Coleus Forskohlii Safety: Blood Pressure, Bleeding and Interactions

Most supplement safety pages are vague on purpose: "generally well tolerated," "consult your healthcare provider," a paragraph about pregnancy, done. This one can be specific, because forskolin's risks are not a list of scattered adverse-event reports. They are predictions. Every caution below follows from one fact — forskolin raises cyclic AMP in whatever tissue it reaches, and it cannot choose the tissue — and each one lands in an organ where a cAMP rise does something you would not have asked for.

That makes this page unusual in a useful way. You do not have to trust an adverse-event database. You can reason it out: find the tissues where cAMP is a control signal, and you have found the side effects. The list is not long, but it includes blood pressure, platelet function, stomach acid, and one absolute contraindication.

The three that matter most, up front. If you take blood-pressure medication, forskolin can add to it. If you take an anticoagulant or antiplatelet drug, or you have surgery coming, forskolin adds bleeding risk. If you have polycystic kidney disease, do not take it at all — cyclic AMP is the signal that makes kidney cysts grow, and forskolin is what laboratories use to make them grow.

Table of Contents

1. One Mechanism, Every Caution
2. Blood Pressure: Vasodilation and Additive Hypotension
3. Platelets, Bleeding and Anticoagulants
4. Surgery, Dental Work and Procedures
5. Gastric Acid, Ulcers and Reflux
6. Nitrates, Vasodilators and Erectile-Dysfunction Drugs
7. Polycystic Kidney Disease: The Hard No
8. Thyroid and Other Hormone Signalling
9. Liver Effects and Drug-Metabolising Enzymes
10. A Different Route Is Not Evidence of Oral Safety
11. Pregnancy, Breastfeeding and Children
12. Product Variability: What "10%" Does Not Guarantee
13. Who Should Avoid It, and What to Watch For
14. Key Research Papers
15. Connections

One Mechanism, Every Caution

Cyclic AMP is a second messenger — the internal signal a cell manufactures when a hormone docks on its surface. It is made by an enzyme called adenylyl cyclase, and it is used by a very large number of tissues for a very large number of purposes. The full mechanism is on the cyclic AMP page; the short version is what matters here.

Almost every drug that raises cAMP does so through a receptor, and receptors are how selectivity happens. A salbutamol inhaler raises cAMP in airway muscle because airway muscle carries beta-2 receptors. Glucagon raises cAMP in the liver because liver cells carry glucagon receptors. The receptor is the address on the envelope.

Forskolin has no address. It crosses the cell membrane and binds adenylyl cyclase itself — the enzyme every cell has. That is precisely why it is a globally used laboratory reagent, and precisely why it is a poor systemic drug. There is no tissue it is aimed at, so there is no tissue it spares.

So here is the safety profile, derived rather than reported. Where is cAMP a control signal?

• Vascular smooth muscle — cAMP relaxes it. Blood vessels widen. Blood pressure falls.
• Platelets — cAMP is their master brake. Clotting is impaired.
• Stomach parietal cells — cAMP drives the acid pump. Acid secretion increases.
• Heart muscle — cAMP increases contractile force and rate. Cardiac effects.
• Kidney cyst epithelium — cAMP drives fluid secretion and proliferation. Cysts grow.
• Thyroid follicular cells — the TSH receptor works through cAMP. Thyroid stimulation.
• Steroid-producing cells — cAMP drives steroidogenesis. Hormone shifts.
• Intestinal epithelium — cAMP drives chloride and fluid secretion. Loose stools.

Every heading in the rest of this page is one line from that list. Nothing here is exotic. It is one molecular event arriving in eight tissues that want different things.

Blood Pressure: Vasodilation and Additive Hypotension

The mechanism. Arteries are wrapped in a layer of smooth muscle whose tone sets their diameter. When cAMP rises in that muscle, protein kinase A reduces its sensitivity to calcium and the muscle relaxes. Wider vessels mean lower resistance, and lower resistance means lower blood pressure. This is not a subtle or theoretical property of forskolin — it is one of the first things ever reported about it.

