This past year I had 4 dx: diabetes 2, chronic lyme, and ended yr. with sleep apnea & restless leg syndrome.

I've seen many post here who have lyme/diabetes too.

I have a Norwegian contact who is close friends with the INTL. Diabetes Assn.

What would you like to see them address for those of us with both illnesses & our countless many other dx/symptoms?

I'll compile list of items and email her to give the Intl. President.

The endocrinologist can't figure out if it is type I or some sort of insulin dep type II. He is also perplexed as to the source of the diabetes.

Lymemomtoo and I have corresponded on this combination and it is helpful to find others dealing with both.

Just off the top:

Type 1 is an autoimmune disease (type 2 is not) so people with type 1 tend to have autoimmune problems with the Lyme, which makes it much harder to treat.

Meds for Lyme tend to affect blood sugars. Interactions between meds and the illness are usually discovered through unexpected lows and highs, which can be dangerous.

Lyme itself can make blood sugars less manageable (any flare of infection can cause highs). GI stuff can cause lows.

There tends to be more thyroid involvement w/Lyme and type 1, our endocrinologist says.

Sugar is necessary for a type 1: to keep blood sugars from going too low. This can make avoidance of yeast harder.

The Bb organism (and yeast) love sugar and so having high blood sugars really makes them comfy.

The stress of having both these illnesses is amazing. It can be hard to find folks who understand having both. My child also suffers from depression a lot.

Doctors do not understand type 1 diabetes, including even the best LLMD's.
Some endocrinologists in turn don't understand chronic Lyme.

In general, healing is harder I think. We assume chronic problems may continue but try to get as much improvement from treatment as possible.

I agree with what Lymemomtoo said, that Lyme and diabetes feed off each other in some way. It's hard to feel optimistic about my child's future, but we definitely try to make the best of things.

That's all I can think of right now. Thanks again for bringing this up.

I can't help but wonder if I would have gotten diabetes without the Lyme. I know I have autoimmune issues but don't know how it all fits together. And I wonder if my LD had been treated right after the Diabetes dx if I would have an easier time with the diabetes now.

Some days it is so terribly difficult to take care of my diabetes when Lyme really has me down (whether physically or emotionally or both). I agree that there is psych stuff with both.

It's hard to test my blood sugar 4-6 times a day when I'm sleeping for 12 or 14 (or even 18) hours a day. I couldn't handle diabetes and LD if I didn't have an insulin pump.

My dad, like tabbytamer's son, got diabetes at an older age than usual and was first dx with type 2 and then later changed to late-onset type 1.

He hasn't been tested for Lyme yet. I wouldn't be surprised if he has it though. We are testing my family members one at a time. (2 out of 5 so far)

There is a LACK OF INFORMATION about Lyme in general but in particular about how abx, esp. long term, relate to diabetes and blood sugar and immune system issues. Even my well known LLMD has never had a type 1 patient before me.

My endocrinologist refused to accept my LD diagnosis until I finally had a WB come back pos. All of her ID friends said I couldn't have it without a bulls eye or a pos ELISA.

I would love to talk to any of you or your children to bounce ideas around or vent or whatever if anyone feels like it.

I think that a lot of my frustration comes from the fact that so few people know how hard diabetes is to live with (especially for kids and young adults) and so few people understand LD and how hard it is too.

My daughter has good control of her blood sugars but with the combined illnesses, it is necessary to test 10-12 times/day, and for 10 years I have checked her at night, at 1 and/or 3am. I have three alarm clocks so I make sure I get up. (I have Lyme too, so sometimes I really want to sleep!)

I don't talk to anyone about these things, nor does my daughter. We know that noone will understand the burdens we live with. There isn't a single doctor who can put it all together for us.

I will e-mail you. There are at least 4 or 5 families on Lymenet dealing with this difficult combination. I hope you are feeling better, and know that there are people out here who do understand what you are going through.

Bb - Borrelia burgdorferi

LD - lyme disease

LLMD - lyme "literate" dr.

IF - infectious dr.

If any of you use other abbreviations in your posts, please show the whole word after the abbreviation for the diabetes president's info so they won't have to guess at our lyme lingo. Thanks so much.

