ALOE VERA

ALOE VERA by Rena Davis, MSc. Copyright © 2007

Scientific Names: Aloe vera L., A. perryi Baker (Zanzibar or Socotrine aloe), A. barbadensis Miller (also called A. vera Tournefort ex Linne or A. Vulgaris Lamark Curacao or Barbados aloe), or A. ferox Miller (Cape aloe). A. vera Miller and A vera L. may not be the same species.

Common names: Cape, Zanzibar, Socotrine, Curacao, or Barbados aloe, aloe vera

The name aloe is derived from the Arabic “alloch” which means a “bitter and shiny substance”. Drawings of aloe have been found in wall carvings of Egyptian temples erected in the fourth Millennium B.C. The Egyptian Book of Remedies (ca. 1500 B.C.) annotates the use of aloe in curing infections, treating the skin, and preparing drugs that were primarily used as laxatives. The Bible references aloe in John 19: 39-40, saying that Nicodemus brought a mixture of aloe and myrrh for the preparation of Christ’s body. Old lore states that Alexander conquered the island of Socotra to obtain control of aloe. The application of aloe for treatment of wounds, genital ulcers, hemorrhoids, and to stop hair loss was recorded by the Greek physician Dioscorides in 74 A.D. In the modern clinical era, the use of aloe began in the 1930’s as a treatment for roentgen dermatitis.

Aloe yields two commercially important products. “Aloe resin” is a solid residue obtained by evaporation of the latex obtained from cells (pericyclic) just beneath the skin. This bitter yellow latex contains anthraquinone barbaloin (a glucoside of aloe-emodin) and iso-barbaloin in addition to a Series of o-glucosides of barbaloin, called aloinosides, chrysophanic acid, and up to 63% resin. A valuable crystalline form of aloin is produced from the resin which contains a mixture of water soluble glycosides. Aloe-emodin exerts dose-dependent growth inhibition of H. pylori through inhibition of N-acetyltransferase (NAT) activity (Wang, 1998). Antibacterial effects have been demonstrated on four strains of methicillin-resistant Staphylococcus aureus (Hatano, 1999). Aloe-emodin is directly viracidal to herpes simplex virus type 1 and type 2, varicella-zoster virus, pseudorabies virus, and influenza virus (Sydiskis, 1991). Aloe gel, a clear gelatinous material obtained by crushing the cells found in the inner tissue of the Inner leaf, is the second commercially important product. The gel is used most frequently in the cosmetic and health food industries. The gel is a rich source of the polysaccharide glucomannan, the component believed to contribute significantly to the emollient quality of the gel.

Aloe vera contains Vitamins C, E, and zinc, which are all important for wound healing. Glycoproteins in aloe gel inhibit and break down bradykinin, a mediator of pain and inflammation. Aloe gel also inhibits Thromboxane which causes inflammation. Aloe gel stimulates fibroblast and connective tissue formation, a healing action rarely found in other anti-inflammatories. The polysaccharides in aloe seem to stimulate skin growth and repair. Aloe increases blood flow to burned tissue, therefore augmenting the healing rate. Aloe gel has been particularly beneficial in healing diabetic leg ulcers because, along with other wound healing capabilities, it lowers blood sugar.

Aloe gel’s antibacterial and antifungal ability compares favorably with the drug silver sulfadiazine, an antiseptic commonly used in the treatment of extensive burns. Aloe vera extract has been shown to kill Pseudomonas aeruginosa, Klebsiella pneumoniae, Serratia marcescens, Citrobacter species, Enterobacter cloacae, Streptococcus pyogenes, Streptococcus agalactiae, Escherichia coli, Streptococcus faecalis, and Candida albicans.

Acemannan, an antiviral component of aloe juice, is a powerful immune system stimulant. It works through enhancement of macrophage activity, the function of T cells and interferon production.
Acemannan has been effective for the treatment of HIV, influenza, and measles. It has demonstrated a direct antiviral effect on HIV by inhibiting glycosylation of glycoproteins. Acemannan, combined with suboptimal non-cytotoxic concentrations of AZT, acts synergistically in inhibition of replication of HIV and herpes simplex virus type 1.

References

Blitz JJ, et al. Aloe vera gel in peptic ulcer therapy; preliminary report. J Am Osteopath Assoc. 1963;62:731-735.

Danhof I. Potential benefits of orally-injested (sic: ingested) internal aloe vera gel. International Aloe Science Council Tenth Annual Aloe Scientific Semina; 1991; Irving, Texas.

