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From: (Steven B. Harris )
Subject: Re: Diabetes and rice
Date: 24 Sep 1995

In <443ur7$> (Merp21) writes:

>My grandma just received news yesterday that she has diabetes. Her
>glucose level is 3+ or something like that. Now there's general
>disagreement among family members on what she should avoid. Someone was
>told from a doctor to avoid rice and such foods because they can raise
>the glucose level. Is there truth to this? What should she avoid and what
>should she eat lots of?
>thanks in advance,

   She should avoid fat, which is what has doubtless made her
overweight in the firstplace (I'm taking a guess here, but most people
with diabetes at that age are quite obese).  Fat not only makes you
fat, but it spoils glucose regulation for more direct reasons.  The
monounsaturated facts (olive oil, avocado, almond oil, Canola) may be
okay, and can be used to replace other kinds of fats, particularly the
animal fats and hydrogenated fats, which are very bad.

  The best diet for diabetics emphasizes complex carbohydrates and cuts
fat.  I would suggest the book "Beyond the Pritikin Diet" if you have
to have one single book.  The book on weightloss by Dean Ornish, M.D.
is also on the right track.

  Understand that most elderly people are not going to radically change
their diets even if the alternative is dying of heart attacks and
having amputations, which is the fate of many a diabetic.  You may have
to come to terms with that.  If you do radically change the diet,
however, a large fraction of diabetes with onset in the later years can
be cured.  By this I mean *cured*-- no need to take medications, and no
more disease and no more disease effects on circulation.

                                        Steve Harris, M.D.

From: B. Harris)
Subject: Re: Where's those Calories comming from?
Date: 7 Jun 1998 05:04:59 GMT

In <> Ed Nichols
<> writes:
>Terranova0 wrote:
>> Doesn't alcohol act like a sugar? It has no "carbohydrates", proper but
>> it is a hydroxal derivitive of hydrocarbons. I know diabetics should
>> approach it with caution, yet many low-carb dieters claim it doesn't
>> interfere with ketosis. What is the lowdown on alcohol digestion?

   The lowdown that concerns diabetics is that alcohol interferes with
the liver's ability to release glucose into the blood between meals.
Diabetics who have insulin on board during those times are likely to
"bomb out" with low glucoses if they drink.  So the rule for diabetics
on insulin and insulin-like drugs (those which cause more insulin to be
made without much sensitivity to sugar levels) is: drink alcohol WITH
meals, if you must drink.

                                           Steve Harris, M.D.

From: B. Harris)
Subject: Re: HIV NON-EPIDEMIC11 -- Duesberg Followers Still Spouting
Date: 15 Aug 1998 06:26:13 GMT

In <>
(Bill Sheppard) writes:

> AIDS is first and foremost a disease of depressed
>cell-mediated immunity (CMI) and must be treated as such _regardless of
>the identity of the triggering agent_. Any effective treatment must,
>from the outset, be targeted to enhance CMI, so that the body regains
>its _own_ antiviral competence. As in the analogy with diabetes, you
>have to treat WHAT PRESENTS, not go after the putative virus that may
>have triggered the pancreatic necrosis.

Bad analogy.  In beginning diabetis (type I) if there are any
pancreatic cells left, you can go after saving them, by doing immune
suppression (to correct immune hyperactivity, triggered by a virus).
That results in a well kid with no need for insulin.  Presumably, if we
could identify the virus infection early (cocksackie B?) and had a good
antiviral for it, we might be able to stop diabetes early THAT way,
also.  Just as we can stop stomach ulcer by treating H. pylori,
shingles by treating H. Zoster, and perhaps even some heart disease by
treating clamydia.

>The triggering agent, as far as
>treatment is concerned, is a moot point.

    Not if you get it early.  And not if it continues to do damage.
Just because you have the ulcer, does not mean it doesn't heal if you
finally treat the infection.  In medicine, it's hardly ever too late to
treat ANY chronic infection.  That's the doctor's reflexes you're
seeing, there.  Remember the Tuskegee experiments and the uproar in
1973?  Do you remember WHY everybody was outraged?  Basically, because
a lot of asymptomatic (black) men who'd had syphilis for 30 years, had
not been treated, as part of an study.  They made them finally treat
them.  And should have.  But if the facts were viewed dispassionately,
there's a lot better reason to treat late state AIDS with antivirals.

>      In AIDS, the exclusive obsession with "attacking the virus"
>results in strategies that further suppress CMI in a disease that
>BEGAN as depressed CMI.

    No.  There are a dozen papers suggesting that CMI improves with
HAART, and I've posted them.  Did you fail to read them?

>  The remisssions seen from HAART, while laudible in
>the short term, are the fortuitous downstrem effect of immune
>suppression, as would be seen with corticosteroids.

   Sez you.  But in the normal course of things, giving somebody with
AIDS and CMV retinitis coricosteroids would cause the disease to
progress, and the patient to go blind.  Only giving these to a patient
with a suddenly overactive immune response would result in containment
of the virus with no damage.  And that's what happens with HAART.

>HAART remissions are
>not intrinsically from any antiviral action -- since the virus is
>already genetically incorporated into host cell genome.

   Non sequeter.  The damage from the virus is not because it's in the
genome, but because it's replicating and the replication products
(gp-160 and so forth) kill cells.  Stop replication, and it doesn't
matter if the virus is in the genome.

>In any rational
>treatment strategy, the infected cells themselves must be eliminated
>which can only be accomplished by a robust CMI response.

   No, in any rational CURE strategy this must happen.  But we don't
have such agents which can do that.  So we settle for good treatment.

> Take a clue
>from the long-term nonprogressors; their common trait is a robust CMI,
>particularly in CD8+ numbers and function.

    Sure, but we have no way to mimmick what their bodies do, or make
other people's bodies do what their bodies do.  When we do, we'll use
it instead of HAART!

>     So if one's Prime Motive in AIDS is truly to save lives long-term
>and end the epidemic, then CMI-enhancement has got to be the central
>object of research.

    Not really, because it may take many years for this to be figured
out, and people are dying NOW.  So you need a 2 pronged research
program: one which supppresses the virus, and the other which aims to
help the immune system do it.  Long term non progressors have the virus
in the genome too, you know.  They just control replication better
(probably by killing off virus manufacturing cells).

> For all his cantankerousness, Fred Shaw seems the
>only person in this NG who recognizes this.
>     Bill (o.c.)

   Fred Shaw has no more sense than God gave a turkey.  Let's see if
the same is true for you.

                                            Steve Harris, M.D.

From: B. Harris)
Subject: Re: FDA does something right (Majik Herbs).
Date: 3 Feb 1999 04:31:42 GMT

In <> "Syd Baumel" <>
>I don't think it's as silly, in this case, as you make it out to be. For
>one thing, I can't understand how researchers - and, through them, the
>forward march of science - can snuff out a potentially significant
>finding on the basis of studies which are quite far from being trivially
>pseudo-replicative. Why wouldn't at least one research group see fit to
>try and truly replicate the original study - and I'm not talking about
>replicating moon phase or what the researchers ate for lunch that day.
>I'm talking major varuiables. Maybe the albino rat is a better model of
>human diabetes than the other strain or two of rats or mice which were
>tested within 24 hours. Shouldn't the logic be: first you replicate
>_really_, then you branch out in search of generalizability? Is there
>some logic I'm missing here because I only have a mail order degree in

    Uh, yes, there is, Syd. Biology just doesn't work that way.  The
odds that one strain of poisoned rat is a great model for the
generation of human type I diabetes, while another strain isn't, are
pretty low.   Too low to spent money on.  I suppose anything's
possible, but resources are too slim to spend on those odds.

   There are a dozen ways to kill islet cells.  In rodent models of
diabetes they are simply poisoned by alloxan or streptozotocin to get
rid of them.  The reason being that you're interested in the effects of
high glucose and no insulin on OTHER cells in the rat's body, which
have no way of knowing how the pancreatic cells met their ends.  So far
as the pancreatic cells, go, though, in humans they are killed
immunologically.  Not poisoned by some artifical chemical.  In fact,
human islet cells are quite resistant to these same chemicals, and if
you implant them into a nude mouse that does't reject them, and then
give the mouse enough alloxan to kill 80% of it's islet cells, the
human cells just laugh at it.  Just as they do in a dish with this
class of oxidative poisons.  So rodents are not even a good model for
this class of nitric oxide poisons in humans, let alone the real
autoimmune process that gives humans diabetes.  Studying antedotes to
poisons in rats (even granting that this is what we have-- and that's
puting the most charitable possible interpretation on it, since I
really doubt that the rat strain is going to make any great difference,
since these are poisons for them all)--- and doing it for poisons
aren't even particularly poisons at those doses for humans (not that
humans ever get them anyway)--- is a really *stupid* way to spend
money.  Sure, you're going to learn something no matter what kind of
science you do.  You'll learn what makes rats easier to poison than
people.  You may learn something new about rat pancreatic cells.  Maybe
there is commercial application, and a new kind of De-Con is in the
offing.  But the point is: do you learn something that will be very
useful to saving people from diabetes type I, or not?  Does any of this
imply that epicatechins "regenerate" pancreatic cells in some generic
process?  And next, will some dweeb like Herb Ass ist understand enough
biology to understand on which particulars an animal model is bad
model, and has nothing to do with trying to practice clinical medicine
on people?  We've seen the answer to that.

   And it appears you're no different.  If you really cannot tell why
your idea that poisoned albino rats might be a great model here for
people with an autoimmune problem, while poisoned Wistar rats, or mice,
are not, you really have no feeling at all for the similarities and
differences in biology.  In which case, I'm really wasting my time
trying to explain it to you.  You just never will get it.  You should
stick with the mail order degree in nuclear physics.

>As for the apparent impracticality (for humans) of the within-24-hour
>effect, with a little bit of thought you can see that this points to a
>very practical possibility: administering e. to children at risk for
>diabetes prophylactically. As you know, I'm no fan of animal research,
>ethically and precisely due to some of the reasoning you use here (what
>does an albino rat "model" that has just been made diabetic by a toxic
>chemical have to do with a human diabetic?).

    Nothing.  But that's not what the model was meant to be used for.
It's being used for investigating the origins of diabetes because the
scientists in this case are idiots.  You've figured this out, but can't
tell them from other scientists using the same model for other
purposes.  That's YOUR problem.

>But it sounds like epicatechin and/or the plants that are rich in it may
>well be safe enough to be used directly in human experiments. I'm boldly
>going out on a limb here (this _is_ an appropriate place for that, isn't
>it?), but has anyone done epidemiologic research to see if a diet rich in
>e. or substances like it (e.g. other biofavonoids, like the catechins in
>green tea) is associated with a lower prevalence of IDDM? Why not see if
>we can build on this (as far as I'm concerned, based on the evidence I've
>seen here and on Medline, not "unreplicated") finding. And what prompted
>those Indian researchers to test e. in the first place? Was there some
>empirical tradition in India of e. or e-rich sources being therapeutic or
>preventive for diabetes? Did you ask yourself this question before
>pouring all that cold water on their reports and siding with the "real
>scientists" who supposedly shot them down? Take that, Steve Harr-ass!

    I didn't have to ask myself that, because I already know the
answer.  Yes, there is such a tradition for these things being
therapeutic for diabetes (of both varieties).  And there are reasons
why they might be, but they have nothing to do with islet cell
degeneration, and a lot to do with capillary damage by high glucose

>...OK. I really don't have time for this now, but I couldn't resist doing
>another broader Medline search on the MeSH terms catechins OR flavonoids
>AND diabetes mellitus. I got 108 hits. It seems this is a most fertile
>area of research, but one that, frankly, is above my head.

Um hummm.