DEADLINE will be Jan. 31 for your input on this folks.

Then what I'll do is send this site page link to my Norwegian friend to pass along to the Intl. Diabetes Assn. President so they are aware of our LYME/diabetes concerns we'd like to have them address.

OTC Gluco Reg - (follow bottle directions) can halt late stage diabetes.

It contains chromium and a lot of acids. Little mineral reacting with a lot of acids to produce hydrogen. (Step one)

One does not have to change their exercise or diet.

It takes TIME! 3 months. From 186 FBS to normal. Saw it happen (mom, age 86)! All the Rxs. made her have diarrhea, so we went the "natural route".

Continued use of the above if Mg levels are low is needed and Mg supplements help too. Chromium will help, but will not sub. entirely for the missing (depleted) Mg levels in the aged.

No Mg connection? Type into a search engine, "Diabetes magnesium". You will find literally thousands of websites to read and learn the connection.

Heredity (genetic) or pathogen that crosses the placental barrier? Do INFANTS, newborns (with high Mg levels) have diabetes?

Keep in mind...Mg is capable of DNA repair.

Bb uses Mg in its enzyme reactions. This is known. So does bartonella.

Besides pathogens, other things can lower our Mg levels...stress, too much calcium in relation to Mg, overdoing sugar (also a ++ charge), fluoride in our water...the list goes on.

Playing with fire. Careful. Lots of $$$ at stake.

A newborn infant of a diabetic mother may develop one, or more, of the following:

� hypoglycemia

Hypoglycemia refers to low blood glucose in the baby immediately after delivery. This problem occurs if the mother's blood glucose levels have been consistently high causing the fetus to have a high level of insulin in its circulation.

After delivery, the baby continues to have a high insulin level, but it no longer has the high level of glucose from its mother, resulting in the newborn's blood glucose level becoming very low.

The baby's blood glucose level is checked after birth, and if the level is too low, it may be necessary to give the baby glucose intravenously.

� macrosomia

Macrosomia refers to a baby that is considerably larger than normal. All of the nutrients the fetus receives come directly from the mother's blood. If the maternal blood has too much glucose, the pancreas of the fetus senses the high glucose levels and produces more insulin in an attempt to use this glucose. The fetus converts the extra glucose to fat.

� ***Even when the mother has gestational diabetes, the fetus is able to produce all the insulin it needs.***

� The combination of high blood glucose levels from the mother and high insulin levels in the fetus results in large deposits of fat which causes the fetus to grow excessively large.

� birth injury
Birth injury may occur due to the baby's large size and difficulty being born.

� respiratory distress (difficulty breathing)

Too much insulin in a baby's system due to diabetes can delay surfactant production which is needed for lung maturation
http://www.musckids.com/health_library/hrnewborn/diabtmom.htm

(The above is from a children's hospital).

Anti-insulin activity in normal newborn cord-blood serum: absence of IgG-mediated insulin binding
JR Bilbao, B Calvo, I Urrutia, A Linares and L Castano
Department of Pediatrics, Hospital de Cruces, Barakaldo-Basque Country, Bizkaia, Spain.
Insulin autoantibodies (IAAs) are present in approximately 60% of type I diabetes patients at onset and are used as predictors for the disease. Although the prevalence of IAAs in the general population has been reported to be <1%, preliminary data have pointed out a higher proportion of IAA positivity in newborn cord-blood serum, and some authors have suggested that they are immunoglobulin G antibodies, resulting from a hypothetical gestational insulitis. To characterize this insulin-binding activity, we analyzed cord-blood sera from 100 healthy newborns, as well as serum from 21 of their mothers at delivery, 179 new-onset type I diabetic patients, and 200 healthy control subjects. IAAs were present in 0.5% of the control subjects and 54% of new-onset type I diabetic patients. On the other hand, 96% of the newborn cord-blood sera showed anti-insulin activity, while it was detected in only 14% of their mothers. No significant differences were observed between cord sera and the general population for islet-cell or anti-GAD autoantibodies. Anti-insulin activity in cord serum was not bound by protein A or protein G, in contrast with type I diabetes-related IAA activity. We conclude that this insulin-binding activity, present in most newborn cord sera and specific to the child, is not IgG mediated. These data, together with the absence of other pancreatic autoimmunity markers in this population, suggest that it is an isolated phenomenon not related to type I diabetes or other pancreatic autoimmune processes and is due to the presence of a cross-reacting molecule in cord blood that has yet to be identified.

