(May 17, 2010; updated July 24, 2010, January 14, 2011, March 2, 2015, April 28, 2015,
      major revision / new version on June 21, 2015; 
updated August 6, 2015, August 28, 2015,
      September 11, 2015, October 10, 2015, January 4, 2016, January 23, 2016,
  January 28, 2016,
      major addition - Type Profile tables added, on April 9, 2016; updated April 22, 2016,
      July 28, 2016, December 13, 2016, May 18, 2017
)
The title graphic above, the following graphic, the table at the end of this article, and the contents within this article combine to present a logical, well-reasoned, and convincing case supporting new names for
  • the seven disparate types of High Glucose Conditions which currently are oft-times called diabetes, with persons having any of the conditions oft-times called diabetic (diabetes / diabetic, old outdated names), which confuses and misleads because when those terms are used without a clarifier, they most often only apply to only one of the High Glucose Conditions, and which one is oft-times unknown

  • one non-glucose anomaly, diabetes insipidus, which can also go by the old diabetes name, with persons having this condition oft-times called the old diabetic name, which confuses and misleads because those terms are often used to only apply to one, some, or all of the High Glucose Conditions

  • the one low glucose condition which doesn't have the old diabetes name in its current name, but which has a name (reactive hypoglycemia) which confuses and misleads because it doesn't result from any reaction to any medication used to treat any of the High Glucose Conditions

January 4, 2016

Signficant Progress Achieved
 
At last, a sign of progress in my campaign to end the use of the "diabetes" and "diabetic" words.

Well, at least one of the changes I've been advocating since 2010 has finally been accepted by the American Diabetes Association, ending the use of the word "diabetic" being used to describe those who have any of the High Glucose Conditions:

- - -
American Diabetes Association
Standards of Medical Care in Diabetes -- 2016

- - -
 
Excerpt:

...

GENERAL CHANGES

In alignment with the American Diabetes Association's (ADA's) position that diabetes does not define people, the word "diabetic" will no longer be used when referring to individuals with diabetes in the "Standards of Medical Care in Diabetes."

...

 - - - end excerpt - - -


Preface:

I've had Insulinitis (old name: type 1 diabetes) for over 55 years, since I got it in March of 1961, at the age of 5. Since 2010,  I've been lobbying for name changes for all of the Diabetes Bubble conditions mentioned above, for multiple reasons, as explained below.

In addition to this enlightening article, to catch up on the recent research into curing or improving the treatments for any of the glucose anomalies, click the graphic link below to access the most recent research information with web research news which uses the old diabetes / diabetic / reactive hypoglycemia vernacular, but at  the following website they have been paraphrased / translated to totally use the new words for glucose anomalies.

This endeavor promotes bursting the diabetes bubble while providing revelations, hope, and encouragement to everyone who has any of the glucose anomalies, who has friends or family members with any of the glucose anomalies, or who is at risk for coming down with any of the glucose anomalies (and that, unfortunately, includes everyone).







The Problem?

Name changes for old outdated diabetes and diabetic words are desperately needed to eliminate the confusion and misleading that transpires when those words are used without clarifiers, which often happens. The following graphic depicts the way in which those two words dominate the descriptions of the conditions in small print in the center, oft-times without clarifying which condition is being described.

How can you tell which of the disparate conditions is being referred to when the exact name for the condition is left off? Oft-times, you can't, and you can only guess at what's actually being referred to, lending itself to confusion, misleading, and misinforming due to the anachronistic, outdated, and unreliable nature of the entire diabetes / diabetic nomenclature:



To those who don't think there's a problem or who are unaware that there's any problem, you will either find reassurance in the following, or you will find the following "Don't Change Anything" area disconcerting.





Don't Change Anything - Keep Things Exactly As They Are

Prior to reading my proposals for name changes, you may be thinking why not leave things the way they are, what's wrong with the way things are, why not leave well enough alone? Back in 2010, I addressed those concerns, and came up with the following powerful reasons many folks might have for leaving things just the way they are and have been for the close to 1,900 years since the old diabetes and diabetic words were first used.



