Horny Goat Weed

Epimedium, known as Horny Goat Weed, is an erectile aid and aphrodisiac used in Traditional Chinese Medicine that just so happens to also increase Testosterone in research animals (has not been looked at in humans). May also be a cognitive booster and heart health agent.

This page features 46 unique references to scientific papers.


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Horny Goat Weed is a herb (Epimedium) that is known for being an aphrodisiac and touted as a Testosterone Booster. It derives its layman names from goats and sheep who acted a bit more frisky after consuming Epimedium that grew near their fields.

It is also sometimes referred to by its active ingredient, Icariin. Icariin is known as a prenylated flavonoid compound and has been shown to exert much of the aphrodisiac effects of Horny Goat Weed. It has also been shown in one rat study to increase Testosterone levels at a rather high dose, and moderate dosages are shown to be beneficial for bone health.

Icariin has not been shown to increase testosterone in females, yet two other compounds in Horny Goat Weed (Icaritin, Desmethylicaritin) have actually increased Estrogen in post-menopausal females. The herb acts as an aphrodisiac in both genders, and the gender-specific hormone increasing could be beneficial for both genders.

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Also Known As

Epidemium, Herba Epimdii, Icariin, Yinyanghuo, Fairy Wings, Rowdy Lamb Herb


Do Not Confuse With

Icariin (active ingredient)


Things to Note

  • Icariin is non-stimulatory.
  • Icariin has pro-erectile properties in males and is seen as a libido enhancer in both genders

Is a Form of


Goes Well With


Caution Notice

Examine.com Medical Disclaimer

Testosterone boosting effects in rats have been noted at a dosage of 200mg/kg of a 40% extract (80mg/kg Icariin), and based on body weight conversions from rats to humans[1] this results in an estimated human dose of:

  • 900mg Icariin for a 150lb person
  • 1,200mg Icariin for a 200lb person
  • 1,500mg Icariin for a 250lb person

Studies that use a lower dosage of Icariin (1-10mg/kg) are approximately equal to:

  • 11-110mg Icariin for a 150lb person
  • 15-150mg Icariin for a 200lb person
  • 18-180mg Icariin for a 250lb person

The human study on postmenopausal women and bone health noted that 60mg Icariin daily was active, and might serve as the lowest active dose currently known. It also appears to fall within the above range of lower active dosages which show benefits in rats.


The Human Effect Matrix looks at human studies (excluding animal/petri-dish studies) to tell you what effect Horny Goat Weed has in your body, and how strong these effects are.
GradeLevel of Evidence
ARobust research conducted with repeated double blind clinical trials
BMultiple studies where at least two are double-blind and placebo controlled
CSingle double blind study or multiple cohort studies
DUncontrolled or observational studies only
Level of Evidence
EffectChange
Magnitude of Effect Size
Scientific ConsensusComments
CEstrogen

No significant influence on serum estrogen levels

CBone Mineral Density

Minor

The rate of bone loss over 2 years has been noted to be reduced with icariin supplementation, although not to a remarkable degree


Studies Excluded from Consideration

  • Excluded due to language barrier[2]

Disagree? Join the Horny Goat Weed Discussion

Table of Contents:


Edit1. Composition and Structure

1.1. Composition

Horny Goat Weed is a common name for the plant genus of Epimedium from the family Berberidaceae. When sold as a supplement, they are standardized for their Icariin content, which is seen as the active ingredient.

The genus of Epimedium contain (specific plants in brackets):

  • Icariin, the prenylated diglycosdie flavonoid known as the active ingredient[3]
  • Structurally similar compound to Icariin, the Epimedium compounds A, B and C[3]
  • Quercetin[3]
  • Ikarioside A and B (wanshanense)[3]
  • Anhydroicaritin and Desmethylanhydroicaritin (wanshanense) [3]
  • Sagittatoside B (wanshanense)[3]
  • Diphylloside A and B (wanshanense) [3]

1.2. Structure

Icariin is known as a 'prenylated diglycoside of Kaempferol'. Specifically, the basic structure has a prenyl- group attached to the Kaempferol molecule (depicted below, its the bendy tail heading upwards from the hexagon) and has two sugar molecules attached to it; a glucose molecule at R2 and a rhamnose molecule at R1. The other three popular molecules found in Horny Goat Weed, Epimedin A-C, have the same following backbone but just different sugars at R1 and R2.