>Here's what I got when I searched for diabetes and tea (57 cites):
>Ooops -- it includes the following "anomalous" study, which I reluctantly
>post here:
>Eur J Clin Nutr 1994 Apr;48(4):279-85
>Is children's or parents' coffee or tea consumption associated with the
>risk for type 1 diabetes mellitus in children? Childhood Diabetes in
>Finland Study Group.
>Virtanen SM, Rasanen L, Aro A, Ylonen K, Lounamaa R, Akerblom HK,
>Tuomilehto J
>Department of Applied Chemistry and Microbiology, University of Helsinki,
>OBJECTIVE: The study was carried out to determine whether coffee or tea
>consumption by the child before diagnosis of diabetes or consumption by
>parents at the time of the child's conception or during pregnancy was
>associated with the risk for childhood type 1 diabetes. DESIGN:
>Case-control study. SETTING AND SUBJECTS: All diabetic children younger
>than 15 years, and diagnosed from September 1986 to the end of April
>1989, were invited to participate. 600 newly diagnosed diabetic children
>and 536 randomly selected population-based children, and their parents
>took part in a nationwide study. RESULTS: The risk for type 1 diabetes
>was increased in the children who consumed at least 2 cups of coffee
>daily [odds ratio (OR) 1.94, 95% confidence interval (CI) 1.08- 3.47],
>and in the children who consumed 1 cup of tea (OR 1.69, 95% CI 1.21-2.37)
>or at least 2 cups daily (OR 2.59, 95% CI 1.60-4.18) when adjusted for
>mother's education, child's age and child's sex. Parents' consumption of
>coffee or tea during conception of the child and mother's coffee
>consumption during pregnancy did not affect the risk for diabetes in the
>children. CONCLUSIONS: We observed an increased risk for type 1 diabetes
>in the children who consumed coffee or tea regularly.
>PMID: 8039488, UI: 94313972
>But then look at this study, which suggests that at least the _catechin_
>component of _green_ tea is preventive against IDDM:
>J Nutr Sci Vitaminol (Tokyo) 1998 Oct;44(5):673-83
>Effects of green tea catechin on hepatic microsomal phospholipase A2
>activities and changes of hepatic phospholipid species in
>streptozotocin-induced diabetic rats.
>Choi JH, Cha BK, Rhee SJ
>Department of Food Science and Nutrition, Catholic University of Teagu-
>Hyosung, Kyungsan-si, Kyungbuk, Korea.
>[Medline record in process]
>In this study, male Sprague-Dawley rats weighing 70 +/- 5 g were divided
>into a control (normal) group and three different diabetes mellitus (DM)
>groups that were supplemented with catechin-free (DM-0C), 0.5% catechin
>dietary (DM- 0.5C), and 1% catechin (DM-1.0C). The animals were
>maintained on an experimental diet for four weeks. At this point, they
>were injected with streptozotocin (STZ) to induce diabetes, and they were
>sacrificed on the 6th day to determine the activities of phospholipase A2
>(PLA2) and the changes of phospholipid species by catechin
>supplementation. In liver tissues, no significant differences were found
>between the PC hydrolysis of a normal group and a diabetic group;
>however, PE hydrolysis of the DM-0C, DM-0.5C, and DM-1.0C groups
>increased by 68.9%, 34.01%, and 26.9%, respectively, compared with the
>normal group. Although the PLA2 activity of the DM-0C group in the liver
>tissues increased 91% compared with the normal group, the PLA2 activity
>of DM-0.5C and DM- 1.0C, which were fed catechin, increased 50% and 56%,
>respectively, compared with the normal group. In the liver tissues,
>peroxide values of the DM-0C, the DM- 0.5C, and the DM-1.0C groups were
>increased 109%, 32.8%, and 46.7%, respectively, compared with the normal
>group. Based on these results for STZ-induced diabetic rats, lipid
>peroxidation seems to be accelerated specifically with the increased PLA2
>activities. Thus if antioxidants like catechin were supplementation, the
>activity of PLA2 and PE hydrolysis can be altered and the accumulation of
>lipid peroxide would be decreased. Therefore we concluded that the
>antioxidant catechin for diabetic animals can significantly reduce PLA2
>activities and lipid peroxide formation.
>PMID: 9919487, UI: 99118132

    Again, not really a study about islet cell regeneration.  You do
recall how this conversation started?

>But then what do we make of this? (Hmmm... Eastern scientists producing
>favourable evidence for one of the West's favourite beverages.)
>J Ethnopharmacol 1995 Mar;45(3):223-6
>Anti-hyperglycemic effect of black tea (Camellia sinensis) in rat.
>Gomes A, Vedasiromoni JR, Das M, Sharma RM, Ganguly DK
>Division of Pharmacology and Experimental Therapeutics, Indian Institute
>of Chemical Biology, Calcutta.
>Investigations were carried out to evaluate the effect of the hot water
>extract of black tea (Camellia sinensis (L.) O. Kuntze (Theaceae) on
>streptozotocin (STZ)-induced diabetes in rats. The extract significantly
>reduced the blood glucose level and was found to possess both preventive
>and curative effects on experimentally produced diabetes in rats. The
>study reveals that, like green tea, black tea also possesses antidiabetic

    This one is more interesting, but still not mechanistic.  Where are
those regenerating islet cells?  And still not relevent to the way
humans get diabetes.  And lastly, as a prophylactic treatment, not
relevent to the way Herb Ass ist proposed to use these compounds in
people.   It's simply irrelevent.

    ONCE AGAIN.  Herb Assist proposes to give epicatechins to human
type I diabetics, most of whom have no islet cells and haven't for
years, because these herbal products "regenerate islet cells."  His
evidence is one group saying they've seen islet cells regenerate when
the stuff is given to RATS or Rat cells, as they are being poisoned by
a RAT poison-- work which has yet to be repeated by any other group in
any convincing way.  And you're now going to take me to task for
calling this kind of lose talk "unscientific."  Gunna teach me how to
interpret science, are you, Syd?  Well, you go right ahead.

>>>As I said, I'm only going by the mostly unabstracted citations I found
>>>searching Medline, so I'm prepared to "stand corrected" by anyone
>>>who can cite a genuine attempt to replicate that failed. Still, it
>>>seems that what we are dealing with here is definately a far cry
>>>from the groundswell of impartial failures to replicate that you
>>>have characterized it to be, Steve.

     We are dealing with a groundswell of failures to save rats which
have had their islet cells destroyed by rat poison, Syd.  That they may
not replicate experiments in which something prevents the poisoning as
it is going on, is getting less and less relevent.  So what if they do?
 So what if they don't?  When Herbassist says (to take a silly example)
that he's going to put diabetic people behind 3 feet of lead because
THIS makes islet cells regenerate, what should we think when we find he
means that it causes them to regenerate, BUT the "evidence" for this is
that a bunch of brass hats from the pentagon have found that this
regeneration happens only if these islet cells are being fried in
marmosets by a gamma ray laser from the D.O.D., and the lead is
interposed to keep it from happening.  And by the way, it doesn't work
with ferrets.  Or at different time sequences.  And humans don't have
the same sensitivity to gamma rays.  And there's no reason to think
that most diabetes is caused by Star Wars weapons anyway.  Get it?
When your evidence for some proposed treatment of a disease is of that
caliber, and that level of artificiality, and that level of
abstractness, it's better to have kept your mouth shut.

>But, as I said, I don't think we're looking at some obscure anomaly
>here; though if we were, and if it could be really replicated, it might
>teach us something useful about the nature of diabetes. I believe that
>even you would argue this in a different context. (E.g. what's different
>about albino rats that would explain their responsiveness to e. and can
>we capitalize on that for humans?)

    And as I said, I've no doubt that a carefully done and replicated
experiment can teach something, no matter what it's about.  But the
question is: is the something worth the money?  Is it worth the
opportunity cost-- the loss of the something else you DIDN'T find out
with the same money?  If you'd been wiser?  As Bastiat said in
economics, you have to learn to see not just what is seen, but what is
unseen.  Not just what is, but what might have been instead.


From: B. Harris)
Subject: Re: colloidal silver research
Date: 25 Apr 1999 08:23:30 GMT

In <> Ed Mathes <>

>Radha wrote:
>> Carey,
>> This is just one alternative I found during a *very* short
>> search that could be worth investigating.  BTW, personal attacks
>> on my credibility do not add any substance to the topic being
>> of discussion.
>>            Treatment of Diabetes with
>>                 Gymnema sylvestre
>> Trials under experimental and clinical conditions have shown
>> significant results in the treatment of diabetes with Gymnema
>> Sylvestre.

    Which doesn't mention that most of the reports are from the same
group, and that numerous other groups got no results in similar animal
systems. In any case, it doesn' matter much. Gymnema is full of
bioflavonoids, and I suppose it's *possible* that it blocks enough PARS
activation to prevent islet cell death in stretozotocin poisoned rats,
if given immediately.  But even if it does, it's hard to say how this
would be useful to people.  We don't get diabetes that way.  Next time
somebody poisons me with streptozotocin, however (much, much harder to
do to a human than a rat, BTW), I'll try to find some Gymnema

From: B. Harris)
Subject: Re: A Question for the ALT crowd, if they can drop into the real world 
	for a minute
Date: 28 Apr 1999 08:58:24 GMT

In <7g56vk$hm4$> "mjdgdc"
<> writes:

>But the history of science, including medicine, continues to teach us
>that, inductive reasoning notwithstanding, just because something sounds
>nutty doesn't mean it is.

   But the problem with induction is just that: because we all have
different expectation values, what sounds nutty me won't sound nutty to
you.  And unlike deduction, there aren't any good (well accepted) ways
to fix these up, and change each others' minds.  Or do better.

>I make this point, and continue to make it, not as a defense of what
>truly is nutty, but just to point out that sometimes things aren't as
>nutty as they sound. When I was in school I found myself assigned to give
>a short talk on the history of diabetes treatment (an old interest of
>mine), and I would often point out that many of the ideas of the giants
>of diabetes were initially considered nutty by their peers. Minkowski
>himself was ridiculed, and MacLoud thought Banting was totally wrong, but
>ended up quite unfairly sharing the Nobel with him. I tend to look to the
>example of Elliot Joslin, whose only goal was the care of his patients.
>When Frederick Allen rejected insulin therapy (it didn't fit his
>"system"), Joslin was its champion, because he saw what good it could do
>for his patients, which was all he cared about.

    Maybe, maybe not.  Joslin decided that since diabetics had a lot of
sugar, that fat and not carbohydrates was good for them.   So these
folks at the Joslin clinic had meals consisting of a little vegetable
and 14 pats of butter.  Right after they stopped dying of ketoacidosis
they started to die like flies of coronary artery disease (that
continued for the next half-century), but Joslin kept on.  His love of
his theory outweighed his love of his patients.  So it goes.

                                      Steve Harris, M.D.

From: "Steve Harris" <>
Subject: Re: nutritional facts on food
Date: Fri, 6 Jul 2001 20:21:05 -0600

"mnt" <> wrote in message
> This is primarily a diet book but goes into nearly all hormone
> interactions, results from diet deficiencies, premature ageing, how to
> fix them. It takes a systems level viewpoint, and the main thrust is
> describing diet related recoveries & healing methods. From her work with
> insulin-resistant patients with Type II diabetes, Dr. Schwarzbein
> concludes that low-fat diets cause heart attacks, eating fat makes you
> lose body fat, and it's important to eat high-cholesterol foods every
> day. Picture cardiologists and dieticians tearing their hair out and
> overweight people cheering as they dive into Eggs Benedict with sausage.
> According to Schwarzbein, the high-carbohydrate, low-fat,
> moderate-protein diet that most dieticians and disease-prevention
> organizations recommend is the culprit that turns people into diabetics,
> makes them age faster and get degenerative diseases, and keeps them fat
> and unhealthy. She supports her theory with case studies of people who
> were sick and miserable on high-carbo, low-fat diets and who sprang to
> life when they "balanced" their diets with more fat and protein.
> Schwarzbein recommends avoiding "man-made carbohydrates"--processed
> carbs--in favor of those you could "pick, gather or milk." She instructs
> patients to eat "as much good fat as their body needs": eggs, avocados,
> flaxseed oil, butter, mayonnaise, and olive oil. Sorry, but fried foods
> and hydrogenated fats are "bad fats," or "damaged fats," as Schwarzbein
> calls them. You can eat as many eggs a day as you want on this plan,
> plus meat (even sausage--as long as it's nitrate-free--and pâté),
> saturated fat, cream, and nonstarchy vegetables. The book includes a
> four-week meal plan and about 15 recipes.


Sorry, but if a low fat diet turned people into diabetics, there would be
high incidence of diabetes in semi-vegetarian populations who eat a low fat
diet. There isn't. Such populations (eg, the Bantu) have the least diabetes.
Populations with the most diabetes are populations who one traditioally ate
a low fat diet, and now eat a processed diet with Crisco (the Pima indians).

