Forskolin in Glaucoma, Asthma and Clinical Research

Long before anyone put forskolin in a weight-loss capsule, medical researchers took it seriously for three specific things: lowering pressure inside the eye, opening constricted airways, and helping a failing heart contract. That work was real, it was published in mainstream journals, and in one case it produced an approved prescription drug. This page reports it properly, because it is genuinely interesting and because it shows what actual clinical evidence looks like next to a marketing claim.

But it comes with a condition attached, stated here at the top and repeated throughout: none of these research strands supports taking an oral coleus supplement, and none of them can be borrowed to prop up the weight-loss claim. The eye studies used drops on the eye. The asthma studies that worked used a powder inhaled into the lungs. The heart studies used intravenous infusion of a chemically redesigned molecule under hospital monitoring. A different route of administration is a different intervention — as different as the distinction between a nicotine patch and a cigarette, or between insulin injected and insulin swallowed. If a sales page cites the glaucoma or asthma literature to sell you capsules, it is misusing it.

First Principle: The Route Is the Intervention
Why the Eye Was a Sensible Place to Look
The Eye-Drop Studies, 1983 Onward
Oral Combination Products in Glaucoma
Glaucoma: What the Evidence Does and Does Not Support
Airways: Literally the Same Mechanism as an Inhaler
Inhaled Forskolin: Where the Signal Was Clearest
The Oral Asthma Trial
Asthma: The Verdict, and a Hard Warning
Heart Failure: The Strand That Became a Real Drug
Cystic Fibrosis: Forskolin as a Clinical Test
Other Research Strands, Honestly Labelled
Why None of This Reaches the Weight-Loss Claim
Key Research Papers
Connections

First Principle: The Route Is the Intervention

This is the idea that makes the rest of the page readable, so it goes first.

When you change how a drug enters the body, you change almost everything about it: the concentration reached at the target, how fast it arrives, how long it stays, how much of it is destroyed on the way, and which other tissues are exposed. Route is not a detail of delivery. Route is part of the drug.

Consider what "50 mg of forskolin" means by each route:

As eye drops: a tiny quantity applied directly onto the cornea, producing a high local concentration in the front of the eye and almost nothing anywhere else. The rest of your body barely sees it.
Inhaled as a dry powder: delivered straight onto airway smooth muscle, which is the target. High local concentration, fast onset, low systemic dose.
Intravenously: the entire dose enters the bloodstream at a controlled rate, with no absorption barrier and no liver first pass. This is why it is done under continuous monitoring.
Swallowed as a capsule: the dose must survive stomach acid, cross the gut wall — difficult, because forskolin is essentially water-insoluble — then pass through the liver, which is built to dismantle exactly this class of greasy plant diterpene. Whatever survives is diluted through the whole body. Nobody has published a well-replicated account of what blood concentration this produces in humans.

So the strongest evidence for forskolin comes from the three routes that bypass the oral problem entirely. That is not a coincidence — it is the researchers telling you, through their choice of route, that the oral route did not look workable.

Why the Eye Was a Sensible Place to Look

Glaucoma is a group of diseases in which the optic nerve is progressively damaged, usually in association with raised pressure inside the eye. The damage is painless, silent, and irreversible. Lowering intraocular pressure is the only intervention proven to slow it, and it is one of the better-evidenced treatment principles in all of medicine.

Pressure inside the eye is a plumbing balance. A structure behind the iris called the ciliary body continuously secretes clear fluid — aqueous humour — into the front of the eye, and that fluid drains out through a mesh of tissue near where the iris meets the cornea. Raise production or block drainage and the pressure rises.

Crucially, aqueous humour production is under cyclic-AMP-linked control. That is not a speculative link: it is the established reason beta-blocker eye drops such as timolol lower eye pressure — they reduce beta-adrenergic, cAMP-mediated secretion by the ciliary epithelium. Beta-blocker drops have been standard glaucoma therapy for decades.

Now the puzzle that makes forskolin's eye story worth telling. If lowering cAMP with a beta-blocker lowers eye pressure, then raising cAMP with forskolin should raise pressure. It does the opposite. Applied to the eye, forskolin lowers intraocular pressure — and it does so, according to the original work, by reducing aqueous inflow, not by improving drainage. The ciliary epithelium's response to sustained cAMP elevation is evidently not a simple mirror of its response to cAMP suppression. This is a real and unresolved wrinkle in the physiology, and it is one reason the eye work attracted attention rather than being dismissed.

