diabetes FAQ: general (part 1 of 5)

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Edward Reid

Apr 14, 2015, 12:04:19 AM4/14/15
Archive-name: diabetes/faq/part1
Posting-Frequency: biweekly
Last-modified: 30 May 2010 (excludes change list and Table of Contents)

Changes: add aspartame topic in research section (14 July 2005)
fix Avogadro's number (15 Dec 2006)
correct U of Louisville link (10 March 2009)
add a point to the mg/dl vs mmol/l table (27 Feb 2010)
clarify conversion section (30 May 2010)



Copyright 1993-2010 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)
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?
Helping with the diagnosis (DM or hypoglycemia) and waiting
Exercise and insulin
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 meter?
I've heard of a non-invasive bG meter -- the Dream Beam?
What's HbA1c and what's it mean?
Why is interpreting HbA1c values tricky?
Who determined the HbA1c reaction rates and the consequences?
HbA1c by mail
Why is my morning bg high? What are dawn phenomenon, rebound,
and Somogyi effect?
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
What is Humalog / LysPro / lispro / ultrafast insulin?
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 -- barely 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)?
Extreme insulin resistance
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?
Could you recommend some good magazines?
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?
Is aspartame dangerous?
IN CLOSING (found in all parts)
Who did this?


Subject: Where's the FAQ?

This FAQ attempts to answer the questions which have been most frequently
asked in misc.health.diabetes (m.h.d). This is not a complete informational
posting. My only criterion for inclusion is that the topic has frequently
appeared in m.h.d, either by an explicit question, or implicitly by
posting a
related question or a common misconception.

This FAQ is posted biweekly to the Usenet newsgroup misc.health.diabetes.
If you obtained this article by some method other than reading Usenet,
refer to the section on "Online resources: diabetes-related newsgroups"
for brief information on how to obtain access to Usenet newsgroups and
misc.health.diabetes in particular.

Feel free to make copies of this FAQ for your personal use or for a
friend or
relative, including to share with health care providers. If you want to make
this FAQ available to others on an ongoing basis (for example, on a BBS),
please do *not* post or copy the entire FAQ. Instead, post only this
entitled "Where's the FAQ?". This will enable others always to retrieve the
most recent version.

I have removed the outdated informational posting on insulin pumps.

An informational posting on diabetes-related software is posted to m.h.d at
the same time as this FAQ. See below for retrieval information. It was
developed and is maintained by Rick Mendosa <mendosa(AT)mendosa.com>.

I've used ideas and information from many people in writing this FAQ. With a
few exceptions I haven't attempted to identify them, but I thank them all.
The words herein are mine unless otherwise credited.

If you read this and it helps you, please let me know what part helped, and
why. If you read this and can't find what you want, let me know that too.
Such comments will help me decide what is worth working on, and whether.
You'd be surprised how little feedback I get. If you are reading this on the
newsgroup, just reply to this article. If you found this on the web, send
email to <edw...@paleo.org.SPAMNOT>.

These documents -- the FAQ and the software overview -- are available
from the news.answers archives at rtfm.mit.edu. Using anonymous ftp, get
the files:


or in web browser format:


You can reach a formatted version of the FAQ and other documents at


Unfortunately, faqs.org has not updated reliably for the past several
years, so rtfm.mit.edu is the best source for the latest version.


Subject: What's this newsgroup like?

Posting topics range through emotional support, treatment techniques,
psychological factors, health care practices, and insurance. We talk about
our problems, frustrations, depressions and complications to find out how
others handle the same issues and for mutual support. The atmosphere is
generally a highly supportive one, and most participants believe strongly
that this is an important aspect. As in other parts of the net, there
are one
or two regular participants who believe that it is important to question the
motives and/or knowledge of anyone posting a new problem. If you find that
the first response is antagonistic, please wait a few hours. Every
antagonistic response will elicit a dozen sympathetic responses.

Meta-topics include discussions of how to best convey health information on
the Usenet, ethical treatment of other participants, what topics and
information are appropriate for m.h.d, where to find diabetes information,
and what the newsgroup should be like.

Betsy Butler says eloquently:

The positive posts of people who are in great control are very
motivating, but it is also helpful to hear from people who don't find
it so easy. I'm sure there are a lot of people who struggle to keep
control. The people who are having trouble also need to know that there
are others who struggle, and that they are not alone. It can be very
intimidating, and a blow to self-esteem for people to suggest that if
you would just do X, Y and Z, you will be in control. There are 100s of
factors to balance, and I think people need to be reassured that "yes,
it's hard to balance so many things, many of which can't be measured or
that don't act predictably."

Topics closely related to diabetes mellitus which do not have their own
in Usenet are welcome. Examples are diabetes insipidus, hypoglycemia,
intolerance, legal and employment ramifications of chronic illness, effects
on family members, how family members can best provide support, and so on.
misc.health.diabetes tends to be inclusive of anyone who needs it.

The same caveat applies here as in all newsgroups: the advice is worth what
you paid for it. This applies in spades to a critical health topic such as
diabetes. Never substitute informal advice for a physician's care. Advice
given in m.h.d is *never* medical advice.

The variety of individual responses to diabetes is exceeded only by the
variety of individual responses to life. No two patients respond alike, and
many respond *very* differently from others. These differences are
physiological, not just psychological. They reflect not only varying
responses, but the fact that diabetes itself probably has many causes, many
more than the few types currently recognized (see section on types).
When you
read advice, realize that what works (or doesn't work) for someone else may
not work (or may work) for you. When you give advice, try to remember that
most advice is relative to the individual, not absolute. Recognize that you
can't treat your own diabetes by a set of rules, but only by knowing how
own individual body and physiology work and by adjusting to your own


Subject: Abuse of the newsgroup

As mentioned above, a few participants believe that name-calling and abusive
language are more effective than polite discussion, support and interchange
of information. They are wrong, and the vast majority of participants
a more civilized and polite view of humanity. Since misc.health.diabetes is
unmoderated, we all have to live together.

A few m.h.d. participants have received abusive email. Some are afraid to
expose such abuse, having been told that email must always be private.
However, abusive email is no more deserving of privacy than obscene phone
calls or threatening letters. There is no authority to which you can report
abusive email (unless it contains an actual threat, in which can you may be
justified in contacting a law enforcement agency). Steve Kirchoefer
<swkirch(AT)chrisco.nrl.navy.mil> is willing to try to mediate problems with
email. Though Steve has no official authority, he has experience in dealing
with problems on the net and may be able to help clear up such problems.
him complete copies of any abusive email.


Subject: The newsgroup charter

The actual charter which led to the creation of the newsgroup in May 1993
follows. This charter was proposed by Steve Kirchoefer
<swkirch(AT)chrisco.nrl.navy.mil> and approved by a public vote of the
readership, and is the official statement of the scope and purpose of this

1. The purpose of misc.health.diabetes is to provide a forum for the
discussion of issues pertaining to diabetes management, i.e.: diet,
activities, medicine schedules, blood glucose control, exercise,
breakthroughs, etc. This group addresses the issues of management of
both Type I (insulin dependent) and Type II (non-insulin dependent)
diabetes. Both technical discussions and general support discussions
relevant to diabetes are welcome.

2. Postings to misc.health.diabetes are intended to be for discussion
purposes only, and are in no way to be construed as medical advice.
Diabetes is a serious medical condition requiring direct supervision
by a primary health care physician.


Subject: Newsgroup posting guidelines

The following posting guidelines were adopted by a vote of m.h.d
in September 1994.

Posting guidelines for misc.health.diabetes:

Postings to misc.health.diabetes should be compliant with the standards
for all material posted to Usenet. The following articles may be found
in news.announce.newusers, and should be reviewed by all posters:

-Emily Postnews Answers Your Questions on Netiquette
-Answers to Frequently Asked Questions about Usenet
-A Primer on How to Work With the Usenet Community
-Rules for posting to Usenet
-What is Usenet?

Posting to misc.health.diabetes should be compliant with the group charter,
[which is in the previous section].

In addition to the above, the following guidelines are emphasized as
particularly relevant for contributions to misc.health.diabetes:

-No personal attacks or insults. Avoid argumentative debates. Responses
should concentrate on the issues presented.

-No private discussions. Take private discussions to email. When in
doubt, use email.

-Edit responses to avoid unnecessary inclusions of earlier postings.

-Edit subject lines as necessary to remain consistent with the topic.

-Support factual statements with your sources. If you can not recall the
source, then say so. Do not imply authority which you can not actually

Additional information can be found in the general FAQ posted periodically
to this group.


Subject: What is glucose? What does "bG" mean?

Glucose is a specific form of sugar, one of the simplest. It is the form
found in the bloodstream. "Blood sugar" always refers to blood glucose, and
is abbreviated bG. All bG meters are specific for glucose and will not
respond to other sugars, such as fructose, sucrose, maltose and lactose.

Although sucrose (table sugar) is the most common sugar in food, glucose is
also common. Most fruits, fruit juices, and soft drinks contain large
of glucose, and many foods contain small amounts. This means that you
must be
very careful to clean any food residue from your fingers before drawing
for a bG check. Since the normal level of bG is only 1g/L (=100mg/dl), it
only takes a tiny speck of glucose on your finger to contaminate the sample
and give you a falsely high reading. 10 *micrograms* of glucose could raise
the reading enough to cause you to overreact dangerously.


Subject: What are mg/dl and mmol/l of glucose? How do I convert?

This section discusses the conversion ONLY for glucose. The conversion is
different for every chemical. See the following section for conversions for
cholesterol and other substances.

There are two main methods of describing concentrations: by weight, and
by molecular count. Weights are in grams, molecular counts in moles. (If you
really want to know, a mole is 6.022*10^23 molecules.) In both cases, the
unit is usually modified by milli- or micro- or other prefix, and is always
"per" some volume, often a liter.

This means that the conversion factor depends on the molecular weight of the
substance in question.

mmol/l is millimoles/liter, and is the world standard unit for measuring
glucose in blood. Specifically, it is the designated SI (Systeme
International) unit. "World standard"is not universal; not only the US but a
number of other countries use mg/dl. A mole is about 6*10^23 molecules; if
you want more detail, take a chemistry course.

mg/dl (milligrams/deciliter) is the traditional unit for measuring bG (blood
glucose). All scientific journals are moving quickly toward using mmol/L
exclusively. mg/dl won't disappear soon, and some journals now use mmol/L as
the primary unit but quote mg/dl in parentheses, reflecting the large
base of
health care providers and researchers (not to mention patients) who are
already familiar with mg/dl.

Since m.h.d is an international newsgroup, it's polite to quote both figures
when you can. Most discussions take place using mg/dl, and no one really
expects you to pull out your calculator to compose your article. However, if
you don't quote both units, it's inevitable that many readers will have to
pull out their calculators to read it.

Many meters now have a switch that allows you to change between units.
Sometimes it's a physical switch, and sometimes it's an option that you can

To convert mmol/l of glucose to mg/dl, multiply by 18.

To convert mg/dl of glucose to mmol/l, divide by 18 or multiply by 0.055.

These factors are specific for glucose, because they depend on the mass
of one molecule (the molecular weight). The conversion factors are
different for other substances (see following section).