She is correct about trans-fats; they are horrid. If she thinks diabetics
can eat all the saturated fat and cream they like and stay healthy, however,
she's completely out to lunch.

Finally, there isn't anything special about the diabetic heart disease.
Diabetes works synergistically with the other standard risk factors to cause
atherosclerosis. It's like smoking or renal dialysis in this regard.
Diabetics as a group die most often of heart disease, of course, not
diabetes per se. The worse their diabetic control, the better their chance
of getting heart disease. Otherwise, all the same risk factors apply to them
as to anybody else-- except in spades.

Bottom line:

Polysat and monosat fats: good
Sat fats: bad
Trans-fats: ugly.

Total caloric intake is the most important thing of all for a type II
diabetic to watch, however-- far more important than dietary makeup.


From: "Steve Harris" <>
Subject: Re: nutritional facts on food
Date: Sat, 7 Jul 2001 03:42:08 -0600

Spam me and get sued!" <> wrote in message
"Steve Harris" <> wrote:

>>Total caloric intake is the most important thing of all for a type II
>>diabetic to watch, however-- far more important than dietary makeup.

 >Not according to the Endo'99 studies.


COMMENT: Okay, here are a few abstracts for you. Then I want yours.

Note: you can prevent DMII by restricting calories and fat.

Prevention of  DMII by restriction of weight

N Engl J Med 2001 May 3;344(18):1343-50

Comment in:
 N Engl J Med. 2001 May 3;344(18):1390-2

Prevention of type 2 diabetes mellitus by changes in lifestyle among
subjects with impaired glucose tolerance.

Tuomilehto J, Lindstrom J, Eriksson JG, Valle TT, Hamalainen H,
Ilanne-Parikka P, Keinanen-Kiukaanniemi S, Laakso M, Louheranta A, Rastas
M, Salminen V, Uusitupa M; Finnish Diabetes Prevention Study Group.

Department of Epidemiology and Health Promotion, National Public Health
Institute, Helsinki, Finland.

BACKGROUND: Type 2 diabetes mellitus is increasingly common, primarily
because of increases in the prevalence of a sedentary lifestyle and
obesity. Whether type 2 diabetes can be prevented by interventions that
affect the lifestyles of subjects at high risk for the disease is not
known. METHODS: We randomly assigned 522 middle-aged, overweight subjects
(172 men and 350 women; mean age, 55 years; mean body-mass index [weight
in kilograms divided by the square of the height in meters], 31) with
impaired glucose tolerance to either the intervention group or the
control group. Each subject in the intervention group received
individualized counseling aimed at reducing weight, total intake of fat,
and intake of saturated fat and increasing intake of fiber and physical
activity. An oral glucose-tolerance test was performed annually; the
diagnosis of diabetes was confirmed by a second test. The mean duration
of follow-up was 3.2 years. RESULTS: The mean (+/-SD) amount of weight
lost between base line and the end of year 1 was 4.2+/-5.1 kg in the
intervention group and 0.8+/-3.7 kg in the control group; the net loss by
the end of year 2 was 3.5+/-5.5 kg in the intervention group and
0.8+/-4.4 kg in the control group (P<0.001 for both comparisons between
the groups). The cumulative incidence of diabetes after four years was 11
percent (95 percent confidence interval, 6 to 15 percent) in the
intervention group and 23 percent (95 percent confidence interval, 17 to
29 percent) in the control group. During the trial, the risk of diabetes
was reduced by 58 percent (P<0.001) in the intervention group. The
reduction in the incidence of diabetes was directly associated with
changes in lifestyle.  CONCLUSIONS: Type 2 diabetes can be prevented by
changes in the lifestyles of high-risk subjects.

Publication Types:
Clinical trial
Multicenter study
Randomized controlled trial

PMID: 11333990 [PubMed - indexed for MEDLINE]

Fat intake and heart disease in Korea

Am J Clin Nutr 2001 Apr;73(4):722-7

Moderate dietary fat consumption as a risk factor for ischemic heart
disease in a population with a low fat intake: a case-control study in
Korean men.

Suh I, Oh KW, Lee KH, Psaty BM, Nam CM, Kim SI, Kang HG, Cho SY, Shim WH.

Department of Preventive Medicine and Public Health, Yonsei University
College of Medicine, Seoul, Republic of Korea.

BACKGROUND: Dietary fat intake is associated with the incidence of
ischemic heart disease (IHD) in Western countries. In populations in
which both the average dietary fat consumption and the incidence of IHD
are lower than in Western countries, the association of dietary fat
intake with IHD incidence remains unknown. OBJECTIVE: We conducted a
case-control study to examine the association of dietary fat with IHD
incidence in Korean men. DESIGN: The case group consisted of 108 patients
with electrocardiogram-confirmed myocardial infarction or
angiographically confirmed (> or =50% stenosis) IHD who were admitted to
a university teaching hospital in Seoul, Republic of Korea. The controls
were 142 age-matched patients admitted to the departments of
ophthalmology and orthopedic surgery at the same hospital. Dietary fat
intake was assessed by a nutritionist using a semiquantitative
food-frequency questionnaire. Body mass index (BMI), cigarette use,
alcohol intake, exercise, and history of disease were determined during
an interview and examination.  RESULTS: In a univariate analysis, the
mean percentages of energy from total fat, saturated fatty acids, and
monounsaturated fatty acids were significantly higher in the cases than
in the controls. BMI, smoking, and a history of hypertension were
associated with the occurrence of IHD. In multiple logistic analyses,
total fat intake was a significant risk factor (odds ratio: 1.08 for 1%
of energy intake; 95% CI: 1.02, 1.14) after adjustment for BMI and
smoking.  CONCLUSION: In a population with a relatively low fat intake
(19% of energy intake), a moderate increase in total fat intake may be a
risk factor for IHD.

PMID: 11273846 [PubMed - indexed for MEDLINE]

The risk factors which independently correlated
with heart disease is the very large nurse's health study.

N Engl J Med 2000 Jul 6;343(1):16-22

Primary prevention of coronary heart disease in women through diet and

Stampfer MJ, Hu FB, Manson JE, Rimm EB, Willett WC.

Department of Medicine, Brigham and Women's Hospital and Harvard Medical
School, Boston, USA.

BACKGROUND: Many lifestyle-related risk factors for coronary heart
disease have been identified, but little is known about their effect on
the risk of disease when they are considered together. METHODS: We
followed 84,129 women participating in the Nurses' Health Study who were
free of diagnosed cardiovascular disease, cancer, and diabetes at base
line in 1980.  Information on diet and lifestyle was updated
periodically. During 14 years of follow-up, we documented 1128 major
coronary events (296 deaths from coronary heart disease and 832 nonfatal
infarctions). We defined subjects at low risk as those who were not
currently smoking, had a body-mass index (the weight in kilograms divided
by the square of the height in meters) under 25, consumed an average of
at least half a drink of an alcoholic beverage per day, engaged in
moderate-to-vigorous physical activity (which could include brisk
walking) for at least half an hour per day, on average, and scored in the
highest 40 percent of the cohort for consumption of a diet high in cereal
fiber, marine n-3 fatty acids, and folate, with a high ratio of
polyunsaturated to saturated fat, and low in trans fat and glycemic load,
which reflects the extent to which diet raises blood glucose levels.
RESULTS: Many of the factors were correlated, but each independently and
significantly predicted risk, even after further adjustment for age,
family history, presence or absence of diagnosed hypertension or
diagnosed high cholesterol level, and menopausal status. Women in the
low-risk category (who made up 3 percent of the population) had a
relative risk of coronary events of 0.17 (95 percent confidence interval,
0.07 to 0.41) as compared with all the other women. Eighty-two percent of
coronary events in the study cohort (95 percent confidence interval, 58
to 93 percent) could be attributed to lack of adherence to this low-risk
pattern. CONCLUSION: Among women, adherence to lifestyle guidelines
involving diet, exercise, and abstinence from smoking is associated with
a very low risk of coronary heart disease.

PMID: 10882764 [PubMed - indexed for MEDLINE]

Same study: The particular kind of fat matters:

N Engl J Med 1997 Nov 20;337(21):1491-9
Comment in:
 ACP J Club. 1998 May-Jun;128(3):75
 N Engl J Med. 1997 Nov 20;337(21):1544-5
 N Engl J Med. 1998 Mar 26;338(13):917-8; discussion 918-9
 N Engl J Med. 1998 Mar 26;338(13):917; discussion 918-9
 N Engl J Med. 1998 Mar 26;338(13):918-9

Dietary fat intake and the risk of coronary heart disease in women.

Hu FB, Stampfer MJ, Manson JE, Rimm E, Colditz GA, Rosner BA, Hennekens CH,
Willett WC.

Department of Nutrition, Harvard School of Public Health, Boston, MA 02115,

BACKGROUND: The relation between dietary intake of specific types of fat,
particularly trans unsaturated fat and the risk of coronary disease
remains unclear. We therefore studied this relation in women enrolled in
the Nurses' Health Study. METHODS: We prospectively studied 80,082 women
who were 34 to 59 years of age and had no known coronary disease, stroke,
cancer, hypercholesterolemia, or diabetes in 1980. Information on diet
was obtained at base line and updated during follow-up by means of
validated questionnaires.  During 14 years of follow-up, we documented
939 cases of nonfatal myocardial infarction or death from coronary heart
disease. Mutivariate analyses included age, smoking status, total energy
intake, dietary cholesterol intake, percentages of energy obtained from
protein and specific types of fat, and other risk factors. RESULTS: Each
increase of 5 percent of energy intake from saturated fat, as compared
with equivalent energy intake from carbohydrates, was associated with a
17 percent increase in the risk of coronary disease (relative risk, 1.17;
95 percent confidence interval, 0.97 to 1.41; P=0.10). As compared with
equivalent energy from carbohydrates, the relative risk for a 2 percent
increment in energy intake from trans unsaturated fat was 1.93 (95
percent confidence interval, 1.43 to 2.61; P<0.001); that for a 5 percent
increment in energy from monounsaturated fat was 0.81 (95 percent
confidence interval, 0.65 to 1.00; P=0.05); and that for a 5 percent
increment in energy from polyunsaturated fat was 0.62 (95 percent
confidence interval, 0.46 to 0.85; P= 0.003). Total fat intake was not
signficantly related to the risk of coronary disease (for a 5 percent
increase in energy from fat, the relative risk was 1.02; 95 percent
confidence interval, 0.97 to 1.07; P=0.55). We estimated that the
replacement of 5 percent of energy from saturated fat with energy from
unsaturated fats would reduce risk by 42 percent (95 percent confidence
interval, 23 to 56; P<0.001) and that the replacement of 2 percent of
energy from trans fat with energy from unhydrogenated, unsaturated fats
would reduce risk by 53 percent (95 percent confidence interval, 34 to
67; P<.001).  CONCLUSIONS: Our findings suggest that replacing saturated
and trans unsaturated fats with unhydrogenated monounsaturated and
polyunsaturated fats is more effective in preventing coronary heart
disease in women than reducing overall fat intake.

PMID: 9366580 [PubMed - indexed for MEDLINE]

The Dutch view:

Acta Cardiol 1999 Jun;54(3):163-8

Treatment and prevention of coronary heart disease by lowering serum
cholesterol levels; from the pioneer work of C.D. de Langen to the third
"Dutch Consensus on Cholesterol".

Jukema JW, Simoons ML.

Dept. of Cardiology, Leiden University Medical Center, The Netherlands.