The Eye-Drop Studies, 1983 Onward

The foundational work came from Joseph Caprioli and Marvin Sears at Yale.

Caprioli and Sears, Forskolin lowers intraocular pressure in rabbits, monkeys, and man, published in The Lancet in 1983. Forskolin applied topically — as drops onto the eye — lowered intraocular pressure across three species including human volunteers. Evidence tier: early human study, topical route.

Caprioli, Sears, Bausher, Gregory and Mead, Forskolin lowers intraocular pressure by reducing aqueous inflow, published in Investigative Ophthalmology and Visual Science in 1984. The mechanistic follow-up establishing that the effect came from reduced production rather than improved outflow.

More recently, a 2015 open-label study published in the Saudi Journal of Ophthalmology by Majeed, Nagabhushanam, Natarajan and colleagues examined a 1% forskolin eye-drop preparation in open-angle glaucoma and reported pressure reduction. Note the design: open-label, meaning everyone knew who was getting what. For a measurement as susceptible to expectation and technique as tonometry, that is a real weakness. Evidence tier: preliminary human study, unblinded, topical route.

Two hard practical points follow, and they are the most important sentences in this section:

Forskolin eye drops are not an approved glaucoma therapy in most countries. Forty years after the first Lancet report, they are not standard care anywhere. That is itself a finding: the effect was either not large enough, not durable enough, or not reproducible enough to displace the drops we already have.
Never improvise eye drops from a supplement. This deserves to be said in plain language because people do it. An oral capsule is manufactured to oral standards: it is not sterile, not pH-balanced, not isotonic, not free of particulates, and not preservative-controlled. Putting its contents into your eye risks chemical injury to the cornea and bacterial or fungal keratitis, which can destroy vision in days. There is no version of this that is a good idea.

Oral Combination Products in Glaucoma

The modern human literature took a different turn, and this is where honesty about study design matters most.

A relatively small number of research groups — concentrated in Italian ophthalmology — have studied oral combination supplements in patients with primary open-angle glaucoma who were already on maximum tolerated pressure-lowering eye drops. The products combine forskolin with rutin (a flavonoid) and, depending on formulation, B vitamins, homotaurine, carnosine or folic acid.

Representative publications include Pescosolido and Librando, reporting in Clinica Terapeutica in 2010 on an oral association of forskolin, rutin and B vitamins as an addition to pharmacological treatment in open-angle glaucoma; and Vetrugno, Uva, Russo and colleagues, Oral administration of forskolin and rutin contributes to intraocular pressure control in primary open angle glaucoma patients under maximum tolerated medical therapy, published in the Journal of Ocular Pharmacology and Therapeutics in 2012.

These studies generally report a modest additional reduction in intraocular pressure on top of existing drops. That is a clinically meaningful question — patients at maximum tolerated therapy who are still progressing face surgery, so an add-on that worked would matter.

The limitations are substantial and must travel with the finding:

Multi-ingredient products. When a capsule contains forskolin, rutin, homotaurine and vitamins, no observed effect can be attributed to forskolin. This is the single biggest problem with the strand.
Small samples, short follow-up. Tens of patients, weeks to months, in a disease measured over decades.
Frequently unblinded or single-centre. Several are open-label.
Geographic clustering. A body of work from a small number of groups in one country, without independent large-scale replication elsewhere, is a recognised warning sign in evidence appraisal — not proof of anything wrong, but a reason to withhold confidence.
Surrogate endpoint. These studies measure pressure, not vision. Lowering pressure is a validated surrogate in glaucoma, but a small pressure change over eight weeks is a long way from demonstrated protection of the optic nerve.
Publication bias. A small literature on a commercial supplement is exactly where negative results are least likely to appear.

Glaucoma: What the Evidence Does and Does Not Support

Supported: that aqueous humour production is cAMP-linked, and that topically applied forskolin lowered intraocular pressure in early human work. Tier: established mechanism plus early human data, topical route.

Preliminary at best: that an oral multi-ingredient supplement containing forskolin adds a modest pressure reduction in patients already on maximum drops. Tier: preliminary, small, largely unblinded, multi-ingredient, geographically clustered, surrogate endpoint.

Not supported, and dangerous to assume: that a coleus weight-loss capsule from a supplement shop treats glaucoma; that forskolin can replace prescribed drops; or that a supplement is a reason to delay laser treatment or surgery.

