Saw Palmetto

Saw Palmetto is a fatty acid mix from Serenoa Repens that has been touted for its abilities to increase Testosterone (not effective) and suppress prostate growth (effective); may be healthy and good treatment of Benign Prostatic Hyperplasia and abnormal urine flow rates in men.

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Saw Palmetto is a supplement which is derived from the fruit of the plant Serenoa Repens. The supplement (Saw Palmetto) has a caloric value, as it is a concoction of fatty acids.

The fatty acids in question have the ability to block an enzyme that converts testosterone into dihydrotestosterone (DHT), the latter of which is a more androgenic form and can cause hairloss in the genetically susceptible.

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Also Known As

Serenoa Repens

While the active compound(s) are not yet known, it is known that they exist in what is known as the 'liposterolic' fraction of the fruits. If using saw palmetto choose a product that discloses the percentage of the supplement which is this fraction.

Supplementation of saw palmetto tends to be in the range of 160-320 mg, taken once daily, of a product which is 80-90% liposterolic compounds by weight. While it is not confirmed if saw palmetto needs to be taken with food due to the fat soluble nature of this fraction it is advised.

Table of Contents:

Edit1. Sources and Composition

1.1. Origin and Composition

'Saw palmetto' refers to the berries from the dwarf palm tree known as American serenoa repens which have traditionally been used for male fertility and libido and claimed to increase breast size in women.[1]

The ground fruits of saw palmetto, referenced as SRM 3250,[2] have the following composition:

The main mechanism that saw palmetto is known for, inhibition of the enzyme known as 5α-reductase responsible for producing dihydrotestosterone (DHT) from testosterone, is found in the lipid soluble extracts of the fruits[3] with more potency in the saponifiable subfraction.[3]

The bioactives found in saw palmetto tend to be found in the fat-soluble component of the berry

1.2. Formulations and Variants

Supercritical CO2 extracts tend to have a high percentage of unsaturated fatty acids (84%) with lower amounts of fatty acid esters (10%) and less than 2% of other chemical components (phytosterols, aliphatic alcohols, and polypyrenic compounds).[4] It is known under the brand name SABAL SELECT and the reference material number SRM 3251.[2]

This extraction increases the amount of fatty acids as triglycerides relative to the ground fruit (by 6-25 times[2]) and is predominately the unsaturated fatty acids lauric (aka. dodecanoic) and oleic acid with some myristic acid and palmitic acid as the next major components.[4][5][2]

This extraction, in contrast to the raw berries, has certified concentrations of phytosterols (campesterol, β-sitosterol and stigmasterol), carotenoids (46.8μg/g as β-carotene), and vitamers of Vitamin E (gamma and delta tocopherol at 280μg/g and 35.3μg/g).[2]

Supercritical CO2 extracts are one of the basic forms of saw palmetto extracts

There is another extract known as Peroxim® which is an n-hexane extract lipodo/sterolic extract of the fruits.[6]

The extraction known as IDS 89 (Strogen®) is able to inhibit 5α-reductase in vitro with an IC50 of 2,200µg/mL when tested in whole prostate homogenates while having some efficacy at 500µg/mL in both epithelial and stromal prostate cells.[3] This extract was found to be noncompetitively inhibitive.[3]

Edit2. Molecular Targets

2.1. Adrenergic Receptors

Oleic acid and lauric acid obtained from saw palmetto, as well as reference standards of these two fatty acids, appear reduce binding of prazosin to α1-adrenergic receptors.[4] The IC50 for preventing prazosin binding being 41.8-46.3µg/mL and 84-92.1µg/mL for oleic acid and lauric acid respectively[4] and a later study have found that oils from saw palmetto (composition not specified) inhibited binding of both prazosin and tamsulosin to α1-adrenergic receptors.[7]

This reduction of ligand binding is not thought to be competitive as saw palmetto appears to reduce total binding sites of α1-adrenergic receptors and (when tested in isolation) appeared to reduce signalling through the receptor.[7]

When tested acutely in vitro, it seems components of saw palmetto impair the ability of ligands to bind to the α1-adrenergic receptor which reduces the ability of these ligands to increase α1-adrenergic signalling. The net acute effect is a loss of signalling

Oral ingestion of saw palmetto supercritical CO2 extract at 6-60mg/kg in rats over the course of four weeks has been found to increase the Bmax (total binding capacity) of praxosin to α1-adrenergic receptors expressed in the prostate,[8] suggesting a chronic adaptation in opposition to the acute effects.