In the beginning of this century a possible relation was observed between
cholesterol-rich foods, blood cholesterol levels and atherosclerosis by
"pioneers" in this field as Anitschkow and De Langen. In the second half
of this century a definite link was established between serum cholesterol
levels and development of coronary heart disease (CHD). In angiographic
studies it has recently been shown that a decrease in total cholesterol
as well as in low-density lipoprotein cholesterol level results in a
retardation of the progression of vascular disease. Furthermore, clinical
event intervention trials demonstrated that therapy with cholesterol
synthesis inhibitors reduces not only cardiovascular and total mortality,
but also other manifestations of CHD.  These recent results prompted to
revise, for the second time, the Dutch consensus text for lipid lowering
therapy, with the following conclusions.  Hypercholesterolaemia is
treated with a low-saturated fat diet and normalisation of weight. For
individuals, this might result in a reduction of the risk for myocardial
infarction or death and for the population in a decrease of the mean
serum cholesterol concentration and a reduction of the incidence of CHD.
The indication for drug therapy is founded on the expected effectiveness
to reduce the incidence of (new manifestations of) CHD, which is related
to the level of the absolute risk of vascular disease. Treatment with
cholesterol synthesis inhibitors must be considered in (a) patients with
familial hypercholesterolaemia; (b) all patients with a history of
myocardial infarction or other symptomatic vascular disease with a total
cholesterol concentration above 5.0 mmol/l and a life expectancy of at
least five years; (c) persons without known vascular disease with a
combination of diabetes mellitus, hypertension, hypercholesterolaemia,
cigarette smoking and high risk for development of CHD, rising from 25%
per 10 years at the age of 40 years to 35-40% per 10 years at the age of
70 years, with a life expectancy of at least five years. If these
guidelines are followed, the calculated cost-effectiveness is about Dfl.
40,000 per life year gained or less. The consensus committee judges this
reasonable in comparison with other therapeutic interventions in the
Netherlands. Thus by now, with regard to lipids and atherosclerosis, the
definite link has been established between observational medicine and an
effective treatment modality which is applicable in daily practise.

Publication Types:
Historical article

PMID: 10478274 [PubMed - indexed for MEDLINE]

A small study, but showing the energy restriction significantly helps
diabetes, and replacement of sat fat works even better.

Diabetes Care 1999 Jun;22(6):889-95

Comment in:
 Diabetes Care. 1999 Jun;22(6):886-8

Effect of energy restriction, weight loss, and diet composition on plasma
lipids and glucose in patients with type 2 diabetes.

Heilbronn LK, Noakes M, Clifton PM.

Department of Physiology, University of Adelaide, Australia.

OBJECTIVE: To determine the optimal diet for improving glucose and lipid
profiles in obese patients with type 2 diabetes during moderate energy
restriction. RESEARCH DESIGN AND METHODS: A total of 35 free-living obese
patients with type 2 diabetes were assigned to one of three 1,600
kcal/day diets for 12 weeks. The diets were high carbohydrate (10% fat,
4% saturated), high monounsaturated fat (MUFA) (32% fat, 7% saturated),
or high saturated fat (SFA) (32% fat, 17% saturated). RESULTS: Diet
composition did not affect the magnitude of weight loss, with subjects
losing an average of 6.6 +/- 0.9 kg. Energy restriction and weight loss
resulted in reductions in fasting plasma glucose (-14%), insulin (-27%),
GHb (-14%), and systolic (-7%) and diastolic blood pressure (-10%) levels
and the glucose response area (-17%) independent of diet composition.
Diet composition did affect the lipoprotein profile. LDL was 10% and 17%
lower with the high-carbohydrate and high-MUFA diets, respectively,
whereas no change was observed with the high-SFA diet (P < 0.001 for
effect of diet). HDL was transiently reduced on the high-carbohydrate
diet at weeks 1, 4, and 8, whereas higher fat consumption maintained
these levels. The total cholesterol:HDL ratio, although significantly
reduced on the high-MUFA diet (P < 0.01), was not different from the
other two diets after adjustment for baseline differences. CONCLUSIONS:
Energy restriction, independent of diet composition, improves glycemic
control; however, reducing SFA intake by replacing SFA with carbohydrate
or MUFA reduces LDL maximally during weight loss and to a greater degree
than has been shown in weight-stable studies.

Publication Types:
Clinical trial
Controlled clinical trial

PMID: 10372237 [PubMed - indexed for MEDLINE]

Male health professionals study in US: counterpart of the (female) nurses
health study.  Sat fat intake reaches significance for fatal MI; however
the effect is not as strong as in the multicountry studies. It is as
strong as predicted from the effect of sat fat on blood lipids.  Fiber is
a partial confounder. Omega-3 intake comes out looking good (as it does
in many other MI studies, and also in diabetes studies).  Fish good, very
good. Butter not good, but only as bad as its effect on LDLs.  Crisco
bad, very bad.

BMJ 1996 Jul 13;313(7049):84-90

Comment in:
 BMJ. 1996 Nov 16;313(7067):1258
 BMJ. 1996 Nov 16;313(7067):1258; discussion 1259
 BMJ. 1996 Nov 16;313(7067):1259

Dietary fat and risk of coronary heart disease in men: cohort follow up
study in the United States.

Ascherio A, Rimm EB, Giovannucci EL, Spiegelman D, Stampfer M, Willett WC.

Harvard School of Public Health, Boston, MA 02115, USA.

OBJECTIVE--To examine the association between fat intake and the
incidence of coronary heart disease in men of middle age and older.
DESIGN--Cohort questionnaire study of men followed up for six years from
1986. SETTING--The health professionals follow up study in the United
States. SUBJECTS--43 757 health professionals aged 40 to 75 years free of
diagnosed cardiovascular disease or diabetes in 1986. MAIN OUTCOME
MEASURE--Incidence of acute myocardial infarction or coronary death.
RESULTS--During follow up 734 coronary events were documented, including
505 non-fatal myocardial infarctions and 229 deaths.  After age and
several coronary risk factors were controlled for significant positive
associations were observed between intake of saturated fat and risk of
coronary disease. For men in the top versus the lowest fifth of saturated
fat intake (median = 14.8% v 5.7% of energy) the multivariate relative
risk for myocardial infarction was 1.22 (95% confidence interval 0.96 to
1.56) and for fatal coronary heart disease was 2.21 (1.38 to 3.54). After
adjustment for intake of fibre the risks were 0.96 (0.73 to 1.27) and
1.72 (1.01 to 2.90), respectively.  Positive associations between intake
of cholesterol and risk of coronary heart disease were similarly
attenuated after adjustment for fibre intake. Intake of linolenic acid
was inversely associated with risk of myocardial infarction; this
association became significant only after adjustment for non-dietary risk
factors and was strengthened after adjustment for total fat intake
(relative risk 0.41 for a 1% increase in energy, P for trend < 0.01).
CONCLUSIONS--These data do not support the strong association between
intake of saturated fat and risk of coronary heart disease suggested by
international comparisons. They are compatible, however, with the
hypotheses that saturated fat and cholesterol intakes affect the risk of
coronary heart disease as predicted by their effects on blood cholesterol
concentration. They also support a specific preventive effect of
linolenic acid intake.

PMID: 8688759 [PubMed - indexed for MEDLINE]

It's not only the calorie restriction that helps, but the amount of
weight loss.  They are independent factors. Two papers from the same
group and study.
Diabetes Care 1994 Jan;17(1):30-6

Caloric restriction per se is a significant factor in improvements in
glycemic control and insulin sensitivity during weight loss in obese
NIDDM patients.

Wing RR, Blair EH, Bononi P, Marcus MD, Watanabe R, Bergman RN.

Department of Psychiatry, University of Pittsburgh School of Medicine,

OBJECTIVE--To examine the effects of caloric restriction, independent of
differences in weight loss, on improvements in glycemic control, fasting
insulin, and insulin sensitivity. RESEARCH DESIGN AND METHODS--We
randomized 93 obese type II diabetic patients to two different degrees of
calorie restriction (1,674 or 4,185 kJ/day; 400 or 1,000 kcal/day) and
compared the changes in fasting glucose, fasting insulin, and insulin
sensitivity that resulted from a comparable reduction in body weight (11%
of initial body weight). Insulin sensitivity was assessed using the
minimal model analysis of frequently sampled intravenous glucose
tolerance tests. RESULTS--Despite equal weight losses, subjects in the
1,674 kJ/day (400 kcal) condition had lower fasting glucose levels (7.61
vs. 10.13 mM, P = 0.03) and greater insulin sensitivity (1.79 vs.  1.13,
P = 0.04) after weight loss than did subjects in the 4,185 kJ/day (1,000
calorie) condition. Subjects were restudied 15 weeks later when both
groups were consuming a 4,185 kJ/day (1,000 kcal/day) diet. Subjects who
increased from 1,674 to 4,185 kJ (400 to 1,000 calories) had worse
fasting glycemic control in spite of continued weight loss, whereas
subjects who remained on 4,185 kJ (1,000 calories) throughout had further
improvements in both blood glucose and insulin sensitivity with increased
weight loss. CONCLUSIONS--Both degree of calorie restriction and
magnitude of weight loss have independent effects on improvements in
glycemic control and insulin sensitivity.

Publication Types:
Clinical trial
Randomized controlled trial

PMID: 8112186 [PubMed - indexed for MEDLINE]

 J Clin Endocrinol Metab 1993 Nov;77(5):1287-93

Relative effects of calorie restriction and weight loss in
noninsulin-dependent diabetes mellitus.

Kelley DE, Wing R, Buonocore C, Sturis J, Polonsky K, Fitzsimmons M.

University of Pittsburgh School of Medicine, Pennsylvania 15261.

In obese patients with noninsulin-dependent diabetes mellitus (NIDDM),
reducing calorie intake improves glycemic control, often more rapidly
than weight loss.  Conversely, after weight loss has been achieved,
metabolic control can deteriorate once calorie intake is increased, even
if there is no regaining of weight. The current study, therefore, tested
the hypothesis that restricting calorie consumption has an important
role, independent of weight loss, in metabolic regulation of NIDDM
patients. Isotopic determinations of hepatic glucose production (HGP),
post-absorptively and after ingestion of 75 g glucose (dual glucose
isotope method), were made in conjunction with measurement of insulin
secretion and insulin sensitivity in seven obese NIDDM volunteers after
four periods of controlled calorie intake: 1) 7 days of a baseline weight
maintenance diet, 2) followed immediately by 7 days of calorie
restriction (800 Cal/day); 3) followed by a weight loss program that
consisted of 2 months of a very low calorie diet (400 Cal/day) and then 4
weeks of gradual refeeding and 7 days on a weight maintenance diet; and
4) a final week of calorie restriction (800 Cal/day). The initial brief
interval of calorie restriction produced substantial decreases in fasting
plasma glucose, HGP, and fasting plasma triglyceride and increases in
insulin sensitivity and secretion. After a substantial weight loss (12.7
+/- 2 kg), each parameter improved further, with the effect of weight
loss approximately equal to that obtained with initial calorie
restriction. Reimposing calorie restriction after weight loss had little
effect, except that fasting plasma glucose and HGP improved slightly
further. In obese NIDDM subjects, a 7-day period of calorie restriction
produces approximately half of the overall improvement in HGP, insulin
sensitivity, and insulin secretion that is obtained after a substantial
loss of weight. These findings indicate that calorie restriction has an
important regulatory effect on the metabolism of obese patients with
NIDDM that is independent of weight loss.

PMID: 8077323 [PubMed - indexed for MEDLINE]

From: David Rind <>
Subject: Re: Coca Cola Causing Diabetes.
Date: Tue, 30 Nov 2004 21:12:53 -0500
Message-ID: <coj9bb$49t$>

PF Riley wrote:
> On Mon, 29 Nov 2004 18:28:34 -0500, David Rind
> <> wrote:
>>PF Riley wrote:
>>>This is irrelevant to the original question. Eating too much sugar
>>>does not cause diabetes. This is such an annoying yet common
>>>misconception, because people confuse cause and effect. People who
>>>have diabetes have high sugar levels in their bloodstream. This is
>>>CAUSED by the diabetes, not the other way around. You won't raise your
>>>blood glucose levels by eating lots of sugar and "become" diabetic.
>>I think this answer is overly definitive. There's a fair amount of
>>reason to worry that high glycemic index foods (and sugar is such a
>>food) can increase the risk of type II diabetes.
> But given that simple sugars are a relatively recent addition to the
> human diet and believed by some, Atkins notwithstanding, to be a main
> cause of obesity and even hypercholesterolemia in Western society, and
> given that obesity is the major risk factor for type 2 diabetes, could
> it simply be that high sugar intake is a contributing factor to
> obesity, and the obesity causes the insulin resistance and ultimately
> diabetes?
> PF

Yes, that is possible. But there is evidence from animals to suggest
that high glycemic index foods actually promote diabetes independent of
effects on weight. It's not that I think the issue is proven, but rather
that I think your statement that eating sugar won't lead to diabetes is
also not proven and may well turn out to be incorrect.

