[continued from previous message]
continue. There is nothing on the horizon for type 2 diabetes with promise comparable to that of beta cell transplants for type 1. The sequencing
of the
human genome, completed in 2000, provides information for research which is likely to help, but that is for the very long term.
This is distinct from the *treatment* of type 2 diabetes, which has improved quite significantly even since I first wrote the above paragraph. New drugs
are available which improve insulin sensitivity. The UKPDS directly, and the DCCT indirectly, have convinced many more doctors that intensive treatment
of type 2 diabetes is worth the trouble and expense. Support and education programs continue to expand. The UKPDS showed clearly that medical nutrition therapy (MNT, diet with proper medical team support) helps type 2 diabetics greatly even without weight loss, and so more doctors are providing the necessary aid.
But all this is treatment, not cure.
------------------------------
Subject: What's a glycemic index? How can I get a GI table for foods?
The glycemic index, or GI, is a measure of how a given food affects
blood glucose (bG). Some complex carbohydrates affect bG much more
drastically than others. Some, such as white bread, affect bG even more
than sugar (sucrose).
This was quite a surprise when the research was first published in 1981.
It really should not have been such a surprise. "Sugar", meaning
sucrose, decomposes in the gut to equal parts of glucose and fructose. Fructose, as expected, has only a small effect on bG. Even
professionals, it turns out, were swayed in their thinking by the evil
charm of the word "sugar" and failed to take into account the
differences among the many kinds of sugar found in foods.
To use the glycemic index in a real-life diet, you must combine the GI
of various foods using a weighted average. Rick Mendosa's article (see
below) has information on simple calculations for mixed meals, which
recent research has shown to be reliable.
It remains difficult to predict the GI of high fat meals because of the multiple affects of the fat, especially the way it slows the gut. For
example, a baked potato has a very high GI (one of the famous,
unexpected examples), but adding butter to it lowers the GI greatly.
This is a good reason to reduce dietary fat (if you needed another
reason), since doing so makes the effect of carbohydrates more
predictable.
If you don't want to go to the effort of full GI calculations, the
important thing is to understand that foods may affect your bG profile
in ways that you wouldn't expect from categorizations such as "simple
sugar" and "complex carbohydrate". Build your knowledge about your own
response to different foods and meals by monitoring and keeping
records, and avoid assumptions.
Rick Mendosa <mendosa(AT)mendosa.com> has written an excellent and thorough article about the glycemic index. He also maintains a glycemic index
list. I highly recommend that you check out
http://www.mendosa.com/gi.htm
[Thanks to Rick for information he provided for this section.]
------------------------------
Subject: Should I take a chromium supplement?
The short answer is "no". I'll quote the ADA's longer answer, from the May
1994 _Diabetes Forecast_, p.73. The ADA's editorial board says:
Some popular books on diabetes have claimed that chromium, which is
found in many common foods such as animal meats, grains, and
brewer's yeast, is good for people with diabetes. Not so. Though
chromium supplements may benefit people who are significantly
malnourished and have an actual chromium deficiency, there is no
significant evidence that consuming extra chromium helps people
with diabetes who are even close to being well nourished.
Taken at the dosages listed on the bottle, however, chromium is not
likely to be harmful. But your money is better spent on more useful
items!
------------------------------
Subject: I beat my wife! (and other aspects of hypoglycemia)
(not yet written)
------------------------------
Subject: Does falling blood glucose feel like hypoglycemia?
Sometimes. Symptoms of hypoglycemia are divided into the adrenergic and the neuroglycopenic. Adrenergic responses are caused by increased activity of
the autonomic nervous system and may be triggered by a rapid fall in blood glucose (bG) or by low absolute bG levels; symptoms include
weakness
sweating
tachycardia
palpitations
tremor
nervousness
irritability (sound familiar?)
tingling of mouth and fingers
hunger
nausea or vomiting (unusual)
The autonomic nervous system activity also causes the secretion of
epinephrine,
glucagon, cortisol and growth hormone. The first two are secreted
rapidly and
eliminated rapidly. The second two are secreted slowly and remain
active for
4-6 hours, and may cause reactive hyperglycemia.