And remember that reflectance meters have a some error margin due to
both intrinsic limitations and environmental factors, and that plasma
readings are 15% higher than whole blood (as of 2002 most meters are
calibrated to give plasma readings, thus matching lab readings, but this
is a recent development), and that capillary blood is different from
venous blood when it's changing, as after a meal. So round off to make
values easier to comprehend and don't sweat the hundredths place. For
example, 4.3 mmol/l converts to 77.4 mg/dl but should probably be quoted
as 75 or 80. Similarly, 150 mg/dl converts to 8.3333... mmol/l but 8.3
is a reasonable quote, and even just 8 would usually convey the meaning.

Actually, a table might be more useful than the raw conversion factor, since
we usually talk in approximations anyway.

mmol/l mg/dl common
glucose glucose interpretation
------ ----- --------------
2.0 35 extremely low, danger of unconciousness
3.0 55 low, marginal insulin reaction
4.0 75 slightly low, first symptoms of lethargy etc.
5.5 100 mecca
5 - 6 90-110 normal preprandial in nondiabetics
7.0 126 fasting cutoff to diagnose diabetes, per ADA
recommendation established in 1997
8.0 150 normal postprandial in nondiabetics
10.0 180 maximum postprandial in nondiabetics
11.0 200
15.0 270 a little high to very high depending on patient
16.5 300
20.0 360 getting up there
22 400 max mg/dl for some meters and strips
33 600 high danger of severe electrolyte imbalance

Preprandial = before meal
Postprandial = after meal


Subject: Converting mmol/l<->mg/dl of cholesterol, triglycerides, creatinine

To convert mmol/l of HDL or LDL cholesterol to mg/dl, multiply by 39.
To convert mg/dl of HDL or LDL cholesterol to mmol/l, divide by 39.

To convert mmol/l of triglycerides to mg/dl, multiply by 89.
To convert mg/dl of triglycerides to mmol/l, divide by 89.

To convert umol (micromoles) /l of creatinine to mg/dl, divide by 88.
To convert mg/dl of creatinine to umol/l, multiply by 88.


Subject: What is c-peptide? What do c-peptide levels mean?

Thanks to Andrew Torres <andym(AT)ku.edu> for this section.

C-peptide blood levels can indicate whether or not a person is producing
insulin and roughly how much.

Insulin is initially synthesized in the form of proinsulin. In this
form the
alpha and beta chains of active insulin are linked by a third polypeptide
chain called the connecting peptide, or c-peptide, for short. Because both
insulin and c-peptide molecules are secreted, for every molecule of insulin
in the blood, there is one of c-peptide. Therefore, levels of c-peptide in
the blood can be measured and used as an indicator of insulin production in
those cases where exogenous insulin (from injection) is present and mixed
with endogenous insulin (that produced by the body) a situation that would
make meaningless a measurement of insulin itself. The c-peptide test can
be used to help assess if high blood glucose is due to reduced insulin
production or to reduced glucose intake by the cells.

There is little or no c-peptide in blood of type 1 diabetics, and c-peptide
levels in type 2 diabetics can be reduced or normal. The concentrations of
c-peptide in non-diabetics are on the order of 0.5-3.0 ng/ml.


Subject: What's type 1 and type 2 diabetes, and gestational diabetes?

The term diabetes mellitus comes from Greek words for "flow" and "honey",
referring to the excess urinary flow that occurs when diabetes is untreated,
and to the sugar in that urine.

Diabetes mellitus (DM) comes in the following classifications (which some
will argue don't really represent the actual types very well):

type 1 -- characterized by total destruction of the
insulin-producing beta
cells, probably by an autoimmune reaction. Onset is most
in childhood, thus the common (but now deprecated) term
"juvenile-onset", but the onset up to age 40 is not
uncommon and
can even occur later. Patients are susceptible to DKA
ketoacidosis). There seems to be some genetic tendency,
but the
genetic situation is unclear. Most patients are lean. Always
requires treatment by insulin. Not sex-linked. Also
referred to
as IDDM (insulin dependent diabetes mellitus).

type 2 -- characterized by insulin resistance despite adequate insulin
production. A large majority of patients are overweight at
and a majority are female. Most are over 40, hence the common
(but now deprecated) terms "adult-onset" or
"maturity-onset", but
onset can occur at any age. Patients are not susceptible
to DKA
(diabetic ketoacidosis). There is a strong genetic
tendency, but
not simple inheritance. Depending on the individual, treatment
may be by diet, exercise, weight loss, oral drugs which
the release of insulin, or insulin injections -- and usually a
combination of several of these. Also referred to as NIDDM
insulin dependent diabetes mellitus) *even when treated with
insulin* -- a confusing terminology which, unfortunately, is
supported by the ADA.

gestational -- occurs in about 3% of all pregnancies as a result of
insulin antagonists secreted by the placenta. It is
that all pregnant women receive a screening glucose tolerance
test (GTT) between the 24th and 28th weeks of pregnancy to
gestational diabetes early if it occurs, as diabetes can cause
serious difficulties in pregnancy. Sometimes requires insulin
treatment. Not susceptible to DKA (diabetic ketoacidosis).
Usually disappears after childbirth, but about 40% of patients
develop type 2 diabetes within five years. Most
authorities state
that the typical patient is female ...

malnutrition-related -- severe malnutrition sometimes causes diabetes --
hyperglycemia and all the usual symptoms. The reason is
and since this syndrome occurs almost entirely in third world
countries, research on this form of diabetes is nearly

other types -- sometimes called secondary. A catchall for forms not
by the types described above. Causes include loss of the
pancreas (to trauma, cancer, alcohol abuse, or exposure to
chemicals), diseases that destroy the beta cells, certain
hormonal syndromes, drugs that interfere with insulin
or action, and some rare genetic conditions.

These terms are not used entirely consistently. Some doctors will refer to
any diabetic using insulin as type 1, and will refer to the early onset of
type 1 diabetes as type 2 until insulin therapy is required. This usage does
not fit with most modern usage as described above (type 1 is beta cell
destruction, type 2 is insulin resistance). The situation is complicated by
the fact that early in the course of the disease it can be difficult to
determine which type is occuring, especially for patients in their 30's, the
age when the onset of both types is common.

Different patients respond very differently to what is categorized above as
the same disease. The root causes of all forms of diabetes are not
understood, and are likely more complex and varied than the simple
show. Type 1 diabetes likely has a few root causes, and type 2 diabetes
probably has a larger number of root causes.

There are also well documented reports of cases of diabetes with unexplained
combinations of syndromes from types 1 and 2. These are sometimes
referred to
as "type 1-1/2", and the reasons are not understood.

The classification above is not completely standard, and other

About 90% of diabetes patients are type 2 (some 12 million in the US), and
about 10% are type 1 (some 1 million in the US). Discussion on m.h.d
tends to
run about 2/3 type 1, I'd guess. This probably reflects the fact that type 1
diabetes is harder to ignore, and that type 2 seldom strikes the younger
people who are more likely to have net access. Type 2 is *not* less serious.

"1" and "2" are often written in Roman numerals: type I, type II. Because
typography is often unclear on computer terminals, I've stuck with the
numeral version.

Diabetes accounts for about 5% of all health care costs in the US, some
US$90 billion per year.


Subject: Is it OK to discuss diabetes insipidus here? What is it?

Diabetes insipidus (DI) results from abnormalities in the production or
use (two main types) of the hormone arginine vasopressin. The main
symptoms are excessive thirst and massive urination. The excess urine
flow is devoid of sugar. There are no blood glucose abnormalities, and
in fact there is nothing in common with diabetes mellitus except the
excess urination when untreated.

Diabetes insipidus caused by failure to produce vasopressin. This is
known as neurogenic DI (or central DI, or pituitary DI). It can be
treated with hormone replacement (by nasal spray or other routes). DI
caused by failure to use vasopressin (nephrogenic DI) is more difficult
to treat, but several drugs are available which help.

DI is much less common than diabetes mellitus, though a few people have
discussed it on misc.health.diabetes and are reading m.h.d. Such
participation is certainly welcome, but because the number of DI
patients is only 1 or 2 per 10,000 population (25,000-50,000 in the
US), there probably isn't a critical mass for discussion on Usenet.

I'm aware of two organizations which offer support specifically
related to DI.

DIARD publishes a support newsletter, maintains a support network,
distributes information on DI, and promotes education and research
related to DI, and has a web page with information and links:

Diabetes Insipidus and Related Diseases Network
535 Echo Court
Saline, MI 48176-1270
+1 734 944 0078
email: GSMAYES(AT)aol.com
web: http://members.aol.com/ruudh/dipage1.htm

The DI Foundation publishes a quarterly newsletter, Endless Water,
promotes public awareness and understanding of DI, and provides
informational material to patients, medical practitioners and

The Diabetes Insipidus Foundation, Inc.
4533 Ridge Drive
Baltimore, MD 21229
+1 410 247 3953
email: diabetesinsipidus(AT)maxInter.net
web: http://diabetesinsipidus.maxInter.net


Subject: How about discussing hypoglycemia?

Sure ...

To clarify: the term "hypoglycemia" is used to refer to two distinct
conditions. The word just means "low blood glucose". This can occur as
an insulin reaction, the result of too much injected insulin (taken to
treat diabetes) compared to food intake and exercise. But low blood
glucose can also be a chronic condition resulting from abnormalities of
insulin secretion, and this chronic condition is also called

Chronic hypoglycemia may be caused by beta cells which overreact to an
increase in blood glucose (bg) by releasing too much insulin, which
then causes a too-rapid drop in bG. Such a condition, called reactive
hypoglycemia, is usually handled by dietary adjustments, in particular
avoiding refined sugars and large meals which stimulate the
overreaction. This often requires an effort in calculating the diet and
monitoring bG levels that is equal to what anyone with diabetes needs.

Tumors (insulinomas) can cause a steady overproduction of insulin.
These generally require surgical removal.

There are other causes as well. Mayer Davidson discusses some in his
book _Diabetes Mellitus: Diagnosis and Treatment_. But you'll have to
find the Second Edition, because he dropped this chapter from the Third
Edition. I don't believe anyone claims to understand all the causes of
hypoglycemia. The US NIDDK has a booklet online which discusses some of
the less common causes:


So chronic hypoglycemia is closely related to diabetes mellitus in
being a disorder of insulin production and use, and requires many of
the same techniques for its treatment. The two are a natural for
discussion in the same newsgroup. Which is good, since there really
isn't anywhere else in Usenet at present to discuss chronic
hypoglycemia. Welcome.

A hypoglycemia mailing list, HYPO-L, is available and sees moderate
traffic. See the section on mailing lists in part 4 of this FAQ for
subscription information.

Lars Idema maintains a hypoglycemia FAQ and information on a variety of
hypoglycemia resources on the Internet. See his web page at



Subject: Helping with the diagnosis (DM or hypoglycemia) and waiting

Diagnosis of marginal type 2 diabetes, and even more so of
hypoglycemia, can be an iffy task. Single-point blood glucose
measurements often miss significant readings, especially for
hypoglycemia. While I don't recommend self-diagnosis, you can take some
steps on your own to aid your health care team in your diagnosis and
treatment. These are safe and useful steps. The first is purely
monitoring and not treatment or diagnosis on your part. The others are
good advice for anyone who does not have some other medical condition
to contraindicate the action, and are particularly good for those with
type 2 diabetes.

