Thanks for your patience–or if you weren't patient, thanks for not beating
me up over it!

yer janitor,
Dick Dunn rcd@talisman.com Boulder County, Colorado USA

>By the way, is anyone using bee pollen as a yeast nutrient? I've had good
>results. All natural, and probably authentic!

I would love to have you elaborate on the nutrient effects of bee pollen,
how it improves the ferment and how a non-beekeeper can get it. Do you
know the chemical composition? Is it expensive?

BTW, I judged National Best Of Show Meads on New Orleans last week.
Astonishing! Of the three meads:

3- A nicely balanced metheglyn. All of the spices sang in chorus, none were
overpowering, none were hidden. There was a trace of youth that detracted.

2- A beautiful, delicate floral show mead. No flaws, but seemed to fade in
the 15-30 minutes that it took to reach a consensus.

1- A Melomel that was made from blueberries, raspberries and a variety of
honeys which had the cherry-like taste and aroma of a fine Burgundy wine.
It seemed to improve and open like a red wind as the #2 mead faded.
Beguiling. It took BoS.

All of this makes me wonder if a mead should not have a judgung category
for "table life" Most of us take a fair amount of time to drink a mead
during which the mead changes. I would think that a mead that tastes
better, rather than worse, might be rewarded…..Just an interesting topic
for discussion.

DanMcC

The active toxic principals in honey derived from azaleas and
related plants (rhododendron, laurel, and possibly many more
plants in the family Ericaceae) are andromedotoxins (which are
now called something else that I can't remember the name of) and
arbutin. Andromedotoxins are diterpenes (terpenes are common
defensive compounds in many plants – after all, if you can't move
you gotta do something to protect yourself) and arbutin is a
hydroquinone (quinones are also common plant defensive compounds).
Other similar compounds have medicinal uses (digitalis, quinine).
All parts of the plant are poisonous, including pollen. Children
have been poisoned by sucking the nectar from flowers – I can
remember doing this as a child with honey suckle and yes, azaleas.
(must not have gotten enough…) Livestock have also been poisoned.

With regard to making mead on the Forrestal – it's common for prison
inmates here in SC (and probably elsewhere) to make a product called
"buck" from whatever sugary (or sweet-tasting, remember that we're not
talking about rocket-scientists here) stuff they can get hold of. "Buck"
is usually made in 5-gallon buckets, artfully hidden, with bread yeast.
I've never had the pleasure, personally, but it's got to be pretty awful.
I've heard of everything from banana peels to old socks being included.
(Toe-jam lambic, anyone?) I'm sure that young Navy men are at least as
resourceful as SC's prisoners, so Good Luck to you, and maybe, if you
play your cards right, you'll get the chance to make the real thing 😉

Regards,
C
I don't speak for Clemson; they think I'm at work.

meuse@u.washington.edu

Oxidation is caused by the introduction of oxygen into a beverage
(beer/wine/mead) anytime after the bulk of the fermentation is complete.
The "introduction of oxygen" can be caused by splashing too much while
racking/siphoning, or loose caps or corks during storage. In my
experience, excessive splashing or foaming during racking causes a "wet
cardboard" or "stale" character in the finished product, while air creeping
in during storage can introduce sherry-like flavors. Attend a few
beer-judgings (as a steward, if necessary), and you'll see what I mean.

In general, when siphoning, let the outlet end of the tube rest below the
surface of the liquid, and you'll be okay.

Regarding the "Purple loosestrip" honey:

I believe that the plant is "purple loosestrife", and if it's the one I'm
thinking of, then it's that evil weed with the tall purple flower spike
that grows everywhere that there's any water at all. It's a non-native
invader, the botanical equivalent of the zebra mussel. 🙁
If you can get honey from it, then that's the first remotely good use I've
heard of for it. [die, die, evil non-native species!!]

• — Joyce, botanist-at-large

Here in Minnesota we have a plant called purple loosestrife, which is an
exotic aquatic plant which is choking out the native grassy-type plants
along the shorelines of lakes. I'm wondering if that is what the honey is
made out of. It would be nice if a supposedly harmful plant (at least
that's what the Department of Natural Resources tells up) can account for a
decent honey. What could be next, oyster stout made with zebra mussels?

