Know the story.

The patient is a 26-year-old male with chronic, predominantly post-prandial nausea beginning in mid-2020 following a dengue-like illness (not laboratory-confirmed) and a period of significant stress. Initial symptoms were mild and intermittent, with several spontaneous remissions over the first two years. By 2022-2023 the illness evolved into a persistent, load-sensitive pattern characterized by nausea and abdominal bloating rising 30-120 minutes after meals.

The defining feature of this case is reproducible meal-load sensitivity. Through extensive self-tracking, he identified three primary determinants of symptom burden: meal size, eating speed, and fat load. Meals above approximately 500-600 cal, rapid eating, or higher fat content reliably provoke nausea and bloating, whereas smaller meals (generally 300-450 cal), eaten slowly and deliberately, are often tolerated and can prevent flares entirely. Splitting meals and finishing with a brisk walk frequently reduces or aborts active episodes. During flares, his tolerated meal threshold contracts (sometimes <300 cal), contributing to difficulty maintaining caloric intake and weight. Bloating and nausea correlate closely in onset and severity, with bloating typically preceding moderate flares. He also reports intermittent evening vertigo (peripheral spinning without presyncope), episodic 45-minute waves of abdominal pain accompanying nausea, and psoriasis on the forehead.

Objective testing has shown bile reflux with non-erosive gastritis on endoscopy (February 2023), normal gastric emptying, normal CT abdomen, and low gallbladder ejection fraction (22%) on HIDA scan. Hydrogen-dominant SIBO was diagnosed in 2023; rifaximin worsened symptoms. Betaine HCl was trialed repeatedly and consistently exacerbated nausea, culminating in a severe flare in late 2024; acid supplementation is now avoided. PPIs were briefly helpful early but later ineffective or worsening. A bile-reflux-targeted regimen (sucralfate, alginate, bile acid binder, ursodiol) was implemented in late 2025 with partial, inconsistent benefit.

Beginning in late 2024, cycling botanical antimicrobials produced durable reductions in gas and bloating and modest improvement in nausea. Digestive enzymes and bitters became consistently helpful pre-meal supports. Probiotics, prebiotic beverages, and gummy supplements reliably provoke significant gas and bloating and are poorly tolerated. High supplement burden increases stress and symptom fixation; simplifying to liquids and essential agents improved overall tolerance. In early 2025 he developed intermittent pill-sticking and occasional food-sticking sensations that can independently trigger nausea.

A prominent feature of the illness is autonomic modulation. Exercise can rapidly reduce active nausea. High-engagement, socially immersive, or novel environments often correlate with near-normal days despite imperfect diet. Conversely, isolation, rumination, sleep disruption, travel, and missed vagal stimulation sessions cluster with multi-day flares. Consistent vagal stimulation (VaguStim, humming, breathwork) reduces frequency and intensity of post-prandial waves; lapses correlate with worsening. These patterns suggest a significant brain-gut/autonomic component layered on top of meal-load sensitivity.

Laboratory patterns over time include intermittent ANA positivity (occasionally high-titer), chronic low white blood cell and neutrophil counts with relative lymphocytosis, recurrent EBV and HHV-6 reactivation markers, and fluctuating stool markers consistent with mucosal immune activation and barrier stress (elevated secretory IgA, intermittent zonulin, calprotectin, β-glucuronidase). Thyroid testing has shown intermittent TSH elevation; iodine deficiency was identified on prior testing and has been corrected, resulting in improved TSH levels.

In late 2025, treatment expanded to include a structured bile-reflux regimen (sucralfate, alginate therapy, cholestyramine, and ursodiol), cromolyn for mast-cell stabilization, and initiation of mirtazapine in December 2025, later increased to 30 mg in February 2026. Around January 2026, during a period of strict routine - including small/slow low-fat meals, regular medication use, daily vagal stimulation, structured workdays, and improved sleep - he experienced his most sustained improvement to date. Nausea was often brief, lower intensity, and more manageable, and overall productivity approached baseline. Since that time he has been working harder and longer hours than ever, which he reports helps him to ignore/push through flares much faster than he would otherwise. However, this improvement has not been fully durable. Attempts to increase meal size to support weight gain, travel, sleep disruption, stimulant adjustments, or lapses in routine continue to provoke predictable flares. While his functional ceiling is meaningfully higher than earlier in the illness, he remains vulnerable to relapse and requires tight behavioral and dietary control to maintain stability. The current goal is not just partial control under ideal conditions, but durable resilience and the ability to tolerate normal meal volumes and routine variability without recurrence.

Overall, the illness behaves as a load-sensitive post-prandial nausea syndrome with strong autonomic modulation, superimposed on objective findings of bile reflux, gallbladder hypomotility, dysbiosis patterns, and fluctuating immune activation. While functional capacity has improved significantly under tightly controlled conditions, he remains vulnerable to relapse with modest dietary or routine deviations and continues to struggle to increase caloric intake without triggering symptoms.