Icariin is definitely on my top ten list of supplements that I take. I have bought many varieties of this to find the best one.
- What is Icariin?
- My Experience With Horny Goat Weed
- The Health Benefits of Icariin
- 1) Icariin Improves Erectile Dysfunction and Increases, Sex Drive
- 2) Icariin Reduces Dementia and Enhances Cognitive Function
- 3) Icariin is Neuroprotective and Promotes Neurogenesis
- 4) Icariin Lowers Stress and Acts as an Antidepressant
- 5) Icariin Stimulates Bone Growth and Repair
- 6) Icariin Promotes Heart Health
- 7) Icariin Stimulates Blood Vessel Formation
- 8) Icariin Exhibits Anti-Cancer Effects
- 9) Icariin is Anti-inflammatory and Immunoprotective
- 10) Icariin Combats Fatigue
- 11) Icariin Protects DNA and Delays Aging
- 12) Icariin Eliminates Acne
- 13) Icariin Reduces Premature Ejaculation
- 14) Icariin May Fight Jetlag
- Buy Icariin
What is Icariin?
Icariin is an active flavonoid component of the Epimedium plant species commonly known as Horny Goat Weed. Extracts from these plants have long been used in Traditional Chinese Medicine for enhancing libido and male sexual function [R].
Due to its widespread distribution and movement in the body including the brain, icariin exhibits far-ranging biological activities such as antioxidant and anti-inflammatory effects, neuroprotection, anti-tumor activity, as well as promoting overall health in the heart, bones, and a variety of other organs [R, R].
My Experience With Horny Goat Weed
Icariin is one of my favorite supplements and I take it for the PDE5 inhibiting properties. It reliably increases blood flow throughout the body and is great for increasing tolerance to carbs.
It improves cognitive performance for me and is an anti-inflammatory.
The Health Benefits of Icariin
1) Icariin Improves Erectile Dysfunction and Increases, Sex Drive
Icariin inhibits phosphodiesterase type 5 (PDE5), an enzyme that breaks down cyclic guanosine monophosphate (cGMP) [R].
PDE5 inhibition stimulates the NO/cGMP pathway and improves reproductive function in animal models.
This is due to increased cGMP and nitric oxide levels which lead to smooth muscle relaxation, widening of blood vessels and increased blood flow to the penis, facilitating erection [R].
Chronic treatment of icariin was shown to suppress penile smooth muscle cell death in multiple animal studies [R].
Additionally, icariin was shown to significantly increase pelvic nerve length when cultured with nerve fragments, indicating that it may enhance penile rehabilitation in humans [R].
Research indicates that high levels of testosterone are correlated with increased sexual desire in aging males and females, suggesting that icariin may act as a natural aphrodisiac in individuals with diminished libido [R, R].
2) Icariin Reduces Dementia and Enhances Cognitive Function
Beta-amyloid peptides (Aβ) are proteins that cause plaque formation and cell damage in Alzheimer’s disease [R].
Icariin was shown to markedly decrease β-amyloid-induced toxicity in rat adrenal embryonic cells (by inhibiting tau protein hyperphosphorylation, a key biological marker of Alzheimer’s disease )[R].
Icariin improved dementia in aluminum-intoxicated rats by reducing oxidative damage and β-amyloid deposits in the hippocampus. This is in part due to increased superoxide dismutase (SOD), an enzyme that reduces oxidative damage [R].
In rat models with induced brain inflammation, short-term icariin treatment was found to improve spatial learning and memory abilities. This effect is thought to be due to the lowering of pro-inflammatory cytokines (TNF-alpha and IL-B as well as COX-2, an enzyme responsible for fever, inflammation, and pain) [R].
Icariin can also suppress neuroinflammation by inhibiting the activation of microglia, macrophage-like cells in the in the brain nervous system that play a pivotal role in initiating the neuroinflammatory response [R].
In rats with stroke, Icariin protects against cognitive deficits by increasing acetylcholine metabolism in the hippocampus, a key neurotransmitter involved in learning and memory [R].
In addition, Icariin can enhance cognitive function via stimulation of the NO/cGMP pathway. Elevated levels of cGMP and nitric oxide (via icariin inhibition of PDE5) improves brain blood flow, synaptic plasticity, neurovascular dysfunction, and β-amyloid elimination from the hippocampus (memory center) and cortex [R, R, R].
Due to its potent anti-inflammatory, antioxidative and anti-amyloid activity in the brain, icariin may serve as a promising therapeutic option for cognitive disorders such as Alzheimer’s disease and other forms of dementia [R, R].
3) Icariin is Neuroprotective and Promotes Neurogenesis
Icariin was found to suppress neurotoxicity by maintaining intracellular calcium homeostasis in rat hippocampal neurons [R].
