Allies Voice: Would you use an insulin analogue that caused beta cell destruction?
Would you use an insulin analogue that caused beta cell destruction? Depending on the age of diagnosis, and type of diabetes - certain insulin analogues may not be the most ideal for the treatment of your diabetes. A person without diabetes excretes insulin with a pH of approximately 7.2 - 7.4. A person, with or without diabetes, should have a blood pH of 7.35 - 7.45. Here's my question: does the pH of your insulin analogue catalyze beta cell destruction?
The pH of the extracellular fluid can cause interference with beta cell regeneration. For a newly diagnosed Type 1 diabetes - deviating too far off the ideal range of blood pH is potentially stifling. For Type 2 diabetes, the further away from 7.3 the intracellular fluid pH strays, the weaker the might to regenerate. In both circumstances, individuals are at a disadvantage because higher blood glucose predisposes the blood to greater acidity. Wouldn't it make sense for diabetes treatment to mandate restoring the blood pH with an insulin that has a pH of 7.3?
In the US, the majority of insulins prescribed are insulin analogues. In light of a study that evaluated glucose metabolism in "young" and "adult" islets, cultured at different pHs - I had to wonder if some insulin analogue could impair beta cell regeneration / catalyze beta cell destruction. What do you think?
The study found a reduction of insulin secretion at both the acidic and alkaline sides of pH 7.3. Glucose provoked an increase of insulin secretion in both "young" and "adult" islets, as well. Good, that means keeping the body pH as close as possible to 7.3 will help islets (green and golden) respond to glucose. Check.
The study results also demonstrated that "young" islets are more acid tolerant than "adult" islets. Both basal and glucose-stimulated insulin secretions, as well as other parameters of "young" islets were significantly higher than those of "adult" islets in response to low pH. Okay, so like a tired old person, compared to a young vigilante - it would seem logical to lay off the more acidic insulins for the treatment of Type 2 diabetes.
To me, this study alludes that in adult-onset diabetes the administration of an insulin-analogue with an acidic pH lower than 7.3 is detrimental to the preservation and recovery for islets. So why on Earth is Lantus - with a pH of 4.0 (i.e., acid WASHED analogue) - the hottest selling analogue for the treatment of Type 2 diabetes? (Hint: checkout the Sale of the Century blog).
And for the sake of "young" islet preservation, considering the diagnosing event is typically diabetes ketoacidosis (acidic blood + elevated glucose + ketones) -- the choice of insulin to restore blood glucose should be an insulin as close to 7.3 as possible. I'd say go with a combo of NPH and Regular but I hesitate to confirm anything due to the extraordinary "range" accepted for pH in these formulas - clocking in at anywhere from a pH of 6.9 to 7.8!! Talk about a crapshoot!
To summarize:
What does pH have to do with beta cell survival? A lot. Balancing your blood pH has been shown to lend protection to your beta cells as they attempt to recover. For Type 2s this should matter a great deal. For Type 1s this should matter even more. If you have a squirt of insulin (and C-peptide) left in the life of your beta cells - wouldn't you protect it with all your might? Yeah, me too.
Discuss with your doctor the importance of managing your blood pH by using the most appropriate insulin (i.e., closest to a pH of 7.3). Here are your (current) insulin and analogue choices with their respective pH values:
- Lantus (Sanofi-Aventis): pH of 4.0
- APIDRA (Sanofi Aventis): pH of approximately 7.3
- Humalog (Eli Lilly): pH of 7.0-7.8
- Humulin R (Eli Lilly): pH range of 7.0 to 7.8
- Humulin N (Eli Lilly): pH range of 6.9 to 7.5
- NovoLog / NovoRapid (Novo Nordisk): pH of 7.2-7.6
- Levemir (Novo Nordisk): pH of approximately 7.4
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...........so then Allie, according to the chart you posted about the various Insulins and their respective pH:
Lantus (Sanofi-Aventis): pH of 4.0
APIDRA (Sanofi Aventis): pH of approximately 7.3
Humalog (Eli Lilly): pH of 7.0-7.8
Humulin R (Eli Lilly): pH range of 7.0 to 7.8
Humulin N (Eli Lilly): pH range of 6.9 to 7.5
NovoLog / NovoRapid (Novo Nordisk): pH of 7.2-7.6
Levemir (Novo Nordisk): pH of approximately 7.4
everyone then should ideally be using Levemir, Novolog, NovoRapid or/and Apidra as their respective Insulin of choice, since the one's I mentioned are closest to the pH of 7.3, right?
Now all we need is a way to stop whatever is causing the destruction process of the *re-generation* of the beta cells to take place so that the REAL cure can miraculously occur.
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Hey BetterCell,
The insulin analogues manufacturers are irresponsibly dismissing the importance of pH. This screams questionable disregard for patient safety.
An insulin analogue that suppresses beta cell regeneration will cause a number of difficulties like a) metabolic disarray b) hypoglycemic awareness and c) blood glucose control.
Consider the highest and lowest of Humulin Regular + Humulin NPH = 6.9 + 7.8 = 14.7 / 2 =
pH value = 7.35
** Human amino acid sequence
** Human insulin pH +/- .5
The importance of pH has been dismissed by insulin analogue manufacturers at the cost of beta cell recovery.
What kind of an industry profits from causing beta cell destruction?
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Keep in mind, that all of the mentioned Insulins are manufactured differently in the lab and sometimes NEED a different pH adjustment so as to maintain their stability and bio-activity
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Hi Allie,
Thanks so much for such an informative blog! The chart you posted in regards to the insulins pH is vital. Personally, I use the Humulin R and N for numerous reasons. Thanks again!! Julie
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I JUST WANTED TO TELL YOU ALLIE THAT I AM SO VERY IMPRESSED BY WHAT YOU'VE ACCOMPLISHED THUS FAR. BRINGING TO THE ATTENTION OF THE PUBLIC THE ABSENCE OF C-PEPTIDE ALONE IS OF HUGE SIGNIFICANCE, AND WILL INSPIRE OTHERS TO HELP EDUCATE AND RALLY TOGETHER TO GET A BIOIDENTICAL INSULIN BACK ON THE MARKET!
BEST REGARDS,
SAYER JI
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Hi Sayer - I truly appreciate your compliments on my efforts here on "Allies Voice" and beyond
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This is a specious* argument. The tiny amount of insulin given, relative to the total amount of fluid in the body, means that an insulin injection is not going to change the pH of the body. A healthy body (even with diabetes) is quite good at maintaining pH balance. Furthermore no one is squirting insulin directly onto the pancreas; it's injected under the skin (or in special situations, into a vein). Before it gets anywhere near beta cells it has to be carried in the blood - where the pH is maintained at 7.35-7.45 The body is constantly producing acids...eg lactic acid is a byproduct of muscle activity. Yet the body is able to get rid of that and other acids to keep pH within a narrow range. Kidneys are the main regulator of pH, but lungs can be involved too: eg, the smell of ketones on the breath is an indication of the lungs' efforts to remove acidic ketones from the body. There can come a tipping point beyond which the body's buffering systems are overwhelmed and cannot compensate. Then circulation, respirations and brain function shut down, leading to death. But with diabetes that's the result of LACK of insulin, not the pH of insulin given. Bottom line - pH of injected/infused insulin is not a health concern (other than that acidic insulin such as Lantus may sting at the injection site), and does not affect the pH of blood or extracellular fluid. It may vary due to manufacturing processes, or be deliverately adjusted in order to achieve specific actions (eg, the acidic nature of Lantus allows it to be slowly utilized for up to 24 hours).
* Specious - definition: having the ring of truth but actually false
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Hi Judith - Since you proclaim to be a "Diabetes Educator" I'm thankful you're familiar with the definition of specious. Keep that in mind as you pursue your line of work!
