Bushman's hat

Last Updated: September 28, 2022

Hoodia gordonii is a small shrub (falsely said to be a cactus) that is claimed to suppress appetite. It seems the main bioactive (P57) cannot easily reach the brain to do this, and aside from failures of hoodia to suppress the appetite it may also be mildly toxic and imprudent to supplement.

Bushman's hat is most often used for.

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Sources and Composition



Hoodia gordonii (of the family Apocynaceae and formerly the Trichocaulon or Stapelia genera) is a small desert 'cactus' (actually part of the milkweed family[1]) that has traditional usage as a food product and thrist quencher in Africa[1][2] and has similar traditional usage and effects in the body as the related species hoodia pilifera[3] and similar bioactives to the forementioned and the officinale, currorii, and lugardii species.[4][5] The entire genera of Hoodia is sometimes known as veldkos (food from the veld) and due to its usage as a supplement hoodia gordonii may also be called Slimming Cactus.[6] When it blooms, the flowers give off the scent of raw meat which has led to the name of the flower sbeing carrion flowers.[1]

The hoodia plant is widely distributed in arid areas of South Africa and Namibia, and it is used as a food product due to its multi-stemmed succulent with thick, erect, cylindrical, fleshy and fairly hard, glabrous, grey-green to grey-brown stems; it is spiny, but not actually a cactus (cactuses are things in the Cactaceae family).[2] Hoodia gordonii appears to be a protected plant.[7]

The main bioactive appears to be able to be synthesized[8][7] although this may be subject to patent,[4] and industry specifications for hoodia gordonii growers suggest it should be at 0.3% of the plant's dry weight.[9]

Hoodia gordonii is a desert plant that resembles a cactus although it is not phylogenetically related to such. It is a vegetable more than anything, and appears to be traditionally used to suppress the desire to eat or drink water (similar to other famine foods such as Caralluma fimbriata)



Hoodia gordonii has some atypical methylated sugars in the glycosides including D-Thevetose (The), D-Cymarose (Cym), D-Oleandrose (Ole), D-digitoxose (Dig), and 3-O-methyl-6-deoxy-D-allose (MDA) as well as glucose;[2] these abbreviations are used below to illustrate the side chain, with the first one mentioned being the one connected to the basic steroid structure (either the molecule in the first bullet, or Calogenin).

The steroid glycosides contained in Hoodia include:

  • Hoodigogenin A and Gordonoside A, both are the same molecule (12β-tygloyl-14β-hydroxy-pregn-5-en-20-one) and form the base of all Gordonosides and most Hoodigosides (those not based on Calogenin)[10][11][12] and is sometimes also called Tigloyloxydigipurpurgenin II[3]
  • The glycoside based off of the aforementioned known as P57, P57A53, or Glycoside number 12 (Hg.12) with the glycoside chain of Cym-Cym-The;[3][2] known to have appetite suppressing properties, said to be at 0.3% (Industry Spec[9]) and measured from undetectable to 0.43% (4% of samples had over 0.3%[9] and elsewhere the dry weight of the plant itself was noted to be 0.24%[13])
  • Other Hoodigosides are based of the Hoodigogenin A structure and vary by their glycosides including Hoodigoside A (The-Cym), Hoodigoside B (The-The-Cym), Hoodigoside C (The-Cym-Cym-Cym), Hoodigoside D (The-The-Cym-Cym), Hoodigoside E (Glu-The-Cym-Cym), Hoodigoside F (Glu-Ole-The-Cym-Cym), Hoodigoside G (Glu-Cym-The-Cym-Cym), Hoodigoside H (Glu-Cym-Cym-Cym-Cym), Hoodigoside I (Glu-Ole-Cym-Cym-Cym), Hoodigoside J (Glu-Ole-Dig-Cym-Cym), Hoodigoside K (Glu-Glu-Cym)[11][2] Hoodigoside W (Ole-The-Cym-Cym), and Hoodigoside X (The-Cym-Cym)[14]
  • Gordonosides, which are also based off the Hoodigogenin A steroid. These include Gordonoside B (The-Ole-Cym-Cym), Gordonoside C (side chain unidentified), Gordonoside D (Dig-Ole-Cym-Cym), Gordonoside E (Ole-Ole-Cym-Cym), Gordonoside F (Ole-Cym-Cym-Cym), Gordonoside G (four Cyms), Gordonoside H (side chain unidentified), Gordonoside I (Dig-Ole-Ole-Cym-Cym), and Gordonoside L (Ole and four Cyms)[10][2]
  • Hoodigosides that are based off of Calogenin (pregn-5-ene-3β,14β,20β-triol) rather than Hoodigogenin A, but most have glucosides on the opposite side of the Calogenin chain. The most basic is Hoodigoside N (The-Ole; no secondary chain) and adding a diglucoside to the second site produces Hoodigoside M (The-Ole; Glu-Glu). All other structures have either an initial side chain of plus a tigloyl (Tig) group on the end and these include Hoodigoside V (The-Ole-Tig;Glu), Hoodigoside O (The-Ole-Tig;Glu-Glu), Hoodigoside L (The-Ole-Tig;Glu-Glu-Glu), Hoodigoside P (Ole-Cym-Tig;Glu-Glu-Glu), Hoodigoside R (Ole-Ole-Cym-Tig;Glu-Glu-Glu), Hoodigoside Q (Cym-Cym-The-Tig;Glu-Glu-Glu), Hoodignoside T (Cym-Cym-Cym-Ole-Tig;Glu-Glu), Hoodigoside S (Cym-Cym-Cym-Ole-Tig;Glu-Glu-Glu), Hoodigoside U (Cym-Cym-Cym-Cym-Tig;Glu-Glu-Glu)[15] Hoodigoside Y (The-Ole;Glu), and Hoodigoside Z (The-Cym-Cym;Glu-Tig)[14]
  • Unnamed Hoodigogenin A glycosides with the side chains Cym-The-Cym-Cym (18mg/kg),[3] Ole-Mda-Cym-Cym, Cym-Mda-Cym-Cym, Ole-Dig-Cym-Cym, and Ole-Cym-Cym-Cym[2]
  • Hoodistanalosides based on an Orostanol backbone (3,5,14,20-tetrahydroxy-5{6→7}abeo-pregnan-7-al[16]) of which the glycosides that exist are Hoodistanaloside A and Hoodistanaloside B, both with a similar glycoside chain (Tig-The-Ole;Glu) but differ by hydroxyls on the backbone[14]

Total steroids in the raw plant have been noted to reach 2.1% dry weight with P57 being about 11% of total steroids,[13] although supplements are usually standardized to much higher levels (33-80% steroidal glycosides).

Note: The above glycoside chains are named working outwards from the steroid, hence why P57 is listed as Cym-Cym-The while the picture below depicts The-Cym-Cym (as the chain extends out to the left)


The steroidal glycosides in Hoodia are either based off of Hoodigogenin A (synonymous with Gordonoside A) or they are based off of Calogenin. They only differ by what sugars (atypical methylated sugars) are included in their side chains and in what order they exist, having these sugars makes then 'glycosides' (without the sugars, they are 'aglycones' meaning 'without sugar')

Other constituents of Hoodia gordonii that do not fall in the steroidal glycoside category are:

  • Cholesterol and β-sitosterol (collectively 0.5% of an extract of 33% steroidal glycoside[17] or inclusive of stigmasterol they are at 0.39% of an 80% steroidal glycoside extract[18])
  • Fatty acids (collectively; palmitic, linolenic, oleic, stearic, arachidonic, behenic, henatriacontylic, lacceroic, psyllic, and geddic acids) at 20% of a 33% steroidal glycoside extract[17] or 3.12% of an 80% steroidal glycoside extract[18]
  • Alkanes (C31, C33) at 2.9% of a 33% steroidal glycoside extract[17]
  • Vitamin E (as alpha-tocopherol)[18]

The bioactives in Hoodia that do not belong to the steroidal glycosides are not well studied, and at this moment in time there does not appear to be anything remarkable about them; some of the saturated fatty acids get quite long though (34 carbons) which is mildly interesting


Physicochemical Properties

P57 is confirmed to activate the bitter receptor (TAS2R14).[19] Ligands of the bitter taste receptors tend to induce secretion of either GLP-1[20] or CCK,[21] and P57 has been noted to induce CCK as well.[19]

Hoodia is noted to activate the bitter taste receptors, which may have a gustatory influence on appetite regulation

