Subject: diabetes FAQ: treatment (part 3 of 5)
Supersedes: <diabetes/faq/part3_827207059@rtfm.mit.edu>
Date: 1 Apr 1996 18:12:51 GMT
References: <diabetes/faq/part1_828382217@rtfm.mit.edu>
Summary: Discusses questions which have been asked frequently in
         misc.health.diabetes. Likely to be of interest to anyone who has
         diabetes or a friend or relative with diabetes or other blood
         glucose disorder.
X-Last-Updated: 1996/03/08

Posting-Frequency: biweekly
Last-modified: 20 Feb 1996

Changes: add warning about pen refill concentration (7 Feb)
         add mention of pen clicks (20 Feb)

Subject: READ THIS FIRST
========================

Copyright 1993-1996 by Edward Reid. Re-use beyond the fair use provisions
of copyright law and convention requires the author's permission.

Advice given in m.h.d is *never* medical advice. That includes this FAQ.
Never substitute advice from the net for a physician's care. Diabetes is a
critical health topic and you should always consult your physician or
personally understand the ramifications before taking any therapeutic action
based on advice found here or elsewhere on the net.

Subject: Table of Contents
==========================

INTRODUCTION (found in all parts)
  READ THIS FIRST
  Table of Contents
GENERAL (found in part 1)
  Where's the FAQ?
  What's this newsgroup like?
  Abuse of the newsgroup
  The newsgroup charter
  Newsgroup posting guidelines
  What is glucose? What does "bG" mean?
  What are mmol/L? How do I convert between mmol/L and mg/dl?
  What is c-peptide? What do c-peptide levels mean?
  What's type 1 and type 2 diabetes?
  Is it OK to discuss diabetes insipidus here? What is it?
  How about discussing hypoglycemia?
BLOOD GLUCOSE MONITORING (found in part 2)
  How accurate is my meter?
  Ouch! The cost of blood glucose measurement strips hurts my wallet!
  What do meters cost?
  Comparing blood glucose meters
  How can I download data from my One Touch II?
  How can I download data from my Glucometer (tm)?
  Other recordkeeping software
  I've heard of a non-invasive bG meter -- the Dream Beam?
  What's HbA1c and what's it mean?
TREATMENT (found in part 3)
  My diabetic father isn't taking care of himself. What can I do?
  Managing adolescence, including the adult forms
  So-and-so eats sugar! Isn't that poison for diabetics?
  Insulin nomenclature
  Travelling with insulin
  Injectors: Syringe and lancet reuse and disposal
  Injectors: Pens
  Injectors: Jets
  Insulin pumps
  Type 1 cures -- beta cell implants
  Type 1 cures -- pancreas transplants
  Type 2 cures -- not even a dream
  What's a glycemic index? How can I get a GI table for foods?
  Should I take a chromium supplement?
  I beat my wife! (and other aspects of hypoglycemia) (not yet written)
  Does falling blood glucose feel like hypoglycemia?
  Alcohol and diabetes
  Necrobiosis lipoidica diabeticorum
  Has anybody heard of frozen shoulder (adhesive capsulitis)?
  What is pycnogenol? Where and how is it sold?
  What claims do the sales pitches make for pycnogenol?
  What's the real published scientific knowledge about pycnogenol?
  How reliable is the literature cited by the pycnogenol ads?
  What's the bottom line on pycnogenol?
  Pycnogenol references
SOURCES (found in part 4)
  Online resources: diabetes-related newsgroups
  Online resources: diabetes-related mailing lists
  Online resources: commercial services
  Online resources: FTP
  Online resources: World Wide Web
  Online resources: other
  Where can I mail order XYZ?
  How can I contact the American Diabetes Association (ADA) ?
  How can I contact the Juvenile Diabetes Foundation (JDF) ?
  How can I contact the British Diabetic Association (BDA) ?
  How can I contact the Canadian Diabetes Association (CDA) ?
  What about diabetes organizations outside North America?
  How can I contact the United Network for Organ Sharing (UNOS)?
  Could you recommend some good reading?
RESEARCH (found in part 5)
  What is the DCCT? What are the results?
  More details about the DCCT
  DCCT philosophy: what did it really show?
IN CLOSING  (found in all parts)
  Who did this?