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Judith,
While the concept of what you're saying seems logical and would be easy to accept without proof, I'd have to ask for the proof first before dismissing Allie's postulation. Here's why.
I'd agree that if you could take a heterogenous mass of "human" and then add a dropper full of low pH insulin in a beaker and mix the two, that the "human" would quickly neutralize the acidity of the exogenous insulin and be done with it (as long as that particular body had the buffering capacity to do so) - but - obviously, that isn't how it works. And, while I'd totally agree that the body is an amazing bufferer and purifier, it is very reasonable to postulate that great damage could be done on a cellular level if highly acidic exogenous insulin actually reached the cell membrane intact, was caught by a receptor and then entered the cell as a strong acid. There is no question that a lot of drugs, including insulin, do a lot of damage unexpectantly by binding in unexpected ways. For example, Lantus has 6-8x greater IGF-1 receptor affinity than GE human insulin and Glargine shows increased mitogenicity (induction of cell division) as compared to Humulin R in a malignant cell line. (Ref: Kurtzhals P. Shaffer L, Sorensen A, Kristensen C, Jonassen I, Schmid C, Trub T. Correlations of receptor binding and metabolic and mitogenic potencies of insulin analogs designed for clinical use. Diabetes, 2000; 49: 999-1005.)
The question seems to be: is the exogenous insulin molecule able to retain its acidity largely intact until it enters the cell? - that, to me, is a million dollar question.
In further support, exogenous insulin is a very big molecule; one deliberately designed to take a long time to break down in the body. This could also be interpreted to mean that it will move through the body, largely intact, for a considerable amount of time - possibly until it is captured by a receptor and brought into the cell. I'm no celllular biologist - but, I'd love to hear from someone who is, or from someone who has researched the topic and can bring papers to the table.
Anyone got proof behind their pudding? If yes, I'd love to read it.
And Allie, thanks for the post. As often happens, the paper you cited opened my eyes a bit wider. Now I'm looking at testing and balancing my diet to increase my pH. It seems most (or nearly all) people who are fighting dis-ease are acidic and there's at least some writing out there that says you can't heal unless your body is oxygenated and therefore slightly alkaline. Balance your pH and heal, or so the idea goes. Does anyone out there have thoughts on this concept? Is the insulin itself a minor concern compared to the acidic pH of the whole body induced in our systems by the food we're eating?) This isn't scientific and may be junk, but I did find it interesting and plan to research further on the topic: http://home.bluegrass.net/~jclark/coral_calcium.htm
Kelly
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As you probably already know Kelly, a person CAN modify their pH within their body by both the combination of including certain foods in their diet while eliminating others.
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Since you found it necessary to define “specious” for us, I assume you stereotypically consider readers of this blog as uneducated, moronic cretins? I don’t think Allie’s contention was that the minuscule bit of injected, pH-adjusted insulin-containing material would somehow alter the pH of the entire system; merely that injection may have consequences beyond the mere lowering of bG level.
May I say that your own speciousness is revealed by this statement alone:
Bottom line - pH of injected/infused insulin is not a health concern (other than that acidic insulin such as Lantus may sting at the injection site), and does not affect the pH of blood or extracellular fluid.
A more truthful (less specious) bottom line would be this: pH of injected/infused insulin has not been critically investigated as a health concern. A resultant question, then, would be: WHY?
(As the resident conspiracy theorist, I would suggest that it is not profitable for the insulin cartel to know what sort of adverse reactions may be instigated or what biologic pathways may be altered by injecting multiple foreign substances into our bodies as we seek to lower bG. To imply that the ONLY action that occurs is the expected lowering of bG is naïve*, at best. Further, I would suggest that the ruling paradigm for the insulin cartel is this: “If you don’t know the answer, if the answer might bite you in the butt--don’t ask the question.” And consequently, they haven’t. So we, insulin-dependent diabetics, must rely on blind TRUST that insulin producers place patients before profits, and whatever is delivered concomitantly with insulin is magically neutralized/ignored/removed by the body—no harm done.)
*Naïve—definition: one who is artless, credulous, or uncritical; lacking worldly experience and understanding. (And here, I give you the benefit of the doubt; otherwise, I would suggest you are an industry(ies) propagandist, spewing dogma intended to allay fears or promote a fiscal agenda.)
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Thanks Melody and of course, Allie for speaking the truth! Since no genetic insulin can even compare to what the manufacture of my body (God) has provided--there are no side effects to my own insulin. There are many side effects to insulins that have been produced in a lab. Believe me, they are not the real thing! Of course, the worse side effect to synthetic insulin would be not only an allergy from it but death. I believe in helping people bury diabetes and all of the negative stuff that goes along with it. I am grateful to you Melody and many others on this blog. Blessings, Julie
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Melody ~
The opening byline in Judith's post, that she is a "diabetes educator", alone says volumes. I just "love" when people proclaim their credentials as evidence in support of their position. Authority by title doesn't cut it for me either. Authority by evidence goes a much longer way. Judith, if you have evidence in support of your position, it would be great to read it.
Kelly
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I personally think the bigger issue is that there seems to be evidence to suggest that using animal insulin preserves more endogenous insulin secretion in Type 1 diabetics than current forms of synthetic "Human" insulin. Allie has posted studies on this previously.
The exact mechanisms are unclear, but there are many intriguing possibilities.
Since switching to porcine dessicated thyroid hormone from Synthroid, I have seen a decrease in my exogenous thyroid hormone replacement needs. So much so that I am going for a Thyroid Ultrasound and Uptake Scan to determine how much (if any) thyroid hormone my gland is still making, a full 16 years after onset of Hashimoto's Thyroiditis.
Note that there is a large decrease in my oral thyroid hormone needs even after accounting for the ingestion of T3, T2, T1, etc as well as T4. Enough that my Internist agreed that I should have an uptake scan. I am currently on the waiting list.
I also have to note that I use sea salt instead of iodized salt (iodine may be a major trigger in autoimmune thyroid disease ironically), eat very little processed (i.e. salted) foods, and very little soy products. No one knows if soy may be a direct trigger, or simply interfere with thyroid hormone absorption. Due to Celiac, I am also gluten free (gluten may be a trigger as well).
It also appears as though I have retained some residual thyroid function and possibly beta cell function despite 16 and 24 years of autoimmunity respectively. I base this primarily on positive antibodies for Hashimoto's 9 years after my diagnosis (your body can't continue to attack what isn't there ) and my fluctuating insulin and thyroid hormone needs.
On another note, I also started taking my oral thyroid hormone sublingual, for better uptake. This I began doing only very recently, so I can control my dosing more precisely without the variable of intestinal absorption. I suggest that others consider this method as well. You also do not have to wait to eat after taking your pill.
As for Judith, I think she is where I was until fairly recently. I'm not going to attack her because what she says *does* make sense and is "correct"...if you consider that she is giving a textbook answer. And that is what she is trained to do. My first instinct with MY education would be to give the exact same response, perhaps alluding to the possibility of the unknown.
And this is where I stand today. We simply don't know. We can rationalize, we can assume, but we don't know all of the details for certain. We *think* we do, but the human body is complex. We can *assume* "Human" insulin is preferable, but what about the data linking certain GM insulin to an increase in cancer? Or a decrease in residual beta cells function when compared to animal insulin (Allie please cite that study)? Or factor X?
How many "safe and approved" drugs in the past 5 years alone have been pulled or blackboxed due to side effects?!
We just don't have all the answers
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Melody, I think you said it best, so I have little to add. Most of us here are have been reading this blog for some time, so I can understand Judith being incredulous that we would appear to be so "stupid" as to assume the PH of our insulin is the cause of all of our problems. But as you stated, we are primarily concerned with the BIG picture...the fact that there may be some truth to what Allie has been saying all along in regards to animal insulin being a better choice for some diabetics. For MANY reasons, not just one speculation.