1) Get a blood glucose meter and start checking your blood glucose
before meals and at bedtime. Keep records. Also note what you ate, any
exercise, any unusual stress. If you suspect type 2 diabetes, also try
to check an hour after eating. If you suspect hypoglycemia, check any
time you have suspicious symptoms; you may also want to set up a few
runs where you check every 15-30 minutes for up to five hours after

Don't try to make any adjustments based on the readings until you review
them with your doctor -- just keep the record and show it to the
doctor. This will give the doctor more information than any examination
or lab test can give. Furthermore, if you are waiting for an
appointment, this record will put you ahead of the game when you
actually see the doctor. (If during this monitoring you see a dramatic
rise in blood glucose, to preprandial levels of 250 mg/dl [15 mmol/L]
and above, call the doctors and say you need an appointment *now*, not
in a month, not next week, and quote your bg levels.)

As an additional advantage, doing this monitoring on your own will
demonstrate to the doctor that you are willing to put in this kind of
effort. Often doctors are reluctant to ask patients to put in serious
time to monitor their health because so many patients don't follow up.

Blood glucose meters and all the supplies are OTC items. (True in the
USA, and I haven't heard of any country with a different policy.)
However, depending on where you live and what type of insurance or
national medical coverage you have, you may have to pay from your own
pocket if you do not have a prescription or proper pre-authorization.
For a month or so of monitoring, this is probably worth the cost.

2) Increase your exercise level, within levels that are safe in light
of any other medical conditions. In other words, if you are not already
in an exercise program, consult your doctor. Exercise will also help
with other stresses you are under. This is primarily applicable if you
suspect type 2 diabetes, but may help with hypoglycemia also.

3) Improve your diet if you are not already watching it carefully. A
standard diet with moderate calories and fat is good at this stage,
until you see the specialist. If you suspect hypoglycemia, you may want
to be especially careful of eating large amounts at one time, and avoid
concentrated sugars.


Subject: Exercise and insulin

Charles Coughran <ccoughran(AT)ucsd.edu> contributed this section.

The best way to deal with problems associated with diabetes and exercise
begins with understanding of what goes on in the metabolic system of
normal people and what the differences are for diabetics. Only with
such understanding can you make intelligent choices about
pharmacological tactics. Relying on rules of thumb can cause more
problems it solves because of the wide variability of individual
responses and the wide variety of diseases that fall under the rubric
of diabetes. Not to mention, I have seen postings where the rules of
thumb were clearly misunderstood.

While the following is intended for those who take insulin, it may
assist those on oral medications as well. Exercise in this context
means extended aerobic activity, say a minimum of 20 minutes of
jogging. This is a somewhat simplified account but I think it captures
the most important aspects for exercise related bg control. Comments

When a normal person starts to exercise, the insulin output of his
pancreas goes down. At first blush, this seems backward since the
muscles are working hard and therefore require more glucose to be
transported from the blood into the cells. There are two reasons more
glucose can be transported with less available insulin. The first is
that during exercise insulin becomes much more efficient. The mechanism
of this effect is not fully understood, but it helps overcomes the
reduction in circulating insulin.

Second, exercise activates non-insulin mediated glucose transport
pathways. These pathways are not sufficient to handle the load in the
absence of insulin, but do increase the effective insulin efficiency.

When insulin levels decline relative to the counterregulatory hormones
-- glucagon, epinephrine, norepinephrine, growth hormone, and cortisol
-- the liver is stimulated to release stored glucose. The blood glucose
that is being transported into the cells is replaced by that from
hepatic stores. It is this hormonal balance system that keeps the
levels of blood glucose in the normal narrow range during exercise.

For those of us who inject insulin, the first problem is obvious. Our
circulating levels of insulin do not react to exercise. Absent any
correction, when the muscles demand glucose and insulin becomes more
efficient our blood glucose plummets and we become hypoglycemic. This
is the reason for a commonly encountered prohibition to not schedule
exercise when your insulin is peaking. The higher the level of
circulating insulin, the more pronounced the effect.

One solution is to reduce our circulating insulin levels by reducing
insulin intake. Here specific advice starts to be difficult due to the
wide variety of insulins, regimens, and individual variability. The
spectrum spans from a Type II who takes a little NPH to help his beta
cells out to a c-peptide free pumper. I have spoken to diabetic runners
whose tactics would put me in an ambulance, even though our situations
seem to be very similar. You see a lot of advice of the form, "reduce
your insulin 2 units for every hour of strenuous exercise". This kind
of advice ignores real world variability and is sometimes much worse
than useless.

Clearly, someone who takes one shot/day has a much more limited ability
to adjust circulating insulin levels than someone using multiple
injections or a pump.

The other approach is to increase blood glucose levels by eating
carbohydrates timed to arrive at the blood stream in the form of
glucose when it is needed. The easiest way to do that is usually to eat
fast acting carbohydrates during or immediately preceding exercise.
Again, there are rules of thumb around about so many grams of
carbohydrates for a particular length of exercise at some defined
level. Again, they seem to be swamped by individual and circumstantial

Some of us do a combination of both and pump up our bg levels somewhat
before exercise and reduce insulin levels to keep things on an even

The bottom line is to make careful adjustments and test, and test, and
test, to find out how things work for your particular body.

So much for too much insulin. What happens when the circulating insulin
level is too low? When levels are so low that even the increase in
insulin efficiency doesn't overcome the defect, glucose isn't
transported into the cells. Worse, since insulin levels are low the
liver continues to pump glucose into the blood. The result is bg levels
rise with exercise. The muscles get stressed due to lack of fuel and
the metabolism of fats kicks in, ketones start being produced and the
danger of ketosis or ketoacidosis looms. This is the basis for another
rule of thumb which is often misunderstood. The rule is usually stated
"don't exercise when your bg is above 240 mg/dl (13.3 mmol/l) and
ketones are present in the urine". This makes sense because those are
signs that you have inadequate insulin supplies -- that's how many of
us got diagnosed. Exercise in those circumstances will make things
worse, not better. On the other hand, if you are 300 mg/dl (16.7
mmol/l) because you just drank a large regular cola by mistake with
lunch, exercise is a great way to bring that bg down in a hurry. Why
your bg is elevated is just as important as the fact of the elevated
level when deciding whether or not exercise is contraindicated. The 240
is also a somewhat arbitrary number. Some people start throwing ketones
at significantly lower levels.

In short: avoid exercise if your insulin level is too low. Do exercise
if you are sure your insulin level is adequate but your blood glucose
is too high.

Exercise also produces effects at longer time scales. Sometime after
exercise, there is often a take up of blood glucose by the muscles to
replenish depleted stores. This most often occurs an hour or two after
exercise, but has been reported in the range of 1/2 hour to 48 hours.
Again, as is the case during exercise, artificially high insulin levels
will lead to hypoglycemia. The last rule of thumb is to watch for
hypoglycemia after exercise.

*SPECULATION BEGINS HERE* A problem some of us encounter from time to
time is a post exercise bg spike. Blood glucose readings will be
reasonable after exercise but sharply elevated a few hours later. It is
my speculation that this represents circulating insulin levels that
were adequate to deal with exercise induced blood glucose demand with
its attendant insulin efficiency increase, but too low to deal with the
post exercise demand when insulin efficiency has lowered somewhat. It
has been my experience that post exercise elevated bg levels respond to
much less insulin than would be required in a more normal situation. It
appears that insulin efficiency falls off after exercise at some rate
and you can be on the correct side of the curve during exercise and the
wrong side after. This hypothesis is the best of a couple I have come

Regular exercise over time scales of weeks or months can reduce overall
insulin requirements. In addition, as muscles become trained and
improve their internal storage, it feeds back into the amount of
glucose demand present during exercise, and thus into the entire
control cycle.

Diabetes makes exercise, and almost everything else, harder. But, hey,
if it was easy it wouldn't be any fun :-)

There are two very good, readable books from which you can get more
information. The better is Campaigne and Lampman, _Exercise in the
Clinical Management of Diabetes_. Almost as good is _The Health
Professional's Guide to Diabetes and Exercise_ edited by Ruderman and
Devlin and published by the American Diabetes Association.


Subject: Who did this?

Edward Reid <edw...@paleo.org.SPAMNOT>
Tallahassee FL

Edward Reid

Apr 14, 2015, 12:04:22 AM4/14/15
Archive-name: diabetes/faq/part2
Posting-Frequency: biweekly
Last-modified: 9 December 2007

Changes: see part 1 of the FAQ for a list of changes to all parts.



Copyright 1993-2007 by Edward Reid. Re-use beyond the fair use
Subject: How accurate is my meter?

bG (blood glucose) meters are not as accurate as the readings you get
from them imply. For example, you might think that 108 means 108 mg/dl,
not 107 or 109. But in fact all meters made for home use have at least a
10-15% error under ideal conditions. Thus you should interpret "108" as
"probably between 100 and 120". (Similar considerations apply if you
measure in units of mmol/L.) This is a random error and will not be
consistent from one determination to the next. You cannot expect to get
exactly the same reading from two checks done one after the other, nor
from two meters using the same blood sample.

This is generally considered acceptable because variations in this range
will not make a major difference in treatment decisions. For example,
the difference between 100 and 120 may make no difference in how you
treat yourself, or at most might make a difference of one unit of
insulin. With present technology, more accurate meters would be much
more expensive. This expense is only justified in research work, where
such accuracy might detect small trends which could go undetected with
less accurate measurements.

This discussion applies to ideal conditions. The error may be increased
by poor or missing calibration, temperatures outside the intended range,
outdated strips, improper technique, poor timing, insufficient sample
size, contamination, and probably other factors. Contamination is
especially serious since it can happen so easily and is likely to result
in an overdose of insulin. Glucose is found in fruits, juices, sodas,
and many other foods. Even a smidgen can seriously alter a reading.

When comparing meter readings with lab results, also note that plasma
readings are 15% higher than whole blood, and that capillary blood gives
different readings from venous blood.

Visually read strips are slightly less accurate than meters, with an
error rate around 20-25%.

For some meters, strips are available from manufacturers other than the
meter manufacturer. Some m.h.d. readers have compared the strips side-
by-side and found those from one manufacturer to read consistently lower
than the strips from another. The differences are not likely to make a
significant difference in your treatment, but are large enough to be
noticeable and possibly confusing. For this reason it is not a good idea
to change strip manufacturers without comparing the readings from one
with the readings from the other.

I've seen no such direct comparison of meters, but the possibility
exists that some meters might read consistently lower than others. Be
careful when changing meters.

By "error rate" I mean twice the standard deviation from the mean. An
error rate of 15% says that about 95% of the readings will be within 15%
of the actual value.


Subject: Ouch! The cost of blood glucose measurement strips hurts my

The cost of blood glucose measurement strips is a complex interaction
of R&D costs, manufacturing costs, marketing strategy, insurance
practices, and undoubtedly other factors. You can ask on the net if you
want; you'll get lots of comments but no answers.

There are a few of ways of reducing the cost of blood glucose

One is to seek out the best price for the strips; large stores such as
Costco often have good prices, as do some online order suppliers.

A second way is to choose a meter with lower cost strips. Your health
care team may be familiar with and prefer a particular meter, but it's
not likely that they considered cost in making their choice. If you
insist that you need a lower cost system, they should be willing to
work with you. All meters now on the market are adequately accurate for
home use, so if you are getting strips under insurance, you are
generally safe in using the preferred brand under your plan.

At one time, you could use visually read strips (such as Chemstrip bG)
and cut them in half. This type of strip has mostly disappeared from the
market as of 2007 and the prices on any remaining is high, so this is no
longer a viable option.