Subject: My diabetic father isn't taking care of himself. What can I do?
========================================================================

We'll assume your father has type 2 diabetes. See separate section for
definition of types.

Type 2 diabetics, and those who care for them, are in a difficult situation.
Type 2 strikes late in life, so personal habits and patterns are already
formed and solidly engrained. Yet in most cases those habits and patterns are
exactly what must be changed if a newly-diagnosed diabetic is to care
properly for his or her health. This is a difficult psychological problem.

The cornerstones for treating type 2 diabetes are exercise, weight control,
and diet. A high percentage of type 2 patients who apply these therapies
assiduously can control the disease with these therapies alone, without
insulin or oral hypoglycemic drugs. Naturally these are also some of the most
difficult aspects of life to change. There can be no single or simple answer
of how to help or encourage a particular individual find a combination of
therapies which not only controls the disease but also is psychologically
acceptable and which can be incorporated as a lifetime pattern. Helping
depends on knowing the individual's habits, patterns, motivations, desires,
likes and dislikes, and working with all the existing conditions and
everything brought forward from past life.

Doctors and other health care professionals tend to treat type 2 diabetics
with drugs (oral hypoglycemics) and insulin rather than taking the time to
try to get their patients to make the difficult lifestyle changes described
above. This isn't true of all practitioners, but of many. They have good
reason for this tendency: they know all too well (often from painful personal
experience) that most type 2 patients aren't going to make many changes
anyway, and the doctors and other practitioners don't like wasting their time
and breath. So it's likely to fall to friends and relatives who care deeply
to educate themselves about type 2 diabetes and do what they can to encourage
their loved one to make changes. In particular, if the doctor has left the
impression that drugs and insulin are the only treatments, make sure to
counter that impression with information about the value of exercise, diet,
and weight control.

At the same time, it's important to remember that needing oral hypoglycemics
and/or insulin injections as additional tools isn't failure. On the contrary,
a patient who's been actively involved in self treatment already has an
excellent chance of using these additional tools successfully. Those who have
learned to use the exercise - weight control - diet triumvirate will also be
able to utilize insulin and oral drugs as additional treatments when needed.
Choose the appropriate tools and use them effectively.

These treatment choices can interact in positive ways as well. Bringing blood
glucose under control often increases the body's sensitivity to insulin. So
ironically, using insulin may decrease the need for insulin. This is a
positive change which can then be reinforced by the other, interacting
treatments.

You will need far more information than is appropriate for a Usenet FAQ
panel. As a start, call the ADA (see ADA section), get a subscription to
_Diabetes Forecast_ (see journals), and visit a university library and browse
in the diabetes section in the stacks.

Beyond the generalizations above, a few specifics are usually of value:

   Set a good example in your own life. Exercise and eat a good diet.
   The recommendations for diabetics are healthy choices for anyone.

   Share your example. Serve a tasty, low-fat diet to family and friends
   when they are your guests.

   Suggest joint activities. Suggest a walk instead of watching a
   ball game.

   Make sure your diet and activities are visibly enjoyable so your
   guests will accept your invitiation to join you.

Subject: Managing adolescence, including the adult forms
========================================================

Adolescents have special problems in managing diabetes. These include a
variety of physiological problems related to puberty and rapid growth, social
problems related to growing up and the general social pressures of adolescent
life, and the psychological turmoil caused by the expectations of others. I'm
here today to talk about (hey, hold the eggs and tomatoes) expectations.

Actually, this all applies to adults as well, though the subtle points may
differ.

The most important thing to remember, for the adolescent, the parent, and the
health care provider, is


              All Blood Glucose Measurements Are Good.

              There Are No Bad Blood Glucose Readings.


If that doesn't sound right, then please take two steps. First, learn why it
is true. Then chant it like a mantra until you internalize it, so that you
never give off the slightest vibes to the contrary.

