A functional medicine case study for clinicians
Lena was 52 when she booked her first visit. Her intake form listed three concerns: fatigue that hit hard every afternoon around 2 p.m., low-grade headaches roughly four days a week, and bloating that had become a daily fixture. None of these felt urgent to her. She had simply learned to plan her life around them.
Further down the form, almost as an aside, she noted that she had been diagnosed with Hashimoto’s twelve years earlier, shortly after the birth of her second child. She had been given a prescription for desiccated thyroid, took for a short period of time, and stopped. In her words: “I am not very good at remembering to take pills and I didn’t think they were working. I have always thought there was a more natural way for me to get my thyroid back to optimal levels.” She had not had her thyroid checked in years.
Those couple of sentences told me a great deal about where to start, and about the conversation we would need to have.
A Postpartum Clue
The timing of Lena’s diagnosis was not incidental. The postpartum period is the most common window for Hashimoto’s to emerge in women. During the second and third trimesters, the maternal immune system shifts toward tolerance so the pregnancy can be sustained. After delivery, that suppression lifts, and in genetically susceptible women the rebound can unmask thyroid autoimmunity that had been developing quietly for years.
Clinical pearl: Thyroid antibodies often precede clinical disease by years, sometimes decades. A family history of thyroid disease, combined with new fatigue, mood changes, or hair loss in the year after delivery, is a reason to run antibodies rather than attributing everything to sleep deprivation.
The Initial Workup
Rather than ordering TSH alone, I ran a comprehensive blood panel: a full thyroid panel (TSH, total and free T4, total and free T3, reverse T3, TPO and thyroglobulin antibodies), a comprehensive metabolic panel, CBC with differential, iron studies with ferritin, a lipid panel, hsCRP, vitamin B12, and 25(OH)D. Because celiac disease is considerably more prevalent in patients with autoimmune thyroid disease, I also added tTG-IgA with total IgA and HLA genotyping.
Clinical pearl: Each thyroid marker answers a different question. TSH reflects what the pituitary perceives. Free T3 reflects what the tissues are actually receiving. Antibodies tell you why the gland is failing. A TSH-only strategy can confirm that something is wrong, but it cannot tell you what is driving it or whether treatment is reaching the cells.
The results were quite alarming. Her TSH was 57.0 uIU/mL. Free T4 was 0.65 ng/dL and free T3 was 1.9 pg/mL, both below the lab range. TPO antibodies were 378 IU/mL. This is what Hashimoto’s hypothyroidism looks like when it has gone untreated for more than a decade.
The rest of the panel filled in the picture. LDL was elevated at 162 mg/dL, hsCRP was 2.6 mg/L, 25(OH)D was insufficient at 27 ng/mL, and ferritin sat at the low end of the functional range. Her celiac screen was negative.
Clinical pearl: Hypothyroidism reduces hepatic LDL receptor expression, which slows LDL clearance. Before statins were available, thyroid hormone was actually used to lower cholesterol. When you see new or worsening LDL elevation, a thyroid panel belongs in the workup before a lipid-lowering prescription.
The Conversation That Mattered Most
Lena came to me hoping for a natural path, and I think this can be a common misunderstanding for patients and it should be discussed. The functional approach to thyroid disease does not reject hormone replacement. It asks why the thyroid is failing and addresses those causes, and it uses replacement when the gland can no longer meet the body’s needs. A TSH of 57 falls squarely in that category. Every cell in the body depends on thyroid hormone, and overt hypothyroidism at this level carries real risk for cardiovascular disease, metabolic dysfunction, and cognitive decline.
I explained this to Lena, and I also explained that replacement would treat the consequence while the rest of our work would target the cause. That reframe changed her relationship with the medication. She had stopped taking it twelve years earlier because no one had explained why it mattered and she likely did not take it long enough to see if would move the needle with symptoms. We tied her dose to her morning coffee, set up a weekly organizer, and she has not missed a week since.
We started a T4-based regimen first and planned to titrate every six weeks based on TSH and free T3, rather than TSH alone. Choosing the best medication for each patient is very individualized. I tend to use every tool available to me to find the best fit for the patient. The goal here, was to start with T4- based (Levothyroxine) to get the levels up and balanced, see how her body does with converting the T4 to T3 and then see if we need to add in additional T3 (liothyronine) support or a natural desiccated version instead.