Most discussion on m.h.d of the cost of blood glucose measurement strips
has centered on the US. I'm not sure why, though a good guess is that
differences in health care systems and national policies make this
issue more critical to the individual patient in the US. There is no
dearth of non-US participants on m.h.d.


Subject: What do meters cost?

The flip side of expensive blood glucose measurement strips is that the
manufacturers virtually (and sometimes literally) give away the meters
to hook you on their strips. Don't pay full price for a meter; look for
discounts, rebates, and giveaways. There is even a brand of strips which
includes a basic meter in the top of each vial; the price is OK and as
far as I know the accuracy is as good as any.

Make sure you consider the cost of strips as well as the cost of meters,
and find out which your insurance will pay for. The most fully featured
meters don't have such widely advertised deals, though you can probably
find ways of getting them at discount. Decide whether you need a meter
with a lot of extra features or just a basic one. As of 2007, even most
basic meters allow you to download results into a computer.

If you have insurance that pays for strips but not for the meter, you
should not have to pay anything for the meter. Most like it will be
provided to you so that you can use the preferred strips. If not, and if
it's worth the time to you, call the meter manufacturers' customer
service departments or the online suppliers. They will very likely find
a way to get you the meter for free. The manufacturers make most of
their profit on the strips, not on the meters.

As with strips, this discussion of costs applies to the US, and there
has been little discussion of meter costs outside the US on m.h.d.,
probably because fewer tradeoffs are available in most countries.

In Britain, strips are covered by the National Health Service, but
meters may be expensive. However I've also heard of a limited-time One
Touch program providing a full refund for the meter if you submit the
strip wrappers. Likely other companies will compete. (This information
is from the 1990s, and I do not know if it is current.)

Elsewhere? Please post. It's likely that the situation is continuing to
change rapidly, so if the cost of the meter is painful for you,
investigate other options before paying full price -- wherever you live.


Subject: Comparing blood glucose meters

The ADA has a wealth of information on diabetes-related products,
including meters, at


This URL has changed in the past and might change again.


Subject: How can I download data from my meter?

When I originally wrote this section, download capabilities were rare.
Now, almost every meter maker provides this capability, with the
possible exception of some house-brand meters and very small meters. As
a result, I have removed much of the original information.

A great deal of information on diabetes-related software of all kinds
can be found on David Mendosa's web site, http://mendosa.com.

Most meter makers charge extra for the cable and software for
downloading. The cables usually include electronics, and so are not
easily duplicated. Much of the software on David Mendosa's web site is
third party software which can download from a variety of meters.

LifeScan publishes the download protocol, or at least did at one time.
You can download a copy of those specs from

One Touch II: ftp://vic.cc.purdue.edu/pub/lifescan.ot2
One Touch Profile: ftp://vic.cc.purdue.edu/pub/lifescan.pro

Vic Abell <abe(AT)purdue.edu> has long provided a simple free DOS
program, TOUCH2, to download and analyze One Touch II and Profile data.
This was probably the first widely available third-party program to
analyze meter data. TOUCH2 interfaces to the data port of the One Touch,
downloads the data on command, and provides a variety of analytical
displays. I do not know whether it works with all the latest LifeScan
models. It's available in a couple of forms via anonymous ftp from
vic.cc.purdue.edu in the /pub directory, or using a web browser,



Subject: I've heard of a non-invasive bG meter -- the Dream Beam?

*** The following information is incomplete, as another company has
introduced a non-invasive meter for about $8000. It has been discussed
in the newsgroup. Rumors of other non-invasive (and "non-evasive")
meters abound. I won't be trying to keep this section up to date until
the situation stabilizes. ***

*** Note that as of 2007, we are no closer to having a non-invasive
meter than when I wrote the following over ten years ago. A minimally
invasive meter and two or three continuous meters using embedded probes
exist, but their accuracy leaves a lot to be desired.

There is at least one development project in hot pursuit of a bG monitor
which operates by shining light through flesh (through the thumbnail in
one case) and analyzing the light that passes through. Glucose doesn't
affect light much differently from many other substances in the body, so
this is not an easy task. Some field trials have been done, but the
developers have a way to go to reach acceptable accuracy. A successful
product is far from guaranteed, and may be several years away if it
arrives at all.

One estimate is that such a meter might cost about US$1000. Assuming the
per-check cost is zero, this would pay for itself in 1-2 years for many
patients. Look for the insurance companies to throw up some roadblock to
achieving these savings, at least in the US.


Subject: What's HbA1c and what's it mean?

Hb = hemoglobin, the compound in the red blood cells that transports
oxygen. Hemoglobin occurs in several variants; the one which composes
about 90% of the total is known as hemoglobin A. A1c is a specific
subtype of hemoglobin A. The 1 is actually a subscript to the A, and
the c is a subscript to the 1. "Hemoglobin" is also spelled
"haemoglobin", depending on your geographic allegiance.

Glucose binds slowly to hemoglobin A, forming the A1c subtype. The
reverse reaction, or decomposition, proceeds relatively slowly, so any
buildup persists for roughly 4 weeks. Because of the reverse reaction,
the actual HbA1c level is strongly weighted toward the present. Some of
the HbA1c is also removed when erythrocytes (red blood cells) are
recycled after their normal lifetime of about 90-120 days. These
factors combine so that the HbA1c level represents the average bG level
of approximately the past 4 weeks, strongly weighted toward the most
recent 2 weeks. It is almost entirely insensitive to bG levels more
than 4 weeks previous.

In non-diabetic persons, the formation, decomposition and destruction of
HbA1c reach a steady state with about 3.0% to 6.5% of the hemoglobin
being the A1c subtype. Most diabetic individuals have a higher average
bG level than non-diabetics, resulting in a higher HbA1c level. The
actual HbA1c level can be used as an indicator of the average recent bG
level. This in turn indicates the possible level of glycation damage to
tissues, and thus of diabetic complications, if continued for years.

Interpreting HbA1c values can be tricky for several reasons. See the
following section for more details.


Subject: Why is interpreting HbA1c values tricky?

Interpreting HbA1c values is tricky for several reasons: differing lab
measurements, variation among individuals, and misapprehension of the
relevant timeframe.

First trick: several different lab measurements have been introduced
since 1980, measuring slightly different subtypes with different limits
for normal values and thus different interpretive scales.

A National Glycohemoglobin Standardization Program began in 1996,
sponsored by the American Diabetes Association and others. See
reference 1. This program certifies HbA1c assays which conform to the
method used in the DCCT. However, as of 1998 other versions are still
in use in many places, both in the US and elsewhere. When you get a lab
result, be sure to look at what the lab considers to be the normal
range. Most discussion of HbA1c values in m.h.d appears to be based on
the DCCT, where the normal range is approximately 3.0-6.1%. Caveat
lector. (See part 5, Research, of this FAQ for more information on the
DCCT, the Diabetes Control and Complications Trial.)

Second trick: HbA1c levels appear to vary by up to 1.0% among
individuals with the same average bG. See reference 2.

This is very recent research and its implications are not yet clear. The
actual reaction rates governing the formation of HbA1c may vary among
individuals. Some of the variation may be due to differences in
erythrocyte (red blood cell) survival times -- the rough 90-120 day
range noted earlier -- although other work limits this to a small part
of the total variation (see reference 5). Variations in the HbA1c
formation rate may or may not correlate with the rate of damage to
other tissues.

While we await further research, we can only say that differences of
1.0% from one individual to another may not be meaningful.

Although HbA1c varies among individuals with the same average bG, it is
very stable for any given individual. Thus a change of 1.0% in your own
HbA1c is definitely meaningful.

Third and final trick: most medical professionals have been given
incorrect information about the timeframe which HbA1c represents.
Even textbooks normally state the 90-120 day average, as does the
American Diabetes Association in its Position Statement on Tests of
Glycemia in Diabetes (see reference 1).

The longer estimate is based on the assumption that the conversion of
hemoglobin A to HbA1c is essentially irreversible. This was a
reasonable assumption before the reaction rates were actually measured.
See the following section for information about the research which
measured the reaction rates and simulated the consequences.

See the following section for the references mentioned above.


Subject: Who determined the HbA1c reaction rates and the consequences?

In the early 1980s, Henrik Mortensen and colleagues at Glostrup
University Hospital, in Denmark, measured the reaction rates in vitro.
Their results showed the assumption of irreversibility to be untrue. In
fact the reverse reaction (HbA1c to HbA and glucose) proceeds at about
1/8 the rate of the forward reaction, which is very far from
irreversible. Mortensen et alia also built a biokinetic model based on
the measurements, and validated the model by comparing its predictions
to actual patients. See references 3-5.

Among other things, Mortensen's work shows that after a change in
average bG level, the HbA1c level restabilizes after about 4 weeks.
This has several consequences. Clinically, the most important are

First, the HbA1c is an exponentially weighted average of blood glucose
levels from the preceding 4 weeks, with the most recent 2 weeks being
by far the most important.

Second, measuring HbA1c less often than monthly results in unmonitored
gaps between measurements. To use HbA1c as a continuous monitoring
tool, you need to check it at least once a month.

Third, it is worthwhile checking the HbA1c of newly diagnosed patients
as often as once a week to determine the effectiveness of the newly
imposed treatment.

Reference 1: American Diabetes Association, Tests of Glycemia in
Diabetes, Diabetes Care 23:S80-S82, January 2000 Supplement 1.
This specific issue is no longer available online, but the most recent
version is available at http://diabetes.org/cpr/.

Reference 2: Kilpatrick ES, Maylor PW, Keevil BG: Biological Variation
of Glycated Hemoglobin. Diabetes Care 21:261-264, February 1998.
Abstract available on the web at

Reference 3: Mortensen HB, Christophersen C: Glucosylation of human
haemoglobin a in red blood cells studied in vitro. Kinetics of the
formation and dissociation of haemoglobin A1c. Clinica Chimica Acta
134:317-326, 15 November 1983.

Reference 4: Mortensen HB, Volund A, Christophersen C: Glucosylation of
human haemoglobin A. Dynamic variation in HbA1c described by a
biokinetic model. Clinica Chimica Acta 136:75-81, 16 January 1984.

Reference 5: Mortensen HB, Volund A: Application of a biokinetic model
for prediction and assessment of glycated haemoglobins in diabetic
patients. Scandinavian Journal of Clinical and Laboratory Investigation
48:595-602, October 1988.


Subject: HbA1c by mail

You may find it cheaper and/or more convenient to have your HbA1c
measurements done by mail -- and you collect the sample by fingerstick.
As far as I know, the tests mentioned here are as accurate as those done
by major labs.

Diabetes Technologies (http://diabetestechnologies.com) provides a
"Accu-Base A1c Test Kit". The cost is $26 per kit plus $6 S/H, with
discounts for multiples, which includes the laboratory analysis. All
needed supplies are provided, including a lancet and postage to the lab.

The procedure is simple: they provide a capillary tube already attached
to a clip. Stick your finger (using a one-use lancet they provide, if
you wish) and touch the end of the tube to the drop until the tube is
full -- a fraction of a second to a few seconds. Drop the tube into a
small vial with fluid in it (pre-filled) and shake for a few seconds.
Fill out a little paperwork. Pack the vial in a Biopack, padding and
package, all provided and even prestamped. Drop it in the mail. You
provide: writing pen, blood, tissue paper for the excess blood.