Why is it true?

There are two kinds of adolescents (to simplify life enormously): those who
rebel and those who want to please. Ironically, the rebellious are probably
easier to deal with in treating diabetes. "So my blood sugar is 350, so
what?" Bad? No, that's good: you know what's going on, and so does your
child. The point of blood glucose measurement is to respond -- not to be good
or bad -- and only with an accurate report can you and the patient respond.

  [Compulsory digression: 350 mg/dl = 20.0 mmol/L.]

Look what can happen to the eager-to-please child:

   Child: My blood sugar is 350.
   Adult: Oh, that's awful! You must try to be better!
      [next time]
   Child: My blood sugar is ... um [to self: I must be good] 140 ...
   Adult: Oh, that's great!

In short order, the log book looks great but the HbA1c doesn't jibe.

This all happens with the best of intentions from all parties. The child is
trying to please, and is behaving in exactly the ways that elicit approval.
The adult is trying to care for the child's health in the most natural ways.
And the result is one that neither desires.

Thus the positive mantra to replace the half-negative one above:


              All Blood Glucose Measurements Are Good.

           Responding To Blood Glucose Readings Is Good.


. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

An excellent article entitled "Insulin Therapy in the Last Decade: A
Pediatric Perspective", by Julio Santiago, MD, of the St. Louis Children's
Hospital and the Washington University School of Medicine in St. Louis,
Missouri, appears in _Diabetes Care_, volume 16 supplement 3, December 1993,
pp. 143-154. The article discusses many aspects of treating pediatric
diabetes. Santiago spends several pages discussing how to establish realistic
and honest approaches to self-monitoring. I highly recommend the article.

Subject: So-and-so eats sugar! Isn't that poison for diabetics?
===============================================================

This is asked from both sides: the non-diabetic who doesn't understand
diabetes, and the diabetic who gets tired of hearing "I won't put any sugar
on the table" etc etc ad nauseum.

Diabetics should eat a high-quality, healthy diet very similar to that
recommended for everyone. This will include some sugar, and research
indicates that obtaining a moderate amount of carbohydrates in the form of
sugar makes little or no difference in controlling blood glucose levels. There
isn't room here to describe all the aspects of diabetes treatment that make
this so.

No one has suggested a really good, uniformly satisfying answer to the public
know-alls who insist they know more than you do. Feel free to add to this
list:

   That was true before insulin was isolated in 1921.

   Fat is more dangerous than sugar because diabetics have a three-fold
   higher risk of heart disease.

   The whole point of injecting insulin is to balance carbohydrate intake.

   All carbohydrates are converted to sugar in the digestive tract anyway.

Subject: Insulin nomenclature
=============================

The major types of insulin have both generic designations and brand names
used by the manufacturers. Most of the brand names are close enough to the
generic ones that the correspondence is obvious. Novo uses totally different
names. In those parts of the world where Novo has most of the market, the
Novo brand names are used in place of the generic names. To facilitate
communication between Novo users and others, here is the correspondence:

   Generic      Novo
   -------      ----
   Regular      Actrapid
   NPH          Protophane
   Lente        Monotard
   Ultralente   Ultratard

Subject: Travelling with insulin
================================

Insulin does not need to be kept cold.

Insulin is stable at body temperature. This is not surprising when you realize
that the beta cells often store the insulin they produce for days before
releasing it.

A general guide to how long it is safe to store insulin at various
temperatures:

   Refrigerated          a few years
   Room temperature      several months
   Body temperature      a few weeks

Do not allow insulin to freeze. Do not expose insulin to temperatures
significantly above body temperature. I don't know how much heat is required
to destroy insulin, but leaving it in a closed car in the sun would be a very
bad idea.

Short of such extremes, degradation is gradual. You should always be alert for
gradual changes in your blood glucose anyway, since individual sensitivity to
insulin changes over time for reasons unknown. Your normal dosage adjustments
will handle minor degradation that might occur, say, from keeping insulin in
a very hot room for several weeks.