More so, although I can think of some cases where GM insulin may be preferable, I also think that patients should be given the choice, as opposed to having their "choice" made for them.
With a disease as hard to manage as Type 1 diabetes (or an insulin using Type 2), a person should have access to whatever tools they see fit to maintain their health.
My 2 cents..
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Hi Sarah.......
Speaking about 2¢, it would be good if Insulin(porcine-derived that was not contminated w/crap from China and India) was available and was not cost prohibited. 2¢ for a Life sustaining Hormone sounds reasonable.
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P.S. I suppose if I wanted to copy Judith's elitest position, I should have stated my name as following:
Sarah-Microbiology and Immunology Major (Pre-Med)
Hehe...
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I must say Allie's blog has opened my eyes...after doing further research it appears that porcine insulin may be the best option available for those struggling with the mood swings and potential hypoglycemia unawareness drugs like Lantus may cause. I ordered Hypurin pork insulin from Canada (no prescription needed). It cost $140 plus $15 for shipping. At this point I don't care what it costs. Lantus was driving my close friend into deep depression and was starting to send her sugars on a roller coaster ride.
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Cost IS a big issue, and it's a shame that most places offer no coverage. I do happen to live in Canada, but porcine insulin (or thyroid hormone) is not covered by any provincial health plan that I know of. I don't mind paying $16 per month for thyroid hormone, but right now all of my diabetes supplies and insulin are "free" (covered after I pay 3% of my income annually as a deductible).
I am trying to see if I can somehow get special approval coverage so I can try switching to porcine insulin. As a student, I just can't afford to pay for my insulin when the GM insulin is paid for. At least right now.
It really ticks me off that animal insulin is not covered...even for those that need it to stay out of the hospital (i.e. hypoglycemic unawareness with GM insulin). The government would rather pay $10,000 for a hospital stay than $150 for a bottle of insulin...go figure.
As I said, I do live in Canada, so I'm not complaining by any means...diabetics in the U.S. without insurance are much worse off than I could ever be. But I am frustrated with the bigger picture...even though animal insulin is available in Canada (thank God), you have to go out of your way to get it, and no provincial health plan will pay for it. My plan will pay for Lantus, Humalog, etc. with no questions asked, no restrictions. But if you NEED animal insulin, and you can't afford it, you are screwed. Perhaps there are loopholes, which I intend to find out.
Diabetics should be offered the choice of animal or GM insulin in plain sight, and it should be available for the same cost as GM insulin through government programs.
Like Bettercell said, 2 cents sounds about right to me.
Pay now or pay later...
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Sorry Saver, forgot to add that I am glad you were able to get animal insulin. I hope your friend is doing better. I cannot wait to see if I notice a difference on animal insulin.
Best Wishes.
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Sarah,
Please do relay how you're doing on porcine and what you've noticed when you get further in to using it. I'm just into my second vial now of Porcine Hypurin Isophane after switching from Humulin U (Ultralente) (I hoarded a 2 year stock before it was pulled from the market.) It's going just fine. I'd say I have noticeably less fatigue and the "ride" is about the same as the Ultralente. I'm not really noticing any perceptible differences in lows or highs. It's a little more peaky than the UL; but, certainly manageable and predictable enough not to want to switch to something else. I also did numerous lab tests to allow a before and after picture (if it has any value is another question entirely) and feel better about what I'm putting into my body in regard to overall health risks.
I'd love to hear more stories of how things are going for others. I was very nervous making the switch; but, I'm glad I did.
Kelly
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Allie,
Trying to contact you. Like your new blog -- congrats! Give me a shout at bevsklar@yahoo.com, when you have time.
Thanks,
Bev
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I don't think the acidity of the insulin injected can make any difference. The typical blood volume of a normal-sized human is 5 liters. Let us suppose that the typical amount of insulin injected per day is 50 units, or 0.5 cc. Then that means that the total acidifying insulin in the body amounts to one ten-thousandth of the person's total blood volume, which is not enough to affect the pH measurably.
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Sanktpauli:
The problem is: it isn't just the "dropping" of 0.5 cc of insulin into 5 liters of blood. I think the question is: how much of the intact, low pH insulin molecule gets to the pancreas, hits a receptor and enters a cell? The question is: how acidic is the body it's dropped into to begin with? The question is: if damage from the level of acidity does occur, does it occur faster than regeneration of new cells? The question is: has anyone looked at this in a true research forum, or is it all assumption or a shrugging that it doesn't matter anyway, the thinking being that if someone's diabetic anyway, the pancreas is shot, so what's a little more cell death? Has anyone really looked at this question and seriously tried to answer it?
Kelly
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It would take a well-designed protocol to prove or disprove the hypothesis of blood pH affected by recombinant insulin, insulin analogues, and natural vertebrate insulin. First and foremost the fact that natural vertebrate insulin has been discouraged for use and developed an unfair bias is a sad state of affairs in diabetes treatment. As a person with Type 1 diabetes for almost 23 years - it's unfortunate that a CHOICE for safer,
natural, and likely less expensive (produced in quantities of 5% of the insulin-dependent market) was never proposed. Ever wonder why Big Pharma keeps more money in the bank for marketing and law suits than they spend of Research and Development?
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Some inferences in science are made on the basis of empirical studies and experiments, where the data are not available. Other inferences in science can be made by simple calculation, where the physical laws governing the situation and the values of the forces operating within it are already known.
In this case, since we know the average pH of normal blood is around 7.39 (averaging in arterial and venous pH, both of which vary diurnally), we know the pH of various insulins, and we know that the ratio between the blood mass and the mass of insulin injected per day in a diabetic is typically ten thousand to one, we can calculate the difference in the total pH of the solution that would be made by injecting each type of insulin. Whether the insulin was the most highly acidic or most highly alkaline substance known to organic chemistry, injecting such a relatively small amount compared to the total mass would produce a difference too small to measure. This necessarily leads to the conclusion, without the need to experiment, that the pH of insulin cannot matter to beta cells bathed in blood.
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Sanktpauli,
Sometimes it's just better to say: "I don't know."
This was one of those times.
Kelly
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Regarding choice of insulin pH and beta cell attack, there is one theory most of you have dismissed regarding Allie’s hypothesis re: beta cell destruction.
Those who seek to ridicule or denigrate issues related to insulin pH present a simplistic approach—inferring that it is the height of stupidity to imply that a few miniscule drops of acidic insulin will result in acidifying the bloodstream. I don’t think anyone is making such a claim, but the first artifice in the argument suggests that the insulin is injected into the bloodstream. NOT. These opponents further fail to acknowledge that an infinestimal amount of ricin or botulism can have cascading, catastrophic effects on a biologic system—yet “in total volume” it could be claimed that this is an impossibility.
Likewise, the pH of insulin may be only the instigator of a cascading chain of events—none of which are of benefit to a biologic specimen. As an alternative theory, isn’t it possible to envision this scenario:
One’s immune system is always on alert for foreign protein ‘invaders’ (insulin/analogs are such invaders). The pH of injected insulin may be little more than an attention getter—the parade vanguard waving a banner labeled ABNORMAL—that stimulates the immune system.
Once the immune system has been alerted by this banner, it rushes to attack foreign proteins (insulin), but also recognizes that since beta cells produce insulin, it is also necessary to shut down the source, causing inflammatory response and destroying beta cells.
Keep searching for the truth, Allie. You are asking the RIGHT questions.
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Although insulin is of course not normally injected into the bloodstream (it is in some circumstances, such as when the patient has high insulin antibodies or is in ketoacidosis), the only way it can affect the beta cells with its pH is by traveling subcutaneously to the bloodstream to come into contact with the beta cells, so this is the point of measuring the impact of its influence on pH of the entire bloodstream.
