u/CindyLu2458

A few people have DM'd asking about this since it's come up in earlier threads, so consolidating into one post rather than answering the same questions individually. Full transparency: this is our program.

Quick facts, since these are the questions that keep coming up:

• Two tracks: the General Fellowship (adult-focused functional and integrative psychiatry, open to psychiatrists, PMHNPs, PAs, psychologists, dietitians, and other providers) and the Pediatric Fellowship (child/adolescent-specific, nutrient status and ADHD, PANDAS/PANS, gut-brain considerations in autism and anxiety, environmental triggers). There's a bundled option if you want both.
• Format is self-paced coursework plus live faculty sessions, built to work around a full clinical schedule, not instead of one.
• Enrollment for the current cohort closes August 31, 2026.
• Scholarships are available based on financial need or early-career status, worth asking about directly on a free discovery call rather than assuming it's out of reach.

If you've been reading this subreddit for a few weeks and wondering whether a structured program like this is worth it versus piecing things together from articles and podcasts, that's a fair question, and the honest answer is "depends on how deep you want to go and whether you want it to count toward something formal." Happy to answer specifics in the comments, including the PMHNP-specific angle if that's relevant to you (scope, what counts toward CE, etc.).

Not the only training option out there. Genuinely curious what else people here have used or are considering.

A polarizing topics in pediatric functional psychiatry...

The Feingold-style elimination of artificial food dyes/additives has shown a small but statistically significant effect on hyperactivity in some blinded trials, particularly in children with pre-existing sensitivity, significant enough that the EU now requires warning labels on foods with certain dyes. A broader "few foods" elimination diet has shown benefit for a subset of children with ADHD in blinded studies, especially those with concurrent allergic/atopic conditions.

However the idea that eliminating gluten, dairy, or sugar broadly improves ADHD symptoms in the general pediatric ADHD population isn't well supported by blinded trials. And restrictive diets in children carry real risks (nutritional adequacy, disordered eating patterns, social burden) that need to be weighed seriously.

What I have seen:
- Artificial dye elimination: reasonable to trial, low risk, modest evidence base.
- Structured "few foods" elimination with reintroduction: more rigorous option for suspected food-triggered symptoms, ideally with dietitian involvement given nutritional risk in a growing child.
- Broad, unstructured restriction (cutting gluten/dairy/sugar indefinitely without reintroduction testing): not well evidence-supported for the general ADHD population and carries real downsides.

Curious if others have run structured elimination/reintroduction protocols with pediatric patients, and what you've observed, including cases where it didn't help.

Not a formal AMA, but opening the floor: if you started in a conventional psychiatric or pediatric practice and later incorporated functional/integrative approaches, what actually changed?

A few questions if you want a starting point:

• What made you start looking outside standard treatment algorithms?
• What's something that surprised you, either more effective or less effective than expected?
• How do you talk to patients about combining approaches without sounding like you're dismissing conventional care?
• What's been the hardest part clinically, or in terms of colleague/institutional pushback?

Open to both adult- and pediatric-focused clinicians, curious how the answers compare across populations. Students and researchers, feel free to ask questions in the comments.

For anyone working with kids and adolescents, PANDAS (Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal infections) and the broader PANS (Pediatric Acute-onset Neuropsychiatric Syndrome) category are worth having on your differential. They are under-recognized and frequently misattributed to primary psychiatric onset.

The pattern to watch for:

Abrupt, dramatic onset of OCD symptoms and/or severe eating restriction, often within 24–72 hours, in a previously healthy child

Frequently accompanied by other new symptoms: tics, regression (handwriting, math skills), separation anxiety, urinary frequency, sleep disturbance

Often follows a documented or suspected infection (strep in PANDAS; broader infectious/inflammatory triggers in PANS)

A relapsing-remitting course tied to subsequent infections is a strong clue

Why it matters: kids presenting this way are sometimes treated purely as new-onset OCD or anxiety without investigation of an infectious/inflammatory trigger, which can delay appropriate treatment (which may include antimicrobial, anti-inflammatory, or immunomodulatory approaches alongside standard psychiatric care, depending on presentation and workup).

Not every abrupt-onset OCD case is PANDAS/PANS. This is a specific clinical picture requiring careful history and workup (strep titers, other infectious/inflammatory markers, symptom timeline), not a diagnosis to reach for reflexively.

Pediatricians and child psychiatrists: how often are you seeing this in practice, and what's your workup look like when you suspect it?

For anyone working with kids and adolescents, PANDAS (Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal infections) and the broader PANS (Pediatric Acute-onset Neuropsychiatric Syndrome) category are worth having on your differential. They are under-recognized and frequently misattributed to primary psychiatric onset.

The pattern to watch for:

Abrupt, dramatic onset of OCD symptoms and/or severe eating restriction, often within 24–72 hours, in a previously healthy child

Frequently accompanied by other new symptoms: tics, regression (handwriting, math skills), separation anxiety, urinary frequency, sleep disturbance

Often follows a documented or suspected infection (strep in PANDAS; broader infectious/inflammatory triggers in PANS)

A relapsing-remitting course tied to subsequent infections is a strong clue

Why it matters: kids presenting this way are sometimes treated purely as new-onset OCD or anxiety without investigation of an infectious/inflammatory trigger, which can delay appropriate treatment (which may include antimicrobial, anti-inflammatory, or immunomodulatory approaches alongside standard psychiatric care, depending on presentation and workup).