2.2. Cholinergic Receptors

Oleic acid and lauric acid obtained from saw palmetto, as well as reference standards of these two fatty acids, appear to have affinity for muscarinic receptors with IC50 values (for reducing binding of N-methylscopolamine/NMS in brain tissue) of 70.6-91.3µg/mL and 157-163µg/mL respectively.[4]

Chronic ingestion of 0.6-60mg/kg of a supercritical CO2 extract of saw palmetto has been found to decrease the Bmax (total binding affinity) of NMS in the bladder at all tested doses, with limited dose-dependent effects.[8]

2.3. Ion Channels

Both oleic acid and lauric acid have once been noted to reduce binding of isradipine to 1,4-DHP (dihydropyridine) receptors,[4] which are calcium channel antagonistic receptors.[9] The IC50 of oleic acid in preventing isradipine binding was 33.3-50.6µg/mL whereas the IC50 for lauric acid was 65.7-79.5µg/mL.[4]

2.4. 5α-reductase

A supercritical CO2 extract used in trials (SABAL SELECT[10]) has been tested for its actions on rat 5α-reductase where it was found that two constituent fatty acids, oleic acid and lauric acid, inhibited the activity of this enzyme with IC50 values of 54.3-54.5µg/mL and 66.2-67.6µg/mL respectively.[4] This inhibitory action was of similar potency to the fatty acids obtained from other sources when compared to those obtained via saw palmetto.[4]

One human study attempting to assess 5α-reductase activity in response to 160mg of a lipidosterolic extract found that after one week of supplementation that both serum testosterone and DHT were unaffected compared to baseline.[11]

Edit3. Pharmacology

3.1. Phase I Metabolism

Saw palmetto has been noted to have an inhibitory effect on CYP2C8 activity, thought to be relevant due to possessing an IC50 value of 15.4+/-1.7μg/mL.[12]

Edit4. Cardiovascular Health

4.1. Cardiac Tissue

One study in rats giving 60mg/kg of the supercritical CO2 extract found that four weeks oral supplementation increased the binding of prazosin to its receptor (α1-adrenergic) in cardiac tissue by 30.5%, an effect not noticeable at 6mg/kg or lower while no dose (0.6-60mg/kg) influenced muscarinic receptor Bmax (maximal binding capacities of a ligand).[8]

Edit5. Inflammation and Immunology

5.1. Mechanisms

In keratinocytes given an inflammatory stressor (LPS), a mixture of saw palmetto with L-Carnitine and Alpha-Lipoic Acid at 0.1% of the medium (ratios unspecified) had antiinflammatory actions as assessed by changes in some biomarkers (CCL17, CXCL6, and Leukotriene B4).[13]

An antiinflammatory effect has been noted with Permixon® in prostatic cells (BPH-1, WPMY-1, and PC3) at concentrations of 10-56µg/mL by reducing the expression and content of chemokine receptor (MCP-1/CCL2) and adhesion factors (VCAM-1).[14] This effect has been replicated in another study using the BPH cell line of benign prostatic hyperplasia where several genes involved in inflammation were downregulated leading to the inflammatory effect of a few cytokines (IL-6, IL-15, and IL-17) being suppressed.[15]

Edit6. Interactions with Hormones

6.1. Androgens

A supercritical CO2 extract used in trials (SABAL SELECT[10]) has been tested for its actions on rat 5α-reductase where it was found that two constituent fatty acids, oleic acid and lauric acid, inhibited the activity of this enzyme with IC50 values of 54.3-54.5µg/mL and 66.2-67.6µg/mL respectively[4] (lauric acid has been noted to reach peak efficacy at 200µM[3]). This inhibitory action was of similar potency to the fatty acids obtained from other sources when compared to those obtained via saw palmetto[4] and elsewhere fatty acids tested at even higher concentrations (2mM) found efficacy with myristic acid[3] known to also be present in saw palmetto.[4]

Other studies assessing saw palmetto noted that an n-hexane extract of a saw palmetto extract (Permixon®) in insect cells expressing the DNA for 5α-reductase inhibitied the type I 5α-reductase isomer with an IC50 of 4µg/mL while also inhibiting the type II isomer at 7µg/mL;[16] this potency was hypothesized, but not confirmed, to be due to aliphatic fatty acids which are known to interact with this enzyme[17] and other studies using this extract have found efficacy at a concentration of 10µg/mL[18][6] inhibiting up to 72-76% of both isoforms; an efficacy comparable to finasteride (83%) at its own therapeutic concentration of 5nM.[6]