Icariin was also found to inhibit β-amyloid-induced neurotoxicity (by increasing CART (cocaine and amphetamine-regulated transcript) in cortical neuron cells). Found widely in the brain, CART functions in preventing energy loss and preserving mitochondrial function [R, R].
Mitochondria are known to play a key role in increasing energy production for neuronal survival during a stroke [R].
4) Icariin Lowers Stress and Acts as an Antidepressant
5) Icariin Stimulates Bone Growth and Repair
Icariin increased hip and lower spine bone density in postmenopausal women by inhibiting bone destruction (bone break down) marker deoxypyridinoline and maintaining osteocalcin, a bone formation marker [R].
Icariin stimulated the generation of cultured human bone (osteoblast) cells by increasing bone morphogenetic protein (BMP-2) production, a key protein involved in bone and cartilage formation [R].
Icariin was also found to enhance production of primary osteoblasts (by increasing bone formation markers ALP, osteocalcin, COL-1 and OPG and decreasing RANKL, a protein involved in osteoclast formation) [R].
Icariin inhibits the formation and bone-resorbing action of osteoclasts by increasing OPG/RANKL ratios in bone cells [R].
Osteoprotegerin (OPG) is known to inhibit RANKL activity which plays a role in osteoclast formation and bone destruction [R].
In addition, Icariin can suppress osteoclast formation by decreasing superoxides, reactive oxygen species that are required for osteoclast survival and activity [R].
Icariin can inhibit cartilage and bone degradation in arthritic mice (by inhibiting cathepsin K, an enzyme that breaks down cartilage and bone) [R].
6) Icariin Promotes Heart Health
Icariin improved heart function and reduced tissue death in rats with an acute heart attack (myocardial infarction) by activating the PI3K-Akt pathway, which plays a critical role in cell survival [R].
Icariin prevented heart muscle cell death during reoxygenation following an acute heart attack by increasing Bc1-2 (an anti-cell death factor) and decreasing Bax ( a pro-cell death factor). These effects are in part due to activation of the PI3K/Akt pathway, which increases Bc1-2 in heart muscle cells [R].
In another study, icariin inhibited heart muscle cell death by suppressing matrix metalloproteinase (MMP) activity in rats with heart failure. MMPs are enzymes involved in heart remodeling after injury [R].
Icariin improved heart function by reducing oxidative damage in the mitochondria of diabetic rat hearts [R]. Icariin improves blood flow to the heart by widening heart vessels via inhibition of Ca2+ channels, which helps reduce the risk of heart stroke and tissue death [R].
Hardening of arteries (atherosclerosis) is a common cause of stroke and heart attack. Icariin can reduce the risk of hardening of the arteries by lowering cholesterol levels in the blood [R].
Multiple studies show that icariin can promote new heart muscle cell formation by inducing cell death, increasing reactive oxygen species generation, and activating the P38 MAPK and NF-kappaB pathways in mouse embryonic stem cells, indicating that icariin may have a potential application in heart tissue engineering [R, R, R].
7) Icariin Stimulates Blood Vessel Formation
New blood vessel formation improves stroke-related tissue injuries and wound healing by increasing oxygen and nutrients to the affected area [R].
Icariin can stimulate blood vessel growth (by activating the MEK/ERK and PI3K/Akt/eNOS pathways) in human blood vessel cells. These pathways are associated with the generation, movement and structural shaping of blood vessel cells during blood vessel growth [R].
8) Icariin Exhibits Anti-Cancer Effects
In human stomach cancer cells, icariin was able to suppress tumor cell movement and invasion (by inhibiting the Rac1-dependent VASP pathway, which is involved in cellular motility) [R].
Another study showed that Icariin was able to suppress the attachment and movement of stomach cancer cells (by inactivation of protein kinase A (PKA), an enzyme known to promote cell production and survival) [R].
Icariin inhibited human gallbladder cancer cell production and induced cell death by suppressing NF-κB activity. The NF-kB pathway plays a key role in cancer cell survival by increasing anti-cell death factors survivin and Bc1 [R].
Icariin triggered human liver cancer cell death (by activating the ROS/JNK-dependent mitochondrial pathway which plays a key role in initiating cell death) [R].
9) Icariin is Anti-inflammatory and Immunoprotective
Icariin was able to reduce intestinal inflammation and improve disease symptoms in mice with irritable bowel syndrome (by inhibition of STAT1 and STAT3 phosphorylation which is responsible for activating and increasing Th1 and Th17 T-cells and pro-inflammatory cytokines) [R].
Icariin improved airway inflammation in asthmatic rats (by adjusting the Th1/Th2 cytokine imbalance in the lung tissue). Icariin also inhibited the activation of the NF-κB pathway in lung tissue, which is involved in inflammation [R].