The influence of pH on the bloodstream is not that of an infective agent such as botulism, where a very small dose can have disproportionate effects very quickly through the entire body. In the case of changing the pH, the acidifying or alkalinizing effect has to operate by the net impact of the substance on the pH of the entire fluid system into which it is dumped. In other words, it is a physical, not a biological mechanism. So changing the pH of 5 liters of blood by putting 0.5 cc of insulin into it per day is like pouring tomato juice into the Atlantic and waiting for the ocean to turn red.
Immunological responses are the reaction of antigens in the body to foreign substances. A different pH does not attract an immunological response, because then the entire body would reject itself in a massive auto-immune attack every time it falls into acidosis, which does not happen in patients who suffer acidosis, such as diabetics and renal patients. Thus it cannot be happening in response to an anomalous pH of insulin either.
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Sanktpauli,
I think you might want to reread the blog - it looks like you've missed the point. The question isn't whether injecting 0.5 cc of low pH insulin into 5 liters of blood has any impact; I don't think anyone is disagreeing on that. The question is on a cellular/receptor level specifically having to do with exogenous GE insulin, i.e.: what effect does exogenous GE insulin have on beta cells - it's a molecule that has been deliberately designed NOT to degrade quickly. It remains intact in the blood stream for a long time (18-36 hours). It is highly plausible that at some point, the molecule will degrade at the point it has reached the beta cell and is then received intact. It's more like asking what effect a cyanide pill that's encased in a basketball of mass will have when it's dropped into a bloodstream, not just blood. Surely the basketball's exterior will be neutralized; but when it finally degrades leaving only the cyanide, what will the cyanide hit? and if the cyanide basketball is a specific molecule designed to be received by a certain type of cell, as is the case of GE insulin and the pancreas, what effect will IT have once it dissolves on location? It's this other question I think the rest of us are focusing on.
Kelly
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Now you're changing the thesis. If you think there is some destructive mechanism in the genetically engineered insulin molecule which can damage beta cells INDEPENDENTLY OF THE pH DIFFERENCE, you are making a new argument. Since pH is a mechanical effect, it will always be buffered by the pH of the surrounding medium, so any deviant pH of the GE insulin molecule will always be rendered insignificant by the surrounding blood. A purported alternative damaging mechanism in the GE insulin molecule is purely imaginary, since no evidence yet exists of it, nor has anyone stated what it could be or how it would work. Until we have further evidence for it and detail about it, this is just an empty hypothesis.
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Ahh, Sanktpauli,
Alas. First, now you see what the rest of us are talking about; welcome to the conversation. And second, you present the perfect response of Big Pharma - described by Marsden Wagner of the World Health Organization as "anti-precautionary medicine", i.e. go ahead and assume no harm is done until it's proven harm was done and only then stop. It should be the other way around - prove the medicine or intervention does no harm before using it on people. In reality, the way it is, western medicine is, in particular and in vast majority, one big human experiment after another with tragic consequence after tragic consequence of exactly the policy of which you speak.
Kelly
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Kelly--
Thanks for expressing my opinions. I wrote the following yesterday . . . then stuck it in my 'draft' folder instead of posting it here. I offer this as MY reply to Sanktpauli . . . but it is merely an echo of your message:
I contend that you are using industry-friendly strawmen arguments. What power do you think individuals have beyond anecdotal observations, and 'empty' hypotheses? But just as we CANNOT prove that there is a damaging mechanism, neither can industry prove that there isn't. Unfortunately, since money & power lie with industry (and their puppets--advocacy groups/sponsored medical experts & researchers), and since 'discovering' such damaging mechanisms would impact negatively on their bottom lines--NO ONE IS LOOKING.
I would ask--have you actually injected yourself with a foreign hormone--multiple times a day over a course of 50 years? Have you actually had the opportunity to compare (internally) differences between natural hormones and manmade hormones? Have you enough experience to detect subtle but recognizable changes within your unique biologic system that are cause for concern and point to ‘insulin’ as causative? Some of the hypotheses I encounter (from individuals) regarding synthetic insulin as causative are no less far-flung and unprovable than the still-unproven hypotheses, fuzzy-logic and all, that garnered FDA approval for this problematic drug
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Hi Melody.........This argument is becoming complex, because what is at stake, is complex........Human Lives and what is put into their Bodies exogenously with a benefit or risk(or a combination of both)that may or may not occur.
There is always the *Risk-Benefit Ratio* that exists in Medicine. This applies whether the medicine is derived in the lab or from botanical sources(Phytoceuticals).
The choices as far as T1DM management are concerned become even more limiting if a person does not have the additional $$ to purchase animal/porcine derived insulin, does not have adequate health care insurance and lives in a country where "what we have is what you get" type of existence.
To have T1DM and thus be dependent on exogenous Insulin is made very clear in the beginning. Where respiration is induced into the fetus at birth for the continuance of Life, Insulin (GM or animal derived) then becomes our sustenance and continuation as well.
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Melody,
To make matters worse, often industry DOES look at the "damaging mechanisms", but they deliberately choose not to publish the information because it would damage their bottom line. It's completely dishonest. We just never hear about the negative evidence.
Case in point: The Wall Street Journal recently wrote an article about a study where the researchers found that manufacturers failed to publish negative research and it inflated the reported effectiveness of all 12 of the antidepressants studied. (Source: Wall Street Journal - January 17, 2008; Page D1A.)* The researchers found that the average "effect size" of the antidepressant Zoloft, for example, rose 64% by the failure to publish negative or questionable data on the drug.
So gee, if you only publish the good data and not the bad, and that's all the doctors prescribing the drug have to go on, guess what? Damage, death occur. But, hey, they knew it would. They just chose not to publish it so we could make an informed decision on whether or not to put it in our bodies.
So a major question is: why isn't it illegal for manufacturers not to disclose information that would put their "wunderdrug" in a "bad" light (read also as an "honest" light)? They do this strictly as a means to increase their revenues, regardless of the fact that it misleads doctors, and harms patients. Sanktpauli - they might have already done the research on low pH and beta cell death. We're just not privy to it.
But, hey, if they did and they were to publish that negative research - as is the case with antidepressants - and the new "wunderdrug" doesn't perform better than a placebo when they take all of the research into account, then the FDA won't let them sell it and they're out billions. Can't have that now. Those poor pharmaceutical companies. People will just have to suck it up, eh Sanktpauli? The effect of pH on beta cells? Who cares? (oops. I mean, we did care, but we buried that evidence a long time ago and look - Now we're billionaires!)
Kelly
* To read this article, scroll 3/4's down the page to the title: Antidepressants Under Scrutiny Over Efficacy at: http://ltcadministrator.com/index.php?page=News
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The universally accepted rule in science is that the person advancing a hypothesis has to supply some positive arguments and evidence for it before it can be taken as having any merit worth considering. Imagining that there could be some mechanism or data to support a hypothesis is not a sufficient basis for advancing the hypothesis and expecting others to take it seriously. The electricity fairy may cause the light to go on when I turn the switch on my lamp, but unless someone explains to me some mechanism consistent with the known laws of science and shows me some data for assuming that a fairy is doing this work, I will not entertain the hypothesis.
Now in this case, the initial hypothesis was that the acidity of the GE insulin molecule was somehow damaging beta cells. The only way that acidity can act on the beta cells is by operating through the buffering medium of blood WHICH IS PRESENT EVEN WHERE THE INSULIN MOLECULE MEETS THE INSULIN RECEPTORS. The problem with the hypothsis is that the deviation of the GE insulin molecule from organic insulin is relatively small and would encounter a profound buffering effect from the surrounding blood before doing anything to the beta cells, so significant damage is mechanically impossible.