Why the last point is not merely academic. Glaucoma destroys peripheral vision silently. By the time you notice, the nerve fibres are gone and they do not come back. Every month spent on an unproven supplement instead of proven therapy is a month of possible irreversible loss. Nobody has ever recovered vision lost to glaucoma. If you have glaucoma or raised eye pressure, use your drops, keep your appointments, and if you want to try an adjunct supplement, tell your ophthalmologist so it can be added to — not substituted for — a monitored treatment plan. See Glaucoma for the full clinical picture.

Airways: Literally the Same Mechanism as an Inhaler

Of all forskolin's proposed uses, bronchodilation has the cleanest theoretical case, because the mechanism is not analogous to an existing drug class — it is the mechanism of an existing drug class.

When you use a salbutamol (albuterol) inhaler, the drug docks at beta-2 adrenergic receptors on airway smooth muscle. Those receptors activate adenylyl cyclase, cAMP rises inside the muscle cell, protein kinase A is activated, the muscle relaxes, the airway widens, and you can breathe. Every reliever inhaler on earth works through the cAMP rise.

Forskolin produces that same cAMP rise without needing the beta-2 receptor. In theory this is genuinely attractive, for one specific clinical reason: in severe or poorly controlled asthma, beta-2 receptors can become desensitised after heavy reliever use — pulled off the cell surface, so the inhaler stops working as well. An agent acting downstream of the receptor would in principle still work when the receptor did not.

That is a serious pharmacological idea, and it is why the asthma work was done. It is also, unfortunately, where the story stops being encouraging.

Inhaled Forskolin: Where the Signal Was Clearest

The most convincing asthma data used forskolin delivered directly into the airway.

Lichey, Friedrich, Priesnitz and colleagues reported in The Lancet in 1984 on the effect of forskolin on methacholine-induced bronchoconstriction in extrinsic asthmatics — a challenge-protection study, the standard way to demonstrate bronchoprotection.

Kaik and Witte reported in Wiener Medizinische Wochenschrift in 1986 on forskolin's protective effect against acetylcholine provocation in healthy volunteers, comparing two doses against fenoterol and placebo.

Bauer, Dietersdorfer, Sertl, Kaik and Kaik, Pharmacodynamic effects of inhaled dry powder formulations of fenoterol and colforsin in asthma, published in Clinical Pharmacology and Therapeutics in 1993. This is the key reference: inhaled dry-powder forskolin (as colforsin) compared head-to-head against inhaled fenoterol, an established beta-2 agonist, in people with asthma. Measurable bronchodilation was demonstrated. Evidence tier: human clinical pharmacology study, inhaled route.

So the pharmacology worked when the compound was put where it needed to be. And then — this is the part that matters — nothing happened. More than three decades later there is no forskolin inhaler approved anywhere. Beta-2 agonists remained the standard, joined by inhaled corticosteroids, long-acting agents and combination inhalers, all with vastly larger evidence bases.

Why? The published record does not fully explain it, and it would be wrong to guess with confidence. What can be said is that a compound with a demonstrated effect that is never developed usually has a problem the abstract does not show: too short-acting, too irritating, too weak relative to comparators, or no advantage worth the development cost. The one thing an undeveloped positive result does not mean is that the compound was suppressed or overlooked. Forskolin was never overlooked; it is one of the most-studied natural products in pharmacology.

The Oral Asthma Trial

There is one trial that used the oral route, and it is the closest thing in this entire literature to a test of a swallowed forskolin product.

González-Sánchez, Trujillo, Trujillo-Hernández and colleagues, Forskolin versus sodium cromoglycate for prevention of asthma attacks: a single-blinded clinical trial, published in the Journal of International Medical Research in 2006.

A few dozen asthma patients in Mexico received either oral forskolin or inhaled sodium cromoglycate for attack prevention, and the reported attack rates were broadly comparable. Evidence tier: small randomised trial, single-blinded, oral route.

Read carefully before drawing anything from it:

Single-blinded is a weak design for a symptom-based outcome. "Number of asthma attacks" depends on patient reporting and on clinician judgement, both of which are exactly what blinding protects.
Sodium cromoglycate is a weak comparator by modern standards. It is not what current guidelines recommend as controller therapy; inhaled corticosteroids are. Matching a weak comparator is not the same as matching standard care.
Small, single-centre, unreplicated. No independent group has reproduced it in the two decades since.
Non-inferiority claims need much larger samples. Showing that two treatments are similar is statistically harder than showing they differ, and a few dozen patients cannot do it.