Indian pharmacologists described it before the molecule was even famous. Lindner, Dohadwalla and Bhattacharya published Positive inotropic and blood pressure lowering activity of a diterpene derivative isolated from Coleus forskohlii: forskolin in Arzneimittel-Forschung in 1978, and Dubey, Srimal, Nityanand and Dhawan published pharmacological studies on coleonol as a hypotensive diterpene in the Journal of Ethnopharmacology in 1981. The blood-pressure-lowering effect is in the compound's founding literature. Evidence tier: established in animal pharmacology and in monitored human intravenous studies.

What this means in practice.

• If you take medication for high blood pressure, the effects can add. That includes beta-blockers, ACE inhibitors, angiotensin receptor blockers, calcium-channel blockers, diuretics and nitrates. The result of additive hypotension is not usually dramatic — it is light-headedness on standing, unsteadiness, fatigue, occasionally a faint. In an older person, a faint is a hip fracture.
• If you already have low blood pressure or orthostatic symptoms, be more careful, not less. People with postural orthostatic tachycardia syndrome, autonomic dysfunction or a habitually low reading have no headroom.
• Other blood-pressure-lowering supplements stack too. Beetroot or nitrate products, hawthorn, high-dose fish oil, magnesium at bowel-tolerance doses, and several others all push the same direction.
• "It lowers blood pressure" is not a reason to take it for hypertension. No trial has shown that a coleus supplement usefully treats high blood pressure, and an unmonitored, non-selective, poorly characterised vasodilator is not a substitute for a medication with decades of outcome data. See Hypertension.

Practical step: if you take it anyway, know your baseline. Measure your blood pressure sitting and standing for a few days before starting, and again in the first week. A supplement that moves a number you are not measuring is a supplement whose effect you will only discover by feeling unwell.

Platelets, Bleeding and Anticoagulants

This is the most under-reported risk in forskolin marketing, and mechanistically it is one of the most solid.

The mechanism. Cyclic AMP is a platelet's off switch. Your own blood-vessel lining uses it deliberately: healthy endothelium releases prostacyclin, prostacyclin raises cAMP inside passing platelets, and raised cAMP keeps them from activating and clumping where they are not needed. This is how your circulation stops itself clotting continuously.

Forskolin raises platelet cAMP directly. Siegl, Daly and Smith demonstrated inhibition of aggregation alongside stimulated cAMP generation in intact human platelets in Molecular Pharmacology in 1982. This was established so early and so clearly that Agarwal and Parks proposed forskolin as a potential antimetastatic agent in the International Journal of Cancer in 1983 largely on the strength of its antiplatelet action. Evidence tier: established in human platelets in vitro.

The interactions that follow.

• Anticoagulants — warfarin, and the direct oral anticoagulants such as apixaban, rivaroxaban, edoxaban and dabigatran. These work on the clotting cascade rather than on platelets, but adding platelet inhibition on top increases overall bleeding risk.
• Antiplatelet drugs — aspirin, clopidogrel, ticagrelor, prasugrel, dipyridamole. Same target, additive effect. Anyone on dual antiplatelet therapy after a stent is at the highest risk here.
• Other antiplatelet supplements — high-dose fish oil, ginkgo, garlic extract, high-dose vitamin E, curcumin, nattokinase. People taking a "stack" often have four or five of these without realising they all pull the same lever.
• Anti-inflammatory drugs — ibuprofen, naproxen and similar drugs have their own antiplatelet effect and irritate the stomach lining, which combines badly with forskolin's effect on gastric acid (below).

Signs to take seriously: bruising more easily or in unusual places, nosebleeds that take longer to stop, bleeding gums when brushing, blood in urine or stool, black tarry stools, cuts that keep oozing, or unusually heavy periods. Any of these while taking forskolin is a reason to stop and speak to a clinician — not a reason to wait and see.

Surgery, Dental Work and Procedures

This gets its own section because it is actionable and frequently missed.

Stop forskolin at least two weeks before any planned surgery, dental extraction, biopsy, endoscopy with possible intervention, or injection procedure. Two weeks is the standard interval advised for supplements with antiplatelet activity, and it exists because platelets live about eight to ten days and the affected population needs to turn over.

The reason it matters is that forskolin brings two surgical liabilities at once: impaired platelet function, which increases bleeding, and a blood-pressure-lowering effect that interacts with anaesthesia, which itself drops blood pressure. Neither is welcome on an operating table.