Don't Change Anything - Keep Things Exactly As They Are

  1. The Power of Optional Exactitude for any High Glucose (and one normal glucose) Condition

    You can iterate the nature of the condition, exactly, by simply using clarifying words (long list), and don't worry if the long
    words are misleading or not well understood or left off (as often happens), that would simply lend itself to the ideas expressed in reason '2' which follows:
type 1 diabetes
juvenile diabetes
insulin dependent diabetes
prediabetes
type 2 diabetes
adult diabetes
non-insulin dependent diabetes
maturity onset diabetes of the young
latent autoimmune diabetes
gestational diabetes
neonatal diabetes
diabetes mellitus
other diabetes mellitus
diabetes insipidus

  1. The Power of Fuzzing Out / Confusing / Misleading

    You can refer to all High
    Glucose Conditions and one normal glucose condition or to any single condition (see reason '1') by using a single word.  However, when using the word, many ignore the non-glucose condition, and use it as if the word only applies to High Glucose Conditions.

    How can one tell what you're referring to? Most often, they can't, and they just have to guess when you use
    a single word for all or any High Glucose and/or one normal glucose condition, and oft-times no one will know the condition or conditions you're talking about for sure (all, only all High Glucose Conditions, or only some or one of the conditions, and which ones or one, good luck on figuring that out).
Think of it as kind of a code, where the word can and will mean different things to different people, and you can use it for any / all of the conditions listed in reason '1', kind of like a work of art, it's simply a matter of interpretation, isn't vagueness grand?

diabetes
diabetic
  1. The Power of Long-Lived Training / Supporting the Way Things Are

    Into conformity? Into
    close-minded thinking? Into the way things are? Averse to change? Fearful of radical revolutionary notions? Love to castigate clarity and freethought and open-mindedness and reliability as unwelcome?

    Love to stick your head in the
    sand, resistant to change? Not to worry, reasons '1' and '2' give you that power. Stay with it, ignore all the disadvantages of it, close your minds, stay with the way things are no matter what. Feel the power, what a rush.
  1. The Power of Old Diabetes and Diabetic Words in Dictionaries Focused on Urination, Not Causes / Not Treatments / Not Risks

    For
    close to the first 1,800 years of the about 1,900 years the diabetes and diabetic words have been used, folks had no clue regarding disparate causalities, disparate treatments, or disparate risks.
The diabetes and diabetic words, as presented in the definition in most common dictionaries, has nothing whatsoever to do with any of that. What's the common theme in the dictionaries? Excessive urination, basically all that was known about the conditions until the last 100 years.

Don't you really like having a condition / disease named for excessive urination? Isn't it a relief not having to read about causes or treatments or risks when looking up the word up in a dictionary and which is focused on a symptom that's not even present when treatments work?

Thank goodness the diabetes and diabetic words are still around, and widely used,  especially considering the way the exact clarifier (type) is frequently left off - see reason '2'.
  1. The Power of Built-in Direct or Implied Support of Almost Everyone

    Heck, since almost everyone is into reasons '1' and '2' above, having been trained to think that way since birth, and since all of the powerful organizations set up to fight one or more of these conditions has the core word in their club name, easy for folks to feel the power of reason '3'.
Easy for folks to resist the cumbersome changes that would be required if new words fixed the areas of reasons '1' and '2' that are problematic. Easy to just go along with the overwhelming majority, not stick one's neck out, to ignore the problems presented in reasons '1' and '2', and to reject the fixes for the problems.

Heck, it's kind of like rejecting someone saying "The emperor has no clothes." Sure, the emperor has no clothes, but why not just go along with the emperor pretending he's well-dressed?

After
all, almost everyone else is, including doctors and most of the persons who have the conditions, so the fact that the emperor has no clothes, who cares, why stick one's neck out, why join yours truly, why risk change, why fix a problem that almost everyone else doesn't even admit is a problem (and even if they do in their heart of hearts, they're doing a good job of pretending they don't)?
  1. The Power of the Internet / Media / Books Support for the Way Things Are

    Change is exceedingly difficult in most cases. Since the old way of talking about the condition(s) has been around so long (about 1,900 years) almost everything available (in print and via the internet) uses the old way of talking about things.
Heck, even yours truly, when I post internet articles about the conditions, I'm hard-pressed to avoid referencing the old lingo as it's everywhere, it's habit, it's unstoppable, it cannot be changed, not by anyone (well, other than yours truly who, some would say, has deluded himself into believing it can be changed), not by any doctor, not by any leader, not by any group (especially not by any group that has diabetes in its name), it's endemic in the medical field and ubiquitous and permanently deeply embedded in our culture, as solid as a rock!