This trial is worth reporting because it exists and because pretending otherwise would be dishonest. It is not worth acting on.

Asthma: The Verdict, and a Hard Warning

Supported: that cAMP elevation relaxes airway smooth muscle, and that inhaled forskolin produced measurable bronchodilation in small human studies. Tier: established mechanism plus small human studies, inhaled route.

Preliminary and unreplicated: the single-blinded oral prevention trial. Tier: preliminary.

NOT SUPPORTED: oral coleus supplements as asthma treatment, as controller therapy, or as anything to be used in an attack.

Now the warning, without hedging. Asthma kills people, and it kills them through undertreatment. A rescue inhaler works in minutes because it is delivered straight to the airway. A swallowed capsule of poorly absorbed plant extract cannot possibly do that, and there is no scenario in which reaching for one during breathlessness is anything other than dangerous. Equally, quietly stopping a preventer inhaler because a supplement is "working" is how a stable asthmatic becomes an emergency admission — inhaled corticosteroids reduce airway inflammation you cannot feel, so the deterioration is invisible until it is severe.

If you have asthma: keep your reliever with you, keep taking your preventer, keep your action plan, and if you want to try a supplement, tell the clinician who manages your asthma. See Asthma for the full picture and the interactive asthma visualization for what is happening in the airway.

Heart Failure: The Strand That Became a Real Drug

This is the most instructive strand of all, and the least talked about, because it ends with an actual approved medicine — and with a conclusion that is bad news for the capsule.

The mechanism. In heart muscle, rising cAMP increases the force of contraction (positive inotropy) by enhancing calcium entry and handling. In blood vessels, rising cAMP relaxes the wall and widens the vessel. So a cAMP-raising agent should make the heart pump harder and reduce the resistance it is pumping against — the combination cardiologists call an inodilator, and a genuinely desirable profile in acute decompensated heart failure. This is not new territory: existing drugs including milrinone reach the same endpoint by blocking cAMP breakdown rather than by increasing its production.

What was studied in people. The relevant human work used intravenous infusion under continuous haemodynamic monitoring in hospital. Kramer, Thormann, Kindler and Schlepper reported effects of forskolin on left ventricular function in dilated cardiomyopathy in Arzneimittel-Forschung in 1987. Baumann, Felix, Sattelberger and Klein published a comparative study of forskolin's cardiovascular effects against dobutamine and sodium nitroprusside in patients with idiopathic congestive cardiomyopathy in the Journal of Cardiovascular Pharmacology in 1990. Real haemodynamic changes were measured. Evidence tier: small human studies, intravenous route, monitored setting.

What happened next, and why it is the whole argument. Rather than develop forskolin itself, chemists in Japan built a water-soluble derivative — colforsin daropate — which was approved there as an intravenous drug for acute heart failure.

Sit with that for a moment. Pharmaceutical developers with full knowledge of the molecule, real financial incentive, and the ability to run trials did not produce a forskolin pill. They rebuilt the molecule to be water-soluble and gave it by drip. The reason they had to is the reason the capsule is doubtful: natural forskolin does not dissolve or absorb well enough to be given any other way.

The frequent retelling — "forskolin is used as a heart medicine" — compresses that into something misleading. The accurate version: a chemically modified, water-soluble relative of forskolin, given intravenously under monitoring, is an approved heart-failure drug in one country. Nothing in that sentence endorses a capsule, and anyone with heart failure, arrhythmia or unstable cardiovascular disease should stay well away from self-experimenting with a compound that alters cardiac contractility and vascular tone. See Heart Failure.

Cystic Fibrosis: Forskolin as a Clinical Test

Here is a use of forskolin that genuinely touches patient care today, and it is not a treatment at all — it is a measurement.

Cystic fibrosis is caused by a faulty chloride channel called CFTR, and CFTR opens in response to cAMP-driven phosphorylation. So if you grow a miniature tissue — an organoid — from a patient's own intestinal cells and add forskolin, working CFTR channels pump chloride and fluid into the organoid and it visibly swells. Broken channels do not, and it does not.

This is the forskolin-induced swelling assay, described by Dekkers and colleagues in Nature Medicine in 2013 as a functional CFTR assay using primary cystic fibrosis intestinal organoids. It has been used to help predict whether an individual patient — including patients with rare mutations too uncommon for a clinical trial — is likely to respond to CFTR-modulator drugs.