David Rind

From: David Rind <>
Subject: Re: Coca Cola Causing Diabetes.
Date: Wed, 01 Dec 2004 07:21:49 -0500
Message-ID: <cokd12$e2r$>

Daniel Prince wrote:
> David Rind <> wrote:
>>I think this answer is overly definitive. There's a fair amount of
>>reason to worry that high glycemic index foods (and sugar is such a
>>food) can increase the risk of type II diabetes.
> Is this increase in risk independent of the increase in risk caused
> by the weight gain that high glycemic index foods cause?

There is concern that it is an independent risk (based mainly on animal
models). Again, I am not saying that such a risk has been definitively

David Rind

From: Steve Harris <>
Subject: Re: Statins do NOT protect against Azlheimer's
Date: 13 Feb 2005 14:22:12 -0800
Message-ID: <>

>>I'm not sure most people on this ng realize that this kind of condition
is not just a painful burning of the hands and feet, it can result in
amputation of the extremities.  There tends to be a 'yawn, big deal'
attitude whenever PN from statins is brought up (not from you personally,
Jim - more the general tone of the group).  However, if it results in the
loss of a limb, yes, it is a very big deal. <<


Yes, and if wishes were horses, then fools would ride.

You're making an unwarrented assumption. The neuropathy of diabetes
contributes to amputations ONLY because it contributes to foot wounds,
but without the diabetes, such wounds heal and are no big deal.
Amputation in diabetes is due to the vascular disease and poor
infection handling capability, which are in turn ALSO caused by the
diabetes. Without diabetes, peripheral neuropathies caused by other
conditions (aging being most common, followed by various toxins,
compression syndromes, etc.) very rarely result in amputation, because
circulation and infection handling capacity in the leg remains fine.

Thus, your assumption that statin neuropathy would result in amputation
is not warrented. If anything, by decreasing peripheral vascular
disease risk, I would expect that statins probably decrease amputation
risk. Again, it's poor arterial circulation that leads to foot loss,
not numbness per se. If I had to choose between nerve or artery damage
in my legs, I'd take the nerve damage.


From: Steve Harris <>
Subject: Re: Statins do NOT protect against Azlheimer's
Date: 13 Feb 2005 18:05:34 -0800
Message-ID: <>

>>Are you suggesting that more neuropathy in diabetics with less
peripheral vascular disease (is diabetic peripheral vascular disease
equivalent to arteriosclerosis - I don't know) will equate to net fewer
amputations?  <<


Yes, it could well be. Needs to be proven, of course.

Diabetes results in both large and small vessel arterial disease, but
it is almost entirely the large vessel disease (endovascular thickening
progressing to plaque and/or clot-- all considered stages of
atherosclerosis) which results in really deep nonhealing ulcers,
gangrene, and amputation. This disease in diabetics is not all that
different from that in standard atherosclerosis, save for being nastier
and perhaps a little more peripheral. Diabetics do indeed get a lot of
pressure ulcers from just the neuropathy and stress, but they're
usually not deep, and if arterial circulation is good, the underlying
tissue will be found to be alive and such ulcers usually eventually
heal without deep infection.

This question comes up quite alot in physical exam, by the way.  An
ulcer will occur  in a diabetic foot and the question will arrise of
what the risk for gangrene is, since the patient is diabetic and
there's no way of knowing what shape his small arteries are in. But
it's not the small arteries that are important.. If pulses are
detectable in the main 2 foot arteries (by feel or by doppler) then
with good wound care the progosis for healing is (again) also good.


From: Steve Harris <>
Subject: Re: Can DiabetesT2/IR cause Obesity?
Date: 2 Jul 2005 20:32:57 -0700
Message-ID: <>

>>Now my doubts are:-
Whether obesity is a reason/cause of getting Type 2 diabetes OR Type 2
diabetes with deficient action of insulin is the cause/reson of making
a person obese(central obesity)--may be due to conversion of excess
glucose into fats? <<


Insulin is a pro-storage molecule. Too much action will encourage fat
deposition, but people with insulin resistance have too little action,
even if they have high levels. Thus, this is not result, but cause.
Much data of manipulation of fat in type II diabetics showing you can
influence insulin sensitivity that way.

Yes, going on insulin injections makes it very difficult to get rid of

>>How a type2 patient can get deficient secretion of insulin in early
stages? <<

They generally don't. Not till later stages when the pancreas gives up.

>>Can excess BG level cause low secretion of insulin?

No.  Excess BG causes insulin to be made if the body is capable of
doing it.


From: John De Armond
Subject: Re: New with questions
Date: Tue, 05 Jul 2005 04:14:37 -0400
Message-ID: <>

On Mon, 04 Jul 2005 14:09:47 -0400, Dolciani <>

>Please excuse the crosspost, I'm not sure where to post this.
>A little background:  I've just started testing. I've been having problems
>with my feet lately, with burning and pain.  I'm also overweight and not
>very active, and frequently have a dry mouth. When I heard that my aunt was
>recently diagnosed with T2, I thought I'd like to check my BG to see if I
>should be concerned (this is something I just didn't want to even think
>I bought a Relion Newtek meter and started testing.  After initially
>getting amazingly low readings, I realized that I wasn't using enough
>blood.  The first reading I took with a larger drop was AM fasting at 140.
>I was shocked, to say the least.  Eating higher carb meals, I get in the
>140s to 150s 1 hour after eating, highest so far was 155, and in the 130s
>to 140s 2 hours after eating.  With much lower carbs I'm averaging in the
>low 120s before breakfast, and in the low 110's to 120's at other times.

I hate to say it but "welcome to the club".  Here are some URLs.  <<<<< PAY ATTENTION TO THIS ONE
And probably the most important one,

Dr. Bernstein is on the leading edge of diabetes treatment, being one
himself, being the first to do home glucose testing, etc.  I highly
recommend the book.  I use a slightly relaxed form of his lifestyle
method of diabetes management and have normal, non-diabetic BG, A1C
and lipid panel numbers.

>Today I finished the last of the Relion strips.  The meter read 110.  I
>immediately re-tested with my new meter, an Ascensia Contour, and got a
>reading of 89.
>First, why such a large difference in the numbers?

First off, the RElion meter you have isn't very impressive.  I bought
one and was not impressed.  OTOH, the Relion Ultima is a quite nice
meter.  It is cheaper to operate than the one you bought.  I have
tested it extensively against my One Touch Ultra using both my blood
and calibration solutions and find that the two agree within 3 points
or so.

There is ONE BIG DIFFERENCE.  The One Touch will refuse to produce a
reading if the sample volume isn't correct.  The Relion will, more
often than not, produce an incorrect reading if there is too little
blood. Flooding the end of the strip with blood works best.  For the
difference in price if I'm paying for the strips, I can milk a little
more blood.

Second, your test method must be correct.  Follow all the instructions
including stimulating circulation in the area you're about to
puncture.  I suggest tossing the Relion lancet device and getting a
One Touch one.  I like it the best of all I've tested.

I've found that I get erroneous readings if I spend too much effort
trying to coax the blood out of an inadequate puncture.  Probably I
work out some interstitial fluid along with the blood.  I want to see
the drop of blood pop right up there within a second or so of

Even though the Relion instrument isn't rated for "alternate site
testing" (drawing blood from your arms, leg, palm, etc), my testing
indicates that it works just fine.  I do almost all my testing on my
arms.  It is absolutely essential that you massage the test site for a
bit before puncturing to stimulate circulation.  Otherwise the BG
concentration in the rather stagnant blood in that area may be far
off.  I suggest you compare results between your fingers and your arms
before you rely on arm testing.  The advantage to arm testing is, at
least for me, the puncture is totally and completely painless.

>Secondly, any advice on where to go from here?
>I'm worried but I really don't want to go to the doctor for this. I do not
>want a diagnosis of diabetes on my medical record if I can avoid it.  I'd
>rather try to get more normal numbers through LC eating and exercise.

That is a very valid concern.  Once you have the diabetes diagnosis on
your record, forget ever being able to buy individual health, life,
disability or long term care insurance.  I've learned that the hard

Some have suggested running out and buying insurance and then going to
the doctor.  In the case of health insurance, that will do you for one
year.  Then you'll be underwritten as a diabetic and in most states,
refused renewal.  In most states, individual health insurance is not
required to be guaranteed renewal.  It's a whole new world every year.

A diagnosis on your record may even affect your future employment
possibilities.  As the person who writes the checks for my company's
group insurance, I'm well aware of what having a chronically ill
person on the payroll does to rates.  I've been told by my agent to
expect my group rate to about double next year because of my
diagnosis.  Small companies in particular, have great incentive to
either not hire you or to figure out how to get rid of you once they
find out.

You can't let this problem go untreated so you have one of two

Find a doc who will work for cash and not keep records in your name.

Since you'll be self-treating anyway if you plan on having good
control, that is the route I'd go if I had it to do over again.  Read
that web site I flagged above with the "pay attention" flag.  Lots of
good information.

You can buy your testing supplies without a prescription, as you've
already found out.  In most states you can buy some forms of insulin
over the counter without a prescription. Unfortunately this doesn't
cover the basal insulins and the best fast acting ones.

You may be able to nip this problem with diet and exercise alone if
you haven't nuked your beta cells too much yet.  I probably could have
had my doc caught my problem a year earlier.  Now I'm on the needle.

I highly, highly recommend getting the Bernstein book.  His plan is a
little bit too austere for me and probably for you too, but since
you're not a type 1 and still have some functioning beta cells, you
probably will do OK doing a little less.

His plan is based on a very low carb diet, exercise and lots and lots
of testing.  Testing is the only feedback you get on how well you're

As someone else mentioned, you need to watch your lipids closely, as
high cholesterol goes hand in hand with diabetes.  Mine had always
been below normal, then suddenly shot up a few years ago.  That should
have clued at least my doc to look for diabetes but it didn't.  My bad
cholesterol was near 400 at my diagnosis.  It is now smack in the
middle of the normal range even though I eat lots and lots of meat.
That's a secondary benefit of the low carb diet.

Something to think of when you need to go to your regular doc.  Using
your meter and OTC insulin if necessary, get your sugar down to the
normal range before having blood work done.  If there is a chance the
doc will run an A1C test then you need to have had it down for at
least a couple of months, as this test represents your average BG
level over that period.  This procedure is especially useful if you
have to give blood for an insurance physical.

In many cities (Atlanta, for example) there are walk-in clinics where
one can have any sort of blood test performed anonymously.  These
sprung up to service the (potential) AIDS community but they're
equally useful for the rest of us.  When I lived in Atlanta and long
before diabetes, I'd routinely have a workup done before taking an
insurance physical just to make sure.  This gave me the opportunity to
correct any problems before I went on the record.

If you can't control with diet and exercise alone, then you have to
decide whether to go with an oral drug, insulin or a combo.  There is
a lot of debate both in the medical and diabetic communities about
which is best.

I'm firmly on the side of insulin.  I don't like taking a lot of
pills, I don't like the side effects and I don't like the cost.  If
you're lucky, insulin therapy will give your pancreas a rest and a
chance to heal itself.  It may recover part or most of its
functionality, whereupon diet and exercise again do the job.  I wasn't
that lucky but many people are, especially when the disease is caught

It is important to use diet and exercise to keep the required insulin
as low as possible because excess insulin is known to do a number of
bad things (fat storage, for instance) and is suspected in a number of
other bad things (heart disease, for instance).

Bernstein calls this the Law of Small Numbers.  Small numbers -  BG,
insulin dose, carbs, etc won't hurt you.  If you only need a unit or
two of insulin to cover a meal, it's hard to make an error. If your BG
is only a little high and you require only a unit or two of insulin,
it's hard to make a mistake.

OTOH, if you are so insulin resistant and/or are eating so many carbs
that you need 20 or 30 units then it is very easy to mis-figure and
end up in a bad hypo (low blood glucose) condition.  Even mild hypos
are pretty miserable.  The only hypo incidents I've suffered have been
after deviating from my plan, eating something carb rich and then
trying to dose over it with lots of extra insulin.

I should note that everything I've written here I've learned on my
own.  My "diabetic counseling" involved being handed some scripts for
supplies so my insurance would pay for them and some oral instructions
on how to work up the correct insulin doses.  I'm really thankful
that's all I received, judging by some of the stuff I've read since
then.   The ADA's diet and treatment plan - what most
non-diabetes-specialist docs rely on - is so bad that I'd probably
have gone blind by now.  As it is, my very tight control has reversed
the vision problems I had at diagnosis.