Neuroglycopenic responses are caused by decreased activity of the central nervous system and are triggered only by low absolute bG levels; symptoms include
headache
hypothermia
visual disturbances
mental dullness
confusion
amnesia
seizures
coma
The above information is from Mayer Davidson's _Diabetes Mellitus: Diagnosis and Treatment_.
Remember, as always, that individual responses vary greatly. The exact
set of
symptoms encountered will vary. It's not impossible that some of the
symptoms
will fall in the other category for some individuals.
------------------------------
Subject: Alcohol and Diabetes
This section provided by Peter Stockwell <peter(AT)sanger.otago.ac.nz>.
Having diabetes does not prevent the consumption of alcoholic drinks,
but there are some considerations:
- Alcohol can metabolised to produce energy and so has dietary
consequences.
- Alcohol promotes the uptake of blood glucose into liver glycogen
causing a drop in bG.
- Many alcoholic drinks contain sugar, particularly mixed drinks.
- The symptoms of drunkenness and hypoglycaemia are similar - alcohol
may mask the effects of a hypo.
- Diabetics must remain sober enough to care for themselves (perform
injections on schedule, etc).
- Excess alcohol consumption can cause increased serum triglycerides.
Few difficulties arise if following points are observed.
Acceptable in moderation:
- Red wines.
- Dry or medium-dry white wines.
- Dry sherries.
- Dry light beers (lagers, light ales fermented with low residual
sugar).
- Spirits (whiskey, gin, vodka, etc) with "diet" mixers.
Use with extreme caution due to high sugar content:
- Sweet wines or sherries.
- Ports.
- Heavy or dark sweetened beers (stout, porters, etc which have
high residual sugar).
- Wine coolers.
- Spirits with normal mixers.
- Cocktails.
- Liqueurs.
Use with extreme caution due to very high alcohol concentration:
- Neat (undiluted) spirits.
General rules:
- Simple drinks (wine, beer) are more reliable than complex mixed
drinks, especially in company where you have less control over
the contents or concentration.
- Drink with or after food to avoid hypo problems.
- Approach anything with caution if you are in doubt.
- Low alcohol beers are not necessarily preferred - many of them are
rather sweet.
- Alcohol provides about 7 cal/g of food energy. Some is lost in the
urine, but most is converted by the liver into forms which can be
used for energy elsewhere in the body or stored as fat.
Clearly these succinct rules are simplified and there are exceptions to
them (for example, there are dry ports) but they are intended as a
general guide. I make no attempt to define the term moderation, this
will depend on the individual.
------------------------------
Subject: Necrobiosis lipoidica diabeticorum
Necrobiosis lipoidica diabeticorum (NLD) consists of oval plaques,
usually on
the lower legs. It may start as small red spots or raised areas, which
develop a shiny, porcelain-like appearance. The plaques often turn a light color due to extracellular fat (the "lipoidica"). They are often itchy or painful. Typically the spots turn a brownish color, which fades slowly but
is permanent.
NLD is not related to any other complication of diabetes. In particular, NLD does not presage eye, kidney or vascular problems.
NLD is much more common in diabetics, who account for perhaps 2/3 of all
cases. Many of the remainder develop diabetes, and NLD should be
considered a
warning sign of diabetes. Reports vary widely on exactly who is most at
risk.
About 1% of diabetics have some degree of NLD ... plus or minus 1%,
depending
on which report you read. Some reports say NLD occurs more often in young women, but some textbooks disagree.
The real dangers seem to be ulceration, infection, and the stress from the appearance. Ulceration sometimes occurs spontaneously, and often as a result
of trauma.
Ulceration is often a result of scratching or trauma, and the ulceration
from
scratching sometimes heals very slowly. Thus avoiding scratching and trauma decreases the amount of ulceration, though some ulceration will occur
anyway.
