influence on health, role of food and diet, (nutrition
Ray Sahelian, M.D.
February 1 2016
A prostaglandin is any member of a group of compounds
derived from fatty acids containing 20 carbon atoms, including a 5-carbon ring.
Prostaglandins have a variety of biochemical and physiological effects,
including hormonal effects. Since the types of foods we eat influences the
prostaglandins made in the body, foods therefore influence the hormonal status
within the body.
The prostaglandins together with the thromboxanes form the prostanoid class of fatty acid derivatives; the prostanoid class is a subclass of eicosanoids.
herbs that influence prostaglandins
There are many herbs and supplements that have an influence on prostaglandins, here are a few:
Curcumin is an
extract from turmeric.
Phase I clinical trial of oral curcumin: biomarkers of systemic activity and compliance.
Clin Cancer Res. 2004.
Curcumin, a polyphenolic antioxidant derived from a dietary spice, exhibits anticancer activity in rodents and in humans. Its efficacy appears to be related to induction of glutathione S-transferase enzymes, inhibition of prostaglandin E(2) (PGE(2)) production, or suppression of oxidative DNA adduct (M(1)G) formation.
Mangosteen is a
fruit and its extract is sold as a dietary supplement.
Inhibitions of histamine release and prostaglandin E2 synthesis by mangosteen, a Thai medicinal plant.
Biol Pharm Bull. 2002.
The fruit hull of mangosteen, Garcinia mangostana has been used as a Thai indigenous medicine for many years. These results suggest that the 40% ethanol extract of mangosteen has potent inhibitory activities of both histamine release and prostaglandin E2 synthesis.
Preliminary studies on the anti-angiogenic potential of pomegranate fractions in vitro and in vivo.
We previously showed pomegranate seed oil and fermented juice polyphenols to retard oxidation and prostaglandin synthesis, to inhibit breast cancer cell proliferation and invasion, and to promote breast cancer cell apoptosis.
Prostaglandin gel is a medication used to soften and thin the cervix (opening to the womb or uterus). It may be used if you are past your due date, or have a large baby near or past your due date.
Future medications that inhibit the action of prostaglandin D2 should delay male pattern baldness.
Prostaglandin E1 has been used for the first time in the treatment of peripheral arterial occlusive disease 30 years ago. Although widely used, the exact mechanism of the known beneficial effects is not completely understood. A strong vasodilation is induced after intra-arterial administration of PGE1, but is not seen, when PGE1 is intravenously infused. For patients with peripheral arterial occlusive disease stage III or IV not eligible for arterial reconstruction, Prostaglandin E1 (PGE1) therapy not only has significant beneficial effects over placebo on ulcer healing and pain relief but also increases the rate of patients surviving with both legs after 6-months follow-up.
Prostaglandin E1 may be beneficial for some patients with erectile dysfunction.
J Clin Neurosci. 2016. Efficacy and safety of prostaglandin E1 plus lipoic acid combination therapy versus monotherapy for patients with diabetic peripheral neuropathy. PGE1+LA combination therapy is superior to PGE1 or alpha lipoic acid monotherapy for improvement of neuropathic symptoms and nerve conduction velocities in patients with diabetic peripheral neuropathy.
Prostaglandin E2 is a principal mediator of inflammation in diseases such as rheumatoid arthritis and osteoarthritis. Nonsteroidal anti-inflammatory medications (NSAIDs) and selective cyclooxygenase-2 (COX-2) inhibitors reduce Prostaglandin E2 production to diminish the inflammation seen in these diseases, but have toxicities that may include both gastrointestinal bleeding and prothrombotic tendencies. In cells, arachidonic acid is transformed into Prostaglandin E2 via cyclooxygenase (COX) enzymes and terminal prostaglandin E synthases (PGES). Accumulating data suggest that the interaction of various enzymes in the Prostaglandin E2 synthetic pathway is complex and tightly regulated.
COX2-derived bioactive lipids, including prostaglandin E2, are potent inflammatory mediators that promote tumor growth and metastasis through stimulation of cell proliferation, invasion, and angiogenesis.
Feeding rodents an omega-3 diet was is associated with a reduction in prostate tumor prostaglandin E (PGE)-2 levels.
Prostaglandins are produced from the enzyme-controlled oxidation of fatty acids. There are several dozen prostaglandins, and each seems to have very different and very specific functions.
Prostaglandins, for practical purposes, can be classified in three groups, depending on which fatty acid they were made from. Series 1 prostaglandins use linoleic acid as the starting point, while Series 3 prostaglandins use linolenic acid as the base fatty acid. Series 1 and 3 prostaglandins are considered the "good" prostaglandins, while Series 2 are considered the "bad" prostaglandins.
Series 1 prostaglandins are made from gamma linoleic acid (whose parent fatty acid is linoleic acid). This series of prostaglandins relax blood vessels, improve circulation, lower blood pressure, decrease inflammation, improve nerve function, regulate calcium metabolism, improve T-cell function, and lastly, prevent the release of something called "arachidonic acid" from cells. Arachidonic acid, or AA, is what Series 2 prostaglandins, or the "bad" prostaglandins, are made from.
Series 2 prostaglandins promote platelet aggregation (clot formation); inflammation; sodium retention; and may influence heart disease, blood clots, increased cortisol production, etc.. Reducing prostaglandins series 2 is a good option to stay healthier.
Series 3 prostaglandins are formed from the fatty acid found in fish oil: EPA (whose parent essential fatty acid is linolenic acid). The most important job of Series 3 prostaglandins is to prevent AA from being released by cells, thus preventing the production of bad Series 2 prostaglandins.
Function and mechanism of action
Prostaglandins have an influence on practically every organ in the body. As an example, in the area of female function, prostaglandins have an impact on ovarian, uterine, placental, and pituitary function to regulate reproduction. Prostaglandins play important roles in ovulation, luteal function, implantation, maintenance of gestation, microbial-induced abortion, parturition, postpartum uterine and ovarian infections, and resumption of postpartum ovarian cyclicity. Prostaglandins have both positive and negative effects on reproduction; they are used to synchronize estrus, induce parturition, and treat retained placenta, luteinized cysts, and chronic endometritis.
Prostaglandin inhibitor, blocker
is a mild prostaglandin inhibitor, another prostaglandin inhibitor is
Prostaglandin and allergy
Prostaglandins, small lipid molecules derived from arachidonic acid by COX enzymes, are critical mediators of allergic inflammation. The understanding of their role in allergic lung inflammation has been hampered by the very short biologic half-life of these mediators, which has made studies difficult in human subjects.
NSAIDs and Prostaglandins
Long term use of aspirin and similar agents, also called non-steroidal anti-inflammatory drugs (NSAIDs), can decrease the incidence of certain malignancies, including colorectal, oesophageal, breast, lung, and bladder cancers. The best known targets of NSAIDs are cyclooxygenase (COX) enzymes, which convert arachidonic acid to prostaglandins (PGs) and thromboxane. COX-2 derived prostaglandin E(2)(PGE(2)) can promote tumour growth by binding its receptors and activating signalling pathways which control cell proliferation, migration, apoptosis, and/or angiogenesis. However, the prolonged use of high dosages of COX-2 selective inhibitors (COXIBs) is associated with unacceptable cardiovascular side effects. Thus it is crucial to develop more effective chemopreventive agents with minimal toxicity. Recent efforts to identify the molecular mechanisms by which PGE(2) promotes tumour growth and metastasis may provide opportunities for the development of safer strategies for cancer prevention and treatment.