Two further points. Tell your surgeon and anaesthetist about every supplement, not just the ones that sound medical. Pre-operative questionnaires ask about medications, and patients routinely answer without mentioning capsules bought online — which is exactly how an unexplained intraoperative bleed happens. And if surgery is unplanned or urgent, say what you have been taking, even if you took it that morning.

Gastric Acid, Ulcers and Reflux

The mechanism, which is almost too neat. The stomach's acid-producing parietal cells are switched on by histamine acting at the H2 receptor, and that receptor signals through adenylyl cyclase and cAMP to activate the proton pump. This is exactly the pathway that H2 blockers — famotidine, cimetidine, ranitidine — were designed to interrupt.

Forskolin pushes that pathway in the opposite direction. Stimulation of acid and pepsinogen secretion by forskolin in isolated gastric glands was reported by Chew in the American Journal of Physiology in 1983, and forskolin has been a standard tool in gastric physiology ever since for exactly this reason. Evidence tier: established in isolated gastric tissue.

Consequences:

• Active peptic ulcer disease — increasing acid secretion into an existing ulcer crater is directly counterproductive, and combined with impaired platelet function it is the specific combination that turns an ulcer into a bleeding ulcer. See Peptic Ulcer Disease.
• Reflux disease — more acid means more to reflux. See GERD.
• It can work against acid-suppressing therapy. If you take a proton-pump inhibitor or an H2 blocker, forskolin is pushing the accelerator while your medication holds the brake.
• Loose stools and increased bowel activity are the most commonly reported complaints in the small oral trials, and they have the same origin: cAMP drives chloride and fluid secretion by the intestinal lining. This is not a "detox" effect. It is secretory diarrhoea, mildly.

Nitrates, Vasodilators and Erectile-Dysfunction Drugs

Cells run two closely related cyclic-nucleotide systems: cyclic AMP, which forskolin raises, and cyclic GMP, which nitric oxide raises. In smooth muscle they converge on the same outcome — relaxation — through overlapping downstream machinery.

That convergence is the basis of a theoretical but reasonable concern:

• Nitrates (glyceryl trinitrate, isosorbide) work through cyclic GMP to dilate vessels. Adding a cAMP-driven vasodilator risks additive hypotension.
• Phosphodiesterase-5 inhibitors for erectile dysfunction — sildenafil, tadalafil, vardenafil — work by preventing cyclic GMP breakdown. They already carry a hard warning about combination with nitrates for precisely this reason. Adding a third vasodilating agent is not sensible.
• Cyclic-AMP-active heart drugs — milrinone and related phosphodiesterase-3 inhibitors work by slowing cAMP breakdown. Forskolin increases cAMP production. Same variable, two directions of attack, unpredictable together.
• Forskolin has actually been injected into the penis as part of compounded multi-drug mixtures for erectile dysfunction refractory to standard therapy — a specialist procedure performed under urological supervision, and one more example of a route that has nothing to do with a capsule. It is not evidence that oral forskolin does anything for erectile function.

Evidence tier for the interaction concerns: theoretical, mechanistically grounded, not documented in human interaction studies. That combination — plausible and unstudied — is the reason to be cautious rather than reassured.

Polycystic Kidney Disease: The Hard No

Of everything on this page, this is the one absolute contraindication, and it deserves to be understood rather than just obeyed.

In autosomal dominant polycystic kidney disease, the kidneys fill progressively with fluid-filled cysts until function is lost. Cyclic AMP is the central driver of that process. Inside the epithelium lining a cyst, elevated cAMP does two harmful things simultaneously: it drives chloride-and-fluid secretion into the cyst cavity, so the cyst fills, and it switches the lining cells into a proliferative mode, so the cyst wall grows. Yamaguchi, Nagao, Wallace and colleagues showed that cyclic AMP activates the B-Raf and ERK proliferative pathway in cyst epithelial cells from human polycystic kidneys, published in Kidney International in 2003.

The clinical proof runs in the opposite direction, and it is strong. Tolvaptan, the drug approved to slow progression in this disease, works by blocking the vasopressin V2 receptor specifically in order to lower cAMP in those cells. The pivotal trial — Torres, Chapman, Devuyst and colleagues, Tolvaptan in patients with autosomal dominant polycystic kidney disease, in the New England Journal of Medicine in 2012 — showed slowed kidney growth and slowed decline in function.