There are some images of NDL lesions at
http://tray.dermatology.uiowa.edu/DermImag.htm
No particularly good treatment seems to be known. Topical steroids (that is, creams) are the most common first choice. The ulcerations usually heal if
cared for properly, and drastic measures are not called for in most cases. William Biggs reports that skin grafts may be necessary in cases of severe ulceration, but do not tend to give results that are cosmetically
attractive.
Other treatments reported to help sometimes are oral aspirin,
pentoxifylline,
dipyridamole, locally injected steroids, and systemic steroids. No one
claims
to be able to predict what will work on any given patient, and often not
much
of anything is effective. However, the ulcers usually heal if given
supportive treatment. Surgery should be avoided. Ineke van der Pol reports finding relief in Chinese herbal treatments.
STEROID WARNING: locally injected and systemic steroids raise blood glucose
and cause severe problems regulating blood glucose. These should be used
only
as a last resort. Topical steroids (creams and inhalers) cause no such problems.
Note that treatment is not a medical necessity except for ulcerations and infections. Otherwise, the purpose of treatment is to prevent ulcerations
and infections, decrease pain and itching, and improve the appearance.
NLD is the subject of occasional articles in scientific journals on diabetes and on dermatology. Betsy Butler has researched the medical journals,
finding
little beyond what I've reported above -- in her words, "no good answers". _Therapy for Diabetes Mellitus and Related Disorders_, published by the ADA, has a section on necrobiosis lipoidica diabeticorum and its treatment.
Ineke van der Pol has started a mailing list about NLD at
http://groups.yahoo.com/group/necrobiosis.
I thank the following people, especially Betsy, who posted the information
from which I derived this section:
Betsy Butler Polley (who says sorry, she doesn't have any information
besides what's here)
William Biggs <reddy_biggs(AT)msn.com>
Tari M. Birch <tm_birch(AT)pnl.gov>
Terence Griffin (who also says he doesn't have any other info)
Bill Barner <barner(AT)mail.loc.gov>
Ineke van der Pol <fluo(AT)chello.nl> (who has no further information
but is happy to correspond about NLD if you wish)
------------------------------
Subject: Has anybody heard of frozen shoulder (adhesive capsulitis)?
Short answers: adhesive capsulitis, aka frozen shoulder, is a painful
condition that limits motion in one shoulder or both. It's not found exclusively in conjunction with diabetes, but occurs sufficiently more often with diabetes to be considered a diabetic complication. Don't be surprised, though, if your doctor isn't aware of this connection. Avoid surgery (which seldom helps) and cortisone (which plays havoc with blood glucose control); take physical therapy seriously; expect to take about two years to recover.
Lee Boylan <lboylan(AT)cisco.com> wrote:
There are three treatments usually offered for frozen shoulder: surgery,
cortisone shots and exercises. Surgery offers the best transfer of
money to
a surgeon but the patient ends up needing to do exercises anyway.
Cortisone offers quick pain relief but not full shoulder relief, so the
patient is told to do exercises. Also, a DMer has drastically changed
insulin requirements after taking a cortisone injection.
Exercise, with alternating hot and cold packs and optional NSAIDs, offers
slow and sometimes painful therapy that gets full or nearly full
restoration of movement. Just don't let it discourage you, because
improvement comes slowly. Keep at it! Eventually, you will have pain-free
motion in your arm.
And I'll re-emphasize what Lee says: DON'T TAKE STEROIDS LIGHTLY. Including cortisone. This warning should not be necessary, but unfortunately some
doctors are unaware of what steroids do to blood glucose. If your doctor doesn't understand how serious a problem this is, insist on including an endocrinologist in your medical team.
Lyle Hodgson <lyle(AT)world.std.com>, who has been through adhesive
capsulitis in both shoulders, wrote:
I suggest anybody who really wants to know about it who can visit
Boston go
to see Dr. Gordon Lupien, who used to be an orthopedic surgeon at Joslin
and, according to a couple doctors I asked, knows more about adhesive
capsulitis in diabetics than anyone else, period.
