Question: Hi doctor,



Please read and review carefully the attached .pdf file, detailing my medical case.



(It was originally written for a lawyer, but is still suitable for reading/review by a doctor.)



Following the review of the document, please answer the following questions?



(1) Do you believe it to be clear "beyond a reasonable doubt" that the patient here (myself) has had a legitimate diabetic condition?



(2) Could anything like the scenario written about very briefly at the end of the document happen in your country, or is this likely only something that an XXXXXXX medical system can do?



(It is a little bit of a joke, just this second question.)



(3) What other commentary do you have about this case or situation?



(4) Please engage in the following hypothetical scenario:



(4A) Imagine that the facts presented in this case are presented to you personally. Given all of the evidence and facts taken together, if such a case were shown to you, plus you were the doctor who ordered the three tests mentioned that came back positive for indication of diabetes, is there any justified way you could possibly withhold diagnosis of diabetes without compromising or incurring risk of liability?



(4B) Assuming such a diagnosis is given by you or a reasonable doctor, would this diagnosis stand, or can a diagnosis of diabetes ever be "undiagnosed" as per standard medical belief of "diabetes is uncurable (at least "officially")?



(4C) Assuming such a diagnosis does stand for the long term: then, if after two years of time following, such a patient as myself were to come back and without any tests new tests done, and asks "Am I a diabetic patient?" Would the answer be yes or no?



(4D) If the answer were yes, where would the basis of such a determination come from? Would it come from the fact that you can see a registered diagnosis of diabetes on my file, which itself was based on evidence collected two years ago?



(4E) If the answer is yes, is it therefore the case that by implication, no explicit new evidence is necessary within the preceding two years for me to be considered a legitimate diabetic, due to the fact that the life-long determination was already made by a doctor on this subject two years ago?



(4F) Take a second scenario: let's say a diagnosis was never obtained two years ago. The same patient, after the same two years, comes up to you and shows you the same evidence from two years ago that, two years ago, may have likely secured him a virtually-ensured diagnosis.



Do you believe you are looking today at a "true diabetic?"



(4G) If so, does anything hold you back from making a diagnosis on this individual for "diabetes," based on only this evidence from two years ago?



(4H) If not, then good. If yes, then is the reason for such reluctance merely caused by medical convention?



Also, can we see the irony of the situation how the same person with the same evidence can be treated differently today, based only on how others decided to treat him two years ago, and not based on any actual change in the aggregate sum of existing evidence accompanying this person?



Thank you for your time.

Hi doctor,



Please read and review carefully the attached .pdf file, detailing my medical case.



(It was originally written for a lawyer, but is still suitable for reading/review by a doctor.)



Following the review of the document, please answer the following questions?



(1) Do you believe it to be clear "beyond a reasonable doubt" that the patient here (myself) has had a legitimate diabetic condition?



(2) Could anything like the scenario written about very briefly at the end of the document happen in your country, or is this likely only something that an XXXXXXX medical system can do?



(It is a little bit of a joke, just this second question.)



(3) What other commentary do you have about this case or situation?



(4) Please engage in the following hypothetical scenario:



(4A) Imagine that the facts presented in this case are presented to you personally. Given all of the evidence and facts taken together, if such a case were shown to you, plus you were the doctor who ordered the three tests mentioned that came back positive for indication of diabetes, is there any justified way you could possibly withhold diagnosis of diabetes without compromising or incurring risk of liability?



(4B) Assuming such a diagnosis is given by you or a reasonable doctor, would this diagnosis stand, or can a diagnosis of diabetes ever be "undiagnosed" as per standard medical belief of "diabetes is uncurable (at least "officially")?



(4C) Assuming such a diagnosis does stand for the long term: then, if after two years of time following, such a patient as myself were to come back and without any tests new tests done, and asks "Am I a diabetic patient?" Would the answer be yes or no?



(4D) If the answer were yes, where would the basis of such a determination come from? Would it come from the fact that you can see a registered diagnosis of diabetes on my file, which itself was based on evidence collected two years ago?



(4E) If the answer is yes, is it therefore the case that by implication, no explicit new evidence is necessary within the preceding two years for me to be considered a legitimate diabetic, due to the fact that the life-long determination was already made by a doctor on this subject two years ago?