So the disease is driven by high cAMP, and the treatment works by lowering cAMP. Meanwhile, in the laboratory, forskolin is one of the standard agents used to induce cyst formation and fluid secretion in models of the disease. A compound whose experimental job is making kidney cysts grow has no business being swallowed by someone whose kidneys are already full of them.

If you have polycystic kidney disease, or a family history of it, do not take coleus or forskolin. This also matters for people who do not know they have it: ADPKD is common enough — and often silent until adulthood — that a family history of "kidney problems," dialysis, or a parent with large kidneys is worth taking seriously before starting a cAMP-raising supplement. See Polycystic Kidney Disease.

Thyroid and Other Hormone Signalling

Thyroid-stimulating hormone from the pituitary controls the thyroid through a receptor that signals via adenylyl cyclase and cAMP. Raising cAMP in a thyroid follicular cell therefore mimics the pituitary's instruction to work. Forskolin is used routinely in thyroid cell biology for exactly this reason.

What that means practically is honest uncertainty rather than a documented problem. There are no human studies of forskolin's effect on thyroid function or on levothyroxine therapy. Evidence tier: mechanism only, theoretical interaction. But if you take thyroid medication or are being monitored for a thyroid condition, this is worth mentioning to your prescriber, and it is a reason not to introduce a new cAMP-raising supplement in the weeks around a dose adjustment or a thyroid function test. See Hypothyroidism.

The same logic covers steroid hormones. Luteinising hormone drives testicular steroid production through cAMP, and forskolin stimulates steroidogenesis in isolated cells. The 2005 body-composition trial in men reported higher free testosterone as a secondary outcome — see the weight-loss page for why that finding should be treated cautiously. Read as a safety matter rather than a benefit, it says: this supplement may have endocrine activity, taken without monitoring, at an exposure nobody has characterised.

Liver Effects and Drug-Metabolising Enzymes

Two findings from animal work deserve mention, both because they are relevant and because they are almost never mentioned in the retail context.

Dose-related liver injury in mice. Virgona, Taki, Yamada and Umegaki reported that dietary Coleus forskohlii extract generated dose-related hepatotoxicity in mice, published in the Journal of Applied Toxicology in 2013. Evidence tier: animal study. Animal hepatotoxicity does not establish human liver injury, and mice were fed proportionally large amounts. But for a supplement taken daily for months with no human long-term safety data, an animal liver signal is not something to leave out.

Induction of drug-metabolising enzymes, and an interaction that runs the "wrong" way. Japanese researchers reported around 2012 that coleus extract induces hepatic cytochrome P450 enzymes in mice, and — more pointedly — that this cytochrome induction mediated an interaction with warfarin, reducing warfarin's anticoagulant effect in animal models.

Read that carefully, because it is genuinely important and it cuts against the simple story:

• Forskolin's platelet effect would tend to increase bleeding risk on warfarin.
• Cytochrome induction would tend to clear warfarin faster, reducing its effect and increasing clot risk.
• These are opposite directions. The net effect in a given person is unpredictable, which is worse than a predictable interaction in one direction, not better.

For anyone on warfarin, the practical conclusion is simple: do not add this supplement, and if you already have, tell the clinic that manages your INR so your monitoring can account for it. Cytochrome induction also means potential interference with other narrow-margin medications metabolised by the same enzymes — a category that includes many antiepileptics, immunosuppressants and antiretrovirals. Evidence tier: animal and in-vitro; no human interaction studies.

A Different Route Is Not Evidence of Oral Safety

A specific argument appears on sales pages and it needs dismantling, because it sounds reasonable: forskolin has been used as eye drops and studied by inhalation, and it is an approved intravenous heart drug in Japan — so it must be safe.

This gets safety exactly backwards. Route determines dose, distribution and which tissues are exposed. A different route is a different intervention, for risk as much as for benefit.

