hormone specialist, and pioneer in therapeutic plasma exchange (TPE) — to explore the emerging science behind physically reducing inflammatory load. We break down:• What actually happens during therapeutic plasma exchange• How inflammation, cytokines, and antigen load circulate in the blood• Why autoimmune disease may be driven by persistent toxin burden• The connection between mold, plastics, metals, and immune dysfunction• Whether TPE can help long COVID, PCOS, cardiovascular disease, and cognitive decline• Who should — and shouldn’t — consider this therapy.

Guest: Pamela Wartian Smith, M.D. , MPH, MS

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Episode 130 : Why Your Mushroom Supplements Don’t Work (and How to Fix It) with Anna Sitkoff, ND

Dr. Anna Sitkoff, naturopathic physician and medicinal mushroom researcher, reveals why so many people try high-quality mushroom products and feel nothing. This deep dive explores extraction methods, fruiting body versus mycelium, proper dosing, and the clinical applications of Lion’s Mane, Cordyceps, Reishi, and Turkey Tail for immune support, gut-brain health, and neurodegeneration. Find her on your socials at:@drannasitkoff @lucidummedicinalsfull episode notes at https://onethingpod.com/sitkoff

Guest: Anna Sitkoff, ND

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\Episode 129. Dr. Lara Briden, Beyond Willpower: Understanding Metabolism Through Biology, Not Blame

Dr. Lara Briden challenges everything you think you know about metabolism, revealing why energy—not weight—is the true marker of metabolic health. This conversation explores how modern life has pushed our physiology into states it was never designed for, and offers a compassionate, science-based approach to understanding your body as a logical system rather than a problem to fix.GUEST INFORMATION:Name: Dr. Lara BridenTitle/Credentials: Naturopathic doctor, author, former evolutionary biology researcherBackground: Has peer-reviewed publications and thesis in evolutionary biology, specializes in women’s health with focus on centering female physiology as normal mammalian function

Guest: Lara Briden

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I answered it correctly. Then he asked me to turn my answer into a three-word sentence, and I got it wrong three times in a row. Not because the task was hard — because my educated brain kept “fixing” the grammar automatically, without noticing I was doing it. That invisible, automatic fix is exactly what a dyslexic child can’t do yet. In thirty seconds, I understood dyslexia better than an hour of brain-scan explanations could have taught me.

My guest is Russell Van Brocklen , a dyslexia researcher — severely dyslexic himself — whose original writing program was funded by the New York State Senate. His core argument will sound familiar if you’ve been reading me for a while: when someone stays stuck for years, the problem is usually not a broken part. It’s a system running in the wrong direction.

Schools teach general-to-specific, weakness-first, well-rounded-before-specialized. Russell argues the dyslexic brain works in exactly the opposite direction — and that when you flip the direction, kids who have been labeled and lowered start moving. Sometimes startlingly fast. The results he reports are his own numbers, from his own cases, and I say so plainly in the episode — but the method itself costs almost nothing to test, and that’s what makes this conversation worth your time.

His approach, in brief: find the child’s specialty — their area of extreme interest (”It’s Saturday morning, you can go anywhere and do anything — what is it?”). Put all the learning material inside that specialty. Ask specific questions rather than general ones. Have them type — never handwrite — and self-correct by reading aloud. And trust his one rule that has stayed with me since we recorded: if you can write it, you can read it.

What strikes me as a clinician is how directly this maps onto chronic illness. The child who stops trying isn’t unmotivated — the motivation collapses when the material lives outside their specialty, the same way a patient’s adherence collapses when a protocol ignores who they actually are. Accommodation without remediation is the $10,000 golf clubs Russell describes in the episode: better equipment for a game that still isn’t yours. And in both worlds, the deepest intervention isn’t a tactic — it’s replacing “something is wrong with me” with “I’ve been taught in the wrong direction.”

If you’re a parent or teacher of a struggling reader — or you were that kid yourself — this one may land somewhere deep.