Factoids:
o Diabetics get "frozen shoulder" more than non-diabetics.
o Women get "frozen shoulder" more than men.
o Everybody I talked to who had ever treated "frozen shoulder" said that
every patient they'd seen with it got over it in two years, no matter
whether they did the exercises or not.
o The exercises and ESPECIALLY PHYSICAL THERAPY help tremendously in
retaining what range of motion you still have and in keeping the pain
(which can be incredible) to a minimum.
o The exact cause and pathology is completely unknown, but often adhesive
capsulitis follows an untreated injury, or bursitis or tendonitis
or even
a period of no stretching exercises.
o Adhesive capsulitis is often mis-diagnosed as a torn rotator cuff,
which
may well be involved but which will heal without the surgery most
orthopedic surgeons prescribe for it. What's more, an often undiscussed
side-effect of the surgery is permanently reduced range of motion,
because tendons are snipped and resewn, and thus shortened.
o If the exact pathology is unknown, it is certain that it involves
scarification of the tissues in the shoulder "capsule", and from what I
understand scar tissue is at least partly caused by glycosulation of
tissues, so good control is (once again) the best prevention .
o Cortisone is often prescribed for non-diabetic patients, and only for
diabetic patients by doctors unfamiliar with the dramatic effect
cortisone has on bloodsugar levels. Dr. Lupien told me cortisone
doesn't
even really have any long-term effect except to reduce the pain for
awhile, and should be avoided completely since it could also
permanently
screw up how your body deals with cortisone.
o Recommended treatment: daily exercises, biweekly physical therapy,
daily
(if possible) swimming, and acetaminephen (Tylenol). Extensive use of
non-steroidal anti-inflammatories is not recommended. These include
aspirin, ibuprofen (Advil/Motrin), and naproxen.
Here's a sort-of-a- self test for adhesive capsulitis:
1. Lay on the floor on your back. Can you raise your arm over your
head in
a 180-degree arc and rest it on the floor without pain or *too* much
stretching?
2. Stand sideways next to a wall, and walk your fingers up the wall until
you can't reach any more. Can you almost press your armpit to the
wall?
If either of these gives you significant trouble -- you can't quite reach
the floor behind your head, you can't touch the wall with your elbow, and
either or both gives you pain -- you may (MAY, MAYBE, MIGHT) have
adhesive
capsulitis.
Two doctors and one physical therapist told me that shoulders tend not to
get the regular stretching that other joints get: a person can go for
long
periods of time without moving the shoulder much out of its usual hanging
position, and then often the movement doesn't count for much. Hips are
stretched at least a little several or many times a day, even with
sedentary types who only sit, stand, sit, stand, walk a little, sit,
etc.:
the tissues are still fairly regularly manipulated so that it is much
harder for them to freeze up.
Lyle, who is always interested to hear what else anyone has learned about
this little-studied, little-mentioned condition
------------------------------
Subject: Gastroparesis
J K Drummond (no longer on the net, but well) contributed this section.
Gastroparesis (gastroparesis diabeticorum if a diabetes complication) is
nerve damage caused delayed gastric emptying. This more common than
recognized irregular digestive slowdown interferes with blood glucose regulation and oral medicine absorption.
Severity ranges from occasionally recurring bothersome symptoms like
nausea, vomiting, constipation and diarrhea to total "stomach paralysis"
-- the inability to consume/absorb any food. This worst stage requires
tube feedings as the sole source of nutrition, IVs for hydration, and
gastric suction for waste elimination. Be aware that "stomach trouble" may
be more serious for one with diabetes and report digestive problems to
your physician. Do not wait until you have had gastroparesis for several
years or end up in the emergency room because you cannot eat. If you
are a health professional, please routinely ask diabetics if they have digestive problems.
Many with gastroparesis are undiagnosed or misdiagnosed and find little information about it. Often they have been used as guinea pigs in
guessing games of hit or miss treatment trials. The scary quest has
only just begun to find answers, reason, and solutions to this lesser
known and mystifying complication of diabetes. There are people who
have found answers in their lonely struggle with gastroparesis.