If I were in your shoes now, the very first thing I'd do would be to
adopt a low carb diet.  You're going to have to do this regardless so
you might as well get it out of the way now.  This is a lifestyle
change that will last the rest of your life.  Permissible foods are
not bad, they're just different.

Order the Bernstein book and read it.

Go here and get the USDA nutritional database:

This will help you track carbs in non-pre-packaged foods.  For
pre-packaged foods, learn to read the labels for carb content.

If you eat fast food, visit the company web sites and get the
nutritional info for stuff you like.  You'll be amazed at how carb
loaded much of the fast food is.

For the first month after diagnosis I spent every available minute on
the net researching diabetes.  I still spend a lot of time in this
pursuit.  I suggest you do too.  You need to decide for yourself how
you want to treat your disease.

For me, it became obvious that the ADA (american diabetes association)
way was far wrong and that the low carb, low BG way was the right way.
My fasting sugar was over 500 when I was diagnosed so I had to do
something quickly to get it under control.  I initially settled on the
following goals:

Fasting BG under 120.
Post meal BG under 160.
No more than 30 grams of carbs a day.

It initially required 60 units/day of Lantus (slow acting, long
lasting insulin) for my basal load and lots of Novolog (fast) insulin
for meals.

Over the next couple of weeks I achieved those goals.  I continued to
lose weight, something I'd started before diagnosis.  As the weight
came off (and hopefully some pancreatic recovery), so did my basal
load requirement.  I'm currently at 30 units/day Lantus. I ratcheted
my goals down to:

Fasting BG 100 or lower
Post meal BG 120 or lower.

I achieved that fairly easily.  Then I started ramping up the
tolerable carbs.  I tested each food I proposed to eat to see how it
impacted my BG and how much insulin I needed to cover it.  I now allow
myself 60 grams of carbs per day but no more than 30 in any one meal.
Different foods affect my BG differently so I further limit my food
combos so that I need 6 or less units of Novolog for cover.  Most
meals need 3 or less.  Law of Small Numbers!

I keep very careful records using my Palm Pilot.  I use two programs
(because neither does everything I want), Diabetes Pilot
( and GlucoseOne
(  DP has a nice food database and the
ability to compute insulin dose based on the carb count and the BG
reading.  GO has a better record format and a built-in timer to remind
you to test your BG a fixed time after each meal.  It also generates
somewhat better reports.

I test my BG:

Upon waking
Before each meal and snack
1.5 hours after each meal and snack*
bed time.

* By initially testing every 10-15 minutes after eating a meal, I
found that my BG peaks 1.5 hours after eating for most foods.

I keep a record of my blood tests, what I ate, the carb count, the
cover insulin required and any subsequent trim dose.  This later is a
small dose of insulin that I use to catch a peak if I see that it is
going too high 1.5 hours after eating.  This requires a very fast
insulin, Novolog being about the fastest.

Very high BG makes you sick, tired and clouds your thinking.  I ached
all over, I could barely get out of a chair, my vision was shot and I
could not think clearly.  I was in a haze.  That was the situation I
was in when I went to my doc.  For some reason I was convinced that I
had liver problems....

If I had it to do all over again, I'd have NOT gone to my usual doc
and had the diagnosis end up on my records.  I'd probably have found a
doc (maybe my regular one, I never asked) who would work for cash
payments and perhaps keep my records under an alias.  I would
certainly have bought a BG meter and started self-treatment based on
what I learned through research.

In my case, the diabetes would have ended up on my record anyway,
since I went undiagnosed for so long that my pancreas is nuked and
I'll be on insulin for the rest of my life or until the cure.  I'm not
holding my breath for the later.

If you can catch yours early then your pancreas might recover to the
point where you don't need insulin.  In any event, all the side
effects will probably reverse.  They did for me.  My eyesight has
returned, I no longer ache, I have energy and my head is clear.  I
feel better than I have in a decade or two.  In that regard, diabetes
was the best thing to happen to me in quite awhile.


From: John De Armond
Subject: Re: First post-dx A1c's are in...
Date: Tue, 16 Aug 2005 01:18:12 -0400
Message-ID: <>

On Mon, 15 Aug 2005 20:26:57 -0700, Michael
<> wrote:

>1.  Doc doesn't want to reduce my meds.  I'm currently on 2000mg
>Metformin; 1000 at breakfast and 1000 at dinner.  Which reminds me...


>2.  Doc doesn't want me testing 1 hour after.  Just 2 hours.

When is your post-meal peak?  You have to figure that out for yourself
and then test at that point.  For me it's 1.5 hours after eating.

>3.  Doc wants my goal to be 180 at two hours after meal.  He feels that
>     the goals suggested on
> are too
>     aggressive and will be setting myself up for frustration and
>     discouragement.

Ah yas, the doc that can't possibly imagine any mere patient having
more self-discipline than himself.  Modern research is showing that
eye damage starts at about 140.  You risk other of diabetes' nasties
if you decide to live with postprandials that high, IMHO.

I clocked in at >500 fasting and >750 at the random test at the doc's
office when I was diagnosed.  Within a month I had my fasting BG down
below 100 and postprandial no more than 140 and most of the time no
more than 120.  I use metformin plus basal/bolus insulin.  My last A1C
was 5.2 and my 14 day average BG from my meter was 85.

I didn't stop eating anything good.  I simply eliminated the highest
carb foods, moderated others and found new low carb things that I like
to eat.  That and frequent testing produced the above results.

I started out allowing no more than 60 carbs a day.  I eased it up to
80 as the metformin started working.  I'm now letting my fasting level
drift a little over 100 as I back down the insulin to speed my weight
loss.  I still keep the postprandial below 140.

After several months of giving my pancreas a nice vacation by keeping
the BG that low, I'm just in the last week seeing some signs of new
activity.  It was essentially dead at diagnosis as indicated by the
C-peptide result.  I'm hoping that I can at least get off the basal
insulin in a few months and then just dose the moderate carb meals I
sometimes eat.

>4.  drop back testing to 3 times a week, unless I don't feel right.

What hideously dumb advice!!!  If you feel low, you really don't need
to test to know what to do.  OTOH, you'll get VERY high before you
actually feel it.  For me, it's in the 400s before I can feel
anything.  Below that I haven't a clue what the meter is going to
show, based only on my feelings.

If you don't test after each mean then how do you know that what
you're doing is correct?  Answer: you don't.  I'm pretty strong willed
but I still require the constant feedback from testing to keep on
track.  I bet you'll need it too.


From: John De Armond
Newsgroups: rec.outdoors.rv-travel
Subject: Re: New Wrinkle
Date: Sat, 20 Jan 2007 15:53:03 -0500
Message-ID: <>

On Fri, 19 Jan 2007 23:31:55 -0600, Bob Giddings <>

>The doc said I might be getting diabetes.  Urk.  So he did a
>blood test.  Today I got the results.
>The good news is that I don't have diabetes.  It's my thyroid.
>We've been pretty close for a long time, and we're still dating,
>but she just isn't putting out like she should.
>Bob, who is mighty glad to have missed diabetes.  Whew.


According to both my doc and my research, hypothyroidism and diabetes
go hand in hand.  My doc checks for both on every checkup.   So far my
thyroid is still in love with me :-)  My coin-flip went the other
direction.  My pancreas has become estranged...

I highly recommend getting a blood sugar meter and checking
occasionally.  The cost is minimal - A Camp Wallyworld brand meter is
$8 and the strips are $22 for 50.  Testing is as simple as pricking
yourself somewhere and applying the blood drop to the strip, waiting
and reading the meter.

The definition of diabetes has become politicized because so many
states allow insurance companies to boot one out upon diagnosis.  The
threshold is now, IMHO too high.  Eye damage starts at about 140.

A normal person should have a fasting BS in the range of 70 to 90,
preferably on the low side and a post-prandial (2 hours after eating)
of 140 or less.

Even if your BS is high, you're still a long way from the needle
(though I prefer the needle to most of the oral meds - insulin works
better, faster and more predictably)  Diet, exercise and oral meds
work.  Strangely enough, vinegar is a proven BS reducer for many
people including me.  Oil and vinegar salad dressing contains enough
to be effective.

A little tip on glucose testing.  Whomever came up with the notion of
sticking holes in the most nerve-dense area of the body - the
fingertip - is either daft or a sadist or both.  Arm testing (pricking
the lower arm somewhere) is becoming popular but doesn't work well for
me.  I have thick skin (SOP for a RORTer) and even with the pricker
set to "sword fighting", not much comes out.

What works for me and 99 times out of 100 is totally and completely
sensation-free (not just pain-free) is pricking the ball of my hand.
The pricker that comes with the Wallyworld tester can't do that.  The
hole in the end is too small and it smears the blood droplet.  Get
OneTouch UltraSoft pricker and make sure you get the "arm attachment".
This is a clear plastic end for the pricker that has a large hole in
the end and lets you see the droplet as it develops.

Press down hard with the pricker, fire it and while continuing to
press, watch the blood drop develop.  It flows much slower than on the
fingertip.  When it's the right size, withdraw the pricker and apply
to the strip.

At your age you need to keep an eye on your BS since diabetes is a
natural byproduct of aging and the hypothyroidism makes it more


From: John De Armond
Newsgroups: rec.outdoors.rv-travel
Subject: Re: New Wrinkle
Date: Sat, 20 Jan 2007 19:32:39 -0500
Message-ID: <>

On Sun, 21 Jan 2007 00:24:49 -0000, Frank Tabor <>

>On Sat, 20 Jan 2007 17:04:35 -0600, Janet Wilder wrote:
>> Things have changed. When I got my CDL, insulin dependent people were not
>> permitted to get a CDL and drive truck. Glad to hear the industry has
>> smartened up.
>I believe that is still true.  John you aren't actually insulin dependent
>are you?

No, not anymore.  It took over a year of very hard work and some luck
for my pancreas to recover enough to go it with oral meds.  I keep
some fast acting insulin (Novolog) on hand for those special occasions
when I want to pig-out on carbs (I'm a sucker for anything Italian)
but not necessary day to day.  I do eat a very low carb diet, mostly
from the fridge and freezer in my truck.

There was a recent notice in The Trucker magazine that said that
someone in Congress tacked on an amendment to some other bill that
forces DOT to let "well regulated insulin-dependent diabetics" drive
without the unobtainable special permit.  Apparently Congress does
occasionally move to slap a bureaucracy.  I couldn't imagine anything
more stupid than forcing a driver to ineffective and life-threatening
lesser treatment in order to keep his job.  Apparently Congress

I haven't investigated that further since I don't need it day to day
but I probably will eventually.  Once this is clarified I'll probably
go to much lower oral meds and per-meal insulin.  I can achieve
non-diabetic BG levels that way.


From: John De Armond
Newsgroups: rec.outdoors.rv-travel
Subject: Re: New Wrinkle
Date: Sat, 20 Jan 2007 22:40:31 -0500
Message-ID: <>

On Sun, 21 Jan 2007 00:38:24 -0000, Frank Tabor <>

>Here in VA, insulin dependent folks can get an Instate CDL.  Not allowed
>to drive out of the state borders.
>I can see the logic behind the restrictions on insulin dependent drivers.
>Due to most drivers schedules, it's sort of hard to keep a good schedule
>of dosing and etc.  I don't necessarily agree or disagree, but just

That logic was valid in the 70s when glucose meters were big boxes in
doctor's offices and insulin was either bovine or porcine in origin
and didn't really work all that well.

Now, literally everything is different.  Glucose meters are relatively
cheap and work with little more than a few molecules of blood.  The
genetically engineered insulins either work almost instantly or last
all day, usually up to 24 hours.  A basal dose of long lasting in the
AM and a fast-acting calculated dose before each meal lets one live a
regular life and eat whenever.

For the very brittle diabetics who have absolutely no pancreatic
activity, there are the pumps that constantly meter in the basal dose.
When the user eats he computes his "bolus", dials that in on the
pump's control panel and shoots it in.  The pump uses the very fast
acting insulin so response is very fast.  The very latest pumps use a
continuous glucose sensor that closes the feedback loop and adjusts in
real time.

On another front, at least one retired scientist who WAS very brittle
has developed a mathematical model of the body's insulin usage.  With
some simple testing one can determine the coefficients to plug into
the model. From there, simply select the ingredients for the food
you're about to eat and shoot fast-acting insulin accordingly.  He has
a mailing list called Diabetes Self-Management and helps people
develop their own models.