So why do drugstores (pharmacies) keep insulin refrigerated, and why are
"insulin cold packs" advertised? The drugstores are mosty just following
standard procedures. For them, it's a simple precaution not worth violating..

As for cold packs, as long as anyone thinks they are needed, someone will sell
them. As noted, you do need to protect insulin from extremes of temperature,
and the cold packs can help at both extremes. In many situations it may be
just as effective to pack the insulin next to a bottle of water, especially
during outdoor activities when you are carrying water anyway.

Always keep your insulin with you! Keep all your medical supplies with you.
Never pack them in checked luggage. Luggage may sit outside in hot sun or
freezing rain. If you are delayed, or your luggage is waylaid, you could be
without supplies packed in luggage.

Meter manufacturers recommend keeping meters and strips from freezing and
extreme heat.

Subject: Injectors: Syringe and lancet reuse and disposal
=========================================================

Disposable syringes can be safely reused as long as you take reasonable
precautions. Recap both ends between uses, and discard the syringe if
dropped, dirty, or damaged (especially if the needle is bent). Discard it
when it becomes uncomfortable to use. This varies a great deal, being half a
dozen uses for some patients and several dozen uses for others. Comfort
depends far less on sharpness than on the silicone coating applied to the
needle at manufacture. Never wipe the needle with alcohol, as this will
remove the silicone coating.

Lancets can also be reused safely with the same caveats.

Syringe disposal has proven controversial. If you want to be conservative,
buy a needle clipper, get a hard plastic bottle designed for medical waste to
put the syringes in, and take the full bottle to a facility approved for
handling medical waste. Your doctor's office may be able to handle it for
you. Intermediate positions use one of these techniques. At the least
conservative, cap the needle carefully and discard in trash which will not be
subject to illicit searching and possible abuse. If you have trouble capping
the needle without sticking yourself, definitely get a bottle to drop the
uncapped syringes in; a bleach bottle may be adequate. Local or state
regulations may apply.

Subject: Injectors: Pens
========================

A pen injector is a device that holds a small vial of insulin and a
disposable needle, and injects an amount measured with a dial. Advantages
include being compact, convenient, easy to use circumspectly in public, and
accurate and simple in dose measurement. The pen device clicks for each unit
(or two depending on the manufacturer) dialed; this can help those with
impaired vision.

The primary disadvantage is cost. The special vials may be difficult to
obtain in remote areas, and widespread shortages have occurred occasionally.
Falling back to a standard syringe is always an option.

Also, the special vial can be refilled from a standard vial using a syringe,
making sure the rubber stopper is not damaged, though the manufacturer will
not recommend this. If you do refill, make sure to use the same concentration
of insulin. This is not a problem in the US, where only U100 concentration is
used. In some parts of the world, U40 concentration is common, but pen
refills are always U100. Make sure to match the concentration.

Pens are more popular in Europe than in the US.

Subject: Injectors: Jets
========================

A jet injector uses no needles, but instead squirts the substance being
injected through a narrow orifice under high pressure, producing a fine
stream which penetrates the skin as easily as a needle. Jets are popular with
anyone who is simply scared of needles, for any reason. The jet disperses the
insulin more than a needle does, which probably results in faster absorption.
This can be an advantage or a disadvantage, and requires careful monitoring
when first used. Technique is just as important as with needles, so jets are
no more appropriate than needles for small children. If a jet is used to
avoid needles, equipment failure forcing a fallback to needles may be
traumatic. High cost is a major factor.

Subject: Insulin pumps
======================

An insulin pump provides a Continuous Subcutaneous Insulin Infusion, or CSII,
via an indwelling needle or catheter. That is, a small needle (similar to
those on insulin syringes) or tube is inserted through the skin and fixed in
place for two or three days at a time. An external box pumps insulin through
the needle steadily.