Most folks with gastroparesis are female, with type 1 diabetes for 20-25
years and are age 25-45 at onset of gastroparesis.
These incomplete lists of symptoms, treatments, helpful & stressful
foods, and social aspects have been compiled mostly from patient reports.
There is no all-patient guarantee of experience. CHECK WITH YOUR DOCTOR!
S Y M P T O M S
Physical Psychological
nausea fatigue- muscle weakness
vomiting fear
constipation frustration
diarrhea stress
bloating
lack of hunger
indigestion
high stomach acidity
reflux
weight loss
inability to control blood sugars
DIAGNOSIS**
Symptoms together with gender &/or years of diabetes (clinical intuition) Gastric Mobility Transit Test
Manometric Motility Study
Diabetics are also subject to all forms of non-diabetic gastropathy so be
aware that tests are necessary to eliminate and/or verify other diagnoses.
TREATMENTS
NUTRITION - MALNUTRITION Dietitians recommend 6 small meals daily
Foods more easily digested Foods increasing symptoms
fruit juices protein foods - meat, eggs
canned fruits & vegetables raw fruits & vegetables
soft starches (white bread dairy products
& rice, mashed potatoes,
cereals) caffeine, chocolate
soups nuts & seeds
baby foods
non-carbonated beverages
jello
Liquid Nutritional Supplement Drinks
Diabetic: Choice dm (Mead-Johnson), Glucerna (Ross Labs)
Ensure Glucerna OS (Ross Labs)
Non-diabetic: Ensure/Ensure plus, Sustacal (Ross Products Div)
Nutrition via:
IVs (fluids or TPN)
Tube feedings (eq. Osmolite or Supplena)
PHYSICAL - Remaining upright at least a half hour after eating,
stomach massage, enemas, glycerine suppositories, stool softeners
(for example, psyllium husk powder: Metamucil and other brands)
DRUGS - May have adverse side effects on other conditions. Ask your MD!
Reduce stomach acid: Zantac, Pepcid, Prilosec, Axid, Cytotec
Increase motility:
Reglan (metoclopramide)
erythromycin
Propulsid (cisapride) (in U.S. only under compassionate use protocol)
bethanechol
domperidone (U.S. availability: compassionate use only, and for
veterinary
use -- it's used to treat fescue toxicosis in horses)
Zelnorm (tegaserod maleate), labeled in the US as of 2002 to treat
women with irritable bowel syndrome (IBS) dominated by
constipation. Zelnorm increases serotonin activity in the bowel by
activating some 5HT4 receptors, which increases serotonin in the
bowel and increases motility. The percentage of IBS patients who
benefit is small but significant. It's not clear why the labeling
is limited to women, though it seems likely to be a combination of
the fact that 2/3 of IBS patients are women and the clinical
studies barely reached statistical significance. If the effects in
gastroparesis follow those in IBS, a small percentage of patients
will see improvement, and some of those will be helped a lot.
Information from the Zelnorm prescribing information on the
http://www.zelnorm.com web site.
Reduce digestive system spasm: dicyclomine
Diarrhea: immodium, clonidine
Nausea/vomiting: marinol, thorazine, ativan, inapsine, zephran, phenergan
Surgical (physical implants or alterations)
portacath or Hickman - IV hydration or Total Peritoneal Nutrition
jejunostomy - tube feedings
gastrostomy - for stomach suction (PEG tube)
gastric resectioning or stomach removal
gastric pacing - digestive pacemakers (experimental). Enterra Therapy by
Medtronic, gastric electrical stimulation (GES) neurostimulator implants
are approved as a humanitarian use device (HUD) since severe
gastroparesis
(refractory to drugs) has less then 4,000 cases per year. More info at
http://www.medtronic.com/neuro/enterra/patient.html
insulin pumps
SOCIAL & PSYCHOLOGICAL ASPECTS
Frustration for patient and physician from the difficulty in balancing
insulin dosages and food intake to achieve level blood sugars with unpredictable slowed digestion.