Storage of hoodia gordonii extract at ambient temperature (21-24°C) less than 60% humidity for 19 months does not degrade the bioactive steroidal glycosides.[18]

Should be preserved at room temperature and normal humidity for little over a year and a half





In vitro, intestinal absorption of P57 appears to be less than 2% when alongside Caco-2 cells at 100-200μM.[22] It appears to be taken up via P-glycoprotein and MRP transporters[23] and is subject to intestinal efflux;[24] the aglycone (Hoodigogenin A) is passively diffused.[25]

Bioavailability of steroidal glycosides (measured in P57 equivalents) in the pig intestine following ingestion of 7.9mg/kg of a hoodia gordonii extract (79.3% steroidal glycosides) appears to be in the range of 41.9-54.2% with a mean value of 46%.[26] Coingestion with a meal slowed the Tmax of the steroidal glycosides,[26] and a similar bioavailability has been noted in mice (47.5%).[27]

While the steroidal glycosides are not perfectly absorbed (and subject to intestinal efflux), there does appear to be absorption of the steroidal glycosides (as glycosides) which has reached 50% in pigs

Buccal absorption has been noted in vitro with P57, suggesting that oral absorption may be possible.[24]

A possible oral route of absorption appears to be possible with the main bioactive



In rats, 15mg/kg of isolated P57 has reached Cmax concentrations in the range of 0.1-3μM.[26]

In pigs, oral ingestion of 7.9mg/kg of steroidal glycosides (79.3% purity) has resulted in a Cmax of 73–115ng/mL P57 at a Tmax of 93-120 minutes.[26]

Oral ingestion of 1,110mg hoodia gordonii to females results noted a Cmax of steroidal glycosides of 92+/-47ng/mL after a Tmax of 45-50 minutes and a half-life of 50 minutes, conferring an AUC of 366-439ng/mL/h (with a trend for increased AUC after 15 days relative to a single dose).[28] The steroidal glycosides were measured in P57 equivalents.[28]

In humans, the standard recommended dose of hoodia appears to increase plamsa concentrations of steroidal glycosides to the low nanomolar range (although within the concentration range where it may act on the hypothalamus, assuming it reaches the brain in similar quantities)



Oral ingestion of a hoodia gardonii extract (conferring 25mg/kg P57) to mice has been noted to increase tissue concentrations of P57 in the liver, intestines, and kidneys to a low level and there was no detectable increase in brain tissue.[27] The tissue:plasma ratios were calculated for the liver (0.02), intestines (0.11), and kidney (0.06) although none could be calculated for the brain.

P57 does not appear to be well distributed to tissues well following oral ingestion, and none has been detected in the brain (which is required for its supposed appetite suppressing effects, thought to be due to direct stimulation of the hypothalamus)



P57 appears to be metabolically stable in the presence of liver cells[23] but appears to be unstable in the stomach (45% degratation in 60 minutes) and moderately unstable in intestinal fluid (8% degradation in 120 minutes);[25] Hoodigogenin A tends to be formed when P57 is degraded, and it itself is stable under all conditions.[25]

P57 appears to be stable in liver cells but instable in the stomach, while the aglycone (Hoodigogenin A) appears to be stable in the stomach and intestines


Phase I Enzyme Interactions

P57 has been noted to inhibit CYP3A4 with an IC50 of 45μM while it has no inhibitory effect on CYP1A2, CYP2C9, and CYP2D6.[23] The aglycone, Hoodigogenin A, appears to be significantly more potent at inhibiting CYP3A4 with an IC50 of 3μM.[25]

Possible CYP3A4 inhibition may occur with Hoodigogenin A, and it is plausible that this may occur to a limited degree following oral ingestion of high doses of hoodia


Cardiovascular Health


Cardiac Tissue

Supplementation of 1,110mg of hoodia gordonii (79.5% steroidal glycosides) was noted to increase pulse and heart rate relative to placebo when taken over 15 days alongside a controlled diet.[28]

An increase in pulse and heart rate has been noted with hoodia ingestion in otherwise healthy persons, which is thought to be associated with possible toxic effects (not clear at the moment)