Note what forskolin's role is: it is the stimulus in a diagnostic test, applied to cells in a dish outside the body. Nobody swallows it. But it is a legitimate answer to "does forskolin have any real place in modern medicine?" Yes — as an irreplaceable laboratory tool, sometimes one that informs a patient's treatment. That is the honest, and rather more impressive, version of forskolin's clinical relevance. Evidence tier: established laboratory and translational method.

Other Research Strands, Honestly Labelled

Anti-metastatic and anti-cancer activity. Agarwal and Parks published Forskolin: a potential antimetastatic agent in the International Journal of Cancer in 1983, based largely on forskolin's antiplatelet action — platelet aggregation assists tumour cells in seeding new sites. Forty years on, this remains a laboratory observation. Tier: preliminary, in vitro and animal. No human evidence. Do not take forskolin for cancer.
Thyroid function. The TSH receptor signals through adenylyl cyclase, so forskolin stimulates thyroid follicular cells in culture — which is why it is a standard reagent in thyroid cell biology. This is a reason for caution about interaction with thyroid medication, not a therapeutic use. Tier: mechanism only.
Psoriasis and skin conditions. Older literature proposed a cAMP deficit in psoriatic skin, prompting interest in forskolin. It did not develop into a therapy. Tier: preliminary, historical.
Urinary stones. The Ayurvedic pashanabhedi or "stone-breaker" indication is the plant's oldest recorded use, but as noted on the main topic page, that name has most often been assigned to a different plant altogether. Tier: traditional use only. For a herb with a comparable claim and its own evidence page, see Chanca Piedra.
Depression and cognition. cAMP and CREB signalling appear in models of antidepressant action, and forskolin is used to probe them experimentally. There is no human trial evidence for forskolin as a treatment. Tier: preliminary, mechanistic.

Why None of This Reaches the Weight-Loss Claim

Supplement marketing uses the legitimate literature as scaffolding: "studied in glaucoma," "investigated in asthma," "approved for heart failure in Japan." Every one of those phrases is technically true and every one is being misused. Stated as a list:

The eye studies used drops on the eye. A capsule is not eye drops.
The asthma studies that worked used inhaled powder. A capsule is not an inhaler.
The heart-failure drug is a different molecule given intravenously. A capsule is not an infusion, and colforsin daropate is not forskolin.
The cystic fibrosis use is a laboratory assay on cells outside the body. Nobody swallows the reagent.
None of these conditions is obesity. Evidence for one indication is not evidence for another. Lowering eye pressure tells you nothing about fat mass.
The doses do not correspond. The oral glaucoma combination products used on the order of 15 mg of forskolin per day; the body-composition trials used about 50 mg per day. These are different exposures of different products for different purposes.

The honest summary of forskolin's clinical record is this: a real pharmacological agent, with genuine effects when delivered directly to a target tissue, which has never been shown to do anything useful as a swallowed capsule. That statement is more interesting than the marketing, and it happens to be true. For the weight-loss claim specifically, see Forskolin for Weight Loss: The Claim Examined.

Key Research Papers

Authors, titles, journals and years appear as plain text. Links are PubMed topic searches rather than numeric identifiers, so no link can silently resolve to the wrong paper.