Additional psychological impact from delayed treatment due to relative
medical unrecognition causing underdiagnosis and even misdiagnosis (ex. as anorexia nervosa if accompanied by vomiting).
Lack of ostomy education.
If/when eating ability returns following thinking that a normal diet could never again be eaten it may cause physical & emotional anorexia.
Often felt burden to friends and family.
Most information was collected by the pioneering health professionals of
the defunct Gastroparesis Communication Network, updated by J K Drummond.
There's an excellent web page on gastroparesis at
http://www.uoflhealthcare.org/tabid/473/Default.aspx
** If you have been or are out of work pursue Medicare/Medicaid & Social Security Options IMMEDIATELY!
------------------------------
Subject: Extreme insulin resistance
Mayer Davidson writes several pages about insulin resistance in his
book _Diabetes Mellitus: Diagnosis and Treatment_. Except for what's in [brackets], the following information is from pp 126-132 of the third
edition or pp 112-119 in the fourth edition. I'd recommend finding a
copy. Most university libraries will have it, even those without
medical schools. It's about $65; if necessary you can order from the Rittenhouse Medical Bookstore in Philadelphia at 215-545-6072.
In this context, "insulin resistance" refers to patients requiring more
than the arbitrary amount of 200 units/day. Davidson uses the term
"insulin antagonism" for the phenomenon which is commonly part of type
2 diabetes.
Davidson cites ten major causes of insulin resistance. The first eight
are obvious major medical problems that you would immediately suspect
were related, so I won't bother listing those. Rarely, insulin is
destroyed at the subcutaneous injection site; this form can be treated
with normal amounts of insulin administered intravenously or
intraperitoneally.
The most common form of insulin resistance is immune-mediated. Everyone
taking injected insulin develops IgG antibodies to insulin. In most,
the antibody levels are low. In about 1 in 1000, the levels are much
higher, from 5 to over 1000 times higher than usual. In Davidson's
words:
The reason for this markedly enhanced response and the
subsequent decline to normal levels is completely unknown.
The antibodies bind to, and neutralize, the insulin.
At one time it was thought that the antibodies resulted from impurities
in the insulin preparations, and that using highly purified
preparations would avoid the problem. This has proven not to be the
case; purified insulin helps but usually does not resolve the problem,
[though it seems to be worth trying].
Also, switching to a different insulin does not help, as the antibodies
bind to beef, pork and human insulin. They may bind to one more than
the others, but the titers of antibody are so high as to neutralize
virtually all of any of the insulins.
Two treatments which are effective are not generally available in the
US.
First, insulin can be treated with sulfuric acid. The modified molecule
retains some biological activity but has reduced affinity for binding
to the IgG antibodies to insulin. This treatment was tested by a
Canadian laboratory in the late 1960s but is available in the US only
by special petition to the FDA. Novo Nordisk Pharmaceutical can provide information at 609-987-5800.
Second, fish insulin works in humans but does not bind to the
antibodies. Cod insulin, for example, differs from human insulin in 33
amino acid positions compared with 3 differences for beef insulin. But nonmammalian insulins are not available in the US at all.
This leaves the two treatments that are actually used on a regular
basis, and a promising new treatment.
Because this condition is rare, there's been little experience treating
it with lispro insulin (Humalog). That experience is promising; it
appears that the structural change in lispro may inhibit the antibody
binding. If this is borne out by further experience, lispro will be the treatment of choice for extreme insulin resistance.
Glucorticoids such as prednisone decrease the extreme insulin
resistance, possibly by inhibiting the production of IgG antibodies. As
the antibodies have a half life of 3-4 weeks, the response is delayed,
during which time bg control is even more difficult due to the effects
of the glucocorticoids. After several weeks the dosage can be reduced
to maintenance levels or eliminated, but relapse is common. Since glucocorticoids have other nasty effects in addition to the problems
listed above, there are significant problems with this course of
treatment.