Keep in mind that the body naturally undergoes diurnal variation in blood pH. Every meal is followed by what physiologists describe as an 'alkalide tide' because of the high alkaline content of most diets, and this changes the blood pH. But when diabetics experience extremely high degrees of blood acidification in ketoacidosis at the onset of their disease, for example, they can still go on to enjoy a prolonged honeymoon period in which the beta cells return to their normal functioning for a while, despite their exposure to a degree of acidification which infinitely exceeds that of contact with the GE insulin molecules. Even diabetics exposed to extreme blood acidification from renal acidosis go on to experience periods when the requirement for injected insulin falls dramatically, suggesting revival of beta cell function consistent with Faustman's theory that the beta cells never completely lose the battle against the immunological attack.
All these factors in sum indicate that acidification from GE insulin molecules cannot be damaging the beta cells. If there are other mechanisms by which this can be imagined to occur, it is the duty of the researchers advancing the hypothesis that such damage is occurring to demonstrate, not of others to refute in the absence of any evidence supporting the hypothesis.
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Hey Sanktpauli , Thanks for pointing it out. I can see where you're coming from. The factors involved in the pH balance of the body are compelling -- possibly more than an insulin analogue. However, from an empirical standpoint... the chemistry in my body feels more *natural* on animal insulin. Every analogue I've used has been another round of roulette. Animal insulin is just a matter of choice.
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Allie—
You may not want to print this, but Sanktpauli is dismissive of our concerns.
I have been wondering about your email-id; Your sanctimonious preaching to a group of chronically ill patients discussing/hypothesizing about their treatment by doctors, the insulin cartel, “our” charities and diabusiness. Your egotism literally jumps off the page, much as did my doctor, who considers himself the local ‘savior of diabetics.”
For over 50 years I have been a Type 1, and I find my boiling point is lowering daily, especially when preached to by those who think they know science and understand completely all the laws of nature. If you KNOW so much, why haven’t you and/or your colleagues cured this damnable disease?
You are absolutely right about a drop of acid in a bolus being like a piss in the ocean and belief in the light fairy. If all scientific hypotheses were based on the laws of nature (as known at the time) and accepted scientific principles, we would never learn anything new, never discover cures, never know a better way. Based on engineering principles, scientists rightly advance the belief that bumblebees cannot fly. But nobody told the bumblebees. Fleming observed the possibilities inherent in penicillin when he observed clear margins surrounding fungal-contaminated Petri plate growth media. Lucky us! Didn’t his colleagues observe the same events, but lacked the intellectual curiosity to investigate? As for the light fairy . . . is that what Ben Franklin (and some of his inquisitive predecessors) was seeking when his intellect was piqued by the curious phenomenon known as lightning? There are a lot of things about nature and science we DON’T understand, but common friendship allows us to share, discuss, and yes—hypothesize.
When you speak of continued attack on beta cells (like it doesn’t happen with any insulin), is there something you don’t understand about ‘insulin doesn’t cure diabetes?’ We are just now beginning to recognize the role of C-peptides in prevention of complications. If our fate depends on medicine men like you (if that’s what you are), or an industry-sponsored think-tank group of scientists that includes you (if that’s what you are), then heaven help all of us. By the way, I will take the genius of Dr. Faustman and the willingness to think and step outside the box over a classically-trained science robot any day. Erosion of academic integrity and honesty has occurred at ever-increasing speed over the past 2-3 decades, as new “scientists” want it all . . . and want it now. (They want power, prestige, recognition and money . . . and any/all of those come before humanity—known as patients.)
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One of the many *Complications* that is associated with T1DM Longevity, is the ability to see through Sham, the acquisition of more Knowledge, and the intuitive-like power of being able to see through mediocre Doctors, thus separating the Physician from those who only dress like one.
Bravo to you Brent.
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Having suffered for 42 years from a highly labile case of type 1 diabetes, I am not an outsider unable to appreciate the perspective of the patient. It is just that having seen so many purported 'cures' over the years which amounted to nothing, I feel that each new one has to be subjected to rigorous scepticism before it can be accepted.
The main problem with Faustman's approach is that any tissue which has profoundly necrotized for a long period of time simply will not regrow, however much you stimulate it, and this may well restrict her treatment to newly-established cases. For example, patients taking calcineuron inhibitors often experience extreme hypertrophy of the gingiva so that the teeth can hardly be seen, since they become buried under the gums. But in those patients whose gums had a long time before severely receded experience no overgrowth at all. The same thing may well happen in established cases of diabetes when given BCG and INGAP polypeptide.
Generally, I think that porcine islet cells encapsulated in a differentially permeable membrance and engrafted into the abdomen is a more promising treatment than Faustman's, and this is already in phase II clinial trials in human patients in Russia. However, even this approach suffers from the drawback that some immunological response to the pig cells seems to persist, which causes a condition of perpetual inflammation throughout the body, and this can itself lead to complications such as accelerated atherosclerosis.
Generally, from my perspective, I don't think that there will be any effective route out of the diabetes trap in my lifetime.
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Sanktpauli—
I apologize for my comments only in the sense that I made a promise to myself that I would never criticize another individual with diabetes for expressing personal attitudes related to diabetes. We are ALL individuals and see this disease through our own eyes (and experiences). I, too, have been a ‘brittle’ diabetic since 1956 to the point where most doctors would rather NOT have me as a patient, since my questions were beyond the scope of their knowledge. I hope you and I are both wrong (BetterCell, you’re included, too) that we will not see a CURE in our lifetime. HOPE is a terrible thing to waste.
I can see from your pragmatic and thoughtful comments that you, too, have thought a great deal about this chronic disease. Please give me your thoughts on the following (send them to otchmoson at Hughes dot net if you don’t want to clutter Allie’s board):
1) Have you studied the “cure” which Dr. Hammerman (Washington Univ., St. Louis) has been trying to get into human trials?
2) I have a friend in England (biochemist/Oxford grad) who claims that Dr. Faustman’s “cure” will lead to diabetics becoming schizophrenic. The rationale for curing diabetes (T1 and T2) is that carbohydrates—particularly those with gluten—are causing most of the immunologic/inflammatory response.
3) For a long time I have considered the possibility that diabetes is an inflammatory- response disease which, for some reason, targets the pancreas and beta cells. One of the studies of collaboration between the U.S./Canada scientists indicated that one of the capsaicin molecules (which reduced inflammation) may lead to a cure.
4) If you are in the same boat as the rest of us, why haven’t you been active in pursuing free choice of insulin for all diabetics in order to more effectively manage the disease? Do you have suggestions regarding how to stop our pharmaceuticals from switching everyone to foreign synthetic hormones—which can only increase the inflammatory/immunogenic response? The Pharmalot.com website yesterday included discussion by a group of dilantin users who have experienced the same kind of pharma-disregard that diabetics have. Without informing patients of subtle changes, medication was marketed as “the same” . . . and patients suffered. This is pretty astounding when you consider that the problem occurred with a small molecule drug. So far, the insulin cartel has deflected all similar issues involving a BIOLOGIC. And patients—knowingly, or otherwise—suffer. http://www.pharmalot.com/2008/05/a-new-version-of-dilantin-is-giving-pfizer-fits/
I have never considered myself as smart as you or many other people in this world. My analysis of problems does not result from straight-line thinking, but rather from circuitous, hypothetical (non-scientific) and miscellaneous observations which often is very unconventional. I don’t think a pragmatic scientist will cure this disease.
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Sanktpauli,
In regard to necrotizing tissue - if you think your pancreas is dead or dying, it is, if you think it isn't, it isn't. I liken mine to being trapped, suppressed by the flood of exogenous insulin it has to deal with, but otherwise fine, thank you very much. Absent a biopsy of MY pancreas, there's no way to know. And any muscle, despite atrophy, can be strengthened, if given the right conditions and exercise.