Pumps don't solve all the problems of treating diabetes for two main reasons:

  1) The infusion is still subcutaneous, so the insulin still must be
     absorbed before it can be used. Insulin from the pancreas goes directly
     into the bloodstream and takes effect much more quickly.
  2) Current pumps are open-loop -- that is, there is no feedback from blood
     glucose (bG) to the pump. The patient must still self-monitor bG and
     program the pump.

Nonetheless, many patients get much better results with a pump than from
intensive therapy without a pump, and those patients tend to be extremely
happy with the pump. It isn't clear at present how to decide whether a given
patient should use a pump. Different studies have obtained varying results,
ranging from 85% success to 85% dropout! Unfortunately, no studies seem to
have been done since the mid-1980s, and it is likely that the pumps and pump
therapy have become much more consistently successful since then. A few
important factors seem clear, though:

  1) Motivation. A meter takes extra effort and attention.
  2) Knowledge. If you aren't already familiar with intensive therapy,
     think more than twice before jumping for a pump. You should
     probably try intensive therapy with multiple injections first.
  3) Treatment team. Successful users are backed by teams of physicians
     and educators who are experienced *with pumps*. Don't try a pump on
     your own (the manufacturers won't let you anyway), and don't try it
     with inexperienced providers -- these are recipes for unnecessary
     failure.
  4) Funding. Pumps represent a nontrivial capital outlay. If you don't
     have insurance or other public programs that will pay for the pump,
     you will need personal financial resources.

Most or all pump manufacturers allow a trial period, so you can try a pump
without financial risk. You will probably know fairly soon whether you want
to continue with the pump.

A long discussion about many aspects of pumps is posted monthly at the same
time as this FAQ. See the section "Where's the FAQ?" for retrieval
information. The insulin pump discussion was developed and is maintained by
Jim Summers <summers@cs.utah.edu>.

Subject: Type 1 cures -- beta cell implants
===========================================

Beta cells can be isolated and implanted, requiring only outpatient surgery
for implantation. But foreign beta cells are quickly rejected without
immunosuppressant drugs. Even with the recent advances in drugs, especially
cyclosporin, using immunosuppressants is much more dangerous than living with
diabetes. As a result, beta cell implantation is not currently used to treat
diabetes.

Current research is investigating two general methods of implanting beta
cells without the use of immunosuppressant drugs. The first (immunoisolation)
encapsulates the beta cells within a barrier so that nutrients, glucose, and
insulin can pass freely through the barrier but the proteins which provoke
the immune response, and the cells which respond, cannot pass. The second
(immunoalteration) involves altering the proteins on the surface of the cells
which provoke the immune response. The first human trial began early in 1993
on immunoisolated beta cells, and human trials were scheduled to begin late
in 1993 on immunoaltered beta cells.

Don't expect these treatments to be available on a standard basis any time
soon. I've been reading about this research for about 15 years, and the
results are always just around the corner. Serious problems remain to be
solved: safety of the immunoisolated implants, long-term survival, ability to
use beta cells from non-human species, perfection of both techniques -- all
these must be resolved before beta cell implantation moves beyond the
experimental stage. Other problems will likely be encountered along the way,
since this is cutting edge medical research. I'll be surprised if it gets out
of the lab before the year 2000; 2010 is probably a better guess. And it may
fail -- it's always possible that unsolvable problems will yet arise.

Finally, it's not yet clear that even completely normal bG profiles will cure
all the problems of type 1 diabetes. Some may be related to the autoimmune
reaction that is the immediate cause of diabetes. This question cannot be
answered until it is possible to normalize bG levels for a period of many
years.

Subject: Type 1 cures -- pancreas transplants
=============================================

Whole pancreas transplants have the same rejection problems as beta cell
implants, and also require major surgery. For these reasons, whole pancreas
transplants are only used 1) in desperate cases in medical schools with
exceptional capabilities, and 2) in conjunction with kidney transplants.

Kidney transplants are (relatively) common in diabetics with advanced
complications. A kidney recipient is taking immunosuppressant drugs anyway,
and the same surgery that implants the kidney can stick in a pancreas with
little extra effort or trauma. As a result, the double transplant is now
recommended, at least for consideration, for any diabetic patient who
requires a kidney transplant.