Blood Pressure

Supplementation of 1,110mg of hoodia gordonii (79.5% steroidal glycosides) was noted to increase blood pressure relative to placebo when taken over 15 days alongside a controlled diet;[28] the magnitude of increase in these normotensive persons ranging from 5.9-15.9 (systolic) and 4.6-11.5mmHg (diastolic) on an individual basis.[28]

An increase in blood pressure has been noted with hoodia ingestion in otherwise healthy persons, but the magnitude of blood pressure increase is actually quite large and a concern




Appetite and Food Intake

Mechanistically, injections of isolated P57 into the rat hypothalamus have increased intracellular ATP concentrations which were associated with reductions in food intake (40-60%);[29] Hoodigogenin A appears to be inactive, and the increase in ATP is thought to underlie appetite reduction seen with P57.[29]

It is thought that P57 increases ATP concentration in the hypothalamus, which is a mechanism known to reduce appetite; this has been seen with intracerebral injections of P57 to rats

6.25–50mg/kg of P57e from hoodia gordonii over one week was able to reduce food intake with more potency on day one (49-55% reduction) than after seven days (12-45%) with irregular dose dependency;[3] 30mg/kg of this bioactive appeared to be more potent than 15mg/kg fenfluramine.[3]

One study mentions preclinical (unpublished) data from a trial where 1,800mg of a Hoodia gordonii extract (79.5% steroidal glycosides) taken twice daily for 15 days reduced appetite by 30% associated with a serum concentration of 100ng/mL total steroidal glycosides; when the authors themselves a trial in mildly overweight women given 1,110mg hoodia gordonii (79.3% steroidal glycosides, said to hit 100ng/mL) twice daily (hour before meals) in a clinical setting for 15 days failed to find significantly more appetite suppression with Hoodia (24%) than placebo (18%).[28]

Although one animal study (using oral supplementation rather than intracerebral injections) has noted positive effects, the human study has failed to outperform placebo


Obesity and Fat Mass


Weight and Body Fat

In rats subject to 6.25-50mg/kg of the isolated pregnane triglycoside, body weight appears to be attenuated which is thought to be secondary to reduced food intake.[3]

In women given 1,110mg of the hoodia gordonii extract (79.5% steroidal glycosides) over 15 days, the lack of appetite suppression was met with a failure to decrease weight or body fat more than placebo.[28] There appear to be some small trials (not found online, but mentioned in this report[30]) which showed promise but were funded by PhytoPharm, a producer of Hoodia gordonii supplements.

Secondary to the influences on appetite (best evidence says that this does not occur to a large degree in humans) there are modifications in weight; no human evidence supports a weight loss effect of hoodia


Interactions with Hormones



Pregnane glycosides from hoodia gordonii (25% purity) at 4-100µg/mL (IC50 in the range of 75-90µg/mL) is able to inhibit forskolin-induced secretion of corticosterone, with 100µg/mL needed to suppress secretion of cortisol or androstenedione.[31] It was noted to reduce HSD3B2 mRNA levels (no include on P450 enzymes nor StAR)

Inhibition of steroidogenesis from pregnane type steroids appears to be reduced 8-fold when the tigloyl group is added to C12, while glycosides on C3 (mostly D-cyamarose) seem to increase it.[31]

There may be an inhibitory effect on steroid synthesis in isolated adrenal cells with a high concentration of steroidal glycosides from Hoodia gordonii (may not be relevant following oral ingestion due to the high concentration)


Safety and Toxicology



In mice, while 400mg/kg appears to be a well tolerated dose of hoodia gordonii (33% steroidal glycosides and 4.7% P57) it appears that 500-1,000mg/kg was associated with some mortality (none at the 750mg/kg dose oddly).[17]

There is apparent toxicity in mice at higher doses, which (if converted to human equivalents and standardized for the steroidal glycoside content) are within the ranges used for nutritional supplementation

Supplementation of 1,110mg of hoodia gordonii extract (79.5% steroidal glycosides) in women over 15 days has resulted in increased serum ALP (a liver enzyme) in the range of 4.7 to 8.8 U/L and was also able to increase total and indirect bilirubin by 0.20mg/dL to 0.58mg/dL and 0.18mg/dL to 0.49mg/dL (respectively).[28] The authors noted that they were unable to find a causative agent (either the steroidal glycosides of something in the unidentified 9.4% of the supplement), and due to no hemolysis nor inductions of other liver enzymes the clinical significance of these findings were uncertain.[28]