Not every abrupt-onset OCD case is PANDAS/PANS. This is a specific clinical picture requiring careful history and workup (strep titers, other infectious/inflammatory markers, symptom timeline), not a diagnosis to reach for reflexively.

Pediatricians and child psychiatrists: how often are you seeing this in practice, and what's your workup look like when you suspect it?

Magnesium comes up constantly for pediatric anxiety, so worth being precise about what's actually known versus extrapolated from adult data.

Mechanism: magnesium modulates NMDA receptor activity and supports GABAergic signaling, both relevant to anxiety regulation, plausible in kids as in adults, though the pediatric-specific mechanistic research is thinner.

Evidence base: most positive trial data for magnesium and anxiety comes from adult studies; pediatric-specific randomized trials are limited in number and generally small. The existing pediatric data (including some ADHD-with-anxiety populations) shows modest positive signal, but the evidence is nowhere near as robust as it's sometimes presented online.

What's not established: optimal pediatric dosing (which varies significantly by age/weight and isn't well standardized across studies), which formulation is preferable in children, and whether benefit is concentrated in kids with documented deficiency versus a general anxiolytic effect.

Clinically: given the thinner pediatric-specific evidence, this is a good example of where checking status (RBC magnesium) before recommending supplementation is more defensible than extrapolating adult dosing directly onto a child.

Anyone testing magnesium status in pediatric anxiety cases? What's your dosing approach when you do supplement?

Lithium at psychiatric (high) doses is well established for bipolar disorder, but "low-dose" or "microdose" lithium (often in the range of 1–5 mg elemental lithium, well below therapeutic bipolar dosing) gets discussed differently in integrative circles, worth separating what's supported from what's speculative.

What's reasonably supported:

• Trace lithium is naturally present in drinking water at varying concentrations, and several large ecological studies have found associations between higher regional lithium levels in water supplies and lower rates of suicide, homicide, and all-cause mortality, notable, though ecological studies can't establish individual-level causation.
• Preclinical and some human research suggests lithium has neuroprotective and neurotrophic properties even at doses far below those used to treat bipolar disorder.
• Small clinical studies have explored low-dose lithium as an adjunct in conditions like treatment-resistant depression, aggression, and some neurodegenerative-risk contexts, with mixed but not uninteresting results.

Where it's thinner:

• Randomized controlled trial data specifically on low-dose lithium for mood or cognitive outcomes is limited, much of the evidence base is ecological, preclinical, or small-sample clinical work, not the large RCTs we'd want before broad clinical recommendations.
• Low-dose lithium is often available over-the-counter as a supplement in the US, which means dosing, purity, and quality control vary widely outside a prescribing/monitoring relationship. A real practical concern distinct from the efficacy question.
• Long-term safety data at low doses (kidney, thyroid function) is much less established than the well-characterized (if real) risks at therapeutic bipolar dosing.

Clinically: this is a good example of a biologically plausible, ecologically interesting intervention that's ahead of its RCT evidence base. Worth knowing about, but worth being precise with patients about what's established vs. promising vs. unproven.

Anyone using low-dose lithium in practice, or have thoughts on where the evidence currently sits? Genuinely curious how people here are thinking about the OTC availability issue too.

Looking for real stories, not case reports, the moments that shifted how you approach patients.

Could be a lab result that reframed a diagnosis, a nutrient correction that resolved something medication hadn't touched, a GI workup that explained a "treatment-resistant" presentation, or even a case where the functional approach didn't pan out and taught you something about its limits.

Clinicians, students, researchers are all welcome to share. Keep specifics de-identified if discussing patients*.*

Nutrient status gets discussed a lot in pediatric functional psychiatry: iron/ferritin, vitamin D, B12/folate, zinc, omega-3 index, but I have seen practice vary.

• What's in your standard workup for a new pediatric ADHD, anxiety, or mood presentation, if anything beyond the standard psychiatric assessment?
• Ferritin comes up a lot in ADHD discussions. Do you treat "low-normal" ferritin in a symptomatic child, or wait for a frank deficiency?
• Have you seen a case where a nutrient correction changed the clinical trajectory, e.g., iron repletion affecting ADHD symptom severity, or vitamin D correction affecting mood in an adolescent?

"Gut-brain connection" gets thrown around a lot, so let's ground it in what's actually established vs. still emerging.

What's well-supported:

• The vagus nerve provides a direct bidirectional communication line between gut and brain.
• Roughly 90% of the body's serotonin is produced in the gut, primarily by enterochromaffin cells,  though gut serotonin doesn't cross the blood-brain barrier, so its role in mood is more about local signaling and vagal activation than a direct "serotonin supply" to the brain.
• Gut microbiota produce short-chain fatty acids (like butyrate) that influence neuroinflammation and blood-brain barrier integrity.
• Dysbiosis and increased intestinal permeability ("leaky gut") have been associated with depression and anxiety in multiple studies, association, not yet proven causation in humans.

What's still emerging/debated:

• Which specific probiotic strains, if any, produce clinically meaningful mood improvements (the "psychobiotic" literature is promising but heterogeneous).
• How much of the gut-mood relationship is bidirectional, likely significant, which complicates causal claims in either direction.

Why it matters clinically: a good reminder to ask about GI symptoms as part of a psychiatric intake, not to jump to a specific protocol, but because GI inflammation and dysbiosis are modifiable variables worth investigating in treatment-resistant cases.

Clinicians, are you incorporating gut health screening into intake? 

(Not medical advice. General clinical discussion only.)