The lab analyzes the sample using HPLC (high performance liquid
chromatography). This is the same as the major labs use. In other words,
Quest or LabCorp take an entire vial of blood and use one drop.

Diabetes Technologies is in Thomasville, GA. Their phone number is
888-872-2443, and their web site is http://diabetestehnologies.com.

Flexsite Diagnostics (http://flexsite.com) offers a single-test kit for
$20, four for $60, and they accept Medicare reimbursement. The test
requires two drops of blood, which must dry overnight on a paper
collector before mailing. They offer priority or express mailing (both
ways) for $10 and $30 additional, although I gather they do not promise
that the test itself will be processed any faster. Darrell Hervey
<bpd318(AT)aol.com> reports that his experience with Flexsite was

Biosafe (http://ebiosafe.com) sells a mail-in "Biosafe Diabetes (A1C)
Test", which uses a collection card similar to the Flexsite procedure.
It is available directly from Biosafe and from various online merchants
for around $25. I have serious problems with Biosafe due to their use of
the term "diabetes test", which implies that A1c is to be used for
diagnosing diabetes, which is totally contrary to ADA recommendations.
They even have another "Diabetes Risk Assessment" kit, which explicitly
uses A1c as one part of the assessment. Because of their recommendations
which are contrary to ADA positions, I cannot recommend the Biosafe

Express-Med used to make a kit which I used once, but they no longer
sell it. It was similar to the kit now sold by Flexsite.

Becton-Dickinson (BD) was advertising a HbA1c kit in 1998. However, the
last time I spoke with someone there, they were only distributing it
through health care organizations (such as HMOs) and plans for
individual sales were indefinite.

A personal note: I used the Diabetes Technologies kit, and a predecessor
supplied by Diabetes Support Systems, for several years starting in
1996. Without this service, I probably would have had at most one HbA1c
measurement per year due to the cost and the inconvenience of visiting
the lab or doctor's office -- and I really needed the tests at times. I
am not currently using the service as of 2007, only because my insurance
provides the test free at Quest.

(Some updates applied December 2007. Other options may be available.)


Subject: Why is my morning bg high? What are dawn phenomenon, rebound,
and Somogyi effect?

This section is written by Charles Coughran <ccoughran(AT)ucsd.edu>.

There are three main causes of high morning fasting bg. In decreasing
order of probability they are insufficient insulin, dawn phenomenon, and
Somogyi effect (aka rebound). Insufficient or waning insulin is simple.
If the effective duration of intermediate or long acting insulin ends
sometime during the night, the relative level of circulating insulin
will be too low, and your blood sugars will rise.

Dawn phenomenon refers to increased glucose production and insulin
resistance brought on by the release of counterregulatory hormones in
the early morning hours near waking. It happens in normal people as well
as in diabetics; in nondiabetics it shows up as measurably increased
insulin secretion around dawn. Dawn phenomenon is variable in strength
both within the population and over time in individuals. It can show up
as either high fasting glucose levels or an increased insulin
requirement to cover breakfast compared to equivalent meals at other
times of day.

Somogyi effect refers to a rebound in bg after nocturnal hypoglycemia
which occurs during sleep with the patient not experiencing any
symptoms. The hypoglycemia triggers the release of counterregulatory
hormones. Somogyi effect appears to be less prevalent than previously
thought. While it does occur, some episodes of hyperglycemia following
hypoglycemia are actually waning insulin levels following an insulin
peak with medium acting insulin. This can be difficult to sort out.

The best way to sort it out is to test every couple of hours from
bedtime to morning.

If your bg rises all, or much of the night, it is a lack of
circulating insulin.

If it is stable all night, but rises sharply sometime before you
wake in the morning, it is dawn phenomenon.

If your bg declines to the point of a hypoglycemic reaction, it is
*possibly* Somogyi effect.

You may have to test on several nights to nail the problem. Once you
have figured out the problem you and your doctor can discuss changes in
your insulin regimen to correct it. The answer depends critically on
your particular circumstances.

Mayer Davidson, in _Diabetes Mellitus: Diagnosis and Treatment_ (p 252
in the 3rd edition) says that Somogyi effect rarely causes fasting
hyperglycemia, and cites studies.

Edward Reid

Apr 14, 2015, 12:04:22 AM4/14/15
Archive-name: diabetes/faq/part5
Posting-Frequency: biweekly
Last-modified: 14 July 2005

Changes: see part 1 of the FAQ for a list of changes to all parts.



Copyright 1993-2005 by Edward Reid. Re-use beyond the fair use provisions
Subject: What is the DCCT? What are the results?

The Diabetes Control and Complications Trial was a large multi-center
trial involving over 1400 volunteer patients with type 1 diabetes. It
began in 1983, ramped up to full speed by 1989, and ended early in 1993
when the investigators felt the results were clear. The volunteers were
all undergoing "standard" treatment when they were recruited, meaning
one or two injections per day. They were randomly assigned to two
groups. One group continued as before. The other group received
intensive treatment aimed at achieving blood glucose (bG) profiles as
close as possible to normal. The intensive treatment involved multiple
bG checks per day, multiple injections and/or an insulin pump, and
access to and regular consultation with a team of treatment experts.

It is particularly important to note that intensive treatment was
defined as a collaborative effort involving the patient and a skilled
team of health care professionals. It was not defined by particular
techniques, although certain techniques were typically used. The
frequent consultations and availability of a professional team were
critical components of intensive therapy.

The results show that the intensive treatment group did indeed achieve
bG levels closer to normal, and that they experienced far fewer
diabetic complications though also more hypoglycemia. In particular,
patients who maintained HbA1c levels around 7% appear to be much better
off than those whose HbA1c hovers around 9%. (See caveats in the
section on HbA1c.) Though it is not possible to separate the effects of
all the aspects of the intensive treatment, it is reasonable to believe
that lowering average bG may be effective even in isolation from the
other aspects of the intensive treatment. In its position statement,
the ADA says

Patients should aim for the best level of glucose control they can
achieve without placing themselves at undue risk for hypoglycemia or
other hazards associated with tight control.

Though type 2 patients were not included in the study, it is generally
believed that the results showing the benefits of tight control apply
to type 2 patients as well.

The entire position statement was published in most of the ADA's
publications (see "could you recommend some good reading") in the
summer and fall of 1993.

The formal report detailing the results was published in The New England
Journal of Medicine, aka NEJM, of September 30,1993 (v 329 pp 977-986).
The following discussion is based on that article.

Several DCCT subjects participate in m.h.d and are willing to answer
questions related to the personal aspects of DCCT participation.


Subject: More details about the DCCT

The study placed subjects into two cohorts, primary prevention or
secondary intervention, depending on duration of diabetes and existing
complications -- the primary prevention cohort were those with
essentially no complications.

Specifically: all subjects met these criteria:

Insulin dependent as evidenced by deficient C-peptide secretion
Age 13 to 39 years at entry to the study
No hypertension, hypercholesterolemia, severe diabetic complications,
or other severe medical conditions
Meet the criteria for one of the cohorts

and were separated into the two cohorts by these criteria:

Primary Secondary
Prevention Intervention
Cohort Cohort

Duration of IDDM 1-5 yrs 1-15 yrs
Retinopathy none detectable very mild to moderate
Urinary albumin < 40 mg / 24 hr < 200 mg / 24 hr

Within each cohort, the subjects were randomly assigned to either
conventional therapy or intensive therapy. Thus the study compared
intensive to conventional therapy in two different cohorts. The two
questions the study was mainly designed to answer were

1) Will intensive therapy prevent the development of diabetic
retinopathy in patients with no retinopathy (primary
prevention), and
2) Will intensive therapy affect the progression of early
retinopathy (secondary intervention)?

Conventional therapy included one or two injections per day, daily self
monitoring of blood or urine glucose, education, quarterly
consultations, and intensive therapy during pregnancy. Intensive
therapy included three or more daily injections or an insulin pump, bG
monitoring at least 4x/day, adjustment of insulin dosage for bG level
and food and exercise, monthly personal consultations and more frequent
phone consultations.

To simplify a lot, the DCCT showed the following changes in the
intensive therapy groups compared to the conventional therapy groups.
Note that '-' shows a decrease, '+' shows an increase, in the number of
patients affected. Patients were judged as affected or not based on
binary criteria, so the results only say how many subjects were
affected, not how severely those subjects were affected.

Intensive therapy compared to conventional therapy:

Primary Secondary
Complication Prevention Combined Intervention
------------ ---------- -------- ------------
Retinopathy(*) - 75% - 55%
Nephropathy(*) - 35% - 45%
Neuropathy(*) - 70% - 55%
Hypoglycemia(*) +200%
Weight gain(*) + 33%
Hypercholesterolemia(*) - 35%

(*) This brief table begs many questions about what exactly was
measured and how. For more details, read the paper.

There were no detectable differences on several measures:

Macrovascular disease
Changes in neuropsychological function
(a feared result of severe hypoglycemia)
Quality of life (based on a questionnaire)

Some limitations of the study: type 1 only, patients young and with
short duration (under 15 years) of diabetes, and short duration of the
study (5-9 years). Measured only number of subjects affected according
to binary criteria, not by measurement of severity of complications.
Excluded patients who already had severe complications and who thus
might benefit the most. The difference between the groups increased
during the study, but there is no proof that the difference would
continue to increase with time.

It is tempting to extrapolate the results to all diabetic patients --
all types, ages, and durations -- and there is at least some support
for doing so. However, the DCCT by itself does not show results for
type 2 patients, older patients, patients who have had diabetes for
many years, or those who already have severe complications. On the
other hand, a different group of subjects might shows differences in
areas such as mortality and macrovascular disease, where the young DCCT
cohorts simply did not have significantly measurable incidence. The
DCCT subjects are being tracked in a followup study which may shed
light on some of the unanswered questions.

Secondary analysis of the data indicates that retinopathy decreases with
decreasing HbA1c. This measure was not part of the study design and is
more difficult to interpret, but still shows clearly a correlation
between HbA1c and retinopathy.


Subject: DCCT philosophy: what did it really show?

It is often stated that the DCCT proved that tight control or lowered
HbA1c reduces complications. This is not the case. The controlled
variable in the DCCT was intensive vs conventional therapy, and
intensive therapy was defined by several factors including a team of
skilled health care professionals acting in partnership with the
patient. The results show that intensive therapy results in both
lowered HbA1c and fewer complications, but do not show that one causes
the other. The lead authors provide a good summary of this point in a
followup (NEJM 330:642, March 3, 1994):

We want to stress that the most valid interpretation of the trial
is that intensive therapy, with the **goal** of achieving blood
glucose concentrations as close to the nondiabetic range as
possible, delays the onset and slows the progression of long-term
diabetic complications. The secondary analyses support the notion
that lower glycosylated hemoglobin values are associated with a
lower risk of progression of retinopathy, but they do not prove
that hyperglycemia in itself causes retinopathy. [emphasis added]

Many of us believe, and believed before the DCCT, that actually
achieving good control aids our health. The DCCT adds weight to this
case but does not prove the point.


Subject: Is aspartame dangerous?

In short, no, except for phenylketonurics.

Aspartame is one of the most intensively studied food additives ever,
and the overwhelming scientific evidence is that it poses no danger.