Identification of a renal-specific oxido-reductase in newborn diabetic mice
(diabetes mellitus / diabetic nephropathy)
Qiwei Yang*, Bharat Dixit , Jun Wada*, Yufeng Tian*, Elisabeth I. Wallner*, Satish K. Srivastva , and Yashpal S. Kanwar*,
* Department of Pathology, Northwestern University Medical School, Chicago, IL 60611; and Department of Biochemistry, University of Texas Medical Branch, Galveston, TX 77555
Communicated by Emanuel Margoliash, University of Illinois, Chicago, IL, June 8, 2000 (received for review February 23, 2000)
Aldose reductase (ALR2), a NADPH-dependent aldo-keto reductase (AKR), is widely distributed in mammalian tissues and has been implicated in complications of diabetes, including diabetic nephropathy. To identify a renal-specific reductase belonging to the AKR family, representational difference analyses of cDNA from diabetic mouse kidney were performed. A full-length cDNA with an ORF of 855 nt and yielding a 1.5-kb mRNA transcript was isolated from a mouse kidney library. Human and rat homologues also were isolated, and they had 91% and 97% amino acid identity with mouse protein. In vitro translation of the cDNA yielded a protein product of 33 kDa. Northern and Western blot analyses, using the cDNA and antirecombinant protein antibody, revealed its expression exclusively confined to the kidney. Like ALR2, the expression was up-regulated in diabetic kidneys. Its mRNA and protein expression was restricted to renal proximal tubules. The gene neither codistributed with Tamm-Horsfall protein nor aquaporin-2. The deduced protein sequence revealed an AKR-3 motif located near the N terminus, unlike the other AKR family members where it is confined to the C terminus. Fluorescence quenching and reactive blue agarose chromatography studies revealed that it binds to NADPH with high affinity (KdNADPH = 66.9 � 2.3 nM). This binding domain is a tetrapeptide (Met-Ala-Lys-Ser) located within the AKR-3 motif that is similar to the other AKR members. The identified protein is designated as RSOR because it is renal-specific with properties of an oxido-reductase, and like ALR2 it may be relevant in the renal complications of diabetes mellitus.
http://www.pnas.org/cgi/content/abstract/97/18/9896

It is known and accepted that during pregnancy Mg and Ca levels drop in the expectant mom. The developing fetus needs those nutrients, esp. Mg (to make ATP) which is stored in the brain, heart, liver and bones.
Here's the Mg - RNA/DNA connection:

1. RNA polymerases which allow DNA to be copied by the messenger. (See section 4 first)

2. Aminoacyl transfer RNA synthetases which permit amino acid fixation on the corresponding t-RNA

3. The elongation factor of the polypeptide chain which allows the binding of aminoacyl t-RNA at the receptor site of a ribosome on m-RNA complex

4. Ribsomal peptidyltransferases which allow the formation of the peptide

And...

4. The physical integrity of the DNA helix appears to be dependent on Mg2+

a. Mg2+ ion decreases the number DNA replication errors

b. Mg2+ ion stimulates DNA repair

c. Most of the known enzymes involved in repairing DNA lesions are dependent on Mg2+ at varying degrees

d. Mg may thus by important in reducing occurrence of neoplasms

5. The physical size of the RNA aggregate is controlled by the concentration of Mg

Here's the Mg - antibody (immunoglobulin) connection:

E. Required by immunological process. Magnesium, immunity, and allergy: Mg is required for several steps of immunological reactions

1. Lymphoblastic transformation, a prerequisite of secretion of antibodies by lymphoblasts, requires Ca2+ and Mg2+

2. Mg is required for synthesis of proteins, immunoglobulins included

3. Antibody-induced complement activation is Mg dependent

4. The antigen-immunoglobulin-complement reaction induces degranulation of the mastocyte

a. The degranulated mastocyte releases various substances, mainly histimine

b. Ca2+ and Mg2+ competition appears to regulate secretion of histamine by the mastocytes

i. Ca2+ ion stimulates secretion of histamine

ii. Mg2+ ion inhibits the secretion

5. Disorders in immunity and allergy-like symptoms have been described in Mg deficiency
Both of the above links can be found here: http://www.mdschoice.com/elements/elements/major_minerals/magnesium.htm

Bottom line...pregnant women must be sure to have adequate Mg and Ca intakes, esp. if they are diabetic, to protect the child.