Icariin has a molecular weight of 676.67g/mol.[4]

Similar compounds would be the compound Icaritin, which has -OH groups where both sugars would be (R1, R2) and Desmethylicaritin which has -OH groups at all R positions. Both of these compounds are found co-existing in the Horny Goat Weed plant.[5][3]


Edit2. Pharmacology

2.1. Intestinal absorption

Icariin is not a stable compound in the human intestine due to enzymes present. Icariin, along with three other compounds native to the parent plant of Horny Goat Weed (Epimedin A, B and C), as prenylated flavonoids, are rapidly digested into their respective metabolites in the intestinal environment via hydrolysis. These four compounds seem to mostly have their rhamnose sugar cleaved off during this process.[6] Co-ingestion of a lactase phlorizin hydrolase (Lactase) inhibitor increased the absorption of the active ingredients, preserving 40-62% of the original Icariin content.[7] Without said lactase inhibitor, bioavailability of straight Icariin is approximately 12%.[8]

Icariin metabolizes to Baohuoside I, which is the same structure but with one less glucose moiety. The loss of the glucose moiety can more than double transit into the intestinal membrane.[9] The absorption of baohuoside (and other related compounds) is outranked by the fast efflux back into the lumen, an active transport mediated by MRP2 and BCRP (Breast Cancer Resistance Protein); inhibiting MRP2 may increase absorption of baohuoside I.[9] These receptors may possibly be overridden, as increasing the concentration of baohuoside I decreases the efflux efficiency.[9] When in the intestines, Baohuoside I does not appear to be further metabolizes, due to an apparent lack of appropriate intestinal glycosidases (in rats and vitro).[10][9]

Efflux of Icariin from the intestinal wall into the lumen occurs via P-glycoprotein efflux pumps.[9]

Fairly poor absorption in the intestines, but looks promising to combine Icariin with P-glycoprotein inhibitors such as Ecdysteroids or MRP2 inhibitors in regards to Icariin's metabolite, Baohuoside I

2.2. Colonic

Icariin, if not absorbed, can be sent to the colon and transformed via bacteria into Icariside II, a potentially more erectogenic compound than Icariin.[11]

2.3. Systemic

After intravenous administration in rats, Icariin at 10mg/kg bodyweight had a half-/-life of 0.562+/-0.2 hours and an elimination rate constant (Ke) of 1.361+;0.556 per 1/h.[12] Another study using Icariin at the same dose via injection, however, noted a half-life of 170+/-75.1 hours suggesting quite a bit of variability (Ye et al. 1999).[13]

After oral ingestion of 4.5mg/kg Icariin in rats, a Cmax of 3.37+/-1.42mg/L, an AUC of 40.6+/-5.73mg/h/L with a half-life of 10.9+/-1.35 hours is seen. Elimination rate constant is 0.064+/-0.1 per 1/h.[14]

A study on Horny Goat Weed dosed at 1.64g/kg (4.38mg/kg Icariin) orally showed a Cmax of 2.41+/-0.2mcg/mL, an AUC of 23.62+/-1.37mcg/h/mL, a Tmax of 1.55+/-0.53 hours and a half-life of 0.11+/-0.07 hours.[8] This study also compared Horny Goat Weed ingestion against a combination of HGW and two other herbs (Nepal dock root and Ficus hirta yahl; three main ingredients of a chinese medicine) and found that the Cmax of Icariin was higher (3.13+/-0.29μg/ml) as was the AUC (30.84+/-3.68mcg/h/mL) the half-life (0.35+/-0.32 hours) and the Tmax was prolonged (2.06+/-0.15 hours) when coingested.[8] It is not known what compound in the 8 herb mixture bettered the pharmacokinetic profile of Icariin.

Another chinese mixture of herbs featuring Horny Goat Weed (Er-Xian) at 4.8g/kg orally, measured parameters (Cmax, AUC, Half life and Elimination Constant)do not reach the level of 4.5mg/kg Icariin, yet Icariin's absorption appears to have been increased as Horny Goat Weed only comprised 19% of the mixture by weight and the results were quite comparable.[14]

The pharmacokinetic profile of Icariin appears to be beneficially influenced by some herbs or components of herbs, we just don't know which ones specifically.