The many claims of harm are all either anecdotal and not supported by
adequate observation, or are based on serious lack of understanding of
how to demonstrate facts scientifically. One of the most egregious is
the claim that studies with aspartame in capsules are invalid and that
it's only dangerous in solution. But d'oh -- if you administer
aspartame in solution, the patient will know whether he/she is getting
aspartame or not. This unblinds the experiment. Refer to Reid's Third
Law: Never Underestimate the Power of Suggestion.

An good set of links to web pages on aspartame is at
http://urbanlegends.about.com/library/blasp3.htm. (Unfortunately the
links open framed by about.com's heading, an unfair practice eschewed
by the vast majority of web sites. Ten demerits for about.com.)

The well known low-calorie sweeteners are pretty much all safe:
cyclamates, saccharin, aspartame, acesulfame, sucralose. Yes, even
cyclamates and saccharin -- the studies which resulted in their banning
turned out to be non-reproducible. I don't list stevia because it has
not been adequately studied, but I know of no significant indications
of danger.

If you don't like a given sweetener, try another. If you think you
respond badly in some way to a sweetener, try another. But unless you
have at least a heterozygous gene for phenylketonuria, it's unlikely
that you'll have a verifiable response to aspartame.

Edward Reid

Apr 14, 2015, 12:04:22 AM4/14/15
Archive-name: diabetes/faq/part4
Posting-Frequency: biweekly
Last-modified: 30 April 2003

Changes: see part 1 of the FAQ for a list of changes to all parts.



Copyright 1993-2005 by Edward Reid. Re-use beyond the fair use provisions
Subject: Online resources: diabetes-related newsgroups

On the Usenet, the misc.health.diabetes newsgroup carries most of the
messages related to diabetes. Volume runs about 200-250 articles/day.
you obtained this FAQ by some method other than by reading m.h.d and you
to participate. If you already have access to Usenet news, just subscribe to
misc.health.diabetes; the exact method depends on the software used at your
site, so you should inquire locally for details. If you do not have
access to
Usenet news, inquire locally about obtaining such access. The key words are
"I want to participate in the Usenet newsgroup misc.health.diabetes". Usenet
is available at most colleges and universities, many companies, all of the
large commercial services (including Delphi, Netcom, America Online,
Compuserve, Prodigy), many smaller local services, most Freenet systems,
and many locally run BBSs. Some of these have selective news feeds, and you
will have to ask them to get misc.health.diabetes before you can subscribe
via their system.

m.h.d is not gatewayed to any mailing list, and to my knowledge is not
archived anywhere as such. However, DejaNews has all of Usenet from March
1995 to present online and available to the public, and plans to extend the
scope farther into the past. You can create a filter specifying only the
newsgroup you want, and then search for key words. See


Another newsgroup, alt.support.diabetes.kids, has a much smaller volume of
articles, about 2-3 per day. Being in the alt.* hierarchy of newsgroups, its
propagation is somewhat restricted compared to misc.health.diabetes. To
obtain access, follow the same instructions as for m.h.d, above.

Other Usenet newsgroups which might be relevant are

rec.food and its subgroups
the sci.med hierarchy
the alt.support hierarchy, especially alt.support.diet
bit.listserv.transplant (only available at sites that carry bit.* --
see the description below of the TRNSPLNT


Subject: Online resources: diabetes-related mailing lists

Several public electronic mailing lists have diabetes-related content. The
main alternative to a newsgroup is the DIABETIC list, which carries about
60-80 messages/day. Its charter is to be "a support and information
group for
diabetics". The overall flavor and atmosphere are different from the m.h.d
newsgroup, so if you find that you are uncomfortable with one, try the
If you subscribe to the DIABETIC list, be prepared for the large volume of
messages. If you have not dealt with this volume of email before, it will be
quite disconcerting to see so many messages appear in your personal mailbox,
and I advise that you consider one of the following methods to avoid being

-- set up a mailbox (aka userid, account, screen name) separate from
your normal personal mailbox in which to receive the mailing list.
You will have to ask locally whether this is possible on your
You may also be able to use your mail program to filter mailing list
messages into a separate mailbox.

-- convert to the digest as soon as you have subscribed. The digest
option collects messages into large postings called digests (a
of the word, as all messages are included in their entirety). This
digest is sent daily, or when its size passes a limit (currently
lines). Convert to digest form by sending a message addressed to the
listserv (see below) with a message body containing

set diabetic mail digest

TYPE_ONE is a low to moderate volume mailing list for discussion of type 1
diabetes, intended primarily as a support group. It carries about 10
messages/day. There is no digest option. If you get any error messages from
"majordomo", be sure to write directly to the list owner,
jamyers(AT)netcom.com, as sometimes the software at netcom prevents him from
replying directly.

DIABETES-EHLB started as an Electronic HighLights Bulletin to distribute
information presented at the ADA conference in June 1996. It was carried
forward as a moderated mailing list. The moderator plans to try to keep
discussions focussed on specific topics.

TRNSPLNT is a low volume mailing list for discussion of organ
transplants. It
carries about 10 messages/day. It is relevant to diabetes because
complications of diabetes often lead to kidney transplants. TRNSPLNT is
gatewayed with the newsgroup bit.listserv.transplant, which is available at
Usenet sites which carry the bit.* hierarchy of newsgroups.

DIABETES-NEWS is a one-way list provided by _Diabetes Interview_
magazine. It
provides a sample, one article per week, from the printed magazine. See the
section on "Could you recommend some good magazines?" for more information
about the printed magazine.

AUTOIMMUNE is a moderated, low volume list carrying technical information
about research on autoimmune disorders, including type 1 diabetes.

HYPO is a moderate volume mailing list for support and information on
hypoglycemia (as a medical condition as opposed to an insulin reaction).

To subscribe to the mailing list in the first column, send a message to the
email address in the second column (or to the alternate if given) containing
the command in the third column. Note that Firstname Lastname is your real
name, such as John Doe. The listserv software will use the email address in
your message header for your subscription. If you have trouble sending email
to the listserv, or if you receive no response, then you will need the help
of someone at your site.

DIABETIC listserv(AT)lehigh.edu subscribe diabetic Firstname

TYPE_ONE listserv(AT)netcom.com subscribe type_one

listserv(AT)shrsys.hslc.org subscribe diabetes-ehlb Fstnm

TRNSPLNT listserv(AT)wuvmd.bitnet subscribe trnsplnt Firstname

diabetes-news-request(AT)lists.best.com subscribe

AUTOIMMUNE maiser(AT)ksg1.harvard.edu Subscribe autoimmune_research

HYPO hypo-request(AT)iceblue.com.au subscribe hypo

NECROBIOSIS necrobiosi...@yahoogroups.com [no command needed]
web page: http://groups.yahoo.com/group/necrobiosis

For up to date information and more diabetes-related mailing lists, see
Rick Mendosa's Online Diabetes Resources FAQ at



Subject: Online resources: commercial services

Most of the information here comes from David Cohler
<ar051(AT)lafn.org>, who
tried out all the online services and sent me his reviews. Thanks, David! I
don't have any information about commercial services in countries other than
the US.

CompuServe has a very active "Diabetes Forum." In many respects, it is the
single most comprehensive online resource for diabetics, featuring active
participation from several dozen countries, an extensive document library,
and an extensive software library. The moderators ("sysops") are quick to
pounce on misinformation and either correct it or delete it. No flaming
allowed. As of late 1995 the main drawback to CIS is price; even under a new
pricing policy, accessing the Diabetes Forum just 20 minutes a day could
result in charges of US$30 per month.

America Online has a diabetes support area. It is newer and smaller than
Compuserve's, but growing. The health forum has a number of information
on diabetes which users can read and download. These files generally contain
good advice and some explanation, but not in-depth explanation.

Also on AOL, each Sunday evening at 8:30 Eastern Time (US) a diabetes
group meets in a "private room" named "Diabetes". For more information,
Jim Lewis <jblewis(AT)aol.com>.

Prodigy has a relatively small but active and very friendly support group
accessed by "jumping" to "Medical Support BB" and then selecting "diabetes"
as the bookmark configuration. The board is monitored by several CDEs.
Although there is some discussion of scientific research, etc., the
preponderance of posts concerns support for people having trouble with
self-management. This is an excellent place for newly-diagnosed
diabetics who
still need a lot of basic information and emotional support. Moderated (no
flaming allowed).

Delphi has an active diabetes support forum, accessed by typing GO REL DIA.
Lisa Crawford <LISA_POOH(AT)delphi.com> is the host and forum manager.

Genie has a miniscule diabetes support area, configured as an RT ("Round
Table," Genie's term for BB). As of May 1995, traffic was at the rate of a
dozen posts per week.


Subject: Online resources: FTP

Demon Internet Services, a UK service provider, donated FTP space for
diabetes-related materials due to the urging and coordination of Ian
Preece <ianp(AT)darktower.com>. This cooperative endeavor was launched
with an empty directory in June 1994.

FTP has taken a back seat to the WWW. However, this site is one of the
very few soliciting donations as a cooperative endeavour.

Using the World Wide Web will be the easiest access to ftp for most new


You can also use a traditional FTP program.

To submit material, upload it to the "incoming" directory. After making
a submission, send email to Ian Preece <ianp(AT)darktower.com> telling him
about the file you have submitted.


Subject: Online resources: World Wide Web

I list a few excellent starting points for diabetes information on the
web. The maintainers of these pages are putting a lot of effort into
providing good information and links to other sites, and I'm not going
to try to duplicate their work here.

One of the best starting points is Jeff Hitchcock's Children with
Diabetes. Don't judge Children with Diabetes by the title alone; it has
extensive links to diabetes information of all sorts and is by far the
most extensive compilation on diabetes that I've seen on the net.


Rick Mendosa <mendosa(AT)cruzio.com> maintains a very extensive list of
online resources for diabetes, including many informational and
commercial web sites, and a list of BBSs. It is very likely the most
complete list available, and because it's simply a list, it is much
easier to read than sites with lots of complex internal links. Rick
also keeps one of the most thorough available lists of glycemic index
values for foods.


Another excellent compilation of links to diabetes-related web sites is
the Diabetes Monitor of the Midwest Diabetes Care Center. It's
maintained by William Quick and is exceptionally easy to navigate.


Yahoo has links on a huge variety of subjects, so if you want more than
just diabetes information you can shorten this URL:


Ian Preece <ianp(AT)darktower.com> is maintaining a web site in
conjunction with the Demon FTP site described above:


You can reach a WWW-formatted version of this FAQ via the URL


or you can get the plain text by FTP from


The American Diabetes Association (ADA) has put its entire set of
Clinical Practice Recommendations online in full. For the most recent
version go to


or start at the ADA home page and follow the link to "For Health Care
Professionals", then "Clinical Practice Recommendations".

Since these are oriented toward health care professionals, they provide
a wealth of detailed recommendations for actual health care practice.

Donald Lehn <dal...@facstaff.wisc.edu> was probably the first to put a
server with diabetes information on the web. Lehn's Diabetes
Knowledgebase has been offline since August 1995, and is apparently
gone for good.


Subject: Online resources: other

Most online resources previously available via other means are now
available via the web. Since these are thoroughly cataloged by the best
of the diabetes web sites (see previous section on "Online resource:
World Wide Web), I've dropped this coverage from the FAQ.


Subject: Where can I mail order XYZ?