And yes, folic acid (which may react with the minerals, produce hydrogen, and destroy any pathogen that may be attempting to cross the barrier).

Many diabetics are chromium deficient. When one mineral drops...it most definitely effects the others.

Marnie, I don't believe you and I have talked directly before. I'm a newer member of 2-3 months to this board.

Marnie, Are you a MEDICAL person? What is your background please? I've noticed lots of posts with medical info galore replying to other posters too.

Since I'll be forwarding this link for the Intl. disabetes president's info, thought they would be interested in your background too.

Sis has stage 3 lyme. She was misdiagnosed and given steroids 4 years ago. The rest is "history"...unfortunately.

When she did not get better using all, I repeat all, the abxs. including the "big guns"...Doxy, Ceftin, IV Rocephin, Tinidazole, Mepron with Azith...many repeated...along with a TON of $$$ supplements...

I began to try to figure out WHY the "traditional" medicine wasn't working.

Piece by piece it became clearer.

Find my Updated Nutshell post and my Long overdue posts (all lyme symptoms are Mg deficiency symptoms) to begin to understand what is going on. Sorry, they are long, so have a lot of paper ready in your printer if you cut, paste and drop them in a MS word file and print them out. I documented them to the best of my ability.

Even when the pathogen is destroyed, the problems/symptoms will be present until the Mg level is restored. Mg has so many functions...from making ATP, to making proteins, to making antibodies (along with Ca), to controlling over 350 enzymes, to REPAIRING DNA damage...we HAVE to restore this electrolyte...carefully.

This takes many months, perhaps even a few years, to do and needs to be done slowly...smaller doses at a time...more often. Timing is critical. Healing takes time.

Aging and disease damage the powerhouses of all our cells - the mitochondria. This is where ATP - energy is made. To make ATP takes the electrolyte Mg (and other ingredients).

When we are Mg deficient (and most Americans are) this is very damaging to our bodies.

Why are we Mg deficient? We don't eat the foods that are high in Mg, we put pesticides on our crops which deplete the minerals, overcook our foods, we add fluoride to our water which binds with Mg to make an insoluable salt, we are stressed out (which depletes the B vitamins and in turn, Mg), we overdo calcium (more reactive) which depletes Mg, we overdo sugar (glycogen is alkaline too)which depletes Mg (sugar also triggers an insulin spike which many pathogens - PFK dependent - love) and this stresses our immune system to the hilt to keep up, etc.

Stepping down from my soapbox ;-)

I am constantly researching.

If you have never seen the movie, First Do No Harm (with Meryl Streep), I highly recommend it. It is based on a true story about the ketogenic diet at Johns Hopkins. Of all the hospitals/universities, they appear to be on top of the nutritional/disease links.
Amazing!

Marnie, I've only been dx since 7-04 and misdx for 34 years.

But I did not know of stage 3 lyme. Are there 3 stages of lyme and can you explain what they are so other newbies like me can learn from veterans like yourself? Thanks!!

Thanks for referral to your links which I am showing in Treepatrol & Tincup's newbie link combo for the Intl. Diabetes President to click on, print, & read. Look for Marnie's name & all the links; reminder; they are LONG so have plenty of paper!

http://flash.lymenet.org/ubb/Forum1/HTML/029917.html

Welcome to this 24/7 educational support group board!

You'll need to click on above links to make it work correctly.

Here's TREEPATROL's and tincup's combination newbie links.

I suggest printing off the links then check them off as she reads as she could spend several months reading all of this.

Thank you Elisa on behalf of all of us.