Can I Take Reishi Mushroom with Lisinopril?

At a glance
- Drug / lisinopril, an ACE inhibitor, FDA-approved for hypertension, heart failure, and diabetic nephropathy, typically dosed 2.5 to 40 mg daily
- Supplement / reishi mushroom (Ganoderma lucidum), sold as capsules, powders, or tinctures; not FDA-evaluated for safety or effectiveness
- Interaction type / pharmacodynamic (overlapping effects on blood pressure and platelet function), not a metabolic or drug-transporter interaction
- Blood pressure concern / laboratory studies report ACE-inhibitory activity from reishi triterpenes; small human studies suggest a modest blood-pressure-lowering effect, though results are not consistent or well replicated
- Bleeding concern / laboratory and small human data suggest reishi can reduce platelet aggregation, which matters most for patients also on antiplatelet or anticoagulant drugs
- Kidney/immune concern / theoretical only; no human trial has tested this combination in patients with immune-mediated kidney disease
- Verdict / this is a "discuss with your prescriber first" situation, not an outright contraindication and not a routine safe pairing
Direct answer
There is no FDA-recognized or guideline-defined interaction between reishi mushroom and lisinopril. What exists is a biologically plausible pharmacodynamic overlap: reishi triterpenes have shown ACE-inhibitory activity in laboratory assays, the same pathway lisinopril blocks, and separate reishi constituents have shown antiplatelet activity in small studies. If these effects occur in a person taking lisinopril, the practical risks are added blood pressure lowering (dizziness, falls, fainting) and increased bleeding tendency, particularly in someone already on an antiplatelet or anticoagulant medication. The human evidence behind both mechanisms is limited to small or early-phase studies, so the size of the effect in a typical supplement user is not established. A physician or pharmacist should be told about reishi use before it is combined with lisinopril, especially in older adults, anyone already at their blood pressure target, and anyone on blood thinners.
What reishi mushroom is and why people take it
Reishi (Ganoderma lucidum) is a polypore fungus used for centuries in East Asian traditional medicine. In the United States it is sold as a dietary supplement, most commonly marketed for general immune support, stress adaptation, and vague cardiovascular benefit claims. Commercial products range widely in dose and standardization, from roughly 500 mg to over 5,000 mg of dried extract per day, and label claims about triterpene or beta-glucan content are not independently verified by the FDA.
Compounds that matter for this interaction
- Triterpenes (ganoderic acids and related compounds): laboratory (in vitro) studies have found that certain ganoderic acids inhibit angiotensin-converting enzyme, the same enzyme lisinopril blocks pharmacologically.
- Beta-glucans and polysaccharides: these carbohydrate-based compounds stimulate immune cell activity, including natural killer cells and cytokine release, which is relevant mainly to patients with immune-mediated kidney disease.
- Adenosine and related nucleosides: these have been associated with reduced ADP-induced platelet aggregation in laboratory and small human studies.
These mechanisms are pharmacologically coherent, but coherent mechanism is not the same as a proven clinical effect at the doses found in commercial supplements. Readers should treat the magnitude figures sometimes quoted online (specific mmHg reductions or percentage platelet inhibition) with caution unless traced to a specific, verifiable study, because dosing, extraction method, and study population vary enormously across the reishi literature.
Regulatory status
Reishi products are regulated in the United States as dietary supplements under the Dietary Supplement Health and Education Act, which means manufacturers are not required to prove safety or effectiveness before marketing (fda.gov/food/dietary-supplements, accessed 2025). Quality and potency are not standardized across brands, so two "reishi" products can deliver very different amounts of active triterpenes.
How lisinopril works
Lisinopril is an ACE inhibitor approved by the FDA for hypertension, heart failure, and kidney protection in type 2 diabetes with nephropathy, among other uses. It blocks the enzyme that converts angiotensin I to angiotensin II, lowering blood pressure and reducing the workload on the heart and kidneys. Lisinopril is not metabolized through the liver's cytochrome P450 system and is cleared largely unchanged by the kidneys, so classic pharmacokinetic interactions, where one substance changes blood levels of another by affecting liver metabolism, are unlikely with most supplements, reishi included.
This matters for interpreting the reishi interaction: the concern here is not that reishi changes how much lisinopril is in the blood. The concern is that both act on overlapping physiological targets (blood pressure regulation and, separately, platelet function) in the same person at the same time.
The blood pressure interaction
This is the mechanism with the clearest laboratory rationale. Ganoderic acids and related triterpenes have shown ACE-inhibitory activity in cell-free enzyme assays. Small human studies of reishi extract in people with mild to moderate hypertension have reported modest reductions in blood pressure compared with placebo, though the studies are small, use varying extract doses, and have not been replicated at scale. Whether the laboratory ACE-inhibition translates into a clinically meaningful additive drop in blood pressure for someone already taking lisinopril has not been directly tested in a controlled human trial.