2.4. Excretion

The major metabolic pathway of Icariin appears to be biliary excretion, or ejecting the Icariin with bile salts into the intestinal lumen to leave in the feces.[15] Coingestion of P-Glycoprotein inhibitors can reduce the elimination of Icariin,[15] possibly by the aforementioned inhibition of intestinal efflux.[9][16]


Edit3. Interactions with Neurology

3.1. Kinetics

Icariin is able to cross the blood-brain barrier[17] and after intravenous injection, Icariin and the three diglycoside compounds (Epimedium A-C) are found in the brain, although mostly Epimedium C. Icariin appeared to be more localized to the sciatic nerve.[18] A study using Icariin liposomes intravenously found about 1.83% of the injected dose to be found in the brain after injection of 20mg/kg Icariin liposomes and neural levels exceeded 0.2mcg/g brain mass.[13]

It can get to the brain, but in a limited amount

3.2. Neuroprotection

Icariin also has the ability to act as a neuroprotectant via inhibiting pro-oxidant and pro-inflammatory markers in response to stress[19][20] and can attenuate cognitive decline induced by D-galactose injections at a dose of 60mg/kg bodyweight (injection).[21] In vitro studies suggest it can also protect neurons from damage induced by Lipopolysaccharide (a pro-inflammatory agent)[22][23] and theoretically against aging as assessed by a senescence accelerated rat model.[24] High dose oral Icariin (75-150mg/kg bodyweight) was associated with improved cognitive biomarkers such as superoxide dismutase and glutathione in these rats.[24]

In one study it was shown to exert protective effects via SIRT1 expression and subsequent PCG-1a expression.[25]


Edit4. Interactions with Bone

4.1. Osteoporosis

In vitro studies suggest that Icariin is more effective than Genistein at preventing osteoporosis as it is more osteogenic (bone-forming).[26] Similar effects have been observed in rats, although not in comparison to Genistein.[27] One study has been conducted in post-menopausal women with a combination of Soy Isoflavones (Genistein at 3mg, Daidzein at 15mg) with Icariin at 60mg a day for 2 years, and bone mineral density loss was greatly attenuated.[28]

4.2. Estrogenicity

Icariin's derivatives, Icaritin and DesmethylIcaritin, have been shown in vitro to possess estrogenic activity in breast cancer cells.[5] This discovery was after it was noted in vivo (rats) to increase the uterine weight of the immature mouse and prolong estrus of the mature mouse.[5] This later led to a study that found Horny Goat Weed in postmenopausal women to increase estrogen levels.[29] As Icariin does not exert pro-estrogenic effects per se but its metabolite (Icaritin) does, the effects of oral Icariin itself are uncertain. Icaritin and Desmethylicaritin are also found in the leaves of Horny Goat Weed themselves.[30][3] Another study in men using 50g of a hot water extract of Epimedium Pubescens did not find any estrogenicity over the study period.[31]

Possible explanations for the above results (estrogenicity in females but not males) may lie in Icariin and related structures possessing both estrogenic and antiestrogenic activities, and the ultimate result being context dependent.[32]

A possible structural explanation for the above effects is hydroxylation at the 4' carbon on the flavonoid backbone, which seems to confer estrogenic effects from flavonoids. The 4' carbon on the Icariin backbone is R3 in the above diagram, as desmethyliscaritin has a hydroxyl group here.[33][34] That being said, the 7' carbon on the A ring may also be implicated in estrogenicity.[5]

Estrogenicity as it applies to Icariin and related compounds is complex, like many bioflavonoid-related compounds. It doesn't seem to be large enough of a concern to negate its potential usage as a Testosterone Booster, however.


Edit5. Interactions with Hormones

5.1. Testosterone

Supplementing with oral Icariin at 1-5mg/kg BW in castrated rats showed significant differences in erectile potency but minimal changes in Testosterone. Specifically, 1mg/kg bodyweight restored testosterone to baseline after penile injury while 5,10mg/kg bodyweight was ineffective.[35] Null results were found in rats with removed testicles, with absolutely no changes in testosterone at 1 and 10mg/kg bodyweight Icariin.[36]

One study using 200mg/kg (of a lower purity, 40%; bioequivalent to 80mg/kg) Icariin over 7 days noted that, in a chemically castrated group (average testosterone level of 0.78+/-0.44ng/mL) was able to increase testosterone to almost triple (10.93+/-2.03ng/mL) the control group (3.01+/-0.41ng/mL).[4] LH and FSH did not differ between groups, and the mechanism of action was hypothesized to be in the testes as previous studies on rats without testes showed absolutely no changes in serum testosterone,[36] although the difference in dosage is also a possibility, as one study was conducted on cavernous crushing noted some difference at 1mg/kg bodyweight, and higher doses were insignificantly suppressive relative to control.[36]

The above oral dose of 80mg/kg pure Icariin, after conversions to humans based on Body Surface Area,[1] appears to be 12.8mg/kg bodyweight Icariin or 1163mg Icariin daily for a 200lb human.

