Prostaglandins - hormone-like substances with great potential
Version 1.1, March 2002 , by Isidore Douffeiy
Prostaglandins are a group of hormone-like substances; like hormones they play a role in a wide variety of physiological processes. Michael W. Davidson of the Florida State University: "Prostaglandins act in a manner similar to that of hormones, by stimulating target cells into action. However, they differ from hormones in that they act locally, near their site of synthesis, and they are metabolized very rapidly. Another unusual feature is that the same prostaglandins act differently in different tissues."
While the general public has a fairly good idea on hormones and their functions, this is clearly not the case with prostaglandins. Arthritis and rheumatism sufferers may know that prostaglandins have something to do with their particular condition, but as prostaglandins have a part in what makes people suffer from arthritis and rheumatism, as well as what alleviates their condition, there is considerable confusion.
The primary error is that people often just talk about prostaglandins in general. A patient may relate to a friend: "The doc told me that I have rheumatic pain because my body produces too much prostaglandins." And because of the name *prostaglandin* which clearly refers to the prostate gland, the patient, if male, may even think that something is wrong with the particular organ.
But what's wrong in this case is his understanding.
There is one specific prostaglandin that indeed plays a role in the male sexual tract, prostaglandin E1. It is marketed under the name Caverject (alprostadil) as a treatment for erectile dysfunction.
In the words of medical researcher A. Lea: "Intracavernous alprostadil (synthetic prostaglandin E1) is a vasodilating agent which acts by relaxing the smooth muscles of the corpus cavernosum and by increasing the diameter of cavernous arteries; this leads to erection."
But as the synthetic prostaglandin E1 needs to be injected into the penis prior to intended sexual intercourse, it has never taken off in the same manner as Viagra did. Prostaglandin E1 has other functions, not at all related to the facilitation of erections. It plays a role in protecting the gastrointestinal tract, and a synthetic prostaglandin E1 is marketed worldwide to protect from gastrointestinal bleeding that may be caused by the consumption of large amounts of painkillers (by rheumatism and arthritis sufferers). The synthetic prostaglandin E1 is usually sold under the brand name Cytotec. The drdoc on-line website describes it as follows:
"Cytotec® (Misoprostol) is a synthetic analogue of Prostaglandin E1 (PGE1). Like endogenous PGE1, Cytotec® exerts a protective effect on the gastrointestinal mucosa by increasing mucus and bicarbonate ion secretion and by increasing mucosal blood flow. In addition, Cytotec® inhibits acid secretion. Naturally occurring PGE1 is ineffective after oral administration because it is unstable in an acid environment; it is also quickly degraded when administered parenterally, giving it no practical clinical utility. However, the structural modifications to naturally occurring PGE1 that led to the development of Cytotec® resulted in an orally active drug with a duration of action that makes it clinically useful."
Misoprostol, as synthetic analogue of Prostaglandin E1, in sufficiently high dosages, also causes uterine contractions. In a number of mainly South American countries, women use high dosages of Cytotec to induce illegal abortions or abortions outside of the supervision of physicians.
Prostaglandins are usually named by letters and numbers: A1, A2... E1, E2... They are named by chemical similarity, not by the similarity of physiological effect. Prostaglandin E2, for example, has nothing to do with erections of the male sexual organ. Its function is in causing labor pains by inducing contractions, and it’s an important pharmaceutical agent in the OB.
For some prostaglandins, it makes quite a difference what we eat, or rather, what fats we eat. By and large, omega-6 fatty acids as they are found in meats and most vegetable oils stimulate the production of inflammatory prostaglandins, while the consumption of omega-3 fatty acids stimulates the production of anti-inflammatory prostaglandins. For this reason, marine fatty acids such as cod liver oil have long been known to ameliorate arthritic and rheumatic conditions. Flax seed, evening primrose oil, borage oil and canola oil are plant products stimulating the production of anti-inflammatory prostaglandins. Evening primrose oil is therefore used by women to manage menstrual pains that are caused by contraction-facilitating prostaglandins.