(4F) Take a second scenario: let's say a diagnosis was never obtained two years ago. The same patient, after the same two years, comes up to you and shows you the same evidence from two years ago that, two years ago, may have likely secured him a virtually-ensured diagnosis.



Do you believe you are looking today at a "true diabetic?"



(4G) If so, does anything hold you back from making a diagnosis on this individual for "diabetes," based on only this evidence from two years ago?



(4H) If not, then good. If yes, then is the reason for such reluctance merely caused by medical convention?



Also, can we see the irony of the situation how the same person with the same evidence can be treated differently today, based only on how others decided to treat him two years ago, and not based on any actual change in the aggregate sum of existing evidence accompanying this person?



Thank you for your time.

Hi,

I am sending the attachment to YYYY@YYYY , "ATTN: Elona Xhardo"

Please read and review carefully the information presented therein, and please let me know what you think. Thank you

Hi,

I am sending the attachment to YYYY@YYYY , "ATTN: Elona Xhardo"

Please read and review carefully the information presented therein, and please let me know what you think. Thank you

Thank you for your response.

There are no stress, familial abnormalities of drugs within the system at that time, 2 years ago.

The only relevant and likely causative factor, was the very *apparent* alcohol-induced pancreatitis and beta-cell damage, as evidenced by the sudden onset of symptoms by that time.

Indeed, in addition to the favorable results of three tests that are correlated with the diabetic condition, the presence of very apparent symptoms, along with their timing, is also high indicative of the shift in the underlying metabolic condition. This is all in addition to multiple privately-measured sugar levels of 200+ done by my.meter, one of which is shown.

Assume that all other test done show levels that are all within the normal reference range. Additionally, the A1C level, measured only one week after the alcohol binge, was also low/normal, as it takes 3 months for any blood sugar issues to manifest.

Adopting the mindset of an investigative frame of mind, is there any reasonable doubt that the underlying metabolic condition of the patient (myself) was that consistent with the genuine (though "artificially-induced/toxin-induced" Type I diabetic condition, at that point in time about two years ago?

(1) If so, what is this doubt based on, that Is not sufficiently mitigated by the several interlocking pieces of evidence, including tests?

(2) If not, and if you have no other access to any additional information, do you believe it is appropriate to acknowledge the apparent diabetic status of the patient by means of rendering an official diagnosis?

(3) In this case, do you believe it is more likely that:
(a) a rendered diagnosis would be a "false positive" of a metabolic dysfunctiom that isnt really present; or, more likely that--
(b) a withheld diagnosis would result in the case of a "false negative," where the non-acknowledged condition had, in fact, been in reality a present condition and altered metabolic dynamic?

Thank you.

Thank you for your response.

There are no stress, familial abnormalities of drugs within the system at that time, 2 years ago.

The only relevant and likely causative factor, was the very *apparent* alcohol-induced pancreatitis and beta-cell damage, as evidenced by the sudden onset of symptoms by that time.

Indeed, in addition to the favorable results of three tests that are correlated with the diabetic condition, the presence of very apparent symptoms, along with their timing, is also high indicative of the shift in the underlying metabolic condition. This is all in addition to multiple privately-measured sugar levels of 200+ done by my.meter, one of which is shown.

Assume that all other test done show levels that are all within the normal reference range. Additionally, the A1C level, measured only one week after the alcohol binge, was also low/normal, as it takes 3 months for any blood sugar issues to manifest.

Adopting the mindset of an investigative frame of mind, is there any reasonable doubt that the underlying metabolic condition of the patient (myself) was that consistent with the genuine (though "artificially-induced/toxin-induced" Type I diabetic condition, at that point in time about two years ago?

(1) If so, what is this doubt based on, that Is not sufficiently mitigated by the several interlocking pieces of evidence, including tests?

(2) If not, and if you have no other access to any additional information, do you believe it is appropriate to acknowledge the apparent diabetic status of the patient by means of rendering an official diagnosis?

(3) In this case, do you believe it is more likely that:
(a) a rendered diagnosis would be a "false positive" of a metabolic dysfunctiom that isnt really present; or, more likely that--
(b) a withheld diagnosis would result in the case of a "false negative," where the non-acknowledged condition had, in fact, been in reality a present condition and altered metabolic dynamic?