A great book to read, if you're interested in building your hope supply, is Bruce Lipton's, The Biology of Belief. It'll turn your scientific understanding of cellular biology on its head.
Kelly
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If your pancreas is fine other than the suppression of its function caused by exogenous insulin around it, then why did you start injecting exogenous insulin in the first place? Obviously because there was something wrong with the beta cells of the pancreas BEFORE there was an exogenous insulin present.
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Sanktpauli,
I've told my story elsewhere in Allie's blog, but in short answer - No, I suffered an injury to my pancreas (and liver) from exposure to a fluoroquinolone antibiotic called Norfloxacin. The toxic exposure resulted in a hyperglycemic condition that was incorrectly treated with insulin as diabetes. Exogenous insulin suppresses endogenous insulin secretion. Over time, I've become dependent on insulin and now I'm working to get off of it. Had the injury been understood for what it was, I wouldn't likely be on insulin today. So, in response, no, there wasn't something wrong with the beta cells of the pancreas before there was exogenous insulin present. My theory is I was zinc deficient, the Norfloxacin caused me to be zinc depleted, and zinc is the trigger, not insulin, for telling the liver to secrete glycogen.
Kelly
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Sanktpauli.......
"Generally, from my perspective, I don't think that there will be any effective route out of the diabetes trap in my lifetime."
That is because the geographic area for the CURE has been moved from, "Just around the corner to
on the Horizon."
So it looks like most of us have been looking or/and standing in the wrong place for a long time.
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Brent....When I was a student in the University many years ago, I had a Professor for a Medical Anthropology course who expressed the same sentiment as you regarding your statement, " I don’t think a pragmatic scientist will cure this disease."
I also experience the same problems w/Physicians as you do.
Her feeling was that many therapeutic modalities(treatments, medicine, *cures*) come more to those who are open-minded and receptive to information but still able to use a critical eye and filter. Sometimes good things come as a side-effect of a medication that is not originally intended for use.
As to your insight regarding Inflammation, I am in total agreement. However, Inflammation does have its therapeutic uses and benefits as in the case of an injury where white blood cells, lymphatic fluid, T cells and more will go to aid and treat the first "assault" to the body. It is only when the Inflammatory Process lingers on(they have exceeded their stay because the threat remains to that part of the cell/tissue/organ) that it then becomes toxic to the integrity of the body. The Medical profession recognizes many Diseases that have a major Inflammatory component. This includes Heart disease, Arthritis and all of the Auto-Immune Diseases(T1DM).
I personally use certain foods(alkaline) as well as certain Neutraceuticles(Tumeric) to counter the excess Inflammation.
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Brent, BetterCell,
I love this line of thinking - I think intercellular inflammation is the absolute key to solving the problem. The concept is also well supported by the research and the current thinking, as I'm sure you're both already aware, is that it's not an auto-immune response (as everyone for the last zillion years has blamed the patient for) but an inflammatory response that results in the creation of an auto-immune response.
Around June of last year, I started tracking my general inflammation level through a CRP test and eating a strong Omega 3 diet, supplementing with about 3000 mg of omega 3's a day and focusing on omega 3 (anti-inflammatory) and omega 6 (pro-inflammatory) food intake. Before I started the Omega-3 eating lifestyle, I took a CRP test (a high sensitivity c-reactive protein test) to test my general level of inflammation. Then, after 6 months, I retested. Pre-omega-3 diet, I was generally "moderately inflammed". Post-omega-3, my general inflammation was reduced to virtually zero. I've stopped taking the daily omega-3 supplement because I seem to be bleeding like a champ without it now. (At this point, I eat virtually no meat and my diet has a high focus on raw foods, so I don't think I have much of an inflammation source anymore.
So - here's my question. I've been asking and looking around to see if there's a test out there for intercellular inflammation. The CRP is good for testing the general inflammation response in your body, but it doesn't really test at an intercellular level. From my research, it all seems to point in the direction that it's a "perfect storm" - i.e. your eating habits, lifestyle, environmental conditions, medications/chemical exposures, etc. pre-diabetic, make you susceptible, and an acute environmental trigger creates an acute inflammatory response that severely impacts neural connectivity and manifests itself in our case first or most evidently in the pancreas, showing itself as hyperglycemia. In short, the beta cell is "inflammed" and can't respond to a blood glucose rise.
My work to heal has been to focus on minimizing the inflammation, working to strengthen and rebuild the atrophy that has likely occurred, and decrease the exogenous insulin as much as possible to give the pancreas some room to respond.
So here's my question - Do you (or anyone else out there) know if there IS a test for intercellular inflammation? I've heard that there is, but I haven't found its specific name yet or who performs it. If there is, I'd track its results to see if, like you BetterCell, eating a low pH generating diet has an impact (or eating capsaicin, or fennugeek, etc.)
Thanks for sharing your thinking!
Kelly
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Hi Kelly......
The JDRF is now looking for Bio-markers that can predict T1DM and various organ complications.
In addition, a research paper was submitted to Elsiver that shows that oxidative stress is increased in T1DM independent of glucose values. What was suggested, was a way to perform a breathe test that would measure oxidative age and thus be used as a bio-marker.
I would be happy to send (Email) these papers to you, if you will send me your Email Address on my Site. Just click bettercell and it will bring you there.
There seems to be different bio-markers used according to what organ, illness is being investigated.
As to Omega 3's, if you are bleeding as you had said, it was good that you had eliminated it from your intake. However, Omega 3 Fish Oils still shows and does have a protective role in Coronary Heart Disease(CHP) which is very prevelant in T1DM within bith genders and maybe more so in women. If you are not bleeding, then maybe 1gm/Omega 3's/Day would be better than the 3gms. you were taking.
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BetterCell & Kelly—
First of all, I do not know of an intercellular test for inflammation. Like you, I have had a C-reactive protein test, which has always been in the low range. I do suspect that these results reflect a moderately good diet, Omegas, Co-Q-10, Wobenzyme, and a variety of other supplements that I have taken over the last several years. The other product I have used is called an AKAI water ionizer, which not only produces alkaline water . . . but a charged water which helps to alkalize the body to its normal state since much of what we consume tends to acidify the body. My question to you relates to inflammation and the possibility that our diabetes resulted from an over-active immune response which eventually becomes “overloaded” with factors causing inflammation. The question is: No matter how good you eat, how well you supplement your nutrition, and how well you hydrate your body with the perfect water, my biggest source of inflammatory response probably comes from dirty air; how do we avoid that? Unfortunately, we have to breathe, and on occasion must step outside the bounds of our ‘protected’ environment. I have found the more I do to reduce inflammation, the more sensitive I have become to all the pollens, molds, chemicals that are part of everyday living. In other words, taking away the cause of inflammation does not reduce your sensitivity.
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There is recent and accumulating evidence that what causes beta cell destruction is initially a disease of the nervous system which induces a response in the beta cells that makes them appear foreign to the immune system, which then attacks them via a process of inflammation. By this hypothesis, the problem is not with an immune system which is misdirected to attack itself as has been assumed, but rather with a primary neuropathy which transforms beta cells so as to induce a normal immune system to attack them.
This new concept has intriguing resonances with the discovery that normoglycemic diabetic serum is neurotoxic in vitro to rabbit nerve cells. If diabetes is primarily a neurological disease, then perhaps many of the complications arise not from the high blood sugar which is just one of the spin-off symptoms of the neurological disease attacking the beta cells and interfering with insulin production. Instead, the complications would arise from the continuing neurological disease causing vascular and other changes throughout the body, beyond the initial beta cell attack, during the whole course of the patient's lifetime. The correspondence between the degree of high blood sugar and the rate of development of the complications would then be due, not to the high blood sugar itself being a cause of the complications, but instead to the fact that the worse the neurological attack on the beta cells and their insulin output, the worse the blood sugar level and the neurological attack on the other tissues of the body. A high degree of complications and high blood sugar would then be just two by-products of the same underlying disease, the primary neuropathy, rather than the high blood sugar being the cause of the complications.