XYZ is most often blood glucose measurement strips, especially for those
who don't live near discount pharmacies and must pay cash for their
supplies. Mail order prices are not always lower than local prices.
Remember that there is an advantage to going to a single pharmacist for
all your drugs, if that pharmacist is knowledgeable about interactions
and tracks all the drugs you use. Adjustments will be slower if you mail
order. Never mail order unless you are certain about what you need.

That said, here are two starting points.

_Diabetes Forecast_ has a long advertising section, part of which is for
suppliers. Nowadays most list their web addresses in the ads. In
addition, each issue of _Diabetes Forecast_ contains a column
summarizing recommendations for ordering health supplies by mail.

Jeff Hitchcock's Children with Diabetes web site has links to quite a
list on suppliers with information online at

I have removed the list formerly kept here because it was years out of
date and done better elsewhere. This leaves no information for those
outside the US, as the above links are mostly focused on US sources. In
the past, this has been much more of an issue in the US. However, web
search engines might be a great help -- googling "diabetes supplies
Australia", without the quotes, yields nearly a million hits. Just be
careful to evaluate what you find.


Subject: How can I contact the American Diabetes Association (ADA) ?

The ADA has local offices in many cities. Check your local phone book first.

To contact the national organization, call 1-800-232-3472 or +1 703 549
This will reach all departments. Or write

American Diabetes Association
1660 Duke Street
Alexandria, VA 22314

The ADA offers aid to diabetic patients, books, and journals ranging
from general to research. All can be ordered by phone. They maintain
lists of physicians with special interest and/or training in diabetes.
New patients and their families needing advice are encouraged to call.
They may be able to help in dealing with bureaucratic problems.

The ADA is on the web at http://diabetes.org. The web site has a great
deal of useful information. It includes lists of ADA publications and
ordering information. One section that is particularly useful is the
ADA's Clinical Practice Recommendations, which are all online in full at


or start at the ADA home page and follow the link to "For Health Care
Professionals", then "Clinical Practice Recommendations".


Subject: How can I contact the Juvenile Diabetes Foundation (JDF) ?

Check your phone book for a local office, or call 1-800-533-2873.

The JDF also has a web site at http://www.jdfcure.com/.

The JDF's motto is "finding a cure for diabetes", though apparently they
mean for type 1 diabetes. They are rather obnoxious in their rejection
of the
value of support and treatment other than a total cure. Despite this
the JDF in fact does a great deal of excellent support work.


Subject: How can I contact the British Diabetic Association (BDA) ?

The British Diabetic Association
10 Queen Anne Street
London W1M 0BD
Telephone 0171 323 1531 (+44 171 323 1531)
CARELINE 0171 636 6112 for information about diabetes

The BDA produces a bi-monthly magazine for members called "Balance".
Membership is UKP 12 a year.


Subject: How can I contact the Canadian Diabetes Association (CDA) ?

The CDA has local offices in many cities. Check your local phone book first.

To contact the national organization, call +1 416 363 3373, or write

Canadian Diabetes Association
15 Toronto St, Suite 800
Toronto, Ontario M5C 2E3

In Canada, call 1-800-847-SCAN.

The CDA is on the web at http://www.diabetes.ca.

The B.C. - Yukon Division of the CDA maintains an information center on the
Vancouver Freenet. It includes contact information for regional divisions of
the CDA. See the section "Online resources: other".


Subject: What about diabetes organizations outside North America?

I can't list them unless someone sends me the information.

Ian Preece <ianp(AT)darktower.com> has started a list, which now has
contact info for several European organizations, at



Subject: How can I contact the United Network for Organ Sharing (UNOS)?

UNOS (United Network of Organ Sharing) has a variety of information
concerning organ transplants and transplant centers. Contact UNOS at
(800)24-DONOR or +1 804 330 8602, or PO Box 13770, Richmond VA 23225, USA.

UNOS has a WWW page at


Email contact is Joel Newman <newmanjd(AT)comm5.unos.org>.


Subject: Could you recommend some good reading?

You mean to curl up with on the sofa? Oh, diabetes ... OK.

My favorite book is Mayer Davidson's _Diabetes Mellitus: Diagnosis and
Treatment_, published by Churchill Livingstone. Though written as a
medical text, anyone willing to plow through an occasional dense
passage and keep a dictionary handy will have no trouble with it. (See
below about medical terminology.) Being written mostly by a single
person, it is much better focussed than the "committee" books which are
so common. And it's very cheap for medical books, US$42 in 1994.

Charles Coughran <csc(AT)coast.ucsd.edu> recommends _Management of
Diabetes Mellitus Perspectives of Care Across the Lifespan_, Debra
Haire-Joshu (editor), Mosby Year Book, 1992, ISBN 0-8016-2429-0. He
says it's as good as Davidson, readable, and aimed at a similar audience.

Coughran and Steve Kirchoefer <swkirch(AT)chrisco.nrl.navy.mil> recommend
_Joslin's Diabetes Manual_ by Krall and Beaser, Lea&Febiger 1988.
Though somewhat lacking in consistency due to the multitude of writers,
it's a useful practical book. The Joslin Institute is world renowned
for its support of diabetes research and treatment, and the price of
the book is reasonable.

Coughran further recommends _Joslin's Diabetes Mellitus_ (13th edition)
edited by Kahn and Weir, 1994. It's another book that suffers a lack of
consistency due to the multitude of writers, but it contains a wealth
of information. Lots of biochemistry and also sections on practical
day-to-day management. Oriented toward health care professionals. 1068
pages, $125.

Terence Griffin <griffin(AT)cam.nist.gov> recommends _Therapy for
Diabetes Mellitus and Related Disorders_. It's a professional level book
compiled and published by the ADA, now in its second edition. See below
for ADA ordering information.

Steve Marschman <sc_marschman(AT)pnl.gov> recommends John Davidson's
_Clinical Diabetes Mellitus, A Problem-Oriented Approach_ (2nd
edition), published by Thieme Medical Publications, New York. Written
from a care-giver's perspective, it is an excellent technical resource
book with medical descriptions of diabetes mellitus, diagnosis,
treatment, complications, and concomitant problems. Price about US$150,
but often available used for much less. (As far as I know, the two
Davidsons, Mayer and John, are not related.)

The American Diabetes Association publishes a number of books with
basic diabetes information of various sorts -- self care, diet,
recipes, etc. Deb Martinson <llama(AT)drizzle.com> especially recommends
_The ADA Complete Guide to Diabetes_, about $6 in paperback and
published in 1996. See the ADA's web site at


or use the phone numbers or address in the following section.

Any university library will have a large number of books on diabetes,
and they will be grouped together on the shelves. Go and browse. The
books mentioned above can be found in most university libraries.

The rest of what I have to talk about is periodicals. See the next


Subject: Could you recommend some good magazines?

_Diabetes Interview_ is a popular monthly tabloid with a variety of
news stories, interviews, and lots and lots of advertising. It's run by
a journalist, Scott King, and it shows. Authority, to this publication,
always lies in people they talk to. They don't appear to read
scientific or medical literature as the basis or support for stories.
They do publish research summaries, but these are at the newswire level
with no apparent critical reading. No critical commentary accompanies

Publisher Scott King has pursued some valuable projects, such as
organizing letter-writing to Ann Landers after she tried to shove
dining-out diabetics into the closet -- Landers published King's own
excellent letter. He has certainly advanced the cause of open
discussion of diabetes in general. But _Diabetes Interview_ has been
sidetracked needlessly at times, such as by allocating seriously
inordinate abounts of space and attention to minor issues such as the
animal/human insulin debate. They also regularly run a paid
advertisement for an herbal product which claims to "restore pancreatic
function" -- probably an illegal claim in the US.

_Diabetes Interview_ offers a sample (one article per week) as an
electronic mailing list and many articles on their web site. See the
section on "Online resources: diabetes-related mailing lists" for
information on the mailing list.

_Diabetes Interview_ subscription information: one year, US$20 in the
US, US$31 in CA and MX, $46 in other countries. Cancel after the first
issue if you don't like it

Diabetes Interview
3715 Balboa Street
San Francisco, CA 94121
phone: +1 415 387 4002
US 800-234-1218

_Diabetes Self-Management_ is a bimonthly magazine containing generally
detailed articles oriented to helping patients with techniques and
skills -- diet, exercise, treatment, outlook, etc. They go into areas
not often covered, such as a recent series by Ann Williams on
low-vision tools and coping skills. The writers tend to have in-depth
knowledge of their fields and the information is well balanced. The
magazine emphasizes practical skills over basic knowledge, and spreads
itself a bit thin by trying to address itself to all diabetics. Those
who dislike Diabetes Forecast will find similar coverage in Diabetes
Self-Management but with more depth and aimed at a better educated

The _Diabetes Self-Management_ web site has full text of numerous
articles from back issues, about two articles from each issue.

_Diabetes Self-Management_ costs US$14/yr, or US$36/yr outside the US
and CA. To order, mail payment, call, or look on their website. They'll
send a free trial issue if you wish.

Diabetes Self-Management
P. O. Box 52890
Boulder, CO 80322
US phone: 800-234-0923

Everything else I have to recommend comes from the ADA (see section on

Here's what the ADA says about its own publications:

_Diabetes_ -- the world's most-cited journal of basic diabetes
research brings you the latest findings from the world's top

_Diabetes Care_ -- the premier journal of clinical diabetes research
and treatment. _Diabetes Care_ keeps you current with original
research reports, commentaries, and reviews.

_Diabetes Reviews_ (in memoriam) -- the comprehensive but concise
review articles in ADA's newest journal are a convenient way for
the busy clinician to keep up-to-date on what's truly new in
research. Sadly, Diabetes Reviews ceased publication at the end
of 1999, a victim of the fact that medical libraries face a
crisis of rising subscription costs but flat budgets. The seven
volumes which were published are still an invaluable resource.

_Diabetes Spectrum_ -- translates research into practice for nurses,
dietitians, and other health-care professionals involved in patient
education and counseling.

_Clinical Diabetes_ -- For the primary-care physician as well as
other health-care professionals, this newsletter offers articles
and abstracts highlighting recent advances in diabetes treatment.

_Diabetes Forecast_ -- ADA's magazine for patients and their
families features advice on diet, exercise, and other lifestyle
changes, plus the latest developments in new technology and
research. It is a valuable tool for patient education.

Now for my own opinions.

_Diabetes Forecast_ is the mass market magazine, intended to be readable
by all literate diabetics. For US$24/year you can hardly go wrong. The
biggest problem with DF is that in the attempt to reach almost
everyone, it aims at a very low reading level -- perhaps eighth grade,
I'm not sure. This makes it tonally annoying and dilutes the
information content. Still, it contains useful information and is
excellent at promoting self-care and a positive self-image for persons
with diabetes.

_Diabetes Forecast_ is also one of the best places to look for
advertisements for diabetes-related products.

The remaining journals are of interest if you want to follow what is new
and under investigation in medical practice and research. The journals
vary in difficulty of reading. Though some knowledge of statistics and
chemistry helps, a general acquaintance with scientific method is
perhaps more important, and a smattering of familiarity with medical
terminology helps most. Luckily, medical terminology is basically
simple -- it mostly consists of putting together roots and affixes to
make specific terms. Learn a few dozen roots and you can make out most
of it. Try to have a dictionary at hand at first.

_Diabetes Care_ publishes papers on clinical research. I find many of
the papers to be interesting and applicable to my own management. With
the demise of _Diabetes Reviews_, DC plans to publish more review
articles as well.