Thank you.

Sending attachment via email as response

Sending attachment via email as response

Okay, may send soon if you have not received

Okay, may send soon if you have not received

The full response of mine to your most recent message is posted below.

* * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * *

You are correct, in that my condition has improved drastically within the last two years.

Today, I cannot get my blood sugar up to 200+, even after consuming hundreds of grams of sugar--whether dextrose or glucose.

You are also correct in distinguishing the effects of an "acute" form of pancreatitis, and differentiating this from the "true" or at least “native” type of diabetic condition, which is a metabolic condition which is generally chronic in nature.

However, the answer may not be perfect--please allow me to pose my explanation as to why.

Firstly, the assumed chronic nature of diabetes is only as "chronic" as their underlying causative factors. For Type II, the underlying factor is, primarily, insulin resistance—it may be chronic if the insulin receptivity is kept low, or it may be reversed once insulin sensitivity is restored.



…



For all intents and purposes, Diabetes is—and always has been—a disease of definition.



At the source, diabetes is a dysfunction of insulin transmission. It occurs along a spectrum, with the primary result and measure of its progress being extracellular concentrations of blood sugar.



In a diagnostic, binary-minded system, such a smooth spectrum must be cut in the middle at some place—the diagnostic threshold.



At the diagnostic level, “diabetes” can be equivalently translated and replaced by the words “condition of metabolic imbalance permitting ‘sugar-levels-above-200-and-accompanied-by-classical-symptoms’.”



Hyperglycemia is in fact needed to be a Type 1 Diabetic—and that level of high sugar is already predefined by the diagnostic criteria, as being exactly 200, and no other number besides 200.



There is no other criteria; there are no other exceptions. Very smart people, a long time ago, set the definitions and criteria very specifically and carefully, so as to—



(1) not include people that were inappropriate to include, and also to—

(2) not exclude people that should be included. 



If, in their wisdom, they decided to set additional parameters or conditions, they would have stated something very clear to do so. It might have been: “If the blood sugar goes over 200 then it is diabetes—unless, we are dealing with the case where he doesn’t always need insulin shots and his blood sugar isn’t THAT much higher than 200 most of the time—in which case, nevermind, we won’t call that case diabetes, we’ll ignore it and pretend there’s no sugar- or insulin-based dysfunction at all within that person’s system.”



No, this wouldn’t make sense. There’s no special exceptions.



This never happened. And, this has never happened for a reason—it is because all diagnostic criteria for diabetes is fulfilled as soon as blood sugar is able to cross above 200 as an apparent result of the dysregulation of insulin transmission, particularly when supported by any additional classical symptoms of the disease.



You and I both obviously recognize that Type I diabetes is a form of diabetes caused by beta-cell dysfunction and destruction.



Normally, the cause of beta-cell destruction in those people who are normally diagnosed with Type I, is a cause of destruction that we consider to be autoimmune.



However, there are other causes of beta-cell destruction. One of them is toxins—whether the toxin is ethanol/alcohol, or any other kind of chemical that, in large enough amounts, can produce beta-cell damage, they produce the same effect that one’s own diabetic-inducing autoimmune condition does. This is very important.



Besides ethanol/alcohol, another toxin that can cause beta-cell damage at the right dose, is known as Streptozotocin. In experiments, they give these to rats (who are not naturally born with Type I Diabetes-associated autoimmune disorder, of course). Once the toxin is administered, however, their beta cells are destroyed—just as with ethanol for both rats and humans. At this point, do they call these rats as animals that are afflicted just with “acute pancreatitis?” No. Do they call them “not-real-Type 1,” or “Special third type?” No. They call them exactly what they are: rats who now have “artificially-induced T1DM”; at this point, experiments can be carried out on the rats, who are classified as having Type I diabetes.



“Diabetes was induced in 12-month old 3xTg mice using streptozotocin (STZ; 90 mg/kg, i.p., on two successive days). Hyperglycemia was verified by sampling blood glucose levels.

From the study 'Experimentally induced diabetes worsens neuropathology, but not learning and memory, in middle aged 3xTg mice':


“In this study, we used DTI to assess brain abnormalities in a rat model of STZ-induced type 1 diabetes at 4 weeks after induction.” 