Grindlay D, Reynolds T. The aloe vera phenomenon: a review of the properties and modern uses of the leaf parenchyma gel. JEthnopharmacol. 1986;16:117-151.

Hatano T, Uebayashi H, Ito H et al, Phenolic constituents of cassia seeds and the anti bacterial effects of some naphthalenes and anthraquinones on methicillin resistant Staphylococcus aureus.

Sydiskis RJ, Owen D G, Lohr JL et al., Inactivation of enveloped viruses by anthraquinones extracted from plants. Antimicrob Chemother 1991 Dec; 35(12):2463-6.

Saoo K et al. Antiviral activity of aloe extracts against cytomegalovirus. Phytother Res. 1996;10:348-350.

Vazquez B, et al. Anti-inflammatory activity of extracts from aloe vera gel. J Ethnopharmacol. 1996;55:69-75.

Wang HH, Chung JG, Ho CC, Wu LT, Chang SH. Aloe-emodin effects on arylamine N-acetyltransferase activity in the bacterium Helicobacter pylori. Planta Med 1998 Mar;64(2):176-178.

Zhang L, Tizard IR, Activation of mouse macrophage cell line by acemannan: the major carbohydrate fraction from aloe vera gel. Immunopharmacology 1996 Nov; 35(2): 119-128.

BETA GLUCANS

BETA GLUCANS by Rena Davis, MSc Copyright © 2007

Scientific Name(s): Beta glucans (Beta-1, 3-glucan), Beta glycans (Beta-1. 3/1, 6-glycan)

Common Name(s): Beta glycans, Beta glucans

Beta glucans have been studied for more than 30 years and have been found to have immune system stimulant properties. In fact, in the 1980s beta glucans were used to make salmon more disease resistant.

Beta glucans are carbohydrates. They are natural compounds derived from a variety of sources including mushrooms (Lentinula Scientific Names: Aloe vera L., A. perryi Baker (Zanzibar or Socotrine aloe), A. barbadensis Miller (also called A. vera Tournefort ex Linne or A. Vulgaris Lamark Curacao or Barbados aloe), or A. ferox Miller (Cape aloe). A. vera Miller and A vera L. may not be the same species.

Common names: Cape, Zanzibar, Socotrine, Curacao, or Barbados aloe, aloe vera edodes), oats, barley, baker’s yeast, algae, and mannin.

In in vitro testing and in mice studies, beta glucans have demonstrated potential immune response through enhanced ability of natural killer cells and macrophase activity. In mice with experimental colon and skin wounds, beta glucans increased tensile strength of wounds by 42% and increased collagen biosynthesis as well.

An all natural dietary supplement, Norwegian beta glucan is sold as a supplement to boost the immune system and protect against colds and flu. It claims to strengthen the body’s natural ability to fight disease-causing organism due to its molecular structure as it binds specifically to macrophage surfaces, activating the immune system and increasing resistance. In another claim, beta glucans are said to pass through the stomach unchanged, due to their acid-resistant nature. Other product claims include beta glucans’ ability to heal bed sores, nail fungus, and ear infections. Beta glucans in human trial in phase I and Phase II HIV research appear promising, but this still requires confirmation.

References:

1. Yadomae T. Structure & biological activities of fungal beta-1, 30glucans. Yakugaku Zasshi 2000; 120(5): 413-31. (Japanese).

2. http://www.immunehealthsystems.com/learning_center.htm Pengelly A. Medicinal Fungi of the world. Modern Phytotherapist 1996; 1/3-8 [review].

3. Artursson P, et al. Macrophage stimulation with some structurally related disaccharides. Scand J Immunol 1987; 25(3): 245-54.

4. Rios-Hernandez M. et al. Immuno pharmacological studies of beta-1, 3- glucan. Arch med Res 1994; 25 (2): 179-80.

5. Sherwood E. et al. Enhancement of interleukin-1 and interleukin-2 production by soluble glucan. Int. J. ImmunoPharmacol 1987; 9(3): 261-67.

6. Baba H., et al. Rapid tumor regression and induction of tumor-regressing activity in serum by various immune modulating agents. Int. J. ImmunoPharmacol 1986; 8(6): 562-72.

7. Suzuki I, et al. Immuno modulation by orally administered beta glucan in mice. Int. J. ImmunoPharmacol 1989; 11(7): 761-69.

8. Suzuki I, et al. Antitumor and immunomodulation activities of a beta glucan obtained form liquid cultured Grifolafrondosa. Chem Pharm Bull 1989 37(2): 410-13.

9. Portera C., et al. Effect of marcrophage stimulation on collagen biosynthesis in the healing wound. Am Surg 1997; 63(2): 125-31.