Of course, I'd have to admit, even a rock will erode over time, but heck, why speed up the process? Resist, refuse to change, stick with the way things are and have been for close to 1,900 years, don't think, just go along, don't act as if you can actually control or influence the way things are, don't for one second believe you can actually make one iota of a difference, just accept it, and deal with it as if absolutely nothing ever can or ever should be done about it.

Or, on the other hand, for those open to change, see the following.





The Problem Put in a Different Way

Put in a different way that those discomforted by the above "Don't Change Anything" area can relate to.

Often, the old diabetes or diabetic word is used to describe only one of the types of diabetes, but which type is not iterated. This common practice misleads and confuses when the old word is only applying to one of the conditions but not the others, and that occurs frequently.

Since the practice of leaving off the exact type oft-times occurs (i.e., using the old diabetes or diabetic word without clarifying which type or types is actually being discussed), it's difficult or impossible to know if all High Glucose Conditions, only one of the many High Glucose Conditions (and not any of the others), a non-glucose anomaly, or some of the conditions (but not others) is / are actually being referred to.

The old diabetes and diabetic words without any clarifier, they originated over 1,900 years ago in a day and age of ignorance regarding the disparate conditions and their disparate causalities, ignorance of the existence of insulin as vital to life, and ignorance of all medications currently used to deal with each of the conditions (all of which were discovered in the past 100 years).

However, the risks of having any of the conditions formerly called diabetes (in children, a rapid descent into ever-worsening health and death, and in adults, a slow descent into ever-worsening health and death) were well-known. The exception to that, the diabetes insipidus condition.




The Solution?

New, modern, clarifying, distinct, appropriate non-misleading non-diabetes and non-diabetic names for each of the widely disparate conditions which have much more in the way of differences than in what they have in common:
  • disparate causalities

  • disparate treatments

  • disparate risks
The solution will
  • End the misleading and confusion caused by the predominant use of the old diabetes and diabetic words without clarifying exactly which type of condition one is referring to

  • Clearly indicate the exact disparate causality, the exact disparate treatments, and the exact disparate risks in having each of the disparate conditions

  • Raise esteem

  • End antiquated misconceptions

  • Separate distinctly disparate conditions into separate clearly distinguishable names

  • Modernize terminology based on all we've learned about the disparate natures of each of the glucose anomalies in the last 100 years








New Terminology for conditions which formerly included the word diabetes, and a new name for reactive hypoglycemia




Insulinitis (Islit)

(formerly called type 1 diabetes or juvenile diabetes or
insulin dependent diabetes or confusingly,
when used without clarifier, diabetes)


Autoimmune destruction of pancreas beta cells (Insulitis, an existing word which rarely is mentioned, unfortunately, as this word marks the condition of Insulinitis as unique in its causality compared to other High Glucose Conditions), or destruction of insulin production due to non-Insulitis causes (such as a malignant pancreatic cancer, a severe case of pancreatitis, or a severe pancreatic wound).

Insulitis (dictionary definition):
 

invasion of the pancreatic islets of Langerhans by lymphocytes that produces an inflammatory or autoimmune response and results in destruction of the beta cells of the pancreas

The itis (dictionary definition) part of both the existing Insulitis word and the new Insulinitis word:
 
a suffix used in pathological terms that denote inflammation of an organ and hence, in extended senses, nouns denoting abnormal states or conditions, excesses, tendencies, obsessions, etc. (telephonitis; baseballitis).


Insulinitis Causality Profile
Insulitis (The Role of Inflammation in Insulitis and β‑cell loss in Insulinitis)
In the overwhelming majority (but not all, see other conditions below, some of which involve Insulitis, others which don't) of Insulinitis cases, invasion of the pancreatic islets of Langerhans by lymphocytes produces an inflammatory or autoimmune response, resulting in total or near-total destruction of the beta cells of the pancreas (rapid, over weeks to months, or slow, over years, the condition of Latent Autoimmune Insulinitis).