From another study, 

“Type 1 diabetes was induced by a single intraperitoneal injection of 45 mg/kg body weight of Streptozotocin … to the overnight fasted rats. Control rats were injected with vehicle alone. Diabetes was confirmed at 72 h post STZ injection, by testing the blood glucose level …”



From another article,

 “Alloxan and streptozotocin (STZ) are widely used for producing artificially induced T1DM"



These are scientists and doctors narrating official published peer-reviewed studies--doctors who have to use words carefully. If there were any debate or controversy at all about calling these rodents Type 1 diabetics, those statements would not have been published, and the premise of these studies would have been undermined.



Granted, in these experiments, we know that the source of the diabetic condition is not autoimmune. Therefore, the immune system will not continuously attack the regenerating beta-cells of the rats, and within several months to a couple years, the rats would have regenerated beta cell functionality.



But so what? During that window of time, they were still functionally diabetic.


It is no question that they have diabetes; moreover, they would not be classified as having Type 2 diabetes, for the reason that insulin resistance is not the cause of their hyperglycemia.



For the same reason, it is no question that I had diabetes—and, just like the rats, I would not be classified or suspected as having Type 2 diabetes—which is the only other kind that there is! This is for the reason that insulin resistance is not the apparent cause of my hyperglycemia… It was ethanol-induced beat-cell destruction that was the cause of my hyperglycemia. Thus, this is the perfect living definition of a Type-1 diabetic state.



Type 1 debates is, definitely, “insulin shortage, resulting in hyperglycemia”
Type 2 diabetes is, definitely, “insulin receptor downregulation (decreasd sensitvity), resulting in hyperglycemia”



For humans, hyperglycemia is 200.



In humans, the only difference is that those who have “native” type 1, sourced by an autoimmune disorder, are rarely able to escape the effects of chronic beta-cell destruction.



The criteria does not depend on how much insulin you think you should receive—or even how much insulin you produce!



This would not make sense. There is uniform and perfect consistency to the diagnostic.



(Interesting note: For both the rats as well as myself, autophagy—the state of fasting—is able to quickly regenerate the beta-cells, curing the source of the problem for those who have an artificially-induced type.)


…




***What I think you mean to say, therefore, in distinguishing my type of diabetes from the standard type of diabetes, is that my form of Type 1 diabetes was of the “artifically-induced” or “toxin-induced” variety of type 1, as opposed to the standard, “natural” variety of Type 1.***

It is also not true that “all diabetics who are Type I must have insulin to survive

.

Three pieces of critical information or statistics to support this:


(1) 75% of Type 1 diabetics produce insulin;

 (2) 50% or more of those diagnosed as Type 1 diabetics can “survive” without insulin (with average diagnostic age of 14, they obviously survived 3 sugary meals a day for 14 years without insulin); and,

(3) My fasting insulin level on the test was lower than the average insulin level of newly-diagnosed Type 1 diabetics in the study cited within my original document.



There are only two types of diabetes (one of insulin-shortage, the other of insulin resistance), and all forms of diabetes must either be one or the other (that is, all instances of blood sugar ever reaching 200+ at any time, must be the result of either a decrease of insulin receptor sensitivity, or a decrease of insulin substance).



Was I able to reach blood sugar of over 200 (with other classic symptoms present, such as sweet-smelling urine, tingling of the feet exacerbated by sugar and/or neuropathy, and others)?



If yes, then it is a diabetic condition; furthermore—



—Was the elevated blood sugar caused primarily by a decrease insulin receptor sensitivity? Or a decrease in insulin substance?



If caused by a decrease in receptor sensitivity/density, then it is Type II; if caused by lowered insulin concentrations and lowered production capacity—whatever the cause of that reduction—then it is called Type 1 diabetes just the same.



Once again, whether the Type 1 diabetes is autoimmune-sourced in its nature, or toxic-damage-sourced in its nature—whether it requires a little insulin to prevent dying, a lot of insulin to prevent dying, or whether the organism can survive without insulin, while simply living with higher blood sugar (meaning, above 200).



There is no diagnostic criteria for any other type, classification or level. There is no level within diabetes that is higher than 200 with any practical differentiation of criteria. You are not a “real” Type I diabetic only once you start taking insulin—or only once your condition is bad enough that you truly do require insulin to survive. There’s no higher number beyond 200 to differentiate the “technical”diabetics from the “real” diabetics.