Limited human evidence has found changes in serum biomarkers that indicate toxicity, although at this moment the clinical relevance is unknown


Genotoxicity and Teratogenicity

Supplementation of 100-400mg/kg hoodia gordonii extract to mice (33% steroidal glycosides and 4.7% P57 overall) failed to exert genotoxic effects (higher doses not tested due to lethality with 1,000mg/kg).[17]

One mouse study (duplicated in Medline[32][33]) used 15-50mg/kg of hoodia gordonii extract (70% steroidal glycosides and 10% P57) during pregnancy noted reductions in maternal food intake associated with reductions in fetal size, with no noticeable effect from 5mg/kg. No dose of hoodia gordonii was associated with deformations to the fetus, nor was pregnancy state altered.

No apparent genotoxicity (damange to the DNA) nor teratogenicity (damage to the fetus), although this may be because higher doses were not tested due to killing mice

1.^Lee RA, Balick MJIndigenous use of Hoodia gordonii and appetite suppressionExplore (NY).(2007 Jul-Aug)
2.^van Heerden FRHoodia gordonii: a natural appetite suppressantJ Ethnopharmacol.(2008 Oct 28)
3.^van Heerden FR, Marthinus Horak R, Maharaj VJ, Vleggaar R, Senabe JV, Gunning PJAn appetite suppressant from Hoodia speciesPhytochemistry.(2007 Oct)
5.^Zhao J, Avula B, Joshi VC, Techen N, Wang YH, Smillie TJ, Khan IANMR fingerprinting for analysis of hoodia species and hoodia dietary productsPlanta Med.(2011 May)
6.^Gathier G, van der Niet T, Peelen T, van Vugt RR, Eurlings MC, Gravendeel BForensic Identification of CITES Protected Slimming Cactus (Hoodia) Using DNA BarcodingJ Forensic Sci.(2013 Jul 18)
8.^Zhang J, Shi H, Ma Y, Yu BExpeditious synthesis of saponin P57, an appetite suppressant from Hoodia plantsChem Commun (Camb).(2012 Sep 7)
10.^Dall'Acqua S, Innocenti GSteroidal glycosides from Hoodia gordoniiSteroids.(2007 Jun)
11.^Pawar RS, Shukla YJ, Khan SI, Avula B, Khan IANew oxypregnane glycosides from appetite suppressant herbal supplement Hoodia gordoniiSteroids.(2007 Jun)
12.^Shukla YJ, Fronczek FR, Pawar RS, Khan IAHoodigogenin A from Hoodia gordoniiActa Crystallogr Sect E Struct Rep Online.(2008 Jul 31)
14.^Shukla YJ, Pawar RS, Ding Y, Li XC, Ferreira D, Khan IAPregnane glycosides from Hoodia gordoniiPhytochemistry.(2009 Mar)
15.^Pawar RS, Shukla YJ, Khan IANew calogenin glycosides from Hoodia gordoniiSteroids.(2007 Nov)
17.^Scott AD, Orsi A, Ward C, Bradford RGenotoxicity testing of a Hoodia gordonii extractFood Chem Toxicol.(2012 Jan)
18.^Russell PJ, Swindells CChemical characterisation of Hoodia gordonii extractFood Chem Toxicol.(2012 Jan)
20.^Dotson CD, Zhang L, Xu H, Shin YK, Vigues S, Ott SH, Elson AE, Choi HJ, Shaw H, Egan JM, Mitchell BD, Li X, Steinle NI, Munger SDBitter taste receptors influence glucose homeostasisPLoS One.(2008)
25.^Madgula VL, Avula B, Pawar RS, Shukla YJ, Khan IA, Walker LA, Khan SICharacterization of in vitro pharmacokinetic properties of hoodigogenin A from Hoodia gordoniiPlanta Med.(2010 Jan)
32.^Dent MP, Wolterbeek AP, Russell PJ, Bradford RSafety profile of Hoodia gordonii extract: rabbit prenatal developmental toxicity studyFood Chem Toxicol.(2012 Jan)
33.^Dent MP, Wolterbeek AP, Russell PJ, Bradford RSafety profile of Hoodia gordonii extract: mouse prenatal developmental toxicity studyFood Chem Toxicol.(2012 Jan)