Insulitis Insulinitis is a polygenetic disease caused by progressive autoimmune infiltration (Insulitis) of the pancreatic Islets of Langerhans, culminating in the destruction of insulin - producing β cells. Genome scans of families with Insulitis Insulinitis suggest that multiple loci make incremental contributions to disease susceptibility.

Genetics / Geography
One's relatives and one's birthplace dramatically impact one's risk of getting the Insulitis-caused type of Insulinitis; however, one can get it even if one has no relatives who have it, and even if one is born in a low-risk area
  • If anyone among your blood relatives has the type of Insulinitis caused by Insulitis, your risk of getting it are increased, the closer the relationship, the higher the increased risk

  • Insulinitis incidence (childhood onset under age 14) is very low (less than 8 cases per 100,000 per year) in Mexico, Central America, South America, sub-Saharan Africa, Asia, Japan, and much of the Middle East, moderately high (from 8 to 20 cases per 100,000 per year) in the United States, central and most of southern Europe, northern Africa and Saudi Arabia, and highest (more than 20 cases per 100,000 per year) in Scandinavia, England, the Italian island of Sardinia, Canada, Australia, and New Zealand; data regarding onset at older ages is difficult to track down
Other Conditions
When the condition or drug causes total or near-total loss of insulin production, as documented in the provided links, Insulinitis results
  • Congenital Rubella, Insulinitis in about 20% of persons with this condition

  • Down's Syndrome, results in a four-fold increase in Insulinitis compared to the general population

  • Pentamidine, which is used to treat Pneumocystis Jiroveci Pneumonia and which may have direct toxic effects on pancreatic beta cells, causing Insulinitis

  • Stiff Person Syndrome, Insulinitis in about 35% of persons with this condition

  • Pancreatitis, Insulinitis if insulin production is totally or near-totally reduced due to chronic pancreatitis

  • Trauma / Pancreatectomy, reasons total pancreatectomies (removal of the pancreas via surgery, causing Insulinitis) may be done include trauma (example: gunshot wound to the pancreas), unmanageable pain from pancreas inflammation due to pancreatitis, certain types of cancer or tumors, and a family history of pancreatic cancer;

    a total or near-total pancreatectomy may result in a total or near-total loss of insulin production (Insulinitis in which Insulitis is not involved)

    in patients without Insulinitis prior to a total pancreatectomy, a pancreatic islet auto-transplantation (in patients with severe and chronic or long lasting pancreatitis that cannot be managed by other treatments) may be done after a total pancreatectomy to try to prevent Insulinitis

  • Turner Syndrome, women have a moderately increased risk of Insulinitis in childhood (also, for those who don't have Insulinitis, a substantially increased risk of Cellosis by adulthood)

  • Vacor - Pyrinuron - Pyriminil (rodenticide poison), Insulinitis results in humans who survive poisoning, suspended for commercial distribution in the U.S. in 1979, can destroy pancreatic beta  cells; when released, in 1975, it killed 20 people within 30 days of its introduction

  • Wolfram Syndrome, onset is at age 6 to 16, progression toward total insulin deficiency may be slower in Wolfram Syndrome than it is in the Insulitis-caused type of Insulinitis; also causes Insipidus in about 70% of those with Wolfram Syndrome
Other Conditions (maybe yes, maybe no)
Studies are conflicting or sparse regarding the Insulinitis causality of
  • Highly Active Antiretroviral Therapy (HAART) drugs, used to treat individuals who have HIV/AIDS, per 1 study it caused Insulinitis in 3 Japanese men (also, studies have shown that it substantially increases risk of Cellosis)

  • Cytomegalovirus infection (maybe, and Insulinitis risk also mentioned in a study which showed increased risk of Cellosis in those who are at least 85 years old)
Cellosis causality is different than Insulinitis causality: lifestyle, weight, diet, and aging are frequently implicated in Cellosis causality, but do not cause Insulinitis; one's risk of Cellosis increases as one gets older, but one's risk of Insulinitis is highest in youth and decreases with age


Insulinitis Type Profile
(derived from Insulinitis Causality Profile)
When all Insulinitis is being referred to, a clarifying Insulinitis Type isn't necessary. However, when a specific type of Insulinitis is being referred to, an additional word or words helps to clarify exactly which one is being referred to.