To summarize:

If there is,



(1) blood sugar over 200, which is primarily caused by

(2) a lowered insulin production capacity,



then the patient is a Type I diabetic, regardless of:


(1) whether the condition is caused by an autoimmune disorder or a toxic exposure;

(2) whether the patient needs a little insulin, a lot of insulin, or no insulin to function without a medical crisis; or,

 (3) whether the diabetes is reversible or not reversible on its own within 2 years.



In hindsight, it therefore does make sense to got his “full step” and acknowledge the former condition of mine as having been Type 1 diabetic. The alternative, as you posed, would be to call it acute pancreatitis. However, is it possible to have acute pancreatitis without exhibiting the manifestations of the dysfunction of insulin transmission?



The answer is yes. Therefore, such a diagnosis would not be specific enough, because in addition to the diagnosed condition of acute pancreatitis, there are additional features resembling a metabolic- and insulin-based dysfunction that are not being identified sufficiently.



The proper diagnosis would, therefore, be “Type I diabetes secondary to acute pancreatitis.” Then, can be undiagnosed in future when the beta-cells regrow. (Look up studies on fasting mice for reversing Type 1 (3 fasts of 5-consecutive days each, over the period of 3 months, and the mice in that experimental fasting group lost their Type 1 diabetic status, compared to the control group which was still diabetic)—it is exactly what I did to fix my beta-cell function over the last two years : D



“Type 1 diabetes not possible in your case,” is not an accurate statement. We need to be careful with our words as clinicians. Too often I have seen doctors use the word “not possible,” when they are only one subtle turn of evidence or perspective away from realizing “the impossible.” It is only human impression, when we have not processed like computer brain all the technicalities of the equation. Very, very few things are truly impossible.



You said “Exactly” to beta cell destruction—but the truth is, from a practical standpoint, beta-cell destruction essentially is Type 1 diabetes, as you cannot have one without the other.



…




What are your thoughts? Do you disagree, or do you find merit and strength in the points and arguments made?



What might your colleagues and superiors say? Please feel free any and all of these documents with any colleagues or superiors to get their opinion as well. I would be curious to hear it as well.

The full response of mine to your most recent message is posted below.

* * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * *

You are correct, in that my condition has improved drastically within the last two years.

Today, I cannot get my blood sugar up to 200+, even after consuming hundreds of grams of sugar--whether dextrose or glucose.

You are also correct in distinguishing the effects of an "acute" form of pancreatitis, and differentiating this from the "true" or at least “native” type of diabetic condition, which is a metabolic condition which is generally chronic in nature.

However, the answer may not be perfect--please allow me to pose my explanation as to why.

Firstly, the assumed chronic nature of diabetes is only as "chronic" as their underlying causative factors. For Type II, the underlying factor is, primarily, insulin resistance—it may be chronic if the insulin receptivity is kept low, or it may be reversed once insulin sensitivity is restored.



…



For all intents and purposes, Diabetes is—and always has been—a disease of definition.



At the source, diabetes is a dysfunction of insulin transmission. It occurs along a spectrum, with the primary result and measure of its progress being extracellular concentrations of blood sugar.



In a diagnostic, binary-minded system, such a smooth spectrum must be cut in the middle at some place—the diagnostic threshold.



At the diagnostic level, “diabetes” can be equivalently translated and replaced by the words “condition of metabolic imbalance permitting ‘sugar-levels-above-200-and-accompanied-by-classical-symptoms’.”



Hyperglycemia is in fact needed to be a Type 1 Diabetic—and that level of high sugar is already predefined by the diagnostic criteria, as being exactly 200, and no other number besides 200.



There is no other criteria; there are no other exceptions. Very smart people, a long time ago, set the definitions and criteria very specifically and carefully, so as to—



(1) not include people that were inappropriate to include, and also to—

(2) not exclude people that should be included. 



If, in their wisdom, they decided to set additional parameters or conditions, they would have stated something very clear to do so. It might have been: “If the blood sugar goes over 200 then it is diabetes—unless, we are dealing with the case where he doesn’t always need insulin shots and his blood sugar isn’t THAT much higher than 200 most of the time—in which case, nevermind, we won’t call that case diabetes, we’ll ignore it and pretend there’s no sugar- or insulin-based dysfunction at all within that person’s system.”