Faustman's 'cure' would then only cause the beta cells to regrow, but would not address the root cause of the attack on the beta cells and the complications, which would be the primary neuropathy. Fixing the disordered immune system would repair only one symptom of the neuropathy, but not the neuropathy itself.
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Sanktpauli....
Then it is reasonable to say that because of the existing neuropathy, complications will still occur despite the variable of blood glucose levels.
The difference being, is that hyperglycemia and the longevity of this existing neuropathy(T1DM) will hasten the inevitable Complications.
What a sad/tragic consequence regarding this Disease.
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Brent,
I think your idea aboutthe AKAI water ionizer is an interesting one. I was just introduced to this idea about 2 weeks ago, so it's a new one to me, but one I'm interested in. It seems to me to all go toward the concept of reducing alkalinity and oxidative stress. On your question of what do I think about our diabetes resulting from an "over-active immune response which eventually becomes "overloaded"...I don't know. In my case, I think I set the stage with my diet and lifestyle (zinc deficiency, stress) so when a toxic exposure hit me, my cells couldn't compensate fast enough for the hit, and the zinc deficiency turned to zinc depletion and the hyperglycemia resulted. Is that an "over-active" immune response? I don't think so. I think my cells weren't able to clear the toxin fast enough, severe inflammation resulted and the immune response was correspondingly huge. I think at that time, had a mindful healthcare practitioner guided me into a severely low inflammatory diet (alkaline, omega-3 rich, omega-6 poor, no high fructose corn syrup or other highly inflammatory low pH products, etc.) I could have nursed my cells back to normal function. Instead, the introduction of exogenous insulin and return to my poor eating and stressful ways, just maintained the status quo and it made the "digging out" of the injury that much harder. Couple that with the expectation that you're diabetic for the rest of your life and I was done. I don't think the biggest source of inflammatory response though is "dirty air". I think all of those things you mention - pollens, molds, in particular - are part of our biological ancestry and our bodies are coded and capable of handling that. I think it's that we're in a hole of sorts right now, trying to dig out. Anything anybody's throwing into the hole just makes it that much harder to get out of it. And that's where the exogenous insulin, the dirty air, the low pH foods, the water come in. I think the #1 thing that's feeding the hole though is that we think we can't get out of it. No hope for healing = no healing.
Kelly
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BetterCell,
Please do. You already have my email.
Kelly
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BetterCell,
Interesting post. I was just reading a paper I came across that looks at the
use of an alkaloid extract of fenugreek dried seeds on diabetic rats for 21 days. The results were pretty dramatic, reducing blood glucose values from 280 mg/dL for the diabetic controls to 141 mg/dL for the fenugreek treated rats. They also measured oxidative stress (using TBARS and nitric oxide) and lipids. What was really interesting to me is that the fenugreek normalized the kidney and liver membranes to "more or less control".
Is the breath test you mention something you can pick up at Super Supplements?
Kelly
P.S. the paper I mention is: N. Helmy Abou El-Soud, M.Y. Khalil, Antidiabetic effects of fenugreek alkaloid extractin streptozotocin induced hyperglycemic rats. Journal of Applied Sciences Research, 3(10): 1073-1083, 2007.
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Hi Kelly
The Breathe Test for Qxidative Stress as a result of Diabetes is only available in Research Labs/Hospitals where Breathe analysis is done. Gas
chromatography and mass spectroscopy are used for the measurement.
I will Email the File to you that describes it more in detail and well worth reading.
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Thanks! I also noticed by Googling "oxidative stress home test" that there is a test out there, but it runs about $80.
Kelly
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BetterCell—
Being a T1 who, over the last 3 years, has also been fighting Lyme Disease, I recognize that inflammation caused by the bacteria—added to diabetes—can make ‘normal’ living quite problematic, at times. I have found that an alkaline-charged water producer, Wobenzyme (enzymes), B6-B12 folic acid, and things like tumeric—all make me more ‘comfortable’ while trying to rid myself of a bacteria that has a cell-wall form, a resistant form (which lives within the body’s cells) and a non-cell-wall form—which floats around in the blood stream. Most medical professionals are totally Lyme Disease-ignorant and combined with T1 diabetes symptomology, they usually are at a loss for recommendations. The pragmatic doctor says antibiotic/antibiotic/antibiotic; and when that fails, intravenous antibiotic
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As you probably are aware of Brent, you DEFINITELY should be using a good Probiotic whenever you are on antibiotic treatment and for at least two weeks after.
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Hi Brent,
I have a great referral for you in regards to the Lyme Disease. Please contact me by email. Julie@diabetesdoneright.com
My Best, Julie
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wow.that just about wore me out reading about beta cell destruction,im actually laughing.im a 35 year short type 1 diabetic.in my time ive uncovered certain truths about insulin sales,and almost got someone fired for leaking information.that was the days of letters not internet.in 1984 i found out how much it cost to produce a 10ml bottle of insulin-6 cents!im sure now that insulin is almost an unaffordable commodity,we could never find out.but i bet i could.i wont though.its hard for anyone making trillions of dollars on someone elses misfortune to be caring or truthful,to bad for the powers that be hhmmm.ow ya my name is mark.nice to meet you all!
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Welcome, Mark--
I'm not surprised at the cost of insulin, and the exploitation of those with diabetes. I was re-reading archives from another d-related blog, and the author explained that in the past 10 years, the cost of computers has gone from $2k to less than $1k (comparable features); on the other hand, blood meter strips have risen from $50 to $100. Meter/strips is a more-than $6 Billion/year business.
I was recently investigating foreign-sourced natural insulin; price quoted for a 10 ml vial (retail) was 35-45. A call-back informed me that the price had been expressed in pesos; actual cost $12-$14 a vial.
When Lilly/Novo systematically/cooperatively removed one after another animal insulin from the market, they insured that the U.S. market was totally captive. Whatever insulin or insulin-like material they care to prepare and sell to us, we can (1) take it or (2) leave it (and die). Good choices; ethical business? corporate morality? no . . . just more profit before patients, profit before EVERYTHING!
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ya ,i agree with ya.i have been prodding a few industry heavies,and as soon as i say these testimonies will be published,they wont answer my questions,maybe i should be sly like the big pharma and lie.nope i have pride.i just get fed up with,price increases without reason.example in canada bc.2005 a 10 bag of needles were 2.99 per bag.the next week i went in they were 7.99....?i almost went berzerk.how can these companies get away with murder.now im gonna get back to work on exposing corruption at pharma companys.
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In re Sanktpauli: "There is recent and accumulating evidence" . . .
Can you provide reference information regarding diabetes being initiated by a nervous disease? Some of this appears to be ‘smoke and mirrors’ offered by the medicine men we call doctors because they really—after 80 years—still don’t have a clue. Your explanation provokes the following questions:
What is the possible connection between a nerve disorder and the inflammation it may trigger then targeting the beta cells? This seems as convoluted as shooting my own dog because my neighbor’s dog attacked me.
Do all of these hypotheses related to the next 20 years of research . . . leading down (possibly) blind paths . . . arise because we cannot do anything as simple as checking the 3-dimensional configuration of the insulin molecule produced in a “normal” human body? Whether you call a small-molecule protein a hormone or a polypeptide or consider it merely a chemical composite like aspirin, it would have been so-o-o easy to extract normal human insulin from cadaver pancreases and compare the product to Novolin or Humulin. Instead, we inject normoglycemic diabetic serum into rabbit nerve cells. The fact is, there is nothing ‘normal’ about diabetic serum; and the abnormalities may actually result from the treatment of the disease rather than the disease itself.