Another study showed that icariin decreased lung inflammation (by inhibiting pro-inflammatory markers TNF-α, IL-6, COX-2 and iNOS in the lung via activation of the PI3K/Akt pathway and inhibition of NF-κB) [R].
Multiple sclerosis (MS) is an autoimmune disease in which T-cells attack them in the brain nervous system (CNS), causing axon damage and disability. Icariin was found to improve disease symptoms in mice with induced MS (by suppressing the production of T cells and Th1 and Th17 cells) [R].
10) Icariin Combats Fatigue
A study showed that icariin was able to reduce physical fatigue and increase endurance in mice during a weight loaded swimming test.
It was found that icariin increased blood glucose, hemoglobin and glycogen levels, factors which are known to improve speed, endurance, and exercise ability.
Icariin also decreased blood lactic acid (BLA) and blood urea nitrogen (BUN) levels indicating that icariin might reduce protein breakdown for energy and delay the buildup of lactic acid, both factors known to prevent fatigue [R].
11) Icariin Protects DNA and Delays Aging
Icariin delays aging in mice by increasing SIRT6. SIRT6 is an enzyme that promotes DNA repair and energy metabolism and inhibits the NF-kB pathway, which is involved in cellular aging, death, and inflammation [R].
12) Icariin Eliminates Acne
A study showed that Icariin was able to inhibit Propionibacterium acnes biofilm formation in part by killing the bacterial cells. Propionibacterium acnes is a bacterium linked to the skin condition of acne, indicating that icariin may be used as a natural anti-acne drug [R].
13) Icariin Reduces Premature Ejaculation
In a double-blind, randomized control trial, PDE5 inhibitors can prolong the time that it takes to ejaculate [R].
14) Icariin May Fight Jetlag
PDE5 inhibitors enhance circadian responses to light and decrease the amount of time necessary for re-entrainment in mice [R].
This helps when you fly eastward. Imagine you fly east 3 time zones from California to New York.
Imagine you fly east 3 time zones from California to New York. If you normally go to sleep at 11 PM California time, then you will be going to sleep at 2 AM New York time.
If you want to go to sleep earlier, you need to wake up earlier and ‘advance’ your cycle so that you go to sleep earlier and you wake up earlier.
Icariin and PDE5 inhibitors help you advance your rhythm. See my interview with the author of this study.
- Icariin Capsules
- Inhibited PDE5 [R].
- Increased cGMP [R].
- Increased neuronal nitric oxide synthase (nNOS), inducible nitric oxide synthase (iNOS), endothelial nitric oxide synthase (eNOS) and nitric oxide [R].
- Increased free form testosterone in the blood [R].
- Activated PI3K – Akt pathway [R].
- Inhibited tau protein hyperphosphorylation [R].
- Increased SOD activity and decreased malondialdehyde (MDA) and β-amyloid in the hippocampus (memory center) [R].
- Decreased amyloid precursor protein (APP), beta-secretase 1 (BACE1), and increased insulin-degrading enzyme (IDE) and a disintegrin and metalloproteinase domain 10 (ADAM10) in the hippocampus (memory center) [R].
- Decreased TNF, IL-1b and COX-2 in the hippocampus (memory center) [R].
- Inhibited NF-kB and JNK/p38 MAPK pathways [R].
- Elevated BDNF and TrkB in the hippocampus (memory center) [R].
- Increased acetylcholine, acetylcholinesterase and choline acetyltransferase in the hippocampus (memory center) [R].
- Controlled intracellular calcium levels in hippocampal cells [R].
- Increased CART [R].
- Increased SIRT1 and PGC-1a, catalase and Prx1 [R, R].
- Decreased CRF, cortisol, IL-6 and TNF-a [R].
- Increased ALP, osteocalcin, COL-1, and OPG, decreased RANKL [R].
- Increased bone morphogenetic protein (BMP) and Runx2 [R].
- Decreased deoxypyridinoline [R].
- Activated Wnt/β-catenin pathway [R].
- Increased core binding factor alpha1 (Cbfa1) [R].
- Decreased superoxide [R].
- Inhibited MMP activity [R].
- Decreased creatine kinase (CK), ischemia-modified albumin (IMA), and lactate dehydrogenase (LDH) [R].
- Increased Bcl-2 and decreased Bax in heart muscle cells [R].
- Activated P38 MAPK and NF-kB pathways [R, R].
- Reduced levels of total cholesterol and LDL Cholesterol in the blood [R].
- Activated MEK/ERK and PI3K – Akt – eNOS pathways [R].
- Inhibited Rac1-dependent VASP pathway [R].
- Inhibition of STAT1 and STAT3 phosphorylation [R].
- Increased blood glucose, hemoglobin and glycogen levels, decreased blood lactic acid (BLA) and blood urea nitrogen (BUN) levels [R].
- Inhibited insulin/ IGF-1 (IIS) pathway, increased DAF-16 targets [R].
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