This inhibitory effect has been shown to reduce DHT synthesis from testosterone in prostatic epithelial cells where most local DHT synthesis takes place and in prostatic fibroblasts associated with the Permixon® extract with an IC50 of less than 10µg/mL (fibroblasts) and of 70µg/mL (epithelial cells).[19]

Saw palmetto, specifically the n-hexane extract, seems to inhibit both isomers of the 5α-reductase enzyme at concentrations which are fairly reasonable assuming oral ingestion of the supplement. These inhibitory effects have been shown to reduce DHT formation in vitro, and while less potent it is seems to be comparable in efficacy to finasteride. It is not certain what molecule(s) mediate this effect, as the potency seen in some extracts is far greater than the dietary fatty acids present in saw palmetto

In regards to the androgen receptor, it has been noted in prostate cells (LNCaP) that while finasteride suppresses the activity of the type II isomer of 5α-reductase alongside other effects (suppression of PSA secretion and downregulation of prostatic androgen receptors) that saw palmetto failed to downregulate the androgen receptor or influence PSA secretion rates.[6]

This extract of saw palmetto failed to influence androgen receptor binding to its promoter in LNCaP cells[6] while another study using fibroblasts from human foreskin noted inhibitory effects on DHT binding to receptors (both cytosolic and nuclear, the latter thought to be the androgen receptor).[20]

Mixed evidence as to the effects of saw palmetto at the level of the androgen receptor

A study using saw palmetto paired with haematococcus pluvialis as a source of Astaxanthin at 800-1,200mg a day (specific dosages and extractions not specified) found an increase in testosterone of 38.04% relative to placebo when used over the course of 14 days that failed to reach statistical significance; a reduction in DHT of unspecified magnitude appeared to reach significance.[21] Other studies assessing saw palmetto on testosterone are similarly confounded with other nutrients[22][23][24][25] with one study using saw palmetto (lipidosterolic extract) in isolation at 160mg over one week failing to influence serum testosterone or DHT concentrations relative to baseline (while finasteride was effective at reducing DHT).[11]

Studies assessing saw palmetto on testosterone are currently highly confounded with other nutrients or have potential conflicts of interest, with a lone study lasting only a week using saw palmetto in isolation; this study failed to find any influence on testosterone or DHT concentrations

Edit7. Peripheral Organ Systems

7.1. Urinary Tract

The mechanisms of saw palmetto that are thought to be relevant for its actions in the lower urinary tract include its suppression of α1-adrenergic signalling, muscarinic receptors, and 1,4-dihydropyridine receptors.[10][8]

A study in rats using saw palmetto extract (supercritical CO2) at 0.6mg/kg, 6mg/kg, or 60mg/kg daily over four weeks has been noted to increase the Bmax values (maximum number of binding sites) for prazosin in the prostate at the two higher doses by 23.6-36.7%, whereas only the higher dose affected the spleen (26.1%) and heart (30.5%).[8] The opposite effect was noted with muscarinic receptors where Bmax decreased in the bladder at the two higher doses (31.8-41.2%) with a decrease in the submaxillary gland at 60mg/kg (17.9%) and slight increase at 0.6mg/kg (13.8%).[8]

7.2. Prostate

6-60mg/kg of the supercritical CO2 extract of saw palmetto, when given to rats orally over four weeks, increases the Bmax of prazosin in the prostate by 23.6-36.7%; 0.6mg/kg was ineffective.[8]

A retrospective study on 320mg Peroxim in men with benign prostatic hyperplasia with PSA less than 10ng/mL found that circulating PSA concentrations appeared to decrease from 5.39ng/mL down to 4.38ng/mL (19%) over the course of the six month study.[26]

Edit8. Interactions with Cancer Metabolism

8.1. Glioma

One study in glioma cells (U87 and U251) using saw palmetto at 1μg/mL found that incubation was able to reduce the protein content of PI3K (known to have a role in promoting invasion of these cell lines[27][28]) and the prosurvival protein Bcl-xL in both cell lines while p53 showed differential effects depending on the cell line.[29]

8.2. Prostate

LNCaP and PC3 cancer cells treated with saw palmetto lipido-sterolic extract (44 or 88μg/mL) found both concentrations were able to decrease cell count at three tested time points (24, 48, and 72 hours)[30] while CD45-/CK5-CK8+ cells excised from prostate adenocarcinoma patients appeared to also have their growth reduced from 44μg/mL of this extract associated with apoptosis and interfered NF-kB activation.[30]