Listen: [episode link] · Also on Apple, Spotify, and YouTube. Or watch video

Highlights: the brain science and where Russell breaks from Yale’s Dr. Sally Shaywitz (8:31) · the specialty method (10:03) · the live demo where I fall in the trap (17:02) · “if you can write it, you can read it” (30:15) · his advice for parents (38:48)

Guest resources: Russell’s site and free guide at dyslexiaclasses.com · Overcoming Dyslexia by Sally Shaywitz · The Craft of Research by Booth, Colomb & Williams

This episode shares one researcher’s approach, based on his reported results. It isn’t medical or educational advice for your specific child — bring it to the professionals who know them.

If this articulated something you’ve struggled to explain to people in your life, forward it to one person who needs it. That’s how this work travels.

— Adam Rinde, ND

Did you know?

• Environmental toxins can influence gut health

• Mold-related toxins may affect the microbiome, gut barrier, and immune system

• Mold/Mycotoxin illness can help explain persistent food sensitivities and chronic symptoms

• The gut may not fully recover until upstream environmental triggers are addressed

So if you cannot figure out your gut concerns after many other corrective measures consider this…

Sometimes the gut isn’t the primary problem—it’s reacting to an ongoing environmental stressor.

Lets dive into this together

Join the webinar live.

July 1, 2026 12:00 pm. PST

Join Webinar

She explains why the microbiome changes during perimenopause, why so many women experience weight-loss resistance, the role of stress and immunity, and how hormone replacement therapy, strength training, protein, and fiber can help women age with resilience.

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In this episode we discuss:

• Cynthia’s near-death health crisis

• The gut-hormone connection

• Immune system aging

• Weight loss resistance explained

• The microbiome and GLP-1

• The gut-bone axis

• Why stress changes everything

Practical strategies for women in midlife

What if menopause isn’t just about hormones?

this conversation, nurse practitioner and author

Cynthia Thurlow explains why your gut microbiome may be one of the biggest missing pieces in women’s health. We discuss weight loss resistance, immune function, GLP-1 medications, bone health, stress, and the surprising science connecting the microbiome to longevity.

Whether you’re in perimenopause, menopause, or helping someone who is, this episode offers practical and evidence-based insights.

connect with Cynthia here

https://www.onethingpod.com/guests/cynthia-thurlow/or https://www.cynthiathurlow.com/

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Key Highlights & Takeaways

• The “Lightbulb” Moment: Lena shares the emotional turning point with her son when she realized his refusal to eat wasn’t resistance, but genuine physical and neurological fear.

• When Pickiness Becomes a Red Flag: Learn how to distinguish between typical developmental pickiness (like a brief change in appetite after an illness) and deeper clinical issues. Red flags include the behavior lasting more than a few weeks, relying entirely on a “beige diet” of carbs and sugars, weight loss, or severe psychological stress surrounding mealtimes.

• Sensory Processing & Mechanics: Discover how heightened senses can make the look, smell, or temperature of food completely overwhelming to a child’s nervous system, leading to gagging or vomiting. We also discuss the hidden mechanical problems of chewing and swallowing, such as pocketing food or premature swallowing.

• The Importance of Postural Stability: Why letting a child’s feet dangle in an adult chair can negatively impact their ability to safely swallow, and how tools like the Stokke chair or a simple footstool can provide much-needed physical grounding.

• The BLOOM Framework: Lena breaks down her holistic methodology for addressing feeding challenges:

  • B - Balanced Health: Identifying systemic triggers like constipation, reflux, or blood sugar imbalances.

  • L - Learned Oral Skills: Assessing the physical ability to appropriately chew and safely swallow food.

  • O - Optimal Microbiome: Healing the gut-brain connection and addressing issues like bacterial overgrowth that drive unnatural cravings.

  • O - Open Exploration: Creating safe, low-pressure environments to explore food without the expectation of taking bites.

  • M - Mealtime Boundaries: Setting age-appropriate and state-appropriate boundaries that guide children without triggering sensory overload.

• Sunlight and the Gut Microbiome: A fascinating look into how environmental factors—specifically red, infrared, and UV light from the sun—play a crucial role in healing gut microbes and supporting digestion.

• A Story of Transformation: A powerful case study of a 12-year-old boy who transitioned from extreme malnourishment and sensory aversions to eating steak, vegetables, and playing sports after addressing his biological and environmental needs.

Resources Mentioned in this Episode

• Lena’s Coaching & Workshops: Visit lenalevinsky.com to learn about her 3-month individual coaching, 8-week group programs, one-off evaluations, and to sign up for her free monthly “Beyond Picky Eating” workshop.