• Eye drops deliver a tiny quantity to the front of the eye. Systemic exposure is minimal. That the eye tolerates a drop tells you nothing about what a daily systemic dose does to platelets or blood pressure.
• Inhaled powder targets airway muscle with a small dose. Its documented side effects were local — cough, throat irritation.
• Intravenous infusion is the highest-risk route of all, which is exactly why it is done in hospital with continuous monitoring: the documented effects include flushing, tachycardia and hypotension. Those effects are the mechanism arriving fast. An approved intravenous drug is not "proof of safety" — it is proof that this pharmacology needs a monitored setting.
• And the intravenous drug is a different molecule. Colforsin daropate is a chemically modified, water-soluble derivative. Its approval says nothing about natural forskolin in a capsule.

Run the argument in reverse and its absurdity is clear: nobody would claim that because a local anaesthetic is safely injected into a gum, drinking a bottle of it is fine.

Two more asymmetries worth naming. The traditional food use does not transfer either. In parts of Gujarat and Rajasthan the fresh root is eaten as a pickled condiment — genuinely reassuring about the food, and irrelevant to a solvent extract concentrated to 10% forskolin taken twice daily for three months. And the trials' clean tolerability reports do not cover the population that worries. Those trials enrolled a few dozen relatively healthy overweight adults for twelve weeks. They did not enrol people on anticoagulants, people with ulcers, people with polycystic kidneys, or anyone at all for a second year.

Pregnancy, Breastfeeding and Children

Do not take coleus or forskolin during pregnancy or while breastfeeding. The reasoning:

• There is no adequate human safety data. Not "reassuring data" — no data. For a compound that alters a universal signalling system, absence of data during organ development is a reason to abstain.
• Traditional sources treat the root as inadvisable in pregnancy. Traditional caution is weak evidence of harm but it is not zero, and here it points the same way as the pharmacology.
• The mechanism raises specific concerns. Vasodilation affects blood pressure and therefore placental perfusion; cAMP influences uterine smooth muscle; and cAMP–CREB signalling participates in developmental gene expression. None of this is documented as harmful in humans, and none of it is a risk worth taking for a supplement with no established benefit.
• Breastfeeding: no data on transfer into milk. Same conclusion.
• Children and adolescents: no safety or dosing data, and no plausible indication. Weight-loss supplements marketed to teenagers are a specific harm worth naming, and this is not an exception.

Product Variability: What "10%" Does Not Guarantee

A risk that has nothing to do with pharmacology: you may not be taking what the label says.

In most countries, botanical supplements are not tested for identity, potency or purity before sale in the way medicines are. For coleus specifically:

1. "10% forskolin" is arithmetic, not a guarantee. It means a tenth of the extract powder by weight should be forskolin, so a 250 mg capsule should contain about 25 mg. Whether it does depends entirely on the manufacturer's testing. Independent testing across the supplement industry regularly finds products that do not match their labels.
2. Higher percentages are less studied, not better. Products advertise 20%, 40%, even 95%. The published trials used a 10% extract. A 40% product at the same capsule weight is a fourfold untested dose.
3. Species identity is a real problem here. Several unrelated plants share these common names: in Brazil, Plectranthus barbatus leaves are sold as "boldo" though true boldo is a different plant entirely, and Plectranthus amboinicus (Cuban oregano, Indian borage) is a different species with no meaningful forskolin. A label reading only "coleus" is not an adequate identification.
4. Plant part matters. Forskolin is in the root and essentially absent from the leaf. If the label does not say root, that is a problem.
5. Standardisation is a chemistry test, not a botany test. Meeting a forskolin percentage does not prove the material came from the right plant, or from the root, or that the compound was not added in purified form to a weak extract.
6. Heavy metals and contamination. This is a root crop, and roots concentrate soil contaminants. Third-party testing for heavy metals and microbial contamination is worth insisting on.
7. Multi-ingredient "fat burner" blends are the worst case. Forskolin frequently appears in stacks with caffeine and other stimulants. Combining an unselective vasodilator with high-dose stimulants is a cardiovascular gamble, and proprietary-blend labelling means you cannot tell how much of anything you are taking.

Who Should Avoid It, and What to Watch For

Do not take it at all

• Polycystic kidney disease, or a family history suggesting it. The clearest contraindication on this page.
• Pregnancy or breastfeeding.
• Children and adolescents.
• Taking warfarin, a direct oral anticoagulant, or dual antiplatelet therapy.
• Active peptic ulcer, recent gastrointestinal bleed, or oesophageal varices.
• Unstable cardiovascular disease — a tachyarrhythmia, uncontrolled heart failure, recent heart attack, or significant valve disease.
• Within two weeks of planned surgery or a dental extraction.
• A bleeding disorder such as haemophilia or von Willebrand disease, or low platelets.