Eric in Minneapolis, Minnesota
bakkee01@tigger.stcloud.msus.edu
"A great person is one who never loses the heart of a child." -Mencius

*************************************************************

"MAD" HONEY DISEASE

I bet some of you thought you have seen or heard it all, not true,

if you don't know about the "grayanotoxin" and "mad" honey disease
or Honey Intoxication caused by consuming honey produced from some
of the most beautiful flower's in the west and other places belonging
to the rhododendron family. It is only fair to point out that most of
these plants do not produce or seldom produce much surplus honey that
can be extracted or are they now or have they ever been even a minor
health risk in the US. But occasionally someone does find enough of
the pure stuff to eat and become sick. It is also believed, and from
my own personal experience with the western wild azalea, that the
nectar from these plants may also be toxic to the bees themselves and
cause occasional unexplained loss of field bees in the areas they
can be found blooming. And yes, I know beekeepers who have tasted
the raw honey from the comb and did live to tell about it as you
would expect as we beekeepers can't resist digging into a freshly
uncapped frame for a taste of that strange new honey. Just about all
of us at one time or another had to spit cotton balls or risk missing
a meal because of a sneak taste of raw honey. If not your day is
coming sooner or later. I know when I was a beekeeper's louse, the head
beekeeper would catch me digging into a comb for a taste and warn me
not to eat that raw honey. I thought "what a cheep boss, he won't
let me stick my fingers in that nice new honey comb", but my day
came more then once when he was not watching and I got into some green
honey and shortly after had gut wrenching cramps, but I learned, a
little slow, but I learned.<G>

U S Food & Drug Administration Center for Food Safety
& Applied Nutrition
Food borne Pathogenic Microorganisms and Natural Toxins
1992 (Bad Bug Book)
_________________________________________________________________

1. Name of Toxin: Grayanotoxin (formerly known as andromedotoxin,
acetylandromedol, and rhodotoxin)

2. Name of Acute Disease: Honey Intoxication

Honey intoxication is caused by the consumption of honey produced
from the nectar of rhododendrons. The grayanotoxins cause the
intoxication. The specific grayanotoxins vary with the plant
species. These compounds are diterpenes, polyhydroxylated cyclic
hydrocarbons that do not contain nitrogen. Other names associated
with the disease is rhododendron poisoning, mad hone intoxication
or grayanotoxin poisoning.

3. Nature of Disease:

The intoxication is rarely fatal and generally lasts for no more
than 24 hours. Generally the disease induces dizziness, weakness,
excessive perspiration, nausea, and vomiting shortly after the
toxic honey is ingested. Other symptoms that can occur are low
blood pressure or shock, bradyarrhythima (slowness of the heart
beat associated with an irregularity in the heart rhythm), sinus
bradycardia (a slow sinus rhythm, with a heart rate less than 60),
nodal rhythm (pertaining to a node, particularly the
atrioventricular node), Wolff-Parkinson-White syndrome (anomalous
atrioventricular excitation) and complete atrioventricular block.

4. Normal Course of the Disease:

The grayanotoxins bind to sodium channels in cell membranes. The
binding unit is the group II receptor site, localized on a region
of the sodium channel that is involved in the voltage-dependent
activation and inactivation. These compounds prevent inactivation;
thus, excitable cells (nerve and muscle) are maintained in a state
of depolarization, during which entry of calcium into the cells
may be facilitated. This action is similar to that exerted by the
alkaloids of veratrum and aconite. All of the observed responses
of skeletal and heart muscles, nerves, and the central nervous
system are related to the membrane effects.

Because the intoxication is rarely fatal and recovery generally
occurs within 24 hours, intervention may not be required. Severe
low blood pressure usually responds to the administration of
fluids and correction of bradycardia; therapy with vasopressors
(agents that stimulate contraction of the muscular tissue of the
capillaries and arteries) is only rarely required. Sinus
bradycardia and conduction defects usually respond to atropine
therapy; however, in at least one instance the use of a temporary
pacemaker was required.

5. Diagnosis of Human Illness:

In humans, symptoms of poisoning occur after a dose-dependent
latent period of a few minutes to two or more hours and include
salivation, vomiting, and both circumoral (around or near the
mouth) and extremity paresthesia (abnormal sensations). Pronounced
low blood pressure and sinus bradycardia develop. In severe
intoxication, loss of coordination and progressive muscular
weakness result. Extrasystoles (a premature contraction of the
heart that is independent of the normal rhythm and arises in
response to an impulse in some part of the heart other than the
sinoatrial node; called also premature beat) and ventricular
tachycardia (an abnormally rapid ventricular rhythm with aberrant
ventricular excitation, usually in excess of 150 per minute) with
both atrioventricular and intraventricular conduction disturbances
also may occur. Convulsions are reported occasionally.