• 🌐 Website: Lena Livinsky Official Website https://lenalivinsky.com

• 📸 Instagram: @lenalevinsky

• 🎧 Podcast: Lena Livinsky Podcast https://lenalivinsky.com/podcast:

• ❤️ Charity Mentioned: This episode supports Children’s Health Defense. If this episode reaches 100 views within 30 days, a donation will be made in honor of our guest.

#PickyEating #Parenting #ChildNutrition #FeedingTherapy #GutHealth #SensoryProcessing #ParentingPodcast #KidsHealth #Nutritio

I said yes to The Anti-Inflammatory Solution, a docuseries from Sarah Otto and the Goodness Lover team that’s coming out May 25, 2026 . I want to tell you why I said yes — and just as importantly, what I hope you take from it, and what I hope you don’t.

Why I said yes

Sarah’s own story — feeling trapped in a body that seemed to be working against her — is the story I sit across from in my office almost every week. She’s not selling a protocol. She’s tracing a question that the people I work with have been asking for years: why does my body keep doing this, and is anything ever going to change?

The conversation I got to have on the series was about vagus nerve and its role in inflammation regulation, the role of inflammation in aging, and impact of inflammation on Mitochondria. I also discussed come botanicals that can help with modulating neuroinflammation .

What I hope you take from it

The systems view. Inflammation isn’t a villain to defeat — it’s a signal inside a loop. When you understand the loop, you stop fighting your body and start listening to it. Several of the experts in the series get to that frame in their own way. Watch for those moments.

What I hope you don’t take from it

That you’re behind. That your body is silently destroying itself. That the answer is another list of 24 foods. That you need 38 experts to be safe in your own body.

Some of the marketing around series like these leans heavily on urgency and fear.

I’d rather you skip it entirely than walk away more anxious than you started.

If you notice yourself tightening up while watching, that’s data — pause, breathe, come back to what you already know about your body.

One question for you?

If you’ve watched a health docuseries before — what actually helped you afterward, and what made things worse?

—Dr. Rinde

P.S. to register for the docuseries go here:

There’s a pattern I see often in my own practice.

A patient arrives with a stack of diagnoses — depression first, then anxiety, then ADHD, sometimes bipolar — each one a slightly different label, each tied to a treatment that didn’t quite work.

The internal narrative becomes some version of “if I just got the right diagnosis, then I’d know the right treatment.”

It’s an intuitive belief. It’s also, by the numbers, mostly wrong.

Here’s the data that doesn’t get talked about much: the correlation between an accurate psychiatric diagnosis and a favorable treatment outcome is weak. Even when ten experts agree on a diagnosis, that agreement doesn’t predict who gets better. So the loop continues — another provider, another label, another medication trial — and the structural reason it continues is rarely surfaced inside the appointment itself.

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That’s the conversation I had with my latest guest on One Thing*: Dr. Steve Rondeau, a naturopathic physician who’s spent the last fifteen years analyzing qEEG brain scans — about 50,000 of them — and asking a different question than the one psychiatry typically asks. Not “what’s wrong with this person,” but “what brain pattern is showing up here, and what environment would actually fit it?”*

His reframe is one I’ve been thinking about all week. He calls it the Husky Phenomenon.

A husky in Arizona looks depressed. Amotivated. Lethargic. If a clinician evaluated the dog in that environment, they might reach for a medication. The same husky in Colorado — running through snow, in his element — looks fine. Better than fine. The dog isn’t broken. The climate is.

Rondeau’s argument, backed by the heterogeneity hiding inside labels like “depression” or “ADHD” once you actually look at the brain data, is that many of the patterns we call disorders aren’t disorders at all. They’re brain patterns mismatched to the environments they’re being asked to function in. The clinical question shifts: not “how do we fix this brain,” but “what environment does this brain actually fit in, and can we move it closer to that?”

I want to be clear about what this is and isn’t. It isn’t a dismissal of conventional psychiatric medicine. Sometimes medications are exactly the right answer. Sometimes therapy is. Sometimes the data points somewhere else entirely — a head injury, a heavy metal exposure, an autoimmune process showing up as a psychiatric symptom. The point isn’t natural-good-conventional-bad. The point is that the diagnostic question we’re starting with — does this person fit one of these labels — may not be the most useful question to start with.