Caprioli J, Sears M. Forskolin lowers intraocular pressure in rabbits, monkeys, and man. The Lancet, 1983. The founding topical eye-drop observation across three species. PubMed search
Caprioli J, Sears M, Bausher L, Gregory D, Mead A. Forskolin lowers intraocular pressure by reducing aqueous inflow. Investigative Ophthalmology and Visual Science, 1984. Establishes reduced production rather than improved drainage as the mechanism. PubMed search
Pescosolido N, Librando A. Oral administration of an association of forskolin, rutin and vitamins B1 and B2 potentiates the hypotonising effects of pharmacological treatments in primary open-angle glaucoma patients. Clinica Terapeutica, 2010. An early oral combination add-on study. PubMed search
Vetrugno M, Uva MG, Russo V, et al. Oral administration of forskolin and rutin contributes to intraocular pressure control in primary open angle glaucoma patients under maximum tolerated medical therapy. Journal of Ocular Pharmacology and Therapeutics, 2012. The most-cited oral add-on study; multi-ingredient product. PubMed search
Majeed M, Nagabhushanam K, Natarajan S, et al. Efficacy and safety of 1% forskolin eye drops in open angle glaucoma: an open-label study. Saudi Journal of Ophthalmology, 2015. A modern topical preparation, tested without blinding. PubMed search
Lichey J, Friedrich T, Priesnitz M, et al. Effect of forskolin on methacholine-induced bronchoconstriction in extrinsic asthmatics. The Lancet, 1984. Bronchoprotection in a challenge protocol. PubMed search
Kaik G, Witte PU. Protective effect of forskolin in acetylcholine provocation in healthy volunteers: comparison of two doses with fenoterol and placebo. Wiener Medizinische Wochenschrift, 1986. Dose comparison against an established beta-2 agonist. PubMed search
Bauer K, Dietersdorfer F, Sertl K, Kaik B, Kaik G. Pharmacodynamic effects of inhaled dry powder formulations of fenoterol and colforsin in asthma. Clinical Pharmacology and Therapeutics, 1993. The clearest bronchodilator signal — by inhalation, not by capsule. PubMed search
González-Sánchez R, Trujillo X, Trujillo-Hernández B, et al. Forskolin versus sodium cromoglycate for prevention of asthma attacks: a single-blinded clinical trial. Journal of International Medical Research, 2006. The one oral asthma trial; weak design, weak comparator, unreplicated. PubMed search
Kramer W, Thormann J, Kindler M, Schlepper M. Effects of forskolin on left ventricular function in dilated cardiomyopathy. Arzneimittel-Forschung, 1987. Intravenous haemodynamic study in a monitored setting. PubMed search
Baumann G, Felix S, Sattelberger U, Klein G. Cardiovascular effects of forskolin in patients with idiopathic congestive cardiomyopathy: a comparative study with dobutamine and sodium nitroprusside. Journal of Cardiovascular Pharmacology, 1990. Direct comparison against two standard intravenous agents. PubMed search
Dekkers JF, Wiegerinck CL, de Jonge HR, et al. A functional CFTR assay using primary cystic fibrosis intestinal organoids. Nature Medicine, 2013. The forskolin-induced swelling assay — forskolin as a translational research tool with real patient relevance. PubMed search
Agarwal KC, Parks RE Jr. Forskolin: a potential antimetastatic agent. International Journal of Cancer, 1983. A laboratory observation resting on forskolin's antiplatelet activity; never translated to human treatment. PubMed search
Ammon HP, Müller AB. Forskolin: from an ayurvedic remedy to a modern agent. Planta Medica, 1985. A contemporaneous review of the plant's transition from traditional use to pharmacology. PubMed search

Live PubMed Searches

External Resources

National Eye Institute — US government patient information on glaucoma, intraocular pressure and proven treatment options.
National Heart, Lung, and Blood Institute — asthma and heart-failure guidance, including what controller and reliever therapy is for.
ClinicalTrials.gov — search "forskolin" to see what has and has not been registered as a trial.
National Center for Complementary and Integrative Health — US government appraisals of botanical evidence.

Connections

All Herbs
Coleus forskohlii (Forskolin) — the main topic page: botany, naming, forms, dosage and cautions.
Forskolin and Cyclic AMP — the mechanism that makes every effect on this page predictable.
Forskolin for Weight Loss — why this clinical literature cannot be borrowed to support the retail claim.
Safety and Interactions — blood pressure, bleeding, gastric acid and drug interactions.
Glaucoma — the disease itself, why pressure control is the only proven intervention, and why delay is irreversible.
Ophthalmology — the full eye-disease library.
Asthma — reliever and preventer therapy, and why substitution is dangerous.
Pulmonology — the full respiratory library.
Heart Failure — where a water-soluble forskolin derivative is used intravenously in one country.
Cardiology — blood pressure, contractility and the drugs that act on them.
Asthma Attack Visualization — an interactive look at bronchoconstriction and what relieves it.
Chanca Piedra — another "stone-breaker" herb, with its own evidence appraisal.

Safety note and disclaimer. Nothing on this page is a recommendation to use coleus or forskolin for glaucoma, asthma, heart failure or any other condition. The studies described used routes of administration — eye drops, inhaled powder, intravenous infusion — that are not available as consumer products, and one of them used a different molecule entirely. Never put a supplement into your eye. Never substitute a supplement for a rescue inhaler, a preventer inhaler, glaucoma drops, blood-pressure medication or a heart-failure regimen; in asthma and glaucoma, doing so risks irreversible harm. Forskolin also lowers blood pressure, inhibits platelet aggregation and increases gastric acid secretion — see the safety page. This site is educational and is not medical advice. Discuss any supplement with the clinician managing your condition.

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