The only disadvantage would seem to be that the pancreas donor must be dead;
whereas a living kidney donor is feasible. Even this is not strictly true, as
a kidney-plus-partial-pancreas transplant from a living donor is possible,
and the partial pancreas contains enough beta cells to produce insulin for
the recipient. However, this procedure is seldom performed.

The following is from Alexandra Bost <alex@unx.sas.com>. Thanks, Alex!

Combination kidney/pancreas transplants are listed in a different queue than
kidney-only. Since the number of people waiting for donor kidneys is quite
long (anywhere from a few months to seven or eight years), the kidney/
pancreas list is often a quicker means of receiving a transplant. For
example, in April 1995 there were 28,519 people on the UNOS [see below]
registrations for a kidney transplant. There were only 247 registrations for
a pancreas transplant and 1,139 registrations for a kidney-pancreas
transplant. [Based on UNOS Scientific Registry data as of February 11,
1994.]

Kidney/pancreas transplants, while still considered experimental at some
institutions, have been approved by Blue Cross/Blue Shield in the following
centers: University of Iowa Hospitals and Clinics, Iowa City; University of
Minnesota Hospital and Clinic, Minneapolis; Ohio State University Hospitals,
Columbus; and University of Wisconsin Hospital and Clinics, Madison. Though
this is for BC/BS only, other insurance companies may follow the BC/BS lead
if pushed.

UNOS (United Network of Organ Sharing) has a list of 109 transplant centers
that have pancreas transplant programs. For more information, contact UNOS
at (800)24-DONOR. (See the section on sources for WWW, email, other phones.)

(end of Alex's part.)

The UNOS handles transplant registrations only in the USA, but can provide
contact information for organ-donation agencies around the world.

The transplant mailing list is an excellent resource. See the section on
online resources: mailing lists.

Subject: Type 2 cures -- not even a dream
=========================================

The treatments described in the preceding sections apply only to type 1
diabetes. Type 2 diabetes is the result of insulin resistance or other forms
of improper use of insulin within the body, not in general to an absolute
lack of insulin. Type 2 patients usually have normal beta cells. There is no
treatment of comparable promise on the horizon for type 2 diabetes.

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, and some (such as white bread) even more than sugar. This was quite a
surprise when the research was first published around 1980 [[[[[need to check
date]]]]].

The problem with using the GI extensively in diet is that it is not additive.
That is, different foods interact to produce a combined GI that cannot easily
be predicted from the separate GIs. 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. Research is continuing, and eventually it may be
possible to predict the GI of a complete meal.

For now, 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.

There have been requests for GI tables on m.h.d. To my knowledge, none is
available in electronic form.

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@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.

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.

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

I thank the following people, especially Betsy, who posted the information
from which I derived this section:

    Betsy Butler <betsyb@vms.cis.pitt.edu>
    William Biggs <william@cortex.ama.ttuhsc.edu>
    Tari M. Birch <tm_birch@pnl.gov>
    Terence Griffin <griffin@cam.nist.gov>
    Bill Barner <barner@mail.loc.gov>

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 <BOYLAN_LEE@tandem.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@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: What is pycnogenol? Where and how is it sold?
======================================================

All sections on pycnogenol are written by Laura Clift <cliftl@aa.wl.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 distrbutors. 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, have high bioavailability, cross the
blood-brain barrier, enable vitamin C to remain in the body for 3 days as
opposed to 3 hours, increase capillary resistance, decrease capillary
fragility and permeability, decrease lower leg volume, strengthen collagen,
and remain active in the body for 72 hours.

Ads make claims that pycnogenol prevent, aid and/or cure 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
and hard to remove in the purification of proanthocyanidin that is mutagenic
(2).

No published work could be found on the bioavailability of pycnogenol in
particular, but oral ingestion of bioflavanoids in general result in a low
bioavailability (3).