In short, there is no excuse for anyone to ever have either a
hypoglycemic or hyperglycemic attack.  All one has to do is pay

My BG was at 750 when my doc finally stumbled onto the diagnosis.  I
should have been in a coma.  I attacked the problem as I do any other
one- a direct frontal assault.  I spent several months packing my
brain with diabetic knowledge, including taking most of a week to use
the Emory U medical library for stuff not yet available on-line.  I
took control of my treatment.  Within a couple of weeks I had achieved
non-diabetic BG.  My doc could not believe the print-out from my
glucose meter :-)

One of the things I learned was that if I could keep my BG in the
low-normal range then my pancreas had a good chance of recovering at
least some functionality.  It seems that glucose is toxic to the
islets that make insulin.  That is indeed what happened.  I set up my
insulin regimen as if I were a Type I with no insulin production. That
let my islets take a vacation.  After about 9 months they were
recovered enough that I could wean myself off the basal insulin and
just shoot for meals.  Of course, when I decided to get a CDL, I had
to wean off the meal shoots and go it with oral meds alone.  Stupid,
stupid, stupid!!!!

Even though I walked a fine line on the lower end of normal BG, I've
never had a serious hypo attack.  I've got a little fuzzy occasionally
in the beginning but a glucose tablet fixed that in minutes.

The major problem with the DOT was the stark no-tolerance
black-and-white policy.  If you use insulin you can't drive.  It made
no room for people like me who were not insulin-dependent but who
could achieve better control (and better health) by using some.  Both
the American Diabetes Association and the government agency that
administers the ADA act were talking ADA suits because the ADA
requires "reasonable accommodations."

I hope that this new law short-circuits that process so taxpayer money
won't be wasted on lawyers.  It's yet to be seen whether DOT digs in
its heels and tries to be intransigent or if they obey the law (what a
concept - a government agency obeying the law.)  Stay tuned...


From: John De Armond
Newsgroups: rec.outdoors.rv-travel
Subject: Re: New Wrinkle
Date: Sun, 21 Jan 2007 14:19:31 -0500
Message-ID: <>

On Sun, 21 Jan 2007 00:30:39 -0500, "Steve Wolf" <>

>The problem isn't with you.  The problem is with the others like you.
>A driver operating the wrong way on an interstate is no longer a drunk.
>More often than not, he or she is a diabetic.

I don't have any data on that but based on intuition, I kinda doubt
it.  Regardless of the numbers, there are FAR more non-commercial
diabetics driving than commercial drivers.

>What you are asking the state to do is to sign off on your ability to
>control your condition.  There is absolutely no doubt in my mind you are
>safe.  But that is a subjective judgement based on extrernal factors.  The
>state cannot make that decision for everyone who is using insulin.

The problem is, diabetes was singled out for special treatment by DOT
(not the states) in contravention of the law.  A CDL holder can drive
with a variety of other conditions that if not controlled, would make
him a hazard.  High blood pressure, for example.  Even if a driver
smokes like a chimney and it takes so many meds to control his BP that
he sloshes with them, as long as the cuff registers under a certain
number, he's good to go.  He can stop taking them the day after and
nobody says a word.

Second, you forget that CDL holders have to have a medical card and
physical.  Unlike other problems such as untreated blood pressure,
heart disease, etc., compliance with diabetes treatment over the long
term CAN be simply tested for.  The A1C blood test effectively reports
the average BG for the last approx 90 days.  The test is so simple
that a home tester is available from the drug store for under $30.  I
do the test every 90 days or so to make sure of my regime.

In addition to the A1C test, modern BG meters store months worth of
readings with a time and date stamp and can be downloaded to a PC. The
meter can be password-protected so that only the doc can download and
reset it.  That meter can also prove compliance.  Sure I can fool the
meter but it's hard to fool the A1C also.

In light of that test being available, there was NO justification for
DOT to blanket-ban insulin use.  The ADA requires 'reasonable

DOT's actions were even more egregious in light of the unintended
consequences.  Drivers who need insulin (oral meds aren't doing it)
simply live with the high BG, constantly doing themselves damage. It's
easy to arm-chair quarterback but if driving is all you know then you
make the tradeoff.

It is common knowledge how to get "good" BG readings for the physical.
Ordinary Humalog insulin is available over-the-counter without a
prescription.  Simply get some, get your BG under control, take the
physical without saying anything and you're good to go.

One last point.  There are many other chronic conditions that cause
similar disorientation and dementia.  This thyroid problem that
started this thread, for instance.  Too much or too little synthroid
will turn one into a space cadet.  Several people in this thread have
described the symptoms.  Yet that receives NO DOT attention.  Only

>Getting old, as so many of us are, sucks.  If AAA wants to perform a
>service, then they should quit drawing attention away from problems that
>affect the majority of their members.  They should examine such things as
>diabetes and age-related driving issues.

And AARP.  I fully agree there, but it won't happen.  With the boomers
turning into geezers, their political strength, their
self-centeredness plus the loss of judgment that comes with age, the
keys will come out of their cold dead hands.  Unfortunately with other
cold dead hands frequently involved.

Geezers, most of 'em anyway, simply won't give up the license without
coercion.  I dad's brother, a pillar of the community, would not.  I
finally had to disable his car.  My dad, bless his soul, did know and
did quit driving.  My mom's going to be like my uncle.  I'll have to
disable her car and probably have a talk with her dealer to prevent
her from simply buying another.

Complaining about CDL holders, whose compliance can be checked with
mechanisms already in place, while ignoring the non-commercial drivers
smacks of crocodile tears, I'm afraid.  Pissing on the match while
ignoring the forest fire.

From: John De Armond
Newsgroups: rec.outdoors.rv-travel
Subject: Re: New Wrinkle
Date: Sun, 21 Jan 2007 15:30:53 -0500
Message-ID: <>

On Sun, 21 Jan 2007 14:06:16 -0500, wrote:

>>I highly recommend getting a blood sugar meter and checking
>>occasionally.  The cost is minimal - A Camp Wallyworld brand meter is
>>$8 and the strips are $22 for 50.
>Not really the way to go for non-diabetics. Low cost urine test-strips
>such as Clinistix or Diastix are more than adequate to reveal
>significant blood sugar anomalies.

NO!!  A thousand times NO!  Diastix don't register anything until the
BG is in the 300 to 400 range.  I confirmed what I read on myself.  I
get a headache between my eyes when my BG hits about 250.  Not a peep
from the Diastix.

About the only use for those is to distinguish between a diabetic coma
and drunkenness.  The other use, what I use them for, is testing for
free sugars or starches in food.  Chew up the substance, stick the
stick in your mouth and if it changes color there is sugar or starch
in the food. After awhile one gains a feel for what shade of color
corresponds to how much sugar.

>>The definition of diabetes has become politicized because so many
>>states allow insurance companies to boot one out upon diagnosis.  The
>>threshold is now, IMHO too high.  Eye damage starts at about 140.
>Total nonsense!! Post-prandial BG levels of 160+ (9.0 Canadian) are
>quite normal amongst the non-diabetic segment of the population.

No use responding to any more of your nonsense.  I suggest you spend a
teeny-tiny bit of time on the net actually learning about diabetes.
The ADA has a plethora of journal papers on the subject.  If you look
hard (I don't have the time to find it for you), you'll find the paper
that shows the relationship graphically between BG and eye damage.

Suggest spending some time here:
and here

These two guys are two highly respected authorities in the area,
especially Dr. Bernstein.  They're sometimes at odds with each other
so you can get two different perspectives.

Dr. Bernstein is one of the pillars of the diabetic research and
treatment arenas.  His methods work - I used them to recover enough to
get off insulin and use a looser form of his diet today.

I highly suggest that you learn something of the developments in
diabetes treatment from the last 20 years before you emulate BEen and
post garbage.  And if you have a doc who says that 160 postprandial is
acceptable then you need to find another doc.  He's repeating the ADA
propaganda verbatim just like mine did.

I tossed the ADA crap in the garbage after scanning it and developed
my own program.  After I brought in non-diabetic numbers, he became
interested and did HIS research.  He no longer uses the ADA stuff.


From: John De Armond
Newsgroups: rec.outdoors.rv-travel
Subject: Re: New Wrinkle
Date: Mon, 22 Jan 2007 00:57:16 -0500
Message-ID: <>

On Sun, 21 Jan 2007 19:26:27 -0500, wrote:

>> I confirmed what I read on myself.  I get a headache between my eyes
>> when my BG hits about 250.  Not a peep from the Diastix.
>Although everyone's repsonse to high BG varies, headache isn't
>generally included amongst the symptoms.

Just scratching my head at the purpose of such a dumb-sh*t comment.

>American kidney-spill threshold = 180 mg//dl = real world 10 mmol/L.

Really?  Hard'n'fast at 180, eh?  Since pretty much everything having
to do with the diabetic population happens over a range, we can
cheerfully ignore that claim.  It really doesn't matter what the
"spill" threshold is for the purposes of criticizing the diastix. What
matters is when it shows up on those lousy test stix.  After logging
close to 100 tests, I know that my threshold is between 300 and 400.
I don't have an explanation for the wide spread other than there is
probably a time element involved.  How long the BG has been at
concentration.  It doesn't really matter since by the time the stick
indicates anything the train wreck is already underway.

>>No use responding to any more of your nonsense.  I suggest you spend a
>>teeny-tiny bit of time on the net actually learning about diabetes.
>>The ADA has a plethora of journal papers on the subject.  If you look
>>hard (I don't have the time to find it for you), you'll find the paper
>>that shows the relationship graphically between BG and eye damage.
>American and Canadian Diabetic Associations are the very last place
>you would look for useful diabetic information. In Canada where
>financial data must be published, the Canadian Diabetes Association
>Top five salaries   $120,000+++

About the salary of an engineer with a few years experience.

>Total eligible amount of tax-receipted gifts = $ 22,021,000
>Total cost of raising that $ 22,021,000 = $ 15,193,000
>And in my experience, their usefulness and info is absolutely

Although I agree fully with your opinion on the ADA, I have to say
that this sounds a lot like envy.  If the top salaries really are in
the 120K range (I neither know nor care) then there are some highly
under-paid executives.  Of all the things the ADA can be rightfully
criticized for, executive compensation certainly isn't one of them.

>>Dr. Bernstein is one of the pillars of the diabetic research and
>>treatment arenas.
>And in the process, ended up with one of the biggest bank accounts on
>the continent!

Yep, envy.  Very bad envy.  I have no idea what Dr. Bernstein's net
worth is but I bet it isn't in the range of say, a good heart surgeon.
His consultation fees are very modest by modern medical standards and
if one can't afford them (he takes your word for it.) then there's no
charge.  Likewise, the books are quite reasonably priced.

More to the point, his methods work.  If you're tough enough to stick
to his dietary regime you'll achieve non-diabetic BG levels.  I'm not
that tough but I'm still close.

>>I highly suggest that you learn something of the developments in
>>diabetes treatment from the last 20 years before you emulate BEen and
>>post garbage.
>With ten years of realizing Hemoglobin A1C glucose levels superior to
>those of most non diabetics, while on up to 100 units of insulin per
>day, I am hardly in need of any kind of totally useless marketing hype
>and nonsense from diabetes associations or Berstein types!
>Annual eye examinations = 100%!

With that kind of insulin consumption you gotta be gobby fat.  That's
serious insulin resistance.  So what's your "superior" A1C?  Mine ran
a consistent 5.1 to 5.2 before I dropped the insulin to get the CDL.
Still under 6.

I had that kind of insulin requirement in the beginning.  But my
research told me that I had a good chance of recovering pancreatic
activity AND markedly reducing my insulin requirements by a) losing
weight and b) keeping BG at the low-normal levels for awhile.

Since insulin also mediates fat storage, that much insulin makes not
getting fatter very difficult.  I worked very hard with my diet,
fairly quickly got my insulin usage under 50 units/day and started
losing weight rapidly.  130 lbs later, no basal dose necessary and
minimal meal dosing (under 10 units, typically, for a moderate carb
meal) resulted.

Instead of pumping insulin in by the gallon, why not learn something
new about diabetes management and lose some of that weight and insulin

>>And if you have a doc who says that 160 postprandial is
>>acceptable then you need to find another doc.  He's repeating the ADA
>>propaganda verbatim just like mine did.
>Having one of the absolutely top internists in the Toronto area, he
>has said nothing about how to treat my diabetes other than "Just keep
>on doing what you've been doing!"