No, this wouldn’t make sense. There’s no special exceptions.



This never happened. And, this has never happened for a reason—it is because all diagnostic criteria for diabetes is fulfilled as soon as blood sugar is able to cross above 200 as an apparent result of the dysregulation of insulin transmission, particularly when supported by any additional classical symptoms of the disease.



You and I both obviously recognize that Type I diabetes is a form of diabetes caused by beta-cell dysfunction and destruction.



Normally, the cause of beta-cell destruction in those people who are normally diagnosed with Type I, is a cause of destruction that we consider to be autoimmune.



However, there are other causes of beta-cell destruction. One of them is toxins—whether the toxin is ethanol/alcohol, or any other kind of chemical that, in large enough amounts, can produce beta-cell damage, they produce the same effect that one’s own diabetic-inducing autoimmune condition does. This is very important.



Besides ethanol/alcohol, another toxin that can cause beta-cell damage at the right dose, is known as Streptozotocin. In experiments, they give these to rats (who are not naturally born with Type I Diabetes-associated autoimmune disorder, of course). Once the toxin is administered, however, their beta cells are destroyed—just as with ethanol for both rats and humans. At this point, do they call these rats as animals that are afflicted just with “acute pancreatitis?” No. Do they call them “not-real-Type 1,” or “Special third type?” No. They call them exactly what they are: rats who now have “artificially-induced T1DM”; at this point, experiments can be carried out on the rats, who are classified as having Type I diabetes.



“Diabetes was induced in 12-month old 3xTg mice using streptozotocin (STZ; 90 mg/kg, i.p., on two successive days). Hyperglycemia was verified by sampling blood glucose levels.

From the study 'Experimentally induced diabetes worsens neuropathology, but not learning and memory, in middle aged 3xTg mice':


“In this study, we used DTI to assess brain abnormalities in a rat model of STZ-induced type 1 diabetes at 4 weeks after induction.” 

From another study, 

“Type 1 diabetes was induced by a single intraperitoneal injection of 45 mg/kg body weight of Streptozotocin … to the overnight fasted rats. Control rats were injected with vehicle alone. Diabetes was confirmed at 72 h post STZ injection, by testing the blood glucose level …”



From another article,

 “Alloxan and streptozotocin (STZ) are widely used for producing artificially induced T1DM"



These are scientists and doctors narrating official published peer-reviewed studies--doctors who have to use words carefully. If there were any debate or controversy at all about calling these rodents Type 1 diabetics, those statements would not have been published, and the premise of these studies would have been undermined.



Granted, in these experiments, we know that the source of the diabetic condition is not autoimmune. Therefore, the immune system will not continuously attack the regenerating beta-cells of the rats, and within several months to a couple years, the rats would have regenerated beta cell functionality.



But so what? During that window of time, they were still functionally diabetic.


It is no question that they have diabetes; moreover, they would not be classified as having Type 2 diabetes, for the reason that insulin resistance is not the cause of their hyperglycemia.



For the same reason, it is no question that I had diabetes—and, just like the rats, I would not be classified or suspected as having Type 2 diabetes—which is the only other kind that there is! This is for the reason that insulin resistance is not the apparent cause of my hyperglycemia… It was ethanol-induced beat-cell destruction that was the cause of my hyperglycemia. Thus, this is the perfect living definition of a Type-1 diabetic state.



Type 1 debates is, definitely, “insulin shortage, resulting in hyperglycemia”
Type 2 diabetes is, definitely, “insulin receptor downregulation (decreasd sensitvity), resulting in hyperglycemia”



For humans, hyperglycemia is 200.



In humans, the only difference is that those who have “native” type 1, sourced by an autoimmune disorder, are rarely able to escape the effects of chronic beta-cell destruction.



The criteria does not depend on how much insulin you think you should receive—or even how much insulin you produce!



This would not make sense. There is uniform and perfect consistency to the diagnostic.



(Interesting note: For both the rats as well as myself, autophagy—the state of fasting—is able to quickly regenerate the beta-cells, curing the source of the problem for those who have an artificially-induced type.)