Pycnogenol does cross the blood-brain barrier in rats when given as an
intraperitoneal injection (4). The same study seems to indicate that
pycnogenol can increase capillary resistance and decrease capillary
permeability in rats. A clinical study on 25 patients indicated an increase
in capillary resistance (5). When administered by intraperitoneal injection
to rats, chemically induced edema of the paw was decreased (6).

There are no published studies on pycnogenol's interaction with vitamin C and
most of the preventions, aids and/or cures claimed. However, procyanidol
oligomers offered no protection for venous disease from hypoxia (lack of
oxygen) (7).

Subject: How reliable is the literature cited by the pycnogenol ads?
====================================================================

Written by Laura Clift.

Masquelier J, Michaud J, Laparra J, Dumon MC. Flavanoids et pycnogenols. Int
J Vit Nutr Res 1979;49(3):307-11.

  Article in French. Abstract states that the article describes pycnogenol
  chemically designating the compound as "pycnogenol" to distinguish it from
  the hundreds of other bioflavanoinds.

Uchida S, Edamastu R, Hiramatsu M, et al. Condensed tannins scavenge active
oxygen free radicals. Med Sci Res 1987;15:831-2.

  Pycnogenol is a free radical scavenger (anti-oxidant) in vitro (outside of
  a living animal, or, in a petri plate).

Lagrue G, Oliver-Martin F, Grillot A. Etude des effects des oliomeres du
procyanidol sur la resistance capillaire dans l'hypertension arterielle et
certains nephropathies. La semaine des Hopitaux de Paris 1981; 57:1399-1401.

  French article. Abstract states capillary resistance increased in 25
  patients. No dose amount or route of administration in the abstract.

Cahn J, Borzeix MG. Etude de l'administration des oligomeres du
procyanidoliques chez le rat: Effets observes sur les alterations de la
permeabilite de la barrier hematoencephalique. La semaine des Hopitaux de
Paris 1983;59:2031-4.

  French article. Abstract states that pycnogenol crosses the blood-brain
  barrier in the rat and affects capillary permeability. Route and dose not
  presented in abstract.

Tixier JM, Godeau G, Rober AM, Hornebeck W. Evidence by in vivo and in vitro
studies that binding of pycnogenols to elastin affects its rate of
degradation by elastases. Biochem Pharmacol 1984;33(24):3933-9.

  Study with (+) catechin and pycnogenol (states they are related substances,
  but act differently, including the results of this study). Pycnogenol
  prevents the break down of elastin in vitro and in rabbits.

Kuttan R, Donnelly PV, DiFerrainte N. Collagen treated with (+)-catechin
becomes resistant to the action of mammalian aollagenase. Experentia
1981;37:221-3.

  (+) catechin is not pycnogenol (see above). Study does not investigate
  pycnogenol.

Reimann HJ, Lorenz W, Fischer M, et al. Histamine and acute hemorrhagic
lesions in rat gastric mucosa: prevention of stress ulcer formation by
(+)-catechin, an inhibitor of specific histidine decarboxylase in vitro.
Agents and Actions 1977;71:69-72.

  (+) catechin is not pycnogenol (see above). Study does not investigate
  pycnogenol.

Markle RA, Hollis TM. Rabbit aortic endothelial and medical histamine
synthesis following short-term cholesterol feeding. Exp Mol Pathol
1975;23:117-23.

Markle RA, Hollis TM. Variations in rabbit aortic endothelial and medical
histamine synthesis in pre- and early experimental atherosclerosis. Proc Soc
Exp Biol Med 1977;155:365-8.

Hollis TM, Furniss JV. Relationship between aortic histamine formation and
aortic albumin permeability in atherogenesis. Proc Soc Exp Biol Med
1980;165:271-4.

  Does not study pycnogenol or any bioflavanoid. Logic may go like this:
  pycnogenol is similar to (+) catechin which can effect histamines. Here are
  some cardiac/circulatory problems that are affected by histamine.
  Therefore, pycnogenol will prevent these diseases. Logic may be OK for a
  hypothesis but is flawed as a conclusion, especially since (+) catechin and
  pycnogenol act differently in most studies (see above).

