← All articles

Mastiha for Functional Dyspepsia: Promising Signal, Weak Control

A 2025 trial found Mastiha improved functional dyspepsia symptoms, but its no-treatment control cannot separate resin effects from placebo response.

Mastiha may ease functional dyspepsia symptoms, but the only randomized trial so far cannot tell us whether the resin caused the improvement. That is a serious problem in a condition where placebo response is large and well documented.

Functional dyspepsia causes upper-abdominal discomfort, early fullness, bloating, burning, or pain without an obvious structural explanation. It is frustrating for patients and clinicians because standard treatments often deliver modest and inconsistent benefits over placebo. Mastiha—the aromatic resin from Pistacia lentiscus var. Chia—has a plausible biological pitch: antioxidant and anti-inflammatory activity, plus a proposed prebiotic effect. Plausibility, however, is the invitation to run a good trial. It is not the result of one.

What the Mastiha trial found

A 2025 randomized, three-way crossover trial enrolled adults who met Rome IV criteria for functional dyspepsia. Participants received Mastiha capsules at 1.4 g per day, Mastiha-water at 20 mL per day, and a no-intervention period. Each phase lasted four weeks, with 14-day washouts between phases. The primary outcome was the Leuven Postprandial Distress Scale (LPDS), a patient-reported measure of dyspepsia symptoms.

Both Mastiha treatments improved LPDS scores relative to no intervention, with p<0.001 for each comparison, according to the Kleftaki et al. trial. Capsules were associated with improvements in upper-abdominal bloating, epigastric burning, and heartburn. Mastiha-water improved quality of life, with p=0.012.

Those results justify interest. They do not establish clinical efficacy. The published abstract does not report the sample size, absolute LPDS scores, effect sizes, standard deviations, confidence intervals, or a threshold for a clinically meaningful LPDS change. A small numerical change can produce a low p-value; a statistically nonzero difference is not automatically a difference patients would feel in daily life.

The missing placebo arm changes the meaning of the result

The trial compared active treatment with no intervention, not with a blinded placebo. That choice is especially limiting in functional dyspepsia. A systematic review and meta-analysis by Bosman et al. found substantial placebo responses in pharmacological functional-dyspepsia trials. Expectations, the treatment setting, and trial features can improve symptoms independently of a drug's pharmacology.

In this design, participants knew when they were taking capsules or Mastiha-water and when they were receiving nothing. The active periods therefore differed in more than resin exposure: they also differed in expectation, attention, routine, and the ordinary tendency for symptoms to fluctuate after a person enrolls during a bad spell.

This is not merely a complaint that symptom questionnaires are subjective. In a double-blind, placebo-controlled study in healthy volunteers, Schol et al. found that corticotropin-release hormone altered duodenal permeability and immune activation. Stress-axis signals can affect gut biology as well as symptom perception. That does not prove expectancy caused the Mastiha result, but it makes an unblinded comparison poorly suited to separate an effect of the resin from an effect of treatment context.

A p-value below 0.001 against no treatment shows that the study periods differed. It does not show how much of that difference came from Mastiha itself.

Why the biology remains plausible

Functional dyspepsia is a disorder of gut-brain interaction, not one disease with one broken switch. Research describes overlapping contributions from impaired gastric motility, visceral hypersensitivity, and low-grade duodenal inflammation or barrier dysfunction. A review of dyspepsia describes these pathways, while Holtmann and colleagues emphasize the bidirectional gut-brain mechanisms that shape symptoms across these disorders.

That gives Mastiha a reasonable hypothesis. If compounds in the resin reduce inflammatory signaling, influence barrier function, or alter the microbiota, they could conceivably affect processes relevant to dyspepsia. A 2025 review of herbal treatments for disorders of gut-brain interaction supports the broader idea that plant-derived bioactives can influence mucosal inflammation, visceral sensitivity, motility, and gut-brain signaling.

But the broader herbal literature is not Mastiha-specific proof. Nor did the Mastiha trial measure gastric emptying, duodenal permeability, biopsies, inflammatory markers, or microbiome changes. Its outcomes were LPDS symptoms and quality of life. The study therefore provides a clinical signal against no treatment, not evidence for antioxidant, anti-inflammatory, or prebiotic mechanisms in people with functional dyspepsia.

The crossover design adds unanswered questions

Crossover trials can be efficient because each participant receives more than one intervention. They also depend on the earlier treatment wearing off before the next phase begins. Here, washouts lasted 14 days after four-week treatment periods.

That may be adequate for a short-lived symptomatic effect, but it is harder to judge if Mastiha truly changes the microbiome—the proposed prebiotic mechanism. Persistent effects could carry into the next phase and muddy the comparison. The abstract does not provide evidence that the washout eliminated carryover, nor does it report how analyses handled period effects or treatment sequence.

The capsule-versus-water pattern deserves the same restraint. Different formulations could contain different active fractions, but the reported symptom-specific findings also involve several comparisons. Without the sample size, effect estimates, and information on correction for multiple testing, readers cannot tell whether the formulation split reflects biology or statistical noise.

A better trial is feasible

Functional-dyspepsia researchers can use blinded placebo controls for gut-targeted products. In a 2024 randomized placebo-controlled trial, Zhang et al. tested Bifidobacterium animalis subsp. lactis BL-99 against placebo in functional dyspepsia and reported symptom improvement with the probiotic. The point is not that probiotics validate Mastiha. It is that a blinded comparator is feasible for an intervention proposed to work through microbiota-related pathways.

A useful Mastiha replication would conceal allocation with matched placebo capsules and a credible placebo beverage, report the number randomized and completing each phase, prespecify primary and secondary outcomes, quantify mean differences with 95% confidence intervals, and test whether washout is long enough. It should also report adverse events and funding or commercial affiliations clearly. Objective gut endpoints would help test the mechanism, though patient-centered symptom relief remains the outcome that matters most.

Should you take it?

The 2025 trial makes Mastiha worth studying, not worth treating as an established therapy for functional dyspepsia. Its dose was 1.4 g per day for the capsule phase, and the abstract reported no safety signals, but it does not provide enough detail to establish safety or effectiveness for routine use.

If you have persistent upper-GI symptoms, get evaluated before self-treating: functional dyspepsia is diagnosed after clinicians consider other causes. For people already diagnosed, Mastiha remains an unconfirmed option with a plausible mechanism and an encouraging but uninterpretable active-versus-no-treatment result. The next study needs to answer the question this one left open: does Mastiha beat placebo?

Comments

No comments yet. Be the first!