10. Levy S. Echinacea, more over; Norwegian Beta glucan is here. Drug Topics 2000 Apr. 17:73.

11. http://www.immunehealthsystems.com/learning_center.htm

12. http://www.immunehealthsystems.com/default1.htm

13. Gordon M. Bihari B. Goolsby E., et al. A placebo – controlled trial of immune modulator, lentinan, in HIV positive patients: a Phase I/II trial. J. Med. 1998; 29:305-330.

L-TRYPTOPHAN

L-TRYPTOPHAN by Robert Pollack, PhD Copyright © 2007

All living forms, including plant life, contain amino acids. Only plant cells are able to synthesize amino acids. Animals obtain the needed amino acids by directly eating protein contained in plants or by eating animals that ate plants.

Of the 20 amino acids that occur naturally in proteins, L-Tryptophan2 is, perhaps, the one which has been the most publicized and received the most attention.

Of the approximately 57 compounds that comprise the nutritional requirements of cells, tryptophan is one of the essential amino acids. In protein, tryptophan occurs in the smallest concentration, 0.5-1.6%, of the amino acids, in contrast to 25% of a group of amino acids termed the large neutral amino acids, LNAAs: isoleucine, leucine, phenylalanine, tyrosine, and valine. The LNAAs are of particular interest because they are transported across the blood-brain barrier by the same carrier system as tryptophan, and play a specific role in the way they influence tryptophan’s passage into the brain.

Body cells, including the brain, obtain their nutritive requirements from the circulating blood and fluids that surround them. However, the brain is very sensitive to the surrounding concentration of materials in the blood supply. In the process of traveling from the blood capillaries (extending through the brain) into the brain itself, there is in operation a control mechanism by which the entrance of nutrients into the brain, such as amino acids, are rigidly controlled: the blood-brain barrier. This barrier protects the central nervous system from the changing metabolite concentrations of the blood and serves to provide a constant chemical environment for optimum brain function.

Tryptophan not only has to compete with the LNAAs for access to the same transport carrier mechanism but compete with them despite the fact that these interfering amino acids (especially phenylalanine) have a greater affinity for the transport system than does tryptophan itself, which tends to decrease the amount of tryptophan that actually crosses the blood-brain barrier into the brain.

The blood level concentrations of tryptophan and its relationship to the LNAAs are expressed as the ratio of the concentration of tryptophan to the concentration of the LNAAs:Tryptophan, Isoleucine, Leucine, Phenylalanine, Tyrosine, Valine.

Changes in the concentration of either tryptophan or the LNAAs in this ratio affects the degree to which the tryptophan can pass through the blood-brain barrier. The higher the level of tryptophan, the greater is its ability to compete with the LNAAs for passage through the blood-brain barrier.

Because the body’s sole source of tryptophan is obtained from the food supply, it would seem logical that an increased intake of protein would augment the blood and brain supply of tryptophan – with a resultant increase in the serotonin level.
Paradoxically, exactly the opposite was observed in animal studies: a protein-rich meal results in a decrease of brain tryptophan. Tryptophan studies showed that the ratio of the plasma tryptophan levels to the sum of the other LNAAs tended to decrease as the dietary protein intake increased; the greater the quantity of protein eaten, the less will be the amount of tryptophan getting across the blood-brain barrier into the brain.

The effect of protein-rich food intake on brain serotonin level becomes even more significant in view of the fact that the daily intake of total protein for the average American is generally greater than the Recommended Daily Dietary Allowances, Food and Nutrition Board, National Academy of Sciences – National Research Council, Recommended Daily Allowances, Revised 1980: “The recommendation for the daily protein intake for the adult female is 44 grams per day and for the adult male, 56 grams per day”. Since an ounce of meat, fish, or poultry contains an average of 7 grams of protein, two three-ounce hamburger patties will provide all of the protein necessary for the average adult woman, and three of these same patties will provide all of the daily protein needed for the average adult male.

SEROTONIN
Once tryptophan enters the brain, it is converted to serotonin, a major neurotransmitter in the brain.

Serotonin performs a number of functions in the body from acting as a powerful vasoconstrictor to its role as a neurotransmitter sending messages throughout the brain. Its best known function is its effect on nerve receptors in the brain involved with the neurotransmission of various types of nerve impulses.

In the central nervous system serotonin plays a role in the regulation of pain, depression, sleep, and appetite. Lower than normal levels of serotonin have been associated with aggressive and anger disorders, suicide, depression, obsessive compulsive disorder, and migraines.