The practical concern is for people who are already close to or below their blood pressure target on lisinopril. Adding a second agent that plausibly lowers blood pressure through a related mechanism could push systolic pressure low enough to cause orthostatic dizziness, falls, or fainting, particularly in older adults.
Who carries the highest hypotension risk
- Adults 65 and older who are already at or near their blood pressure goal
- People also taking a diuretic or a second blood pressure medication, since combined effects can stack
- People with diabetes-related autonomic neuropathy or a known history of orthostatic hypotension
- Anyone recently started on or increased to a higher lisinopril dose, before their blood pressure has stabilized
The bleeding and antiplatelet interaction
Reishi's beta-glucans and adenosine-related compounds have shown reduced platelet aggregation in laboratory and small human studies. Lisinopril itself does not directly affect platelet function, so this is not a lisinopril-specific interaction, but many people prescribed lisinopril for heart failure or after a heart attack are also taking aspirin, clopidogrel, or another antiplatelet or anticoagulant drug for a separate reason. In that situation, adding reishi introduces a third agent with plausible platelet-inhibiting activity.
This concern is most relevant for:
- People taking warfarin, apixaban, rivaroxaban, or a similar anticoagulant alongside lisinopril
- People scheduled for surgery, since agents with antiplatelet activity are typically stopped before elective procedures on a timeline set by the surgical team
- People with chronic kidney disease, a common reason for lisinopril use, since uremia itself can impair platelet function
- People with a recent gastrointestinal bleed, low platelet count, or other bleeding disorder
At typical over-the-counter reishi doses in an otherwise healthy adult not on a blood thinner, the bleeding risk from reishi alone appears to be low based on available data, though "low" is not the same as "zero," and the evidence base is not large enough to rule out an effect in more vulnerable patients.
A theoretical third concern: immune modulation and kidney disease
Lisinopril is prescribed in diabetic nephropathy and other chronic kidney disease partly for its protective effect on kidney filtration. Reishi's beta-glucans stimulate immune activity, including cytokine release. In patients whose kidney disease has an immune or inflammatory component, such as IgA nephropathy or lupus nephritis, immune stimulation from reishi is a theoretical concern that could work against the intended benefit of ACE inhibition. This has not been studied directly in a clinical trial and should be treated as a hypothesis, not an established risk. Patients with immune-mediated kidney disease who are considering reishi should raise it specifically with their nephrologist or primary care clinician rather than assuming it is inert.
What is not a concern here
Because lisinopril is not metabolized by liver enzymes and is not a substrate of the P-glycoprotein transporter, the kind of interaction seen with drugs like St. John's Wort (which alters P-glycoprotein-mediated drug transport) is not expected with lisinopril and reishi. If reishi constituents affect P-glycoprotein at all, the effect on lisinopril's blood levels would be expected to be negligible, since lisinopril's clearance does not depend on that pathway.
Evidence-status interaction assessment
This table distinguishes between interactions supported by existing research and those that are theoretically possible based on biological mechanisms but lack direct evidence, while highlighting claims that require confirmation from a healthcare provider before using reishi alongside lisinopril.
| Claim | Evidence status | What is actually known | What to verify before relying on it |
|---|---|---|---|
| Reishi triterpenes inhibit ACE in laboratory assays | Established (in vitro / preclinical) | Multiple laboratory studies report ACE-inhibitory activity from ganoderic acids | Whether these concentrations are reached in human plasma at commercial supplement doses is not established |
| Reishi lowers blood pressure in humans | Plausible, weakly supported | Small human studies report modest blood-pressure reductions versus placebo | Effect size, consistency, and reproducibility across products vary; not established at scale |
| Reishi adds to lisinopril's blood-pressure-lowering effect specifically | Not established | No published trial has tested lisinopril plasma levels or blood pressure response with and without concurrent reishi | This is inferred from two separate mechanisms, not directly measured together |
| Reishi reduces platelet aggregation | Plausible, supported by small/early studies | Laboratory and small human data show reduced ADP-induced platelet aggregation with some reishi extracts | Clinical bleeding risk at typical supplement doses in a general population has not been quantified |
| Reishi meaningfully raises bleeding risk in a patient also on an antiplatelet or anticoagulant | Plausible, unproven in trials | Mechanistically coherent given overlapping antiplatelet activity | No controlled study of this three-way combination exists; treat as a real but unquantified risk |
| Reishi affects kidney outcomes in patients using lisinopril for nephroprotection | Not established | Beta-glucans stimulate immune activity in laboratory models | No human trial in CKD patients on ACE inhibitors; discuss with a nephrologist if immune-mediated kidney disease is present |
| Reishi changes lisinopril blood levels through liver metabolism or drug transporters | Considered unlikely | Lisinopril is not a CYP450 substrate and is not P-glycoprotein-dependent for clearance | Low priority to investigate further given the drug's known pharmacokinetics |
If you are on lisinopril and considering reishi, bring this table to the conversation with your prescriber or pharmacist. The rows marked "not established" are the ones most likely to be described with false confidence in supplement marketing.