If you’ve been in the diagnosis-chasing loop, or you love someone who has, this is the conversation I most wanted to have on the show this year.

🎧 Listen to the full episode here: [link to episode]

About Dr. Rondeau

Dr. Steve Rondeau is the founder of Axon EEG Solutions and the author of the forthcoming book Think Like a Brain*, out at the end of March. An award-winning naturopathic physician, he began his career in developmental pediatrics looking for objective biomarkers in autism — the experience that shaped his core conviction that mental health deserves the same kind of measurable data the rest of medicine takes for granted. Over fifteen years and more than 50,000 qEEG brain scans later, he’s best known for what he calls the Husky Phenomenon: the idea that many of the brain patterns we label as disorders aren’t broken at all, just mismatched to the environments they’re being asked to function in.*

Connect with Dr. Rondeau Website: axoneegsolutions.com Book: thinklikeabrain.com LinkedIn: Dr. Steven Rondeau

Ever since I was a child, I’ve been drawn to observing patterns and trying to understand situations as interconnected wholes.

I’m sure some of that was temperament, and some of it was adaptation of a child trying to make sense of a world that often felt unpredictable, overwhelming, or difficult to interpret.

Over time, that way of seeing evolved into something clinically useful.

As a physician, pattern recognition has become one of the most important tools I bring into the exam room.

Sometimes symptoms that appear unrelated are actually part of the same physiologic conversation.

I bring that lens into today’s post.

This week I saw a woman with longstanding constipation tendencies whose symptoms reliably worsened during the luteal phase of her cycle.

Not randomly.

Not occasionally.

Predictably enough that she had started organizing parts of her life around it.

Most people think constipation is mainly a food problem. More fiber. More water. Less gluten. Maybe magnesium.

But cyclical constipation often reflects something much larger: an interaction between hormones, gut motility, the nervous system, muscular tension, and digestive signaling.

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During the luteal phase, progesterone levels rise significantly. Progesterone has direct effects on smooth muscle and tends to slow colonic transit in susceptible individuals. For the patient who already leans toward slower motility, this shift can become clinically meaningful.

The result may look like:

• harder stools

• incomplete evacuation

• bloating

• pelvic pressure

• reflux

• increased abdominal tension

• or the feeling that digestion has simply “stalled”

At the same time, many women experience increased nervous-system tension during this phase. The body may feel more inflamed, reactive, contracted, or physiologically “tight.” In patients with underlying IBS-C tendencies, pelvic floor dysfunction, hypermobility, chronic stress physiology, endometriosis, or autonomic dysregulation, these shifts may amplify one another.

There is also growing interest in the role bile acids may play in motility regulation.

Most people think of bile only as something involved in fat digestion, but bile acids also function as signaling molecules within the gut. They help regulate secretion, microbial ecology, and intestinal movement through receptors such as TGR5.

Hormonal shifts may also influence bile acid signaling and digestive coordination and we have seen these mechanisms well demonstrated in pregnancy . Yet whether the smaller hormonal fluctuations of the normal menstrual cycle produce clinically meaningful bile acid changes remains unestablished.

The direct effects of progesterone on colonic smooth muscle and motility are far better supported as drivers of cyclical bowel changes.

That said, certain subpopulations may be more susceptible to bile-related effects, particularly those with underlying bile acid dysregulation, IBS, post-cholecystectomy physiology, altered microbiome states, or preexisting motility disorders (like idiopathic constipation).

In other words: the hormonal fluctuations of the menstrual cycle may theoretically amplify an already-compromised system.

One of the most important shifts for patients is realizing their body may not be malfunctioning randomly.

Patterns reduce fear.

Understanding changes the relationship people have with symptoms.

For patients experiencing cyclical bowel changes, it can be helpful to track symptoms alongside the menstrual cycle for several months rather than viewing each flare as a separate event.

Sometimes the first step is not immediately fixing the pattern, but recognizing that the pattern exists.

Not every cyclical digestive symptom means something serious. But when symptoms repeatedly follow hormonal rhythms, it may be worth asking whether the body is revealing a larger physiologic pattern rather than simply another isolated digestive complaint.

The goal is not perfect control over every symptom or every phase of the cycle.