Clinical pearl: Hashimoto’s is an inflammatory condition, and inflammation impairs conversion of T4 to the active hormone T3. Many Hashimoto’s patients normalize their TSH on T4 monotherapy yet remain symptomatic because free T3 lags. Tracking free T3 alongside TSH tells you whether the medication is actually reaching the tissues.
Replacement addressed what was happening. It did not address why. With TPO antibodies near 400, her immune system was still actively attacking the gland, and that immune activity does not happen in isolation. The next question was what was driving it.
Why Order a Stool Test for a Thyroid Patient?
Lena’s daily bloating was the obvious reason to look at her gut, but the rationale goes deeper. The gut and thyroid influence each other in both directions. Most of the body’s immune tissue lines the intestinal tract, and dysbiosis combined with increased intestinal permeability exposes the immune system to bacterial endotoxin, which drives the kind of systemic inflammation that sustains autoimmunity. Hypothyroidism, in turn, slows gut motility and creates conditions that favor overgrowth. The gut also affects how well oral thyroid medication is absorbed.
I ordered a comprehensive stool analysis with culture and three-sample parasitology. Her beneficial flora were present but suboptimal, which was encouraging but we know we need to do some work in this area. Alongside them, though, the culture grew three dysbiotic Gram-negative organisms at 3+: Enterobacter cloacae complex, Klebsiella oxytoca, and Klebsiella pneumoniae. The yeast culture grew Candida inconspicua and Candida krusei at 2+, and microscopic yeast was reported as rare. Parasitology was negative.
Clinical pearl: Enterobacter and Klebsiella are Gram-negative organisms whose outer membranes carry lipopolysaccharide, one of the most potent inflammatory triggers the immune system encounters. In a patient with active thyroid autoimmunity, a steady endotoxin load from the gut is a plausible contributor to ongoing immune activation, and it is something we can actually change.
The yeast findings carried their own lesson. Candida krusei is intrinsically resistant to fluconazole, and Candida inconspicua shares that reduced susceptibility. A reflexive fluconazole prescription would likely have failed. The culture included a sensitivity panel for both the bacteria and the yeast, and that panel guided our choice of agents.
Clinical pearl: Stool cultures that include sensitivity testing let you select antimicrobials, pharmaceutical or botanical, based on what actually inhibits that patient’s organisms. This is especially valuable with non-albicans Candida species, where empiric azole therapy often disappoints.
Treating the Gut in Phases
Sequencing matters in gut work, so we moved in three phases. The first was dietary: a 30-day Paleo (whole foods/low inflammatory) style reset emphasizing whole foods, with gluten, refined sugar, industrial seed oils, and processed foods removed. Given her autoimmune thyroid diagnosis, gluten stayed out permanently. Removing refined sugar also withdrew an easy fuel source for the yeast.
The second phase was targeted eradication. Guided by the sensitivity panel, she completed a course of botanical antimicrobials for the Gram-negative overgrowth alongside an antifungal agent to which both Candida species were sensitive. The third phase focused on rebuilding: a probiotic, gradual reintroduction of fermented foods, and a slow increase in prebiotic fiber to support the beneficial populations that were already there.
Clinical pearl: Separate thyroid medication from supplements, fiber, and minerals by several hours. Iron, calcium, magnesium, and some botanicals can meaningfully reduce levothyroxine absorption, and an unexplained rise in TSH during a gut protocol is often a timing issue rather than disease progression.
An HPA Axis Result That Didn’t Match Perfectly
Her afternoon energy crash and daily headaches prompted a look at her stress physiology, so I ran a dried urine test for comprehensive hormones (DUTCH). Her sex hormones were consistent with the menopausal transition. The adrenal pattern was more interesting. Her diurnal free cortisol curve was low throughout the day, and her 24-hour free cortisol sat at the bottom of the range, yet her metabolized cortisol was high-normal.