Chemical peel
A chemical peel is a body treatment technique used to improve and smooth the texture of the facial skin using a chemical solution that causes the skin to blister and eventually peel off. The regenerated skin is usually smoother and less wrinkled than the old skin. Thus the term chemical peel is derived. Some types of chemical peels can be purchased and administered without a medical license, however people are advised to seek professional help from a plastic surgeon or dermatologist on a specific type of chemical peel before a procedure is performed.
Alpha hydroxy acid peels
Alpha hydroxy acids (AHAs) are naturally occurring organic carboxylic acids such as glycolic acid, a natural constituent of sugar cane juice and lactic acid, found in sour milk and tomato juice. This is the mildest of the peel formulas and produces light peels for treatment of fine wrinkles, areas of dryness, uneven pigmentation and acne. Alpha hydroxy acids can also be mixed with a facial wash or cream in lesser concentrations as part of a daily skin-care regimen to improve the skin's texture.
AHA peels are used to:
reduce fine wrinkling
treat areas of dryness
reduce uneven pigmentation
aid in the control of acne
smooth rough dry skin
improve the texture of sun-damaged skin
AHA peels may:
cause stinging
cause skin redness
cause mild skin irritation
cause dryness
take multiple treatments for desired results
Beta hydroxy acid peels
It is becoming common for the use of beta hydroxy acid (BHA) peels to be used instead of the stronger Alpha Hyroxy (AHA) peels due to BHA's albility to get deeper into the pore than AHA. Studies show that BHA peels control oil, acne as well as remove dead skin cells to a certain extent better than AHA's, due to AHA's only working on the surface of the skin.
Jessner's peel
Jessner's peel is a combination of salicylic and lactic acids, and resorcinol. It is thought to break intracellular bridges between keratinocytes.
Retinoic acid peel
Trichloroacetic acid peels:
are preferred for darker-skinned patients over Phenol
smooth out fine surface wrinkles
remove superficial blemishes
correct skin pigment problems
Trichloroacetic acid peels may:
require pre-treatment with Retin-A or AHA creams
require repeat treatment to maintain results
require the use of sunblock for several months (this is a must)
take several days to heal depending on the peel depth
Phenol peels
Phenol is the strongest of the chemical solutions and produces a deep skin peel. Recent studies suggest that phenol is most likely only the carrier for another active component in the solution, namely croton oil. In fact, phenol alone produces only a light peel which is ineffective for restructuring the deeper dermal structures (such as wrinkles). The term Phenol/Croton oil peel has been proposed as a more accurate descriptor, but the established terminology phenol peel continues to be the dominant usage, as the role of croton oil in the mix is not as widely understood.
Effects of a phenol chemical peel are long lasting, and in some cases are still readily apparent up to 20 years following the procedure. Improvements in the patient's skin can be quite dramatic. A single treatment usually achieves the desired result.
Phenol peels are used to:
correct blotches caused by sun exposure or aging
smooth out coarse deep wrinkles
remove precancerous growths
Phenol peels may:
pose a risk for patients with heart problems
permanently remove facial freckles
cause permanent skin lightening by reducing the ability to produce pigment
take several months to heal
require increased protection from the sun for life
Anesthesia
Light chemical peels like AHA and glycolic acid peels are usually done in dermatologists'or plastic surgeons' offices. There is minimal discomfort so usually no anesthetic is given because the patient feels only a slight stinging when the solution is applied. If a patient were to request something for pain, an oral pain pill like Tylenol with codeine would be appropriate. Medium peels like TCA are also performed in the doctor's office or in an ambulatory surgery center as an outpatient procedure and are a bit more painful. Frequently, the combination of a tranquilizer like Valium and a pain pill usually suffice. TCA peels often do not require anesthesia because the solution itself has a numbing effect on the skin. The patient usually feels a warm or burning sensation. Phenol is the classic deep chemical peel. The application is very painful and most practitioners will perform it under either general anesthesia, administered by an MD-anesthesiologist or nurse anesthetist. Less often, the procedure is done using very heavy sedation, usually intravenous or intramuscular. But that approach is less desirable for several reasons including possible adverse influences of the phenol upon the heart.