The goal is building a more coherent relationship with the body … one based on understanding, flexibility, and resilience rather than fear and hypercontrol.

In my profession and in the world of health influencers there is a grasping for our attention and before we know it we are walking around like puppets repeating what others say with out doing our own homework.

Over the last 5 years, many people have reached out to me stating they want to work on their gut microbiome and gut-health to address bone density concerns.

They heard somewhere that working on your gut matters.

And my conclusion was based on common sense.

Meaning the following….

The gut is where we absorb minerals, nutrients, compounds that directly support bone modeling and remodeling and therefore health digestion, acid balance, and absorption influence good bone signaling.

That is common sense so it makes sense to “improve gut heath” to improve bone health.

Yet there is much more to the plot and most of the story is in its infancy.

Recently I dug into some research to understand the science and step way from the hype.

What I learned was the story involves the possibility that the microbiome produces bile acids that may bind to receptors in bone that dampen bone turnover.

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Spoiler alert…this has not been proven in humans…yet.

So if you believe this in humans you are betting on future possibilities and not current realities.

Basic Science:

The main mechanism that is being touted is as follows:

Your gut microbiota produce a bile acid called HDCA ( also known as 3α,6α-Dihydroxy-5β-cholan-24-oic acid) . HDCA, is a secondary bile acid that is formed from the primary Acid CDCA/chenodeoxycholic acid (3α,7α-dihydroxy-5β-cholanoic acid).

The production of HDCA requires a process called 6α-hydroxylation facilitated by the microbiome.

The production sort of like this

The Liver makes CDCA → conjugates it with glycine or taurine → secretes into bile → reaches the gut → microbes deconjugate and transform it into secondary bile acids (the one being of interest today is HDCA).

Lets zoom into the gut into more detail.

Picture yourself standing in the gut and observing the following taking place.

1. CDCA undergoes 7α-dehydroxylation to a bile acid metabolite called lithocholic acid (LCA)

2. Then under 7α→7β epimerization LCA is converted to ursodeoxycholic acid (UDCA)

3. Next under 6α-hydroxylation (in mice/pigs) UDCA converts into→ HDCA ← THIS what we are talking about primarily today

4. Finally the secondary bile acids undergo a normal Conjugation/deconjugation cycling. Most are re-cycled into our blood through reabsorption in the gut.

HDCA is abundant in mice and pigs but a minor bile acid in humans, because human gut communities lack robust 6α-hydroxylation.

However some microbiota communities may be contributors to this mechanism more then others.

According to pre-clinical research, here are some to think about.

• Clostridium cluster XIVa / Lachnospiraceae
  Clostridium hylemonae and Clostridium scindens are the most-cited isolates with the relevant 7α-dehydroxylation and hydroxysteroid dehydrogenase machinery that feeds into HDCA synthesis

• Clostridium cluster XI
  Clostridium hiranonis has documented bile acid 7α-dehydroxylation activity and contributes to the secondary bile acid pool that includes HDCA in rodents.

• Bacteroides spp.
  Several (e.g., B. fragilis, B. thetaiotaomicron) carry hydroxysteroid dehydrogenases that participate in upstream epimerization steps; they don’t typically finish HDCA on their own but contribute precursors.

• Eubacterium / Eggerthella
  Eubacterium lentum (now Eggerthella lenta) and related strains have 6β-HSDH activity relevant to murideoxycholic acid (MDCA) ↔ HDCA interconversion.
  

The Bone Connection

Now here is where it comes together.

First…the high level view if you want the bottom line:

Gut microbiota → bile acid (HDCA) → TGR5 receptor → ↓ NF-κB signaling → ↓ osteoclastogenesis

But lets unpack it

TGR5 (also called GPBAR1- G-protein coupled bile acid receptor 1) is a cell-surface receptor that senses bile acids and triggers downstream signaling.

It is present in many tissues including the gallbladder, intestine (especially L-cells), brown and white adipose tissue, macrophages and Kupffer cells, skeletal muscle, certain CNS neurons, and bone cells (osteoclasts and osteoblasts).

When HDCA binds to TGR5 receptors in the bone it raises Cyclic AMP (cAMP)and tamps down osteoclast-driven bone resorption.