6. Associated Foods:

Grayanotoxin poisoning most commonly results from the ingestion of
grayanotoxin-contaminated honey, although it may result from the
ingestion of the leaves, flowers, and nectar of rhododendrons. Not
all rhododendrons produce grayanotoxins. Rhododendron ponticum
grows extensively on the mountains of the eastern Black Sea area
of Turkey. This species has been associated with honey poisoning
since 401 BC. A number of toxin species are native to the United
States. Of particular importance are the western azalea
(Rhododendron occidentale) found from Oregon to southern
California, the California rosebay (Rhododendron macrophyllum)
found from British Columbia to central California, and
Rhododendron albiflorum found from British Columbia to Oregon and
in Colorado. In the eastern half of the United States
grayanotoxin-contaminated honey may be derived from other members
of the botanical family Ericaceae, to which rhododendrons belong.
Mountain laurel (Kalmia latifolia) and sheep laurel (Kalmia
angustifolia) are probably the most important sources of the
toxin.

7. Relative Frequency of Disease:

Grayanotoxin poisoning in humans is rare. However, cases of honey
intoxication should be anticipated everywhere. Some may be
ascribed to a increase consumption of imported honey. Others may
result from the ingestion of unprocessed honey with the increased
desire of natural foods in the American diet.

8. Target Population:

All people are believed to be susceptible to honey intoxication.
The increased desire of the American public for natural
(unprocessed) foods, may result in more cases of grayanotoxin
poisoning. Individuals who obtain honey from farmers who may have
only a few hives are at increased risk. The pooling of massive
quantities of honey during commercial processing generally dilutes
any toxic substance.

9. Analysis in Foods:

The grayanotoxins can be isolated from the suspect commodity by
typical extraction procedures for naturally occurring terpenes.
The toxins are identified by thin layer chromatography.

10. History of Recent Outbreaks:

Several cases of grayanotoxin poisonings in humans have been
documented in the 1980s. These reports come from Turkey and
Austria. The Austrian case resulted from the consumption of honey
that was brought back from a visit to Turkey. From 1984 to 1986,
16 patients were treated for honey intoxication in Turkey. The
symptoms started approximately 1 h after 50 g of honey was
consumed. In an average of 24 h, all of the patients recovered.
The case in Austria resulted in cardiac arrhythmia, which required
a temporal pacemaker to prevent further decrease in heart rate.
After a few hours, pacemaker simulation was no longer needed. The
Austrian case shows that with increased travel throughout the
world, the risk of grayanotoxin poisoning is possible outside the
areas of Ericaceae-dominated vegetation, namely, Turkey, Japan,
Brazil, United States, Nepal, and British Columbia. In 1983
several British veterinarians reported a incident of grayanotoxin
poisoning in goats. One of the four animals died. Post-mortem
examination showed grayanotoxin in the rumen contents.
_________________________________________________________________

Links to this Handbook's Table of Contents and to the
Center for Food Safety and Applied Nutrition's Foods Page
Hypertext last edited: 19 Apr 95 mow@vm.cfsan.fda.gov

*********************************************************************

• —

Kelly
Portland, OR

Anyway, think buckwheat and good luck.

Jeff Smith | '71 HD Sprint 350SX | snsi@win.bright.net | Barnes, WI
"What the world needs now is another folk singer,
like I need a hole in my head." Cracker

Also, is this a listserve?

Roz

I feel that this is a very valuable bit of commentary. I been making meads
and other beverages for many years now. In my experience, I have found that
yeast nutrition is critical to seccessfully fermenting vinous beverages.
Unfortunately, I was forced to discover this thru trial and error, not
having access to a forum such as this in my early days. =20

I would encourage any fledgling mead makers to take Ken's message to heart
with regard to the additoins of yeast nutrient and energizers. Don't over
dose your meads etc.. with these additions, least you get a "salty" flavor
from the nutrient salts.=20

As to the second snip above, I have found that in making ciders, meads, and
wines, it is better to check total acidity and volatile acidity post=
ferment.
During the fermentation process as the yeast modify their environment, the=
pH
drops dramatically. If you have added acid blend or citric acid to your must
before ferment takes place, you can often end up with a overly sour product.
Many recipes call for the addition of acid blend to the must prior to
fermenting. This is OK, IF you have checked your total acidity with a test
kit BEFORE you add the additional acids. An acid test kit is usually less
than $10 at your local brewing supply shop, and is easy to use. It's a
really good investment that can also improve your final products. Another
handy item to have is ph strips for wine. They go lower than do the pH
strips sold for beer making. Again, Ken's post provides key information.

Thanks Ken for your input and for getting me thinking about the subject.

Sl=E1inte!

Kurt