…




***What I think you mean to say, therefore, in distinguishing my type of diabetes from the standard type of diabetes, is that my form of Type 1 diabetes was of the “artifically-induced” or “toxin-induced” variety of type 1, as opposed to the standard, “natural” variety of Type 1.***

It is also not true that “all diabetics who are Type I must have insulin to survive

.

Three pieces of critical information or statistics to support this:


(1) 75% of Type 1 diabetics produce insulin;

 (2) 50% or more of those diagnosed as Type 1 diabetics can “survive” without insulin (with average diagnostic age of 14, they obviously survived 3 sugary meals a day for 14 years without insulin); and,

(3) My fasting insulin level on the test was lower than the average insulin level of newly-diagnosed Type 1 diabetics in the study cited within my original document.



There are only two types of diabetes (one of insulin-shortage, the other of insulin resistance), and all forms of diabetes must either be one or the other (that is, all instances of blood sugar ever reaching 200+ at any time, must be the result of either a decrease of insulin receptor sensitivity, or a decrease of insulin substance).



Was I able to reach blood sugar of over 200 (with other classic symptoms present, such as sweet-smelling urine, tingling of the feet exacerbated by sugar and/or neuropathy, and others)?



If yes, then it is a diabetic condition; furthermore—



—Was the elevated blood sugar caused primarily by a decrease insulin receptor sensitivity? Or a decrease in insulin substance?



If caused by a decrease in receptor sensitivity/density, then it is Type II; if caused by lowered insulin concentrations and lowered production capacity—whatever the cause of that reduction—then it is called Type 1 diabetes just the same.



Once again, whether the Type 1 diabetes is autoimmune-sourced in its nature, or toxic-damage-sourced in its nature—whether it requires a little insulin to prevent dying, a lot of insulin to prevent dying, or whether the organism can survive without insulin, while simply living with higher blood sugar (meaning, above 200).



There is no diagnostic criteria for any other type, classification or level. There is no level within diabetes that is higher than 200 with any practical differentiation of criteria. You are not a “real” Type I diabetic only once you start taking insulin—or only once your condition is bad enough that you truly do require insulin to survive. There’s no higher number beyond 200 to differentiate the “technical”diabetics from the “real” diabetics.



To summarize:

If there is,



(1) blood sugar over 200, which is primarily caused by

(2) a lowered insulin production capacity,



then the patient is a Type I diabetic, regardless of:


(1) whether the condition is caused by an autoimmune disorder or a toxic exposure;

(2) whether the patient needs a little insulin, a lot of insulin, or no insulin to function without a medical crisis; or,

 (3) whether the diabetes is reversible or not reversible on its own within 2 years.



In hindsight, it therefore does make sense to got his “full step” and acknowledge the former condition of mine as having been Type 1 diabetic. The alternative, as you posed, would be to call it acute pancreatitis. However, is it possible to have acute pancreatitis without exhibiting the manifestations of the dysfunction of insulin transmission?



The answer is yes. Therefore, such a diagnosis would not be specific enough, because in addition to the diagnosed condition of acute pancreatitis, there are additional features resembling a metabolic- and insulin-based dysfunction that are not being identified sufficiently.



The proper diagnosis would, therefore, be “Type I diabetes secondary to acute pancreatitis.” Then, can be undiagnosed in future when the beta-cells regrow. (Look up studies on fasting mice for reversing Type 1 (3 fasts of 5-consecutive days each, over the period of 3 months, and the mice in that experimental fasting group lost their Type 1 diabetic status, compared to the control group which was still diabetic)—it is exactly what I did to fix my beta-cell function over the last two years : D



“Type 1 diabetes not possible in your case,” is not an accurate statement. We need to be careful with our words as clinicians. Too often I have seen doctors use the word “not possible,” when they are only one subtle turn of evidence or perspective away from realizing “the impossible.” It is only human impression, when we have not processed like computer brain all the technicalities of the equation. Very, very few things are truly impossible.



You said “Exactly” to beta cell destruction—but the truth is, from a practical standpoint, beta-cell destruction essentially is Type 1 diabetes, as you cannot have one without the other.



…




What are your thoughts? Do you disagree, or do you find merit and strength in the points and arguments made?



What might your colleagues and superiors say? Please feel free any and all of these documents with any colleagues or superiors to get their opinion as well. I would be curious to hear it as well.