Bone resorption is the active breakdown of bone matrix by osteoclasts

Downregulating osteoclast-driven-bone resorption is the same goal of many osteoporotic drugs.

Now we get why this has the potentially to be so important in humans.

Now realize the goal of osteoporosis management is to decrease fracture.

So one reabsorption does not mean less fractures

It only predicts less fractures.

And even more better microarchitecture of bone predicts less fractures.

So we are sorely lacking still in research here

1. we don’t have human trials that predict less fractures

2. we don’t have surrogate markers that predict that DCA leads to better microarchitecture of the bone.

Take Home Message

It is way to early to say this a primary strategy in osteoporosis or osteopenia management.

There is no change to current osteoporosis care based on these finding…yet

To do so would be based on a future promise vs. a proven reality.

However, it may be another impetus to understand you bile-acid-profile and how well your gut is producing DCA.

A few labs I have seen offer this include Diagnostic Health Solutions Lab and Vibrant America.

And another question is how accurate these labs are.

Yet the following conclusion are evergreen.

• We should continue to strive for an enriched microbiome that is diverse and not narrow. Neglecting the microbiome may have some major long term health consequences.

• Rotating and including plant forward foods in our diet is really the best way to assure this.

In the meantime check out some of my other articles on bone strategies by searching osteoporosis in my substack.

main source for this article:
Zheng XQ, Huang J, Yuan WQ, Wu T, Wang H, Liu H, Zhang YD, He JW, Huang C, Song CL. Gut microbiota preserves bone mass through modulating the hyodeoxycholic acid-TGR5 axis. Gut Microbes. 2025 Dec 31;17(1):2593088. doi: 10.1080/19490976.2025.2593088. Epub 2025 Dec 2. PMID: 41331982; PMCID: PMC12688228.

Soon, she may not have to.

Every three minutes, someone new is diagnosed with celiac disease. Eighty-three percent of cases are still undiagnosed. For the patients I see in my clinic, the diagnosis comes with one prescription: avoid. Avoid gluten. Avoid restaurants. Avoid the toaster at your in-laws’ house. Avoid the birthday cake.

For eighty years, that’s been the whole treatment plan.

That’s about to change.

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Over the years I have supported, witnessed, and experienced what it is like to be someone who has to avoid gluten. On the surface and to outsiders, it seems easy… just avoid gluten. What gets left out of that is how extraordinarily difficult that “just” actually is. The psychosocial weight of the disease. The major health impact when a celiac patient gets accidentally glutened. The hours of wondering what did I eat? after every flare.

Right now, 2,500 patients across 15 countries are enrolled in Phase 2 and Phase 3 clinical trials for the first real medications for celiac disease.

For the comprehensive list of every drug in development, the Celiac Disease Foundation maintains an excellent reference page. What I want to do here is translate what these mechanisms actually mean for your Tuesday.

There are six doors being knocked on at once:

• A pill that traps gluten in the gut lumen before it reaches your immune system. (Sequestrants.)

• A pill that breaks gluten into pieces your immune system better tolerates. (Enzymes.)

• A pill that tightens the tight junctions of the gut wall so gluten can’t slip through. (Larazotide.)

• A pill that switches off the enzyme that turns gluten into damage. (tTG inhibitors — the most promising in early data.)

• A pill that calms the immune response after the fact. (IL-15 and lymphocyte trafficking blockers.)

• A treatment that retrains the immune system to stop reacting to gluten in the first place. (Antigen-specific immune tolerance …the vaccine-like approaches.)

And yes there’s even a hookworm trial out there. I might come back to that one in a separate post. It deserves its own honest look.

None of these will let a celiac patient eat a baguette in Paris with no consequences. That’s not the goal…at least not at first. The goal is to give Emma her best friend’s birthday back. To give the executive his Tuesday business lunch back. To give the teacher her Monday morning back when the toaster at her sister’s house had crumbs in it.

An insurance plan for celiac, essentially. Tolerance, not avoidance.

What I’m telling patients in clinic right now

In the past three months, three of my patients have asked me a version of the same question: “Should I try to get into a trial?”