Seems to have the mechanisms to increase testosterone, but no human studies exist on the subject matter.


Edit6. Interactions with Sexuality

6.1. Erections

Icariin is a selective PDE5 (enzyme) inhibitor[37] with an IC50 value between 0.75-1.1mM depending on PDE5 isoform[37] and an EC50 of about 4.62mmol/L in increasing cGMP in the corpus cavernosum of the penis;[38] Icariin has approximately 100-fold greater affinity for PDE5 than other PDE isozymes.[39] This effect can be potentiated by the modification of two hydroxyethyl ether moieties to the compound, which increase this inhibition 80-fold,[40] but this modification is not naturally occurring. At 10mg/kg bodyweight in mice (110mg for a 150lb human) Icariin exerts pro-erectile properties[36] and seems to have more effectiveness following repeated doses.[35][36] It has shown efficacy over 30 days at 5-10mg/kg in an animal model of erectile dysfunction related to blood flow,[41] which correlates to a 55-110mg dose for a 150lb man.

Other compounds in the Epimedium family that have PDE5 inhibitory potential are Icarisid II derived from Epimedium wanshanense (not significantly different in potency than Icariin; approximately half of Viagra)[42]

Secondary to PDE5 inhibition, Icariin appears to be a potent pro-erectile agent. It is clearly outperformed by Viagra

Lower doses (1-5mg/kg) are able to improve neuronal Nitric Oxide Synthase (NOS) expression[36] and inducible (iNOS) expression[35][36] content in addition to PDE5 inhibtion. Effects on iNOS and nNOS do not appear to differ greatly from each other at the dosages of 1mg, 5mg, and 10mg/kg bodyweight,[36] suggesting low doses could also exert benefit but by different means.

Icariin may also promote Nitric Oxide signalling via increasing expression of NOS enzymes, which may work synergistically with the PDE5 inhibition

Icariin has also been linked to increasing neurite growth of major pelvic ganglia in vitro[36] which may be downstream of P13K and MEK/ERK activation.[43]

Beneficial effects on neurons may extend to the pelvis


Edit7. Nutrient-Nutrient Interactions

7.1. Yohimbine

Yohimbine has also been researched into its properties as an erectogenic (boner pill). A study conducted in yohimbine and sildenafil (Viagra), which shares the same PDE5 inhibitory mechanism as Icariin, found that they were synergistic in regards to increasing intercavernous pressure and erections.[44]

Theoretical that Yohimbine and Horny Goat Weed can synergistically be pro-erectile, but this has not directly been demonstrated

7.2. P-Glycoprotein inhibitors

P-Glycoprotein inhibitors such as Ecdysteroids or Capsicum Carotenoids are able to inhibit the efflux protein known as P-Glycoprotein. This efflux protein is responsible for ejecting Icariin into the intestinal lumen after it has been absorbed[9] which is also its main excretory pathway when connected to bile acids to prevent reuptake.[15] Coingestion of Icariin with a P-glycoprotein inhibitor increases the AUC of Icariin, and could plausibly increase the bioactivity of Icariin (although this has not been demonstrated).[15]

P-Glycoprotein inhibitors may increase the bioavailability of Icariin


Edit8. Safety and Toxicity

No designated toxicology studies have been conducted on Icariin, although the highest dosage used in rats currently is 200mg/kg bodyweight Icariin for 7 days which showed no signs of clinical toxicity.

8.1. Case studies

One case study has been published in which a 66-year old man suffered from hypomania (persistently euphoric and irritated mood) and Tachyarrhythmia (abnormal rhythm of the heart and increased Heart Rate) associated with Horny Goat Weed.[45] The side-effects occurred after 2 weeks of supplementation (undisclosed brand and dose), and coingested pharmaceuticals included beta-blockers, statins, aspirin and viagra. Subject had bipolar disorder not otherwise specified prior to the onset of results.[45]

Another case study noted benign rashes develop after ingestion or Horny Goat Weed and Ginkgo biloba; both were taken at the same time, so its not sure which contributed or whether the combination is at fault.[46] Subject was an otherwise healthy 77 year old man taking the compounds orally.

References

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  21. Li F, et al. Icariin isolated from Epimedium brevicornum Maxim attenuates learning and memory deficits induced by d-galactose in rats. Pharmacol Biochem Behav. (2010)
  22. Zeng KW, et al. Icariin attenuates lipopolysaccharide-induced microglial activation and resultant death of neurons by inhibiting TAK1/IKK/NF-kappaB and JNK/p38 MAPK pathways. Int Immunopharmacol. (2010)
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