Feine-Haake G. A new therapy for venous diseases with
3,3,4,4,5,7-hexa-dihydro-flauan. Z Allgemeinmed 1975;51(18):839.

  German article, no abstract translation; chemical name implies (+)-catechin
  was studied.

Blazso G, Gabor M. Oedema-inhibiting effect of procyanidin. Acta Physiol Acad
Sci Hung 1980;56(2):235-40.

  Chemically induced edema of a rat's paw was decreased with intraperitoneal
  injections of pycnogenol.

Subject: What's the bottom line on pycnogenol?
==============================================

Written by Laura Clift. (refs) point to "pycnogenol references" section.

All bioflavanoids are anti-oxidants (1,8,9) and may effect capillary
hyperpermeability (8,9), inflammations (3,8), and edemas (8). However, there
is no bioflavanoid deficiency condition, and they have "no accepted
preventive or therapeutic role in vascular purpura, hypertension,
degenerative vascular disease, rheumatic fever, arthritis, cancer, or any
other condition" (9). This was as of 1988; no mention of bioflavanoids is
made in the 1994 edition of this reference. Most pycnogenol studies and/or
claims come from the early 70's to mid 80's. Promising starts are never
followed up on. Most later studies seem negative (both pycnogenol and
bioflavanoids), especially about the oral route. With all but one study
performed in rodents, there is a very definite lack of information on how
this substance acts in humans and what possible side-effects it produces.

The sales pitch seems to be taken from the 1985 patent. Filing a medical
patent doesn't mean the substance is thoroughly studied and its applications
are determined. A patent is filed when preliminary studies look promising and
you try to come up with every possibly use for the compound, no matter how
far out in left field it may be. If you do not hold the patent for the
application, someone else could conceivably use your compound for that
application and owe you nothing or a very reduced royalty.

In short, patent claims have no medical significance.

Subject: Pycnogenol references
==============================

Written by Laura Clift. This is the section to which the (refs) point.

1. Uchida S, Edamastu R, Hiramatsu M, et al. Condensed tannins scavenge active
oxygen free radicals. Med Sci Res 1987;15:831-2.

2.Yu CL, Swaminathan B. Mutagenicity of proanthocyanidins. Food Chem Toxicol
1987;25(2):135-9.

3. Namgoong SY, Son KH, Chang HW, Kang SS, Kim HP. Effects of naturally
ocurring flavanoids on mitogen-induced lymphocyte proliferation and mixed
lymphocyte culture. Life Sci 1994;54(5):313-20.

4. Cahn J, Borzeix MG. Etude de l'administration des oligomeres du
procyanidoliques chez le rat: Effets observes sur les alterations de la
permeabilite de la barrier hematoencephalique. La semaine des Hopitaux de
Paris 1983;59:2031-4.

5. Lagrue G, Oliver-Martin F, Grillot A. Etude des effects des oliomeres du
procyanidol sur la resistance capillaire dans l'hypertension arterielle et
certains nephropathies. Las semaine des Hopitaux de Paris 1981; 57:1399-1401.

6. Blazso G, Gabor M. Oedema-inhibiting effect of procyanidin. Acta Physiol
Acad Sci Hung 1980;56(2):235-40.

7. Michiels C, Arnould T, Houbion A, Remacle J. A comparative study of the
protective effect of different phlebotonic agents on endothelial cells in
hypoxia. Phlebologie 1991;44(3):779-86.

8. Lonchampt M, Guardiola B, Sicot N et al. Protective effect of a purified
flavanoid fraction against reactive oxygen radicals. in vivo and in vitro
study. Arzneimittelforschung 1989;39(8):882-5.

9. Shils ME. Modern nutrition in health and disease. Philadelphia: Lea and
Febiger, 1988. p472.

Subject: Who did this?
======================
-- 
Edward Reid          ed@titipu.resun.com
PO Box 378           reide@freenet.tlh.fl.us
Greensboro FL 32330

On the World Wide Web:

  mailto:ed@titipu.resun.com