I tell them the same thing I’m telling myself . As many of you know I deal with Celiac I tell them yes, if they’re a good fit and the protocol is solid . Meaning they likely have to be Endoscopy/Biopsy confirmed Celiac to qualify and they need to be able to afford the consequences of a being glutened during a trial that did not work. Obviously these trials cannot be double-blinded . Some patients with Celiac disease have milder presentations and others experience extreme setbacks if glutened. Where someone lies on the spectrum would dictate the trial participation. And remember, These trials are not designed to give you back the bakery. They’re designed to give you back the toaster.

A few honest limits

None of these drugs is approved yet. The earliest realistic timelines I’m seeing put initial approvals somewhere between late 2026 and 2028 and that’s for one or two of the front-runners, not the whole field.

Even when they arrive, they will not be cures. They will not let most Celiac Disease patients eat freely.

The honest picture is closer to insurance than to liberation: you’ll still mostly avoid gluten, but the accidental exposure that today costs you three days in bed may cost you nothing at all. The toaster crumbs become survivable.

That’s still an enormous change.

Imagine Emma now, making the sweet sixteen of her best friend without a hitch.

If one of these works, what's the first thing that would improve in your life? Tell me below.

There’s a moment that stops you in your tracks .

A child is developing normally…hitting milestones, engaging, connecting…and then something shifts. The parents describe it the same way, almost every time: “It’s like the lights went out.”

We tend to look for answers in the brain. Neurology. Behavior. Genetics.

But what if we’ve been asking the wrong first question?

In a recent conversation with Kurt Woeller, D.O. , we explored a different lens—one that starts not with structure, but with metabolic energy. Specifically, the role of mitochondria: the tiny organelles responsible for producing the ATP that powers every cell in the body.

Because when energy and metabolic production falters, nothing works quite right.

The brain struggles. The gut becomes dysregulated. The immune system loses precision. And what we often label as separate conditions—brain fog, chronic illness, even autism—may share a common thread: a system underpowered, stressed, and stuck in a defensive state.

This isn’t just theory. It’s something we can begin to measure.

Tools like the Organic Acids Test offer a window into the metabolic landscape—revealing patterns, bottlenecks, and subtle dysfunctions that don’t show up on conventional labs. Markers like succinic acid don’t give us final answers—but they point us in the right direction. They tell us: look closer.

But here’s the deeper insight that emerged from this conversation:

Healing isn’t something you force.

You can’t override the biology with more supplements, more protocols, more intensity. If the system perceives threat, it will resist. The work becomes less about pushing—and more about creating the conditions where the body feels safe enough to shift out of that protective state.

That means looking beyond the lab results.

It means paying attention to stress, environment, rhythm, and the fundamentals we often overlook: sleep, light, movement, connection.

Because ultimately, mitochondria aren’t just about energy.

They’re about how the body responds to the world—and whether it has the capacity to move from protection… back to healing.

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In This Episode

This episode is both a deep dive into biochemistry and a grounded reminder that true healing starts with restoring balance.

• What mitochondria actually do—and why they matter more than you think

• The difference between mitochondrial dysfunction vs disease

• Early signs of mitochondrial imbalance (brain, gut, immune system)

• How the Organic Acids Test reveals hidden metabolic issues

• Why succinic acid is a key marker to watch

• The role of toxins, infections, and nutrient deficiencies

• How the MitoSwab test evaluates mitochondrial function

• Why pushing treatment too fast can backfire

• The importance of lifestyle, stress, and natural rhythms in healing

🎯 Who This Is For

• Parents navigating autism or developmental concerns

• Practitioners in functional or integrative medicine

• Anyone struggling with fatigue, brain fog, or chronic illness

• Listeners curious about root-cause health and advanced testing

🔗 Connect with Dr. Kurt Woeller:

• ⁠Integrative Medicine Academy⁠

• ⁠Functional Medicine Doc Talk Podcast⁠

• Substack: ⁠drwoeller.substack.com⁠

If you found this episode helpful, share it with someone who needs a new perspective on healing.

For paid subscribers. Thank you for being part of this community. This guide is one of my most-requested clinical resources — a comprehensive, easy-to-reference breakdown of the foods that actively support gut lining integrity, reduce intestinal inflammation, and feed a diverse, resilient microbiome. I’ve organized it into four sections so you can focus on whatever area matters most for you right now. Save it, share it with your household, and bring it to your next appointment if you’d like to talk through how it fits your individual plan.

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