Discuss with a clinician first

• Any blood-pressure medication, or low blood pressure and orthostatic symptoms.
• Aspirin, clopidogrel or regular anti-inflammatory drugs.
• Proton-pump inhibitors, H2 blockers, or reflux disease.
• Thyroid medication or a thyroid condition under monitoring.
• Liver disease, or any medication with a narrow therapeutic margin.
• Nitrates or drugs for erectile dysfunction.
• Glaucoma — not because forskolin is dangerous to the eye, but because it must never displace proven pressure-lowering treatment. See the clinical-uses page.
• Asthma — keep your inhalers regardless.

Stop and seek advice if you notice

• Light-headedness or faintness on standing, or unusual fatigue.
• Easy bruising, prolonged nosebleeds, bleeding gums, blood in urine or stool, or black tarry stools.
• New or worsening heartburn, or upper abdominal pain.
• Palpitations or an unusually fast heartbeat.
• Yellowing of the eyes or skin, dark urine, or persistent right-sided abdominal discomfort.
• Persistent loose stools.

If you take it anyway

The realistic advice, since people will:

1. Choose a product naming the species and the root, giving extract weight and percentage, with third-party testing.
2. Stay at the studied 10% extract rather than a high-percentage product.
3. Take it with food.
4. Measure your blood pressure before starting and during the first week.
5. Tell every prescriber and your pharmacist — and write it on pre-operative forms.
6. Avoid stacking it with other antiplatelet or blood-pressure-lowering supplements.
7. Set a stop date. Human trials ran twelve weeks; there is no long-term safety data whatsoever. Indefinite use is unstudied territory.
8. Stop two weeks before any procedure.

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.

1. Lindner E, Dohadwalla AN, Bhattacharya BK. Positive inotropic and blood pressure lowering activity of a diterpene derivative isolated from Coleus forskohlii: forskolin. Arzneimittel-Forschung, 1978. The founding report of the cardiovascular and blood-pressure effects. PubMed search
2. Dubey MP, Srimal RC, Nityanand S, Dhawan BN. Pharmacological studies on coleonol, a hypotensive diterpene from Coleus forskohlii. Journal of Ethnopharmacology, 1981. Early systematic characterisation of the hypotensive effect. PubMed search
3. Siegl AM, Daly JW, Smith JB. Inhibition of aggregation and stimulation of cyclic AMP generation in intact human platelets by the diterpene forskolin. Molecular Pharmacology, 1982. The antiplatelet effect, demonstrated in human platelets. PubMed search
4. Agarwal KC, Parks RE Jr. Forskolin: a potential antimetastatic agent. International Journal of Cancer, 1983. Rests on the antiplatelet action — included here as further evidence of how strong that effect is. PubMed search
5. Chew CS. Forskolin stimulation of acid and pepsinogen secretion in isolated gastric glands. American Journal of Physiology, 1983. The gastric acid effect, in isolated tissue. PubMed search
6. Seamon KB, Padgett W, Daly JW. Forskolin: unique diterpene activator of adenylate cyclase in membranes and in intact cells. Proceedings of the National Academy of Sciences of the USA, 1981. The mechanism from which every caution on this page is derived. PubMed search
7. Yamaguchi T, Nagao S, Wallace DP, et al. Cyclic AMP activates B-Raf and ERK in cyst epithelial cells from autosomal-dominant polycystic kidneys. Kidney International, 2003. Establishes cAMP as a proliferative driver in cyst epithelium. PubMed search
8. Torres VE, Chapman AB, Devuyst O, et al. Tolvaptan in patients with autosomal dominant polycystic kidney disease. New England Journal of Medicine, 2012. The pivotal trial of a drug that works by lowering cAMP in exactly those cells. PubMed search
9. Virgona N, Taki Y, Yamada S, Umegaki K. Dietary Coleus forskohlii extract generates dose-related hepatotoxicity in mice. Journal of Applied Toxicology, 2013. Animal liver signal; not human evidence, but not nothing either. PubMed search
10. Japanese pharmacology groups reported around 2012 that Coleus forskohlii extract induces hepatic cytochrome P450 enzymes in mice and that this induction mediates an interaction with warfarin, reducing its anticoagulant effect — an interaction running opposite to forskolin's antiplatelet effect. Because the exact journal details should be checked at source, this is given as a topic search rather than a formal citation. PubMed search
11. Godard MP, Johnson BA, Richmond SR. Body composition and hormonal adaptations associated with forskolin consumption in overweight and obese men. Obesity Research, 2005. Included here for its tolerability data and its report of altered free testosterone — an endocrine signal in a twelve-week trial. PubMed search
12. Henderson S, Magu B, Rasmussen C, et al. Effects of Coleus forskohlii supplementation on body composition and hematological profiles in mildly overweight women. Journal of the International Society of Sports Nutrition, 2005. Reported no clinically significant adverse effects and no adverse change in blood counts over twelve weeks — useful, and limited to twenty-three healthy women for three months. PubMed search
13. 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. What forskolin's cardiovascular pharmacology looks like when given intravenously under monitoring. PubMed search
14. Ammon HP, Müller AB. Forskolin: from an ayurvedic remedy to a modern agent. Planta Medica, 1985. A contemporaneous review covering the compound's pharmacology across tissues. PubMed search