Ummm, Canadian medicine.  Kina like military intelligence, isn't it?
If you're happy with your results then by all means, keep doing what
you're doing.  Except for giving bad advice, of course.

This has drifted far afield from the core issue - your horrible advice
that one rely on dip-sticks for diabetes diagnosis.  While a positive
indication DOES indicate diabetes - serious diabetes - a negative
indication (false negative) does not mean "all clear".  For little
more than the cost of a bottle of sticks, one can get the Wallyworld
meter and a 50 count pack of test strips and know for sure.

I'll shut up now so that you can have the last word.  That seems to
mean a lot to ya.


From: John De Armond
Newsgroups: rec.outdoors.rv-travel
Subject: Re: Hamster Trip Report (Long)
Date: Tue, 21 Aug 2007 18:26:17 -0400
Message-ID: <>

On Tue, 21 Aug 2007 13:17:04 -0700, David The Hamster Malone <>

>Yes, my weight (265 lbs) is a problem and that's the first thing I'll
>work on... won't be easy because I'm lazy :-) I guess I'll take stock
>after my appointment with the Diabetes Clinic and see what they
>recommend for excercise and diet.

Damn, that's one fat hamster!

Listen to the chaps at the diabetes clinic but then please do your own research.  The
ADA regimen that these places recommend will kill ya! Lots o' carbs and lots 'o

I highly recommend this doc's advice:

Most of the good stuff from his book is available free under the "articles" section.
In a nutshell, he recommends basically a modified Atkins diet.  Low/zero carbs and
lots of protein.

I tried it for a few months and it worked as advertised.  I could not completely give
up my carbs so now I use a low carb version and a little insulin when I cheat.

If you want to get very scientific about diabetes management, get on the DSM
(diabetes self-management) mailing list.  The guy who operates it was the project
manager of the atomic artillery shell development, a heavy duty physicist and
mathematician and an interesting guy to talk to.  He's developed a mathematical model
of diabetes and insulin response.  He'll work with you to plug in your parameters to
the model.   Then you can calculate how much insulin (or other meds) you need for a
particular meal.  I didn't need that level of management but I did sit back and watch
and was amazed to watch him gain control over one brittle diabetic after another.

This is an invaluable tool:

Our tax money at work :-)  This is a database of just about every food and prep
method you could imagine and their nutrient contents.  Of interest to us is the carb
content.  It is broken down into total carbs, indigestible carbs (fiber) and
digestible carbs.  There's a version that you can download for your PC and another
for your Palm pilot.

>What do you use to check your glucose?

Depends on who's paying.  If it's out of my pocket then I use the Relion (Wal*mart)
unit because the meter only costs $8 and 100 strips about $40 - half that of the
major brands.  If insurance is paying then I use a One Touch.  It uses a tiny blood
sample and the lance is the best I've seen but at a buck a strip, out of my price
range.  One nice feature is that the data can be downloaded to the PC for further
analysis and trending.

All use about the same chemistry so the decision is based on cost and convenience.
Some brands have end openings on the strip and some have side openings.  The
processing time varies widely, from only a second or two to 20 seconds or more.

About obtaining blood samples.  The sadistic pricks at the clinics will tell you to
stab your fingertips, one of the most nerve rich areas of the body.  You'll hate the
bastards for that.

Several meter brands now allow arm testing.  That is, pricking your arm and drawing a
blood sample there.  I tried that but my skin is too tough for the lance, even set on
high.  What I discovered is that the ball of the hand has almost as many blood
vessels as the fingers but practically no feeling.  It is as easy to prick there as
the fingertip but if the lance isn't set too deeply, essentially sensation-free. I've
taught this method to the local clinic and now they're teaching it to other patients.

The fingertip lances have holes that are too small for this.  The blood will contact
the walls and smear out.  The best lance that I've found is the One Touch unit with
the "arm tip" attached.  This is a clear plastic tip with a large hole in the end.
The hole is large enough to let the blood droplet form without contacting the rim.

My technique is to press the tip firmly into my palm and hold it until the little
bubble of skin that pokes through the hole is dark red with blood.  Then I back off
until I'm just barely touching the skin and fire the lance.  It takes only the
tiniest prick to get blood out of that blood-engorged skin and there is almost never
any sensation.

If you're interested in it, I can go into the simplified model that I developed so
that I can calculate how much insulin I need for a given carb load.  This involves
characterizing your system's glucose rise per gram of carb and glucose drop per unit
of insulin.  It involves quite a bit of testing up front but then it works smoothly.
These constants will change as you lose weight and as your pancreas recovers
functionality in response to normal BS so one has to stay on top of it for awhile.

Because I pay for my meds out of pocket, I have developed a hybrid oral/insulin
regime that has a lower total dollar cost than either oral-only or insulin-only.
Frankly, I like the insulin-only regime better because it gives me better control and
it lets me eat a wider variety but the fast acting insulin (Novolog) that I respond
to best is quite expensive.


From: John De Armond
Newsgroups: rec.outdoors.rv-travel
Subject: Re: Part Three - Getting Back - Loooong
Date: Fri, 14 Sep 2007 15:50:44 -0400
Message-ID: <>

On Fri, 14 Sep 2007 08:47:39 -0700, David The Hamster Malone <>

>On Sep 13, 10:01 pm, Neon John <> wrote:
>> There's a conversion table in my glucose meter's manual but I'm too lazy or
>> disinterested or both to go look for it.
>Just multiply by 18.
>David "The metric Hamster" Malone

OK, so translating:

>My first fasting blood sugar
>reading was 6.4... it had been running around 7.1 to 7.2. At first I
>thought it was a false reading but they tested me with another
>(OneTouch I think) and got the same readings.

into normal units, you were at from 127 to 129 and now you're down to 115.  Yeah,
that's great.  Drop a hundred pounds and you won't be a real diabetic anymore.  Are
any meds involved at this point?

Once you get  your sugar down to the normal range (~80-90), your pancreatic function
will likely recover enough that you won't actually be diabetic anymore.  That is,
your pancreas can supply all the insulin you need.  Just like regular people and

Also once you drop the weight you'll have broken the positive feedback loop.
Currently your fat emits an enzyme that interferes with insulin's action.  That
causes higher blood sugar which forces the islet cells to make more insulin.  Insulin
mediates fat storage (causes it to happen) so you store away more fat which further
inhibits insulin's function which causes more to be made, etc.

That is until the islets say "Frig it, we're going on vacation" and shut down,
partially at first and then completely if the problem persists.  Sugar soars and one
day you either wake up in a diabetic coma or you do like I did, stumble to the doc's
with a BG >700 and practically no pancreatic function.  I even had a PA walk in the
room to verify that I was actually NOT in a coma - where her chart told her I should
be at that BG.

If you dump the weight and do the strict low carb diet for awhile, those islet cells
will slowly crank back to full output.  Your sugar isn't high enough at this point to
have done any serious damage.  In effect, the islets had quit working and were
packing their bags but they had not yet left the building along with Elvis.... :-)

I dumped 100 lbs and went from 75 units of long acting insulin in the AM plus
anywhere up to 50 units at meal time to my current situation of no maintenance
insulin and only 10 or 15 units of fast acting when I cheat on a meal.  Plus the oral
meds, of course.  I have about 75 more pounds to go.  75 HARD pounds.  I'd love to
wean myself off the oral meds but I don't think that will happen.  Too much islet
cell damage during my 700 fling.

The good part is, once your system recovers, not only will you be a skinny l'il
hamster, you'll be able to eat more or less normally.  Within reason, of course.
"Normal" does NOT mean becoming a "three hundie" again.


From: John De Armond
Newsgroups: rec.outdoors.rv-travel
Subject: Re: Part Three - Getting Back - Loooong
Date: Fri, 14 Sep 2007 16:03:03 -0400
Message-ID: <>

On Fri, 14 Sep 2007 06:56:04 -0700, David The Hamster Malone <>

>The doc said it takes most people a year or so to fully accept they
>have the problem... hard to believe, but I know it's true - half the
>20 odd people in the education session had been diagnosed with
>diabetes for more than 2 years and not done a damn thing about it. All
>of them had blood sugar readings much higher than mine.

The problem is, very high BG muddles up the thinking process.  In my case, I knew
that something was wrong but I couldn't think clearly enough to figure out what.  I
didn't have the most classic symptoms - deep thirst and lots of pee.  My pee had that
acetone smell of seriously high blood sugar but I didn't know what that meant or even
that it was acetone-y.

My doc certainly didn't help either.  I had a regular checkup every 6 months and even
though the blood test had been showing high for 2 years, the only thing he ever said
was one time he made the comment "your sugar's a little high.  Be careful".  WTF does
that mean?  If I were the suing type.....

The first round of fast-acting insulin cleared the cobwebs out of my mind almost like
flipping a switch.  I addressed this problem like I do most problems - a full frontal
assault.  I turned the restaurant over to the inmates (talking about risk-taking) and
burrowed up with the internet.  Then I drove my l'il MH to Emory U and spent a couple
of days in their medical library reading stuff that wasn't available on-line, at
least not to commoners.  Then I designed my own treatment program.

The low carb Atkins-like diet was the centerpiece.  I'd done Atkins back in the 70s
so I was familiar with it.  I got the Bernstein book, found the USDA database and
found a decent diabetes management software program that ran on winders and my Palm
and could pull in readings from my glucose meter.  Within 6 months I had my A1C
reading down in the 6's and eventually into the 5's.  Fives are normal.  (A1C
measures your long term average glucose level.  It's the overall feedback on what
kind of job you're doing.  Wallyworld has a one-time test kit for under $20.)

Make this your mission for a year and you'll be recovered.  If that mission displaces
your, ah, amateur comedian mission then so much the better.....


From: John De Armond
Newsgroups: rec.outdoors.rv-travel
Subject: Re: Part Three - Getting Back - Loooong
Date: Mon, 17 Sep 2007 16:46:16 -0400
Message-ID: <>

On Mon, 17 Sep 2007 06:53:18 -0700, David The Hamster Malone <>

>I really don't know what's going on with my blood sugar. I tracked it
>for 2 days before and after meals on the weekend. My fasting blood
>sugar each day was 5.8 (104.4) and 2 hours after meals the highest I
>recorded was only 8.0 (144).

Sounds pretty typical for a just-barely Type II.  A postprandial (after-meal) of 140
or below is considered good in most of the literature.  That's my goal. If I can keep
the postprandial around 140 then I'm happy.  Your fasting level will go down as you
lose more weight, most likely.

>In fact my fasting blood sugar both days
>was lower than my wife's at 6.2/1 (111.6) who isn't diabetic at all as
>far as we know. The red wine didn't seem to have any appreciable

If that's her fasting BG then yeah, she's a threshold diabetic.

The threshold has traditionally been 100.  The first deleterious effects are noted at
about 120 and 140 is the threshold for eye damage.  The ADA in a political move, has
pushed the definition back so that (unless things have changed again) the threshold
is now 120.

In one sense the reason is laudable - in the US, getting labeled with the "D word" is
the death knell for any type of insurance except perhaps group medical plans.  Ergo,
the ADA figured that if they pushed back the threshold fewer people would get tagged.
And of course, more people would remain insured which ensures the steady revenue
stream to the docs and drug companies.

The political condition doesn't change the objective facts - non-diabetic people have
FBG levels below 100 and most folks are in the 80 range.  In my informal surveys (do
you know how hard it is to get someone to poke their finger in the name of amateur
science?  A plate of ribs usually works....), 80 to 85 is the sweet spot.

If she's that high on fasting BG then she needs to get with your program.  Her
pancreatic engine is pulling the rig up the hill but if the slope gets any steeper
she's in trouble. See, I can tie this back on-topic :-)

This kind of information is hard to come by in the popular literature which is very
frustrating. <insert your favorite conspiracy theory here about drug companies
controlling the advertising budgets of magazines, etc>  But if you wade into the
medical literature and survive the terminal boredom caused by the turgid language,
this is what you discover.  Incompetent docs simply hand out the ADA party line (info
packet) and forgetaboutit.  Good docs, those that look past the party line, reflect
these facts to their patients.

Reading between the lines, it sounds like the canuck docs you've experienced are
doing a better job.  That's good.  Perhaps they could take a look at your wife?


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