Davidson's recommendation is based on The Good News: insulin resistance
is self-limited and only lasts a few months to a year. He simply uses
as much insulin as is needed in the meantime. U-500 concentration is
available for this purpose. The antibodies delay the action, so even
though U-500 is regular insulin it acts like a lente or semilente in
resistant patients. For unknown reasons, much less U-500 is needed than
the equivalent amount of U-100, 50% to 75% less. Since the situation is difficult to manage and is temporary, Davidson advises not trying for
good bg control, but just avoiding ketosis and the overt symptoms of hyperglycemia (thirst, excess urination, infections).
When insulin sensitivity returns, it can happen quite suddenly.
Davidson starts reducing the high insulin doses when fasting bg is
under 200 mg/dl (11.0 mmol/L). At these times, large amounts of insulin previously bound to the antibodies may be released, so avoiding
hypoglycemia is a major concern. The return to normal sensitivity will
take at least several weeks due to the half-life of the antibodies, and
insulin requirements may fluctuate a great deal during this time. A
fast response to U-500 insulin (2-4 hours from injection to measurably
lower bg) may indicate the decline of insulin resistance.
[This was the movie. Now go read the book.]
------------------------------
Subject: What is pycnogenol? Where and how is it sold?
All sections on pycnogenol are written by Laura Clift
<LauraRuss(AT)aol.com>.
Numbers in parentheses refer to the section on "Pycnogenol references".
Pycnogenol, a.k.a. Revenol, is a substance that has been mentioned in misc.health.diabetes as an aid/cure for several diabetic complications. Pycnogenol is a bioflavanoid, also identified as an oligomeric
proanthocyanidin (OPC) and a procyanidin, which is found in the bark of conifers, specifically the maritime pine (_Pinus maritima_) and the Canadian spruce (_Tsuga canadensis_) and in grape seeds. The substance was
patented in
the US (patent 4,698,360) in 1985 by J. Masquelier of France.
Pycnogenol is sold on several web sites in addition to health food
stores. The
web sites are set up in a pyramid scheme with the claims of quick riches for new distributors. Most of the sales pitches rely on first-person "testimonials". Some pitches include a list of published scientific studies that, according to the pitch, support the claims of the ad. In the following sections I examine the sales claims, investigate the ad's publication list,
and establish a bottom line.
------------------------------
Subject: What claims do the sales pitches make for pycnogenol?
Written by Laura Clift.
Pycnogenol or Revenol (super-enriched pycnogenol) claim to be the world's
most powerful anti-oxidant (vitamin C and E are anti-oxidants). The ads
state
pycnogenol is non-toxic, non-mutagenic, has high bioavailability,
crosses the
blood-brain barrier, enables vitamin C to remain in the body for 3 days as opposed to 3 hours, increases capillary resistance, decreases capillary fragility and permeability, decreases lower leg volume, strengthens
collagen,
and remains active in the body for 72 hours.
Ads make claims that pycnogenol prevents, aids and/or cures the following conditions:
arthritis, cancer, AIDs, stomach pains, aches and pains, aging, abnormal
menstrual bleeding, asthma, atherosclerosis, bruises, diabetic
retinopathies, dry skin, edemas, excessive blood sugar, fatigue, hay
fever,
heart attacks due to vascular accidents, hemorrhoids, inflamed tissue,
internal bleeding, jet lag, kidney disease, menstrual cramps, phlebitis,
poor circulation, skin elasticity, strokes due to cerebral accidents,
stress, ulcers, varicose veins, multiple sclerosis, prostate problems,
sleep disorders, dog and horse cancers, attention deficit disorders, and
increased physical endurance.
------------------------------
Subject: What's the real published scientific knowledge about pycnogenol?
Written by Laura Clift. (refs) point to "pycnogenol references" section.
In a study examining the anti-oxidant action of several bioflavanoids, (-)-epicatechin 3-O-gallate and (-)-epigallocatechin 3-O-gallate were both
more potent than pycnogenol against the free radicals DPPH, superoxide
anion,
OH, and OOH, although not by much (1).
The toxicity of pycnogenol is not established in published reports. Proanthocyanidin mutagenicity is tricky, if it is completely pure it is considered non-mutagenic. However, there is an impurity that is very similar
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