Here's a sample of what you can find in the newsgroups on Super Blue Green Algae. All of the following was written by some guy named Mark Thorsen. SBGA users credit a number of effects to the algae, which is the species called _Aphanizomenon_flos-aquae_. The principal effects are increased feelings of "energy", reduced need for sleep, and reduced appetite. Other algae, such as _Spirulina_ and _Chlorella_, don't cause these effects. So, then, what could be in the algae which causes these effects? What is special about _Aphanizomenon_ that the other algae don't have? Here's a little file I put together about that subject: AN ANATOXIN-A PRIMER Copyright Mark Thorson 1995, 1996 The remainder of this file is divided into four parts: I. What is anatoxin-a? II. Where does anatoxin-a come from? III. What does anatoxin-a do? IV. How can algae users protect against anatoxin-a? PART I. What is anatoxin-a? Quoting from _Toxicon_, volume 17, "Pharmacology of Anatoxin-a, Produced by the Freshwater Cyanophyte _Anabaena_flos-aquae_ NRC-44-1", by Carmichael, Biggs, and Peterson, 1979, page 229: "Anatoxin-a (formerly called very fast death factor) is the term being used for the potent alkaloid neurotoxin produced by the freshwater cyanophyte _Anabaena_flos- aquae_ (Lyngb.) de Bre'b. clone number NRC-44-1." "Its pharmacological properties have been investigated and compared with that of a synthetic anatoxin-a which was derived from L-cocaine." "Anatoxin-a is a potent depolarizing neuromuscular blocking agent possessing both muscarinic and nicotinic activity." Quoting from page 236: "Structurally, anatoxin-a does not resemble decamethonium but instead is similar to the tropane alkaloids, specifically cocaine." Quoting from _Molecular_Pharmacology_, volume 18, "Anatoxin-a: A Novel, Potent Agonist at the Nicotinic Receptor", by Spivak, Witkop, and Albuquerque, 1980, page 391: "The potencies of six nicotinic agonists are compared (Table 2) for their ability to depolarize the frog's sartorius muscle by 10 mV. Interpolations from data published by other authors are cited to show that _anatoxin-a_is_the_most_potent_of_these_six_agonists_." [Italics in the original.] [An agonist is a molecule that binds to the same receptor. Agonists activate the receptor, while antagonists are non- activating and block the binding of the normal activating molecule, hence inhibit the action of the receptor.] Quoting from _The_Journal_of_Pharmacology_and_ _Experimental_Therapeutics_, volume 259, number 1, "Nicotinic Pharmacology of Anatoxin Analogs. I. Side Chain Structure-Activity Relationships at Peripheral Agonist and Noncompetitive Antagonist Sites", by Swanson, Aronstam, Wonnacott, Rapoport, and Albuquerque, 1991, page 378: "Anatoxin-a analogs with 12 different modifications of the 'acetyl' side chain moiety or a site directly influencing the conformation of this moiety were synthesized and evaluated pharmacologically. Fortunately, this extraordinary toxin has a semi-rigid homotropane skeletal structure that restricts the number of stable conformations." [An analog is a modified version of another molecule, e.g. heroin and codeine are analogs of morphine.] Quoting from page 383: "Several modifications of the side chain in anatoxin-a significantly changed the agonistic properties of the neurotoxins at the acetylcholinesterase receptor. No analog thus far tested _in_vitro_ was as potent as the parent compound anatoxin-a." Quoting from _The_Journal_of_Pharmacology_and_ _Experimental_Therapeutics_, volume 259, number 1, "Nicotinic Pharmacology of Anatoxin Analogs. II. Side Chain Structure-Activity Relationships at Neuronal Nicotinic Ligand Binding Sites", by Wonnacott, Jackman, Swanson, Rapoport, and Albuquerque, 1991, pages 390-391: "Such analysis assumes greater urgency with the realization that brain acetylcholinesterase receptors identified by high-affinity tritiated agonist binding are decreased in Alzheimer's disease (see Kellar and Wonnacott, 1990), and that nicotine treatment has given an encouraging result with respect to cognitive performance in Alzheimer patients (Sahakian _et_al_, 1989, 1990). Thus, centrally acting nicotinic agents could have an important therapeutic future in the symptomatic treatment of Alzheimer's disease (see Kellar and Wonnacott, 1990). Anatoxin-a is a useful core structure for such drug design because, as a secondary amine, it readily crosses the blood brain barrier." Quoting from _Journal_of_Neurochemistry_, volume 60, number 6, "(+)-Anatoxin-a Is a Potent Agonist at Neuronal Nicotinic Acetylcholine Receptors", by Thomas, Stephens, Wilkie, Amar, Lunt, Whiting, Gallagher, Pereira, Alkondon, Albuquerque, and Wonnacott, 1993, page 2308: "In these diverse preparations, (+)-anatoxin-a was between three and 50 times more potent than (-)-nicotine and about 20 times more potent than acetylcholine, making it the most efficacious nicotinic agonist thus far described." And a surprise quote from page 2310: "These studies were supported by grants from the R. J. Reynolds Tobacco Co. . . ." PART II. Where does anatoxin-a come from? Quoting from _Toxicon_, volume 17, "Pharmacology of Anatoxin-a, Produced by the Freshwater Cyanophyte _Anabaena_flos-aquae_ NRC-44-1", by Carmichael, Biggs, and Peterson, 1979, page 229: "Toxic strains of freshwater cyanophytes have been implicated in animal poisonings for many years. _Anabaena_flos-aquae_, _Microcystis_aeruginosa_, and _Aphanizomenon_flos-aquae_ are the most common species responsible with the most recent reviews on the subject written by Moore (1977) and Gentile (1971)." Quoting from _Journal_of_Applied_Phycology_, volume 5, number 6, "Anatoxin-a concentration in _Anabaena_ and _Aphanizomenon_ under different environmental conditions and comparison of growth by toxic and non-toxic _Anabaena_ strains: a laboratory study.", by Rapala, Sivonen, Luukkainen, and Niemela, 1993, page 581: "Anatoxin-a-concentration in cells of _Anabaena_ and _Aphanizomenon_-strains and in their growth media were studied in the laboratory in batch cultures at different temperatures, light fluxes, orthophosphate and nitrate concentrations and with different nitrogen sources for growth." "The amount of toxin in the cells of the toxic strains was high, often exceeding 1% of their dry weight." "The highest light flux studied did not limit the growth or decrease the level of the toxin in the cells of _Aphanizomenon_." PART III. What does anatoxin-a do? Quoting from _Toxicon_, volume 30, number 8, "Cardio- Respiratory Changes and Mortality in the Conscious Rat Induced by (+)- and (+/-)-Anatoxin-a", by Adeyemo and Sire'n, 1992, page 904: "Since adequate delivery of oxygen to the brain is of prime importance for central nervous system function, the observation that anatoxin-a-induced hypoxia was accompanied by severe and sometimes fatal acidosis suggests that brain hypoxia at the cellular level may result in the accumulation of lactate via anaerobic glycolysis producing acid-base stress, probable loss of reducing equivalents, and rapid depletion of high-energy phosphate compounds produced through oxidative phosphorylation." Quoting from _Neuropharmacology_, volume 31, number 3, "Behavioural Effects of Anatoxin, a Potent Nicotinic Agonist, in Rats", by Stolerman, Albuquerque, and Garcha, 1992, page 314: "Anatoxin differed from (-)-nicotine because it did not increase locomotor activity in rats made tolerant to the depressant effect of (-)-nicotine. It was unclear whether the tolerant rats were cross-tolerant to the locomotor depressant effect of (+)-anatoxin; the doses of (+)- anatoxin needed to decrease locomotor activity were larger in nicotine-tolerant than non-tolerant rats, but the basal level of activity was also lower. The partial, nicotine- like discriminative effect of (+)-anatoxin was notable because non-nicotinic drugs rarely mimic the discriminative effect of nicotine that is of central origin (Stolerman _et_al_, 1984)." Quoting from _Journal_of_Analytical_Toxicology_, volume 12, "Analysis of Anatoxin-a by GC/ECD", by Stevens and Krieger, 1988, page 126: "At present, the general method employed for the detection of anatoxin-a is a mouse bioassay. After lysis of cyanobacterial cells, up to 1 mL of sample water is injected i.p. into a mouse. Presence of anatoxin-a is inferred if the mouse expires within 10 minutes from respiratory arrest following violent convulsions. With a detection limit of about 5 micrograms toxin/20 gram mouse, the need for a sensitive, chemical analysis exists. The bioassay is inadequate for monitoring sublethal levels of anatoxin-a, . . ." PART IV. How can algae users protect against anatoxin-a? Quoting from _Journal_of_Analytical_Toxicology_, volume 12, "Analysis of Anatoxin-a by GC/ECD", by Stevens and Krieger, 1988, page 126: "Two methods for the detection of anatoxin-a in toxic samples have appeared in the literature--HPLC and GC/MS. Both methods involve cumbersome sample handling, and neither method is designed for trace quanititation of anatoxin-a on a routine basis. The HPLC method used UV detection, required a sample size of 100 mL, and employed 2 liquid-liquid extractions." "Due to the low molar absorptivity of its alpha-beta unsaturated ketone, approximately 8500, the HPLC method lacks sufficient sensitivity necessary for trace anatoxin-a detection." "Presently, a mouse bioassay is the general procedure used for testing the toxicity of a bloom--approximately 5 micrograms/ml anatoxin-a sensitivity. A method that is over three orders of magnitude more sensitive than that bioassay is described here. It is readily capable of detecting and quantitating sublethal levels of anatoxin-a." [Note that in the postings from Cell Tech in response to my files, they cite several specific tests they do on their algae. They perform the test for paralytic shellfish toxin, which happens to be a toxin that _Aphanizomenon_ is known to produce. They test for microcystins, which is a toxin that a contaminating algae in Klamath Lake is known to produce. They test for anatoxin-a(s), which is a different molecule from anatoxin-a that has a similar name, because both were originally discovered in an algae called _Anabaena_. To my knowledge, nobody has ever found anatoxin-a(s) in _Aphanizomenon_. But they do not perform the Stevens and Krieger test on the algae. I wonder why? Could taking the anatoxin-a out of _Aphanizomenon_ be like taking the nicotine out of tobacco?] Chet Day Enjoy brain-engaging and assumption-busting natural health articles: http://members.GNN.COM/chetday/open.htm