It’s my understanding that many T1 diabetics do not regularly go through the ‘honeymoon’ period that once was an accepted interval where the human body was trying to recover from whatever onslaught was affecting the beta cells. Wouldn’t it be acceptable to conclude that the diabetic system—whether responding to neurologic or inflammatory events—was already set up to recognize foreign protein produced by the beta cells; and now, all we have is MORE foreign protein to maintain the disease. Just like the C-peptide, which we now think may be a factor in complications—maybe there are other pancreatic cellular components being destroyed by diabetes.
Is it true that there are other possible sites of endogenous insulin production in the body besides that which is produced in the pancreas? It seems I have read several reports that the brain and the spleen also either produce or have regulatory control over the production of total insulin in the body.
This whole scenario seems like the chicken-and-egg conundrum. Right now, it appears to me, diabetic researchers can’t even differentiate the egg FROM the chicken. Consequently, when we allow/endorse research to be ruled by esoteric semantics instead of returning to basics, and answering long-unaddressed questions, a cure will remain forever around the corner or on the horizon. This is like corporate ‘scientists’ who insist on driving their Hummers to work, donning their lab coats and squandering time and resources as they diligently seek to determine the effect of fly flatulence on global climate change.
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The best statement of this new, contrarian thesis is in A. Lonyai, et al, "Fetal Hox11 Expression Patterns Predict Defective Target Organs," Immunology and Cell Biology, vo. 86, no. 4 (June, 2008) 301-309. It has been found that in mice which naturally develop type 1 diabetes, there are abnormalities in the nerve cells of the cochlea, tongue, salivary glands, and pancreas which precede the expression of beta cell destruction. The theory then is that a perfectly normal mouse immune system attacks these organs simply because of their structural abormality, which makes them look like foreign tissues. The death of the beta cells and the resultant hyperglycemia are then just one symptom of the underlying disease, which is a structural abnormality in the nerves. Thus interventions which restore the beta cells or correct the hyperglycemia won't help, since the complications are being caused by the evolving effects of the structural abnormalities in the nerves over the lifetime of the organism.
An interesting support for this hypothesis comes from the fact that rare cases have been discovered of people with the full range of severe 'diabetic complications, including neuropathy, retinopathy, and generalized athero- and arteriosclerosis, but these people don't have diabetes or any trace of elevated blood sugar. They may just have an extreme version of these genetically determined structural abnormalities which have been able to cause most of the tissues of the body to degenerate over time but which have not, for some reason, affected the beta cells of the pancreas, so there is no high blood sugar. (See Kidney International (1985))
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Sanktpauli.........
Thanks for that lead, A. Lonyai, et al, "Fetal Hox11 Expression Patterns Predict Defective Target Organs," Immunology and Cell Biology, vo. 86, no. 4 (June, 2008) 301-309.
I have just finished reading it and feel that proverbial Door is now opened even more into the etiology of T1DM.
However at the same time the complexity of this disease has increased further.
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Thank you for the interesting week-end reading. This opens up a whole new can of worms that complicates putting together a puzzle with no straight-line, definitive edges. However several questions come to mind:
1) Knowing Dr. Faustman is a childhood genius/prodigy who entered med school as a teenager, I would not take the liberty to second-guess her proceeding with the human CURE she has proposed when her name was also on this research.
2) If genetic predisposition/HOX-11 syndrome is the cause for T1DM's attack on select organs, what determines WHEN the expression of these genes leads to the ultimate destruction of the beta cells? Why do some humans develop diabetes at 3 while others develop it during their teen years or as young adults? Isn't it correct that gene potential is minimized or maximized based on environmental input?
3) If HOX-11 gene expression is truly the 'cause,' I would expect those carrying the genes would be like cystic fibrosis patients, all diagnosed at a very tender age, wouldn't you?
4) Taking a look at the forest rather than at a single tree, I am also wondering why the majority of T1 diabetics around the world are diagnosed in the late fall/winter season of the year? (Southern hemisphere has predominance of spring/summer diagnoses--which, again, is THEIR fall/winter season.)
5) Assuming that since 1956, I've had this genetic predisposition, why haven't I become DEAF, lost salivary components, and the only expression that bothers me is high blood sugars?
6) If this new hypothesis is valid, shouldn't ALL T1 diabetics RAIL at the thought of doctors and diabusinesses making billions of dollars for merely treating high-blood-sugar, which may or may not control the outcome?
7) Doesn't this also point out that ALL of the new synthetic insulin products that are patented and dreadfully expensive, in reality are no better than natural insulins?
8) Then, of course, I still asking (and no one answering)--why can we study genetic abnormalities and identify complexes while we still CANNOT provide an actual 3-dimensional, spatially correct model of human insulin before, during and after diagnosis?
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Since the theory that the immune system is not the initial trigger for diabetes expression is new, of course there are many details of it which have not been worked out. I can suggest a few answers a priori on basic principles, however, pending further experiments.
I suspect that all patients do not express the disease at the same time because they all do not have the same genetic loading with the condition that causes the abnormality in the nervous system. This could then explain why the immune system reacts at different speeds to the foreign tissue signal. Alternatively, since both the abnormality of the nervous system and the immune attack it induces have to cooperate for diabetes to become manifest, the different ages at which people become diabetic could be due to different sensitivities of their immune systems to this apparently foreign tissue.
The clustering of new cases in the autumn months could be the result of colds priming the immune system to become more vigilant and active at that time, so that the immune system finally becomes ready to respond to the neurological abnormalities the patient has inherited. T-cell activation by one stimulus is already known to induce heightened immunological response to other triggers.
The neurological abnormalities Faustman and colleagues found in mice represent just one possible set of genetic alterations to the nervous system, which in mice seems to come to expression mainly in Sjogren's Syndrome with its associated deafness. In type 1 diabetic humans, the panoply of neurological abnormalities may be different, so they are not deaf any more frequently than normal populations. However, they do have a much higher than normal rate of multiple sclerosis, which prior to this new, neurologically focused hypothesis, had no explanation.
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Brent, Sanktpauli,
In regard to the question of the majority of diagnoses occurring in the fall/winter, I'd add a little food for thought: isn't it interesting that this is also the time that most of the antibiotics are administered? In my case, I showed diabetic symptoms 2 days after taking a fluoroquinolone antibiotic. In a recent Canadian study of over a million seniors, the same thing happened to nearly 3% of the people (on just 3 of the drugs from the fluoroquinolone family which are all virtually identical in structure). I wouldn't rule out that in a large percentage of the population manifesting diabetes, that antibiotic exposure was the trigger and the subsequent application of exogenous insulin served to sustain the condition.
Kelly
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Brent.....
"Is it true that there are other possible sites of endogenous insulin production in the body besides that which is produced in the pancreas?"
From a Medical Anthropological POV,
the answer to that question is yes. There are other cultures who have a different concept regarding this Disease.
It is strange that after thousands of years, if not longer(1500 BC) the mystery regarding the Etiology of this Disease remains as elusive as ever.
There is a hole in the Butterfly Catcher's Net.
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hi allie.just wondering if talking about insulins,in this topic is ok,ive used the search but come up with no answers.ive noticed using humalog and lantus that,it causes some type of brain lapse?or i cant think as fast on this insulin,i went for 1 full day eating little as in 1000 calories,and using humulin r,just fast.i noticed heightened brain function,i did this test 3 times in a mnth.and i thought faster and clearer on those days?is it because ive had type1 for 34 years?and a change just heightens my awareness,i dont know.
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I've had the same experience numerous times - the less exogenous insulin I have in my system, the better my brain function, the less my fatigue.
I switched to porcine isophane insulin about 2 months ago. This last couple of weeks, I've been able to minimize using the short acting insulin to just a few units a day - my brain function is definitely improved.
I have no doubt that what you're saying is true.
Kelly
Kelly
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