One trial (open label uncontrolled) using a formulaton of saw palmetto with seven other herbs (based off of PC-SPES[31]) found an improvement in PSA levels in the 10 subjects enrolled with hormonal refractory prostate cancer.[32]

Edit9. Interactions with Aesthetics

9.1. Hair

Male pattern baldness, officially known as androgenic alopecia, is an androgen-dependent hair loss heavily dependent on circulating concentrations of dihydrotestosterone (DHT) which is produced by the 5α-reductase enzyme.[33] There are two isomers of this enzyme with 5α-reductase type II being more heavily implicated in hair loss leading to the selective 5α-reductase type II inhibitor, finasteride, being investigated with success in preventing baldness associated with androgens (regardless of biological sex[34][35]). Despite the abundance of type II isoforms in hair follicles, inhibiting both type I and type II may be more effective as dutasteride (inhibitor of both) outperforms finasteride.[36][37] Saw palmetto is thus studied in male pattern baldness due to having inhibitory actions against both isoforms of the enzyme.[4]

The liposterolic extract of saw palmetto (200mg of 85-95% liposterolic content) paired with 50mg β-sitesterol and some B-vitamins (Biotin at 100mcg and niacin at 15mg) in 10 otherwise healthy men with androgenic alopecia over the course of 18-24.7 weeks found that 60% of the subjects had their hair improved (investigator assessed) compared to one subject in placebo although no objective measurements were taken.[38] A later study assessing usage of 320mg saw palmetto over the course of two years in otherwise healthy men with male pattern baldness noted that 38% of subjects treated with saw palmetto reported an increase in hair growth which performed less effectively than 1mg finasteride (66%); saw palmetto appeared to work primarily at the crown of the head whereas finasteride was effective at the crown and frontal regions.[39]

Edit10. Interactions with Medical Conditions

10.1. Benign prostatic hyperplasia (BPH)

Saw palmetto is implicated in benign prostatic hyperplasia (BPH) as it has affinity for both 5α-reductase (in an inhibitory manner[4]) and α1-adrenergic receptors,[4] both of which are molecular targets for BPH (assuming inhibition of α1-adrenergic receptors).[40]

In regards to prostate specific antigen (PSA), a biomarker of prostate cancer, treatment of cells with the Permixon® mixture of saw palmetto has been noted to inhibit 5α-reductase enzymes at 10µg/mL (up to 72-76% with similar potency between isoforms) without influencing secretion of PSA[18][6] even when the culture is stimulated with testosterone or DHT;[18][6] this effect differs from finasteride which, at its therapeutic concentration, suppresses DHT-induced increases of PSA.[6] This discrepancy is thought to be due to how PSA is regulated by androgens[41] and how saw palmetto does not interfere with androgen signalling in the prostate cell.[6]

It has successfully been used in a number of trials to treat BPH.[42][1] It also increases urine flow and decreases nocturia.[43][20]

In men with urinary symptoms caused by BPH (no prostatic cancer and PSA less than 10ng/mL) given 320mg saw palmetto (Permixon®) for six months, a restrospective analysis[26] found an improvement in urinary symptoms when saw palmetto was used alone as well as when used alongside an alpha-blocker, although saw palmetto alone showed better responses on mean void volume and intermittence in urinary flow while combination therapy had a more rapid improvement in maximum flow.[26]

Another study using saw palmetto alongside tamsulosin (α1-adrenergic receptor antagonist) over 6-12 months in men with BPH found combination therapy more effective than tamsulosin alone[44] while combination therapy with Selenium (50mcg) and lycopene (5mg) alongside the supercritical extract of saw palmetto (320mg) appeared to perform equally to 400mcg tamsulosin after a year in improving urinary and erectile symptoms;[45] adding tamsulosin to this combination therapy further increased benefits.[45]

Saw palmetto appears to be effective in reducing prostate size and the symptoms assosiated with benign prostatic hyperplasia. While effective on its own it appears to be more effective when paired with the reference drug tamsulosin (Flomax), an alpha-blocker

Edit11. Safety and Toxicology

11.1. General

Saw palmetto contains tannic acids, which bind to iron and reduce bioavailability.[46] Minor sexual dysfunction has also been reported, possibly through pro-estrogenic effects. Beyond that, side-effects are not discernable from placebo.[47]

Two case-reports have repoted pancreatitis from Saw Palmetto.[48][49] In one incidence liver damage was reported.[50]

There is one case study of a young girl (11 years of age) given saw palmetto for treatment of telogen effluvium who experienced hot flashes that ceased when the supplement was no longer taken; it was seen as probable that this side-effect was due to the supplement used.[51]


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