The seeds of Simmondsia chinensis are commonly processed to remove the fatty acids (Jojoba Oil) from the rest of the seeds (Jojoba Meal), with the former having market value as a cosmeticeutical and the latter usually seen as a waste product.
Components of Jojoba Oil, which comprise about half of the seeds by weight, include:
Eicos-11-enol (47.3% total oil)
Docos-13-enol (45.8% total oil)
Tetracos-15-enol (6.0% total oil)
Octadec-9-enol (0.9% total oil)
The 4-methylsterols Obtusifoliol, Gramisterol, Citrostadienol, and Cycloeucalenol
Cycloartenol, 24-methylenecycloartenol, and Cyclobranol
The sterols mentioned above (last three bullet points) comprise 0.4% of the oil by weight, and the division of sterols in this 0.4% is high in sitosterol (63%), 24-methylcholesterol (18%) isofucosterol (7%) and stigmasterol (7%).
Components of Jojoba Meal include:
Simmondsin (aka. 2-cyanomethylene-3 hydroxy 4,5 dimethoxy cyclohexyl-d-glucoside)
Simmondsin appears to have a marked suppressive effect on appetite, as the first toxicological investigation into Jojoba meal (after the oil was extracted) noted that 5-10% of Joboba meal in the diet reduced food intake to a degree where rats died from emanciation after 94 days. It appears to exert its mechanism of action in the intestines, as injections of large doses of Simmondsin fail to suppress appetite (and also fail to exert toxicity, which occurs with high doses of Simmondsin).
Simmondsin appears to have a same profile of effects after ingestion as Cholecystokinin, and the satiety induced by oral Simmondsin appears to be abolished with the CCKA receptor antagonist Devazepide. It did not appear to be direct activation of the receptor, but indirect through the Vagus Nerve; Vagotomy partially abolishes the effect.
Simmondsin appears to interact with the Vagus Nerve in the intestines and vicariously through Cholecystokinin (CCK) receptors to suppress food intake
When lean rats are fed Simmondsin for 8 weeks up to 0.5% of the diet noted that 0.15% of the diet reduced weight gain by 6% while 0.5% lowered weight below that of baseline despite being fed ad libitum, noted after 1 week but then maintaining weight up to 7 weeks. 0.25% has been tested in other studies in lean rats and shown efficacy.
When obese rats are fed Simmondsin for 16 weeks at 0.25-0.5% of the diet, dose-dependent reductions in food intake and weight are noted with the respective doses reducing carcass weight after 16 weeks by 17% and 26%. Obese rats appear to be more sensitive to appetite suppression relative to lean rats.
This appetite suppressing effect has been noted in other species such as dogs, and is commonly observed in toxicology tested insofar it was been thought to result in death of some rats at very high doses via reductions in food intake.
Appears to have repeated evidence for appetite suppression in rats, and the potency of low doses of Simmondsin appear to be quite remarkable
The fatty acid component of Jojoba seeds is sometimes referred to as Jojoba Liquid Wax (JLW) or Jojoba Oil and is the fragment used in cosmetics, and appears to have been used topically by native americans in the regions Simmondsia Chinensis grows (southern US and Mexico) for bruises and wound healing.
The liquid wax of Jojoba has displayed wound healing mechanisms in vitro, where 0.5-1% JLW solution was able to increase the wound repair capabilities of fibroblasts and keratinocytes (via PI3K-Akt-mTOR, as it was abolished by rapamycin) and was effective as platelet lysate (clinically used wound dressing agent) in inducing repair mechanisms.
Ingestion of 750mg/kg isolated simmondsin for 14 weeks is sufficient to kill mice (5/8) with the remaining mice experiencing hepatotoxicity and intestinal hemorrhage. Oddly, no appetetite suppression nor toxicity was noted with injections.
Ingestion of 250mg/kg Simmondsin in rats for 5 days fails to find any toxicological signs in the pancreas, liver, intestines, testes, or kidneys. Simmondsin up to 0.5% of the diet in lean rats for 8 weeks failed to alter the weight of the liver, and caused a slight increase in percent of kidney weight relative to body weight (absolute kidney weight did not change, and this study did not weight loss due to food intake reduction); the same lack of organ weight changes were noted over 16 weeks in obese rats. Histological examination did not note any remarkable abnormalities.
Pregnant rats fed Simmondin appear to reduce their own food intake, which was deemed the reason birth weight in the offspring was reduced; no other development abnormalities were noted.
In regards to blood parameters, 0.5% of the diet as Simmondsin appears to be associated with reductions of red and white blood cells as well as total lymphocytes with no significant effects at lower doses; replicated from a previous study using 0.5% Simmondsin for 52 days. There did not appear to be alterations in blood clotting, and feeding Simmondsin for 8 weeks and then ceasing ingestion for 8 weeks reverses the decline.