Inhibitions of histamine release and prostaglandin E2 synthesis by mangosteen, a Thai medicinal plant.
Nakatani K, Atsumi M, Arakawa T, Oosawa K, Shimura S, Nakahata N, Ohizumi Y.
Department of Pharmaceutical Molecular Biology, Graduate School of Pharmaceutical Sciences, Tohoku University, Sendai, Japan.
The fruit hull of mangosteen, Garcinia mangostana L. has been used as a Thai indigenous medicine for many years. However, its mechanism of action as a medicine has not been elucidated. The present study was undertaken to examine the effects of mangosteen extracts (100% ethanol, 70% ethanol, 40% ethanol and water) on histamine release and prostaglandin E2 synthesis. We found that the 40% ethanol extract of mangosteen inhibited IgE-mediated histamine release from RBL-2H3 cells with greater potency than the water extract of Rubus suavissimus that has been used as an anti-allergy crude drug in Japan. All extracts of mangosteen potently inhibited A23187-induced prostaglandin E2 synthesis in C6 rat glioma cells, while the water extract of Rubus suavissimus had no effect. The 40% ethanol extract of mangosteen inhibited the prostaglandin E2 synthesis in a concentration-dependent manner with relatively lower concentrations than the histamine release. In addition, passive cutaneous anaphylaxis (PCA) reactions in rats were significantly inhibited by this ethanol extract as well as by the water extract of Rubus suavissimus. These results suggest that the 40% ethanol extract of mangosteen has potent inhibitory activities of both histamine release and prostaglandin E2 synthesis.
Screening of several Indonesian medicinal plants for their inhibitory effect on histamine release from RBL-2H3 cells.
Ikawati Z, Wahyuono S, Maeyama K.
Department of Pharmacology Ehime University School of Medicine, Shigenobu-cho, Ehime 791-0295, Onsen-gun, Japan.
Twelve alcoholic extracts and 12 hexane extracts of plant materials selected on the basis of medicinal folklore for asthma treatment in Indonesia were studied for their activity in inhibiting histamine release from RBL-2H3 cells (rat basophilic leukemia cell line), a tumor analog of mast cells. The results of screening indicated that five alcoholic extracts (Plantago major leaves, Eucalyptus globulus leaves and fruit, Cinnamomum massoiae cortex, Vitex trifolia leaves) and two hexane extracts (Eucalyptus globulus leaves, Vitex trifolia leaves) inhibited IgE-dependent histamine release from RBL-2H3 cells. The inhibitory effects were found to be more than 80% for extract concentrations of 0.5 mg/ml. The results indicate that the extracts contain active compounds that inhibit mast-cell degranulation, and provide insight into the development of new drugs for treating asthma and/or allergic disease.
Cinnamomum cassia
Cassia (Cinnamomum aromaticum, synonym C. cassia) is an evergreen tree native to southern China and Vietnam. Like its close relative, Cinnamon (Cinnamomum zeylanicum, also known as "true cinnamon" or "Ceylon cinnamon"), it is used primarily for its aromatic bark, which is used as a spice, often under the culinary name of "cinnamon". The buds are also used as a spice, especially in India and in Ancient Rome.
The Cassia tree grows to 10-15 m tall, with greyish bark, and hard elongated leaves 10-15 cm long, that have a decidedly reddish colour when young.
Cassia is a close relative to the cinnamon (Cinnamomum verum, Cinnamomum zeylanicum, or "true cinnamon"), Saigon Cinnamon (Cinnamomum loureiroi, also known as "Vietnamese Cinnamon"), Camphor laurel (Cinnamomum camphora), Malabathrum (Cinnamomum tamala) and Cinnamomum burmannii (also know as "Indonesian Cinnamon") trees. As with these species, the dried bark of cassia is used as a spice. Cassia's flavour, however, is less delicate than that of true cinnamon; for this reason the less expensive cassia is sometimes called "bastard cinnamon".