_Diabetes_ is the ADA's journal primarily for basic research. Some of
the articles are interesting, but they run much more toward
biochemistry and mechanisms of metabolism. As important as basic
research is, few of the reports say little of value directly to

_Diabetes Spectrum_ is oriented toward health care practitioners.
It consists of reprints of important articles (sometimes several on
a topic) and summaries of related articles, plus original
commentaries from other authors. As such, it provides a broad
overview of topics for readers who don't have time to track down
lots of separate original articles. If you only have time to read
one technical publication, _Diabetes Spectrum_ is perhaps the best
choice -- the only competitor for this place is _Clinical Diabetes_.

_Clinical Diabetes_ contains focussed articles written specifically
for health care practitioners. It's very readable and to to the
point, another good choice for those wanting higher level reading
but not research articles.

The ADA has price structures for regular members and professional
members. A basic regular membership with _Diabetes Forecast_ is
US$24/year (in the US, $41.93 in Canada, $39 in Mexico, $49 elsewhere,
all in US funds). The other ADA journals will set you back about
US$90-120/year apiece. A professional membership allows you to pick and
choose journals at the listed rates; if you plan to get either
_Diabetes_ or _Diabetes Care_ you should enter a professional
membership to get the best prices. Credentials are not required for a
professional membership.

The ADA takes checks, money orders, Visa, Mastercard and American
Excess. Unfortunately, orders of books from outside the USA incur an
additional $15 shipping charge.

You can get more ADA info online, including an online catalog for all
books and magazines, at


Phone numbers

+1 703 549 1500
+1 703 549 6995 fax

or write

American Diabetes Association
Subscription Services
1660 Duke Street
Alexandria, VA 22314

Edward Reid

Apr 14, 2015, 12:04:23 AM4/14/15
Archive-name: diabetes/faq/part3
Posting-Frequency: biweekly
Last-modified: 10 March 2009

Changes: see part 1 of the FAQ for a list of changes to all parts.



Copyright 1993-2009 by Edward Reid. Re-use beyond the fair use provisions
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
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 have a choice in treating
patients with type 2 diabetes. They can prescribe drugs (oral hypoglycemics)
and insulin, or they can try to get their patients to make the difficult
lifestyle changes described above. (Many patients need both.) The latter
effort is time consuming and often frustrating, as doctors too often see
patients failing to make any change at all.

Friends and family can help by learning about type 2 diabetes, and doing
you can to encourage your loved one to make diet and lifestyle changes. If
this supports the plan a treatment team is urging the patient to follow, you
will add your support for difficult changes. If the doctor (or the whole
treatment team) falls down on the educational and motivational
structure, you
can fill in some of the gaps. Your effort is well spent in either case.

In particular, if a 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
a patient who's been actively involved in self treatment already has an
excellent chance of using these additional tools successfully. Those who
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
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

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
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,
problems related to growing up and the general social pressures of
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

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
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
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.
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
know-alls who insist they know more than you do. Feel free to add to this

That was true before insulin treatment became available in 1922.

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 May also be known as
------- ---- --------------------
Regular Actrapid Soluble
NPH Protophane Isophane
Lente Monotard
Ultralente Ultratard Zn (Zinc suspension)

The recently developed lispro (generic name) insulin is sold as Humalog by
Eli Lilly. Novo has no comparable insulin as of July 1996, although they
undoubtedly have research in progress.


Subject: What is Humalog / LysPro / lispro / ultrafast insulin?

Except as otherwise noted, this info comes from an article on p396 of the
March 1994 _Diabetes_ by researchers at Eli Lilly.

Insulin is a protein. Proteins consist of sequences of amino acids. Human
insulin has the amino acid lysine at position B28 and proline at position

Insulin molecules naturally pair off (like people) and combine into dimers.
The dimers interact with small amounts of zinc and combine into
hexamers, the
form sold as "regular" insulin.

From another source, now forgotten: the time required to disassociate the
hexamer into the dimer, and then the dimer into the monomer so that it
can be absorbed, is the main reason for the delay in the action of
insulin and the reason for injecting it 30 to 45 minutes before meals.

Switching the B28 and B29 positions on the protein has no effect on the
normal activity of the insulin but inhibits the formation of the dimer and
the hexamer. Thus the insulin is in monomeric form when injected and can be
absorbed immediately.

The name LysPro comes from the names of the amino acids, lysine and proline,
that occupy the swapped positions. According to an article in the August
Diabetes Forecast, the spelling 'lispro' is now preferred.

Challenges in the development include the biochemical process for
swapping the
amino acids, and making the result reasonably stable in the monomeric form.

From another source, now forgotten: US FDA approval was not automatic,
the insulin molecule has been modified. In fact, several other amino acid
exchanges have been tried and met with unacceptable side effects.

Some points from the article in the August 1996 Diabetes Forecast:

Patients with gastroparesis, or taking acarbose, should be careful with
lispro. Gastroparesis is a condition caused by neuropathy which causes
the stomach to empty slowly and erratically. (See the section on
gastroparesis later in this section.) Acarbose is a drug which slows
the absorption of carbohydrates from the intestine. Either may result
in lispro insulin acting too quickly.

Response to lispro is variable. Some patients love it, others hate it.
On the average, it does not change bg control either for better or for
worse, but some patients definitely find it one or the other. Eli Lilly
is promoting lispro for convenience, not for better control.

Doctors and patients are still experimenting with the best regimens for
using lispro insulin. "Best" clearly varies from one patient to another.
Typically lispro insulin is injected very close to mealtime.

An obvious concern is that hypoglycemic reactions might be more common
with a
faster acting insulin. A paper presented at the 1996 ADA Scientific Papers
conference studied this possibility:

Reducing the Incidence of Hypoglycemia with a Novel Insulin Formulation
J. Anderson, R. Brunelle, A Pfeutzner et al.
Indianapoils, IN and Bad Homberg, Germany

In fact, they found the rate of hypoglycemic incidents slightly lower among
those using lispro insulin. They found no difference on most other measures,
including especially HbA1c. I've only seen the abstract of the paper, so I
know nothing about their methodology. (They also state the lispro forms
hexamers just like regular insulin but that the hexamers dissociate much
quickly. I don't know who to believe, but from a practical point of view it
doesn't matter.)


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. (Specifically, according to Jens Brange's
_Stability of Insulin_, Regular/Actrapid insulin stored at 40C will
lose 5% of its potency after 14 weeks.)

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

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. (Two readers have reported that solidly
frozen and rethawed regular insulin works just fine. I've been unable
to locate any studies documenting the degradation of insulin at extreme

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, a
local hospital, or a pharmacy 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

Local or state regulations apply in many places and limit your choices.
Know the laws for your area! Where sharps containers are required, the
pharmacy where you purchase the container will probably dispose of the
full container for you.


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.

Some pen units only allow setting a multiple of two units of insulin,
which many find inadequate. Get a model which measures a multiple of
one unit, which should be easy to find among current models.

The primary disadvantage is cost, up to twice as much per unit of
insulin compared with standard vials. 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

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, but are being heavily
promoted 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


Subject: Insulin pumps

An insulin pump provides a Continuous Subcutaneous Insulin Infusion, or
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

1) The infusion is still subcutaneous, so the insulin still must be
absorbed before it can be used. Insulin from the pancreas goes
into the bloodstream and takes effect much more quickly.

2) Current pumps are open-loop -- that is, there is no feedback from
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 the manufacturers have little motivation to fund the studies, as
advertising is more cost-effective for them. 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 pump 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

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.

I have removed the oudated insulin pump discussion previously posted here.


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
diabetes. As a result, beta cell implantation is not currently used to treat

Current research is investigating two general methods of implanting beta
cells without the use of immunosuppressant drugs. The first
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
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. (As of early 1997, I haven't had the
opportunity to try to locate the followup to these trials.)

An article in the Journal of Clinical Investigation, September 1996,
describes a successful experiment which implanted immunoisolated porcine
(pig) islets into monkeys. An accompanying editorial describes the state of
islet transplantation. Both are online in full, linked from the issue
contents page at


In early 2000, a lot of hype appeared about the "Edmonton protocol" trials.
While an important step, this is still only a small step on a long journey.
They made improvements in technique and graft survival, but no progress on
the serious problems of beta cell supply (each patient needed beta cells
from two cadaver donors) or of immunosuppressant use (they used drugs,
albeit carefully).

Don't expect these treatments to be available on a standard basis any time
soon. I've been reading about this research since the mid-1970s, 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 or grow usable cells for grafting in
the laboratory, 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 2005; 2015 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
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


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.

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 January 1998 there were 38,380 people on
the UNOS [see below] registrations for a kidney transplant. There were
only 355 registrations for a pancreas transplant and 1604 registrations
for a kidney-pancreas transplant. [Based on UNOS Scientific Registry
data as of January 28, 1998.]

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. [Information from January
2000. Check to see whether additional centers have been approved.]

UNOS (United Network of Organ Sharing) has a list of 124 transplant
centers that have pancreas transplant programs. For more information,
contact UNOS at (800)24-DONOR or see their web page at


(See the section on sources for additional contact info.)

The UNOS handles transplant registrations only in the USA, but can
provide contact information for organ-donation agencies around the
world. Organ allocation became a political football in the US in the
late 1990s, and the details of allocation and waiting lists may change.

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

(Thanks to Alexandra Bost for much of the information in this section.)


Subject: Type 2 cures -- barely 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 at the
with beta cell insufficiency developing later while the insulin use defects
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

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


[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


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

irritability (sound familiar?)
tingling of mouth and fingers
nausea or vomiting (unusual)

The autonomic nervous system activity also causes the secretion of
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

visual disturbances
mental dullness

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
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
- 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
- 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
About 1% of diabetics have some degree of NLD ... plus or minus 1%,
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
scratching sometimes heals very slowly. Thus avoiding scratching and trauma
decreases the amount of ulceration, though some ulceration will occur

There are some images of NDL lesions at


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

Other treatments reported to help sometimes are oral aspirin,
dipyridamole, locally injected steroids, and systemic steroids. No one
to be able to predict what will work on any given patient, and often not
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
as a last resort. Topical steroids (creams and inhalers) cause no such

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,
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

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.


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,
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
even really have any long-term effect except to reduce the pain for
awhile, and should be avoided completely since it could also
screw up how your body deals with cortisone.

o Recommended treatment: daily exercises, biweekly physical therapy,
(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

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

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

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
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,
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!


Physical Psychological

nausea fatigue- muscle weakness
vomiting fear
constipation frustration
diarrhea stress
lack of hunger
high stomach acidity
weight loss
inability to control blood sugars


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.


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

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)
Propulsid (cisapride) (in U.S. only under compassionate use protocol)
domperidone (U.S. availability: compassionate use only, and for
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
(refractory to drugs) has less then 4,000 cases per year. More info at
insulin pumps


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


** 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

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

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

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

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
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
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
and remains active in the body for 72 hours.

Ads make claims that pycnogenol prevents, aids and/or cures the following

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
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
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

No published work could be found on the bioavailability of pycnogenol in
particular, but oral ingestion of bioflavanoids in general results 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
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
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

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

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

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

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

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
was studied.

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

Chemically induced edema of a rat's paw was decreased with
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
oxygen free radicals. Med Sci Res 1987;15:831-2.

2.Yu CL, Swaminathan B. Mutagenicity of proanthocyanidins. Food Chem Toxicol

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;

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.
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