We at Health System 7 have more than 40 years of clinical experience in the use of Strophantin, BUT here is a logical and clean approach for everyone.
What we Know:
🔹 1. g-Strophanthin = Ouabain
A cardiac glycoside, chemically similar to digoxin, which binds to and modulates the sodium-potassium pump (Na⁺/K⁺-ATPase).
🔹 2. Widely Used in Research
- In cell biology, ouabain is a classic agent for modulating intracellular sodium/calcium dynamics, used to model hypertension, arrhythmias, and cell signaling.
- It plays a role in studying signal transduction, oxidative stress, and even apoptosis in cardiomyocytes and neurons.
- Studies regularly use ouabain in vitro and in animal models to mimic or understand cardiac stress, hypertrophy, and arrhythmogenic behavior.
➡️ So the molecule is clearly “bioactive” and scientifically relevant.
❌ What Mainstream Clinical Medicine Says
- Ouabain is not recommended due to:
- Poor oral bioavailability (especially in North American pharmacological literature).
- Lack of modern double-blind RCTs.
- Preference for better-known glycosides like digoxin.
- It’s sometimes labeled as “toxic”, despite clinical experience suggesting otherwise—especially in low or sublingual doses.
The Hidden Contradiction:
Mainstream cardiology:
“Strophanthin doesn’t work. It’s old, irrelevant, possibly placebo.”
Mainstream research:
“Let’s use ouabain to trigger very specific changes in the heart at the ion-pump level, to model cardiac pathology.”
➡️ This discrepancy is not scientific—it’s political and epistemological.
Why This Contradiction Exists
1. Separation Between Basic Research and Clinical Medicine
- Researchers use ouabain to study mechanisms, not treatments.
- Clinicians demand evidence from RCTs, not cellular responses.
2. Pharma Economics
- Ouabain is non-patentable, low-cost, and plant-derived.
- Zero commercial incentive to fund large-scale trials.
3. Historical Suppression & Bias
- In Germany, Strophanthin had a long clinical history—widely used before being discredited in English-speaking circles (especially post-WWII).
- Its decline coincides with the pharmaceuticalization of cardiology.
To Cardiologist:
I – “If g-strophanthin is so clinically irrelevant, why is it still the molecule of choice in thousands of ion-channel and cardiomyocyte studies? Are we to believe it’s powerful enough to simulate heart dysfunction in the lab but too weak to heal it in a patient?”
II – “I follow what the lab benches around the world use to model cardiac stress. If ouabain is effective enough to model it, it deserves reconsideration in healing it.”