Most of the spice sold as cinnamon in the United States and Canada (where true cinnamon is still generally unknown) is actually cassia. In some cases, cassia is labeled "Chinese cinnamon" to distinguish it from the more expensive true cinnamon (Cinnamomum zeylanicum), which is the preferred form of the spice used in Mexico and Europe [1]. "Indonesian cinnamon" can also refer to Cinnamomum burmannii, which is also commonly sold in the United States, labeled only as cinnamon.
Cassia (Cinnamomum aromaticum) is produced in both China and Vietnam. Up to the 1960s Vietnam was the world's most important producer of Saigon Cinnamon, a species which has a higher oil content than Cinnamomum aromaticum, and consequently has a stronger flavor. Saigon Cinnamon is so closely related to cassia that it was often marketed as cassia (or, in North America, "cinnamon").
Of the three forms of Cassia, it is the form which commands the highest price. Because of the disruption caused by the Vietnam War, however, production of another form of cassia, Cinnamomum burmannii, in the highlands of the Indonesia on island of Sumatra was increased to meet demand, and Indonesia remains one of the main exporters of cassia today. Indonesia Cassia has the lowest oil content of the three types of Cassia and consequently commands the lowest price. Saigon Cinnamon, only having become available again in the United States since the early 21st century, has an intense flavour and aroma and a higher percentage of essential oils than Indonesian cassia. Cinnamomum aromaticum has a stronger and sweeter flavor, similar to Saigon Cinnamon, although the oil content is lower. In China Cassia is known as Tung Hing.
Cassia bark (both powdered and in whole, or "stick" form) is used as a flavouring agent, for candies, desserts, baked goods, and meat; it is specified in many curry recipes, where cinnamon is less suitable. Cassia is sometimes added to true cinnamon but is a much thicker, coarser product. Cassia is sold as pieces of bark (as pictured below) or as neat quills or sticks. Cassia sticks can be distinguished from true Cinnamon sticks in the following manner: Cinnamon sticks have many thin layers and can easily be made into powder using a coffee or spice grinder, whereas Cassia sticks are extremely hard, are usually made up of one thick layer and can break an electric spice or coffee grinder if one attempts to grind them without first breaking them into very small pieces.
Cassia buds, although rare, are also occasionally used as a spice. They resemble cloves in appearance and flavor. Cassia (called ròu gùi; ?? in Chinese) is used in traditional Chinese medicine, where it is considered one of the 50 fundamental herbs.
A 2003 study published in the DiabetesCare journal[2] followed Type 2 diabetics ingesting 1, 3 or 6 grams of cassia daily. Those taking 6 grams shows changes after 20 days, and those taking lesser doses showed changes after 40 days. Regardless of the amount of cassia taken, they reduced their mean fasting serum glucose levels 18-29%, their triglyceride levels 23-30%, their LDL cholesterol 7-27%, and their total cholesterol 12-26%, over others taking placebos.
The effects, which may even be produced by brewing a tea from cassia bark, may also be beneficial for non-diabetics to prevent and control elevated glucose and blood lipid levels, However Chemist Richard Anderson says that his research has shown that most if not all of cinnamon's antidiabetic effect is in its water-soluble fraction, not the oil (The ground cinnamon spice itself should be ingested for benefit, not the oil or a water extraction). In fact, some cinnamon oil-entrained compounds could prove toxic in high concentrations.
Cassia's effects on enhancing insulin sensitivity appear to be mediated by polyphenols [4]. Despite these findings, cassia should not be used in place of anti-diabetic drugs, unless blood glucose levels are closely monitored and its use is combined with a strictly controlled diet and exercise program.
There is also much anecdotal evidence that consumption of cassia has a strong effect in lowering blood pressure, making it potentially useful to those suffering from hypertension. The USDA has three ongoing studies that are monitoring the blood pressure effect.
Though the spice has been used for thousands of years, there is concern that there is as yet no knowledge about the potential for toxic buildup of the fat-soluble components in cassia, as anything fat-soluble could potentially be subject to toxic buildup. There are no concluded long term clinical studies on the use of cassia for health reasons.
European health agencies have warned against consuming high amounts of cassia, due to a toxic component called coumarin.