Free cortisol reflects what the tissues are exposed to. Metabolized cortisol reflects total production. When metabolized cortisol is adequate but free cortisol is low, the adrenal glands are producing enough; the body is simply clearing it quickly. That pattern is more often associated with hyperthyroidism, and Lena was profoundly hypothyroid. Her chronic gut inflammation was one plausible contributor, but the broader lesson is that real patients do not always match the textbook, and the treatment plan should follow the patient rather than the pattern.
Clinical pearl: Starting thyroid hormone accelerates cortisol clearance. In a patient whose free cortisol is already low, beginning replacement without supporting the HPA axis can leave them feeling worse before they feel better. Addressing both at the same time made Lena’s transition noticeably smoother.
HPA support was built around fundamentals: protein at breakfast and regular meals to stabilize blood sugar (her 2 p.m. crash was partly a blood sugar story), a consistent sleep window, morning light exposure, and ten minutes of daily breathing practice that she chose herself. We also repleted vitamin D, ensured selenium intake through food, and deliberately avoided high-dose iodine, which can aggravate thyroid autoimmunity, particularly when selenium status is inadequate.
Three Months Later
At her twelve-week recheck, TSH had fallen to 2.1, but free T3 was still only 2.4 pg/mL and her afternoon fatigue had not fully lifted. This was the conversion problem in action. We adjusted her regimen to include a T3 component, and by six months her TSH was 1.6, free T4 1.18 ng/dL, and free T3 3.0 pg/mL.
The downstream markers told the rest of the story. TPO antibodies fell from 378 to 164 IU/mL, a reduction of more than half. hsCRP dropped from 2.6 to 0.8 mg/L. LDL came down from 162 to 118 mg/dL without a lipid-lowering medication, and 25(OH)D rose to 52 ng/mL. Her repeat stool analysis no longer showed significant dysbiotic bacterial growth, and yeast was not cultured.
Clinically, her bloating had resolved apart from the occasional heavy meal, her headaches had dropped from four days a week to roughly once a month, and the afternoon crash was gone. At her follow-up she said this was the first time anyone had explained why any of it mattered.
Clinical pearl: Thyroid antibodies fluctuate, and many patients never fully normalize them. A sustained downward trend, paired with falling inflammatory markers, is a meaningful signal that immune activity is quieting. Recheck antibodies periodically rather than relying on a single value.
Additional Immune Regulation Support
At the same visit, with her gut treatment underway and her thyroid replacement stabilizing, we added low-dose naltrexone (LDN) to support immune regulation. At low doses, naltrexone briefly blocks opioid receptors, and the body responds by increasing its own endorphin and enkephalin signaling. These pathways help regulate immune cell activity, and LDN also appears to reduce TLR4-mediated inflammatory signaling. The evidence in Hashimoto’s is still early and comes mostly from small studies and clinical experience. For a patient whose antibodies remained high despite progress elsewhere, it offered a low-risk way to calm immune activity directly while the root-cause work continued. One practical point matters for any clinician adding LDN to a thyroid patient’s plan: as immune activity quiets, some patients need less thyroid hormone. We rechecked her labs after being on LDN for 8-12 weeks and saw that her thyroid function maintained stable and her TPO antibodies went down from 164 IU/mL, to 72 IU/mL.
What This Case Teaches
A conventional approach would have gotten one important thing right. Lena needed thyroid hormone, and a TSH of 57 leaves no room for debate. But that approach would likely have stopped there, and her bloating, headaches, gut inflammation, HPA dysregulation, rising LDL, and active autoimmunity would each have been handled separately, if at all.
Equally, a version of functional medicine that withheld replacement in favor of gut protocols and supplements would have failed her. The strength of this case is that both were done at once. Replacement stabilized her physiology while the rest of the plan went after the reasons her immune system had turned on her thyroid in the first place.
Learning to Think This Way
Cases like Lena’s are where a systems-based framework earns its value: knowing which labs to order and why, how to read a stool culture beyond its flags, when a DUTCH result should change your plan, and how to sequence interventions so they support each other rather than compete.
The ADAPT Practitioner Training Program is where that foundation is built. Over the course of the program, you learn the full clinical framework behind a case like this one, from comprehensive lab interpretation and stool analysis to HPA axis assessment and treatment sequencing, and you practice applying it to real patient cases. We are now taking deposits for the upcoming cohort. If this way of thinking resonates with you, it is a good time to take a closer look.”