Live PubMed Searches

1. coleus forskohlii + safety + adverse effects
2. forskolin + platelet aggregation inhibition
3. forskolin + blood pressure + vasodilation
4. forskolin + gastric acid secretion + parietal cell
5. cyclic AMP + cyst growth + polycystic kidney disease
6. herbal supplement + perioperative bleeding risk
7. Coleus forskohlii + hepatotoxicity + cytochrome P450
8. dietary supplement label accuracy + botanical identity
9. intracavernosal forskolin + erectile dysfunction

External Resources

• NIH Office of Dietary Supplements — US government fact sheets on supplement safety, interactions and regulation.
• National Center for Complementary and Integrative Health — appraisals of botanical safety and evidence, including guidance on telling your clinicians what you take.
• MedlinePlus — plain-language drug and supplement information from the US National Library of Medicine.
• US Food and Drug Administration — supplement regulation, recalls and adverse-event reporting.

Connections

• All Herbs
• Coleus forskohlii (Forskolin) — the main topic page: botany, naming, forms, dosage and full cautions list.
• Forskolin and Cyclic AMP — the single mechanism from which every risk on this page is derived.
• Forskolin for Weight Loss — the claim most people are weighing these risks against, and why it is not supported.
• Glaucoma, Asthma and Clinical Research — why an approved intravenous or topical use is not evidence of oral safety.
• Polycystic Kidney Disease — the absolute contraindication, and the disease that explains why.
• Hypertension — why additive blood-pressure lowering matters, and what treats high blood pressure properly.
• Heart Failure — contractility, vascular tone and why these effects belong in a monitored setting.
• Cardiology — the full cardiovascular library, including antiplatelet and anticoagulant therapy.
• Peptic Ulcer Disease — where increased acid secretion plus impaired platelets is the worst combination.
• GERD — reflux, and why a supplement that raises acid output works against your treatment.
• Hypothyroidism — the TSH receptor signals through cAMP, the basis of the theoretical thyroid interaction.
• Lab Tests — the blood tests worth knowing your baseline on before starting any supplement.

Safety note and disclaimer. This page is educational and is not medical advice, and it is not a licence to self-manage a medication regimen. Coleus forskohlii has no established benefit for weight loss and real, mechanistically predictable risks: it lowers blood pressure, it inhibits platelet aggregation, it increases gastric acid secretion, animal studies show dose-related liver injury and induction of drug-metabolising enzymes, and it is contraindicated in polycystic kidney disease and in pregnancy. There is no long-term human safety data at all. Tell every prescriber, pharmacist, surgeon and anaesthetist what supplements you take, stop antiplatelet supplements two weeks before any procedure, and never delay or replace proven treatment for glaucoma, asthma, high blood pressure, heart disease or kidney disease with a supplement. If you develop unusual bleeding, faintness, palpitations or signs of liver trouble, stop taking it and seek medical advice.

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