Monitoring if a clinician approves the combination
If, after review of the full medication list, a prescriber decides the combination is reasonable to try, a structured monitoring approach reduces the chance that a problem goes unnoticed.
Blood pressure
- Record home blood pressure twice daily (morning and evening) for about a week before starting reishi to establish a personal baseline, using a validated upper-arm cuff.
- Continue twice-daily monitoring for several weeks after starting reishi.
- A systolic reading consistently below 100 mmHg, or any episode of dizziness on standing, near-fainting, or fainting, should be reported to a clinician promptly; fainting or chest pain warrants urgent evaluation.
Bleeding
- Watch for easy bruising, unusually prolonged bleeding from minor cuts, blood in urine or stool, or unusual fatigue that could reflect blood loss.
- If also taking warfarin, an INR check after starting or stopping reishi is a reasonable precaution to discuss with the prescriber, since a bleeding-relevant supplement change can complicate interpretation of INR trends even though the mechanisms differ.
Kidney function
- If chronic kidney disease is present, routine creatinine and potassium monitoring on the schedule your clinician already uses is appropriate, since any additive blood pressure drop could transiently affect kidney filtration.
What to tell your doctor or pharmacist
Supplement use is commonly left out of conversations with prescribers, which limits a clinician's ability to anticipate interactions. When discussing reishi, provide:
- The exact product name, manufacturer, and the dose per capsule or serving
- How many doses per day you take or plan to take
- Every other supplement, herbal product, or over-the-counter medication you use
- Your most recent home blood pressure readings, if available
Ask your pharmacist to search specifically for "Ganoderma lucidum," the scientific name, since supplement products are not always indexed consistently under prescription drug interaction checkers.
Should you stop lisinopril to take reishi instead?
No. Lisinopril is prescribed for specific, evidence-based reasons, including blood pressure control, heart failure management, and kidney protection in diabetes. Reishi is not an FDA-approved substitute for any of these indications, and stopping an ACE inhibitor abruptly can cause a rebound rise in blood pressure in some patients and removes the drug's cardioprotective and renal-protective effects. Any interest in adding reishi should be discussed while continuing lisinopril as prescribed, not as a reason to stop it.
Evidence boundary: what this article can and cannot tell you
Established: Lisinopril's mechanism, approved indications, and pharmacokinetics are well documented in its FDA label. Reishi is regulated as an unproven dietary supplement under DSHEA, with no FDA safety or efficacy review before marketing.
Plausible but unproven: Reishi triterpenes inhibiting ACE and reishi compounds reducing platelet aggregation are both supported by laboratory and small human studies, but no trial has measured what happens when reishi is combined with lisinopril specifically, in blood pressure response, bleeding events, or kidney outcomes.
Not established: A safe or "interaction-free" reishi dose alongside lisinopril, the actual magnitude of added blood pressure lowering in a typical patient, and any real-world effect on kidney disease outcomes in patients using lisinopril for nephroprotection.
If you cannot get a claim about this combination verified against a primary study, treat it as unconfirmed rather than as settled fact, including specific numbers you may see quoted elsewhere online.
Frequently asked questions
Can I take reishi mushroom while on lisinopril?
Does reishi mushroom interact with lisinopril?
Is reishi mushroom safe with lisinopril?
Can reishi mushroom lower blood pressure too much when combined with lisinopril?
Should I stop lisinopril if I want to take reishi mushroom?
Does reishi mushroom affect kidney function in people taking lisinopril?
How long before surgery should I stop reishi mushroom if I take lisinopril?
What supplements are generally lower-risk with lisinopril?
Will my pharmacist know about the lisinopril-reishi interaction?
This article summarizes pharmacological mechanisms and general findings from laboratory and small human studies of reishi mushroom, along with the FDA-labeled pharmacology of lisinopril. It does not provide individualized medical advice, diagnosis, or dosing instructions. Specific numeric findings attributed to individual studies should be verified against the primary literature before being treated as established fact. This draft is pending qualified clinical review before publication.
