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