Insulitis Insulinitis
The overwhelming cause of Insulinitis in most, not all cases, is the autoimmune Insulitis condition, helpful to add that word when the autoimmune Insulitis causality is solely being focused on. Note that polygenetic causality is also entailed.

The Insulinitis related to Other Conditions (causalities) are detailed below.
Insulinitis related to Other Conditions
When one of the following conditions or drugs causes total or near-total loss of insulin production, the following Insulinitis Type results (see the table above for details):
  • Congenital Rubella Insulinitis
  • Down's Syndrome Insulinitis
  • Pentamidine Insulinitis
  • Stiff Person Syndrome Insulinitis
  • Pancreatectomy Insulinitis, if insulin production is totally or near-totally lost due to a total or near-total pancreatectomy
  • Pancreatitis Insulinitis, if insulin production is totally or near-totally lost due to chronic pancreatitis
  • Trauma Insulinitis, if insulin production is totally or near-totally lost due to trauma
  • Turner Syndrome Insulinitis
  • Vacor/Pyrinuron/Pyriminil Insulinitis
  • Wolfram Syndrome Insulinitis
Insulinitis releated to Other Conditions (maybe yes, maybe no)
Studies are conflicting whether or not the following conditions or drug causes the following Insulinitis Type results - see Insulinitis Causality Other Conditions (maybe yes, maybe no) area above for details:
  • Alpha Interferon Insulinitis
  • Highly Active Antiretroviral Therapy Insulinitis
  • Cytomegalovirus Insulinitis

Insulinitis abnormal states or conditions,
excesses, tendencies, obsessions


The overwhelming cause of Insulinitis is Insulitis, but even in the non-Insulitis type of Insulinitis, the itis part of that description that is applicable for all who have Insulinitis, regardless of causality, is the part denoting abnormal states or conditions, excesses, tendencies, obsessions:

  • abnormal states or conditions: the abnormal states being the glucose going too low as a result of insulin guessing which exceeded the "right" amount - this occurs in everyone who has Insulinitis from time to time, and can lead to unconsciousness or seizures or loss of cognizance (something I've been able to avoid since January of 2014) or the glucose going too high (too high can be life-threatening if not countered with exogenous insulin), and the abnormal condition being the total or near-total lack of endogenous insulin production that everyone who has Insulinitis must battle with probabilistic exogenous insulin guesses


  • excesses: the excesses entail constant 24 by 7 by 365, 366 every leap year, monitoring of the impact of the multiple insulin guesses taken every day and night (many doing so by awakening during the night to ascertain if additional insulin needs to be dosed to battle a high or rapidly rising glucose level or if a glucose-raising substance needs to be ingested to battle a low or rapidly falling glucose level)


  • tendencies: the tendencies vary for each of us who has Insulinitis. Myself, I tend to call insulin dosing a guess, I tend to call so-called control of the condition a myth as all control was lost when we got Insulinitis and I tend to use the phrase "deal with" rather than "control", I tend to wake up many times at night to check if I need to do as detailed in the excesses area above, I tend to wear my continuous glucose monitor devices on my right wrist and upper left forearm, I tend ...

    ... to wear my Omnipod insulin pump controller on my left wrist, I tend to experiment with diets from time to time to ascertain whether they're helpful or not, I no longer tend to have severe lows (haven't had any since January of 2014, though before then, I was having an alarming number of them), I tend to get angry about having Insulinitis when insulin guesses yield glucose levels higher or lower than expected / desired, and I tend to hate every last thing about the old diabetes / diabetic vernacular (and there's more, but I'll leave it at that for now)


  • obsessions: all of the above, which includes the obsession of constantly thinking about Insulinitis in order to try to avoid the glucose going too low, to react with glucose-raising substances when it does, and to try to avoid the glucose from going too high, and to endeavor to guess at the "right" insulin to dose at all times, especially when the glucose goes too high as well as when a lot of glucose-raising substances have been ingested to deal with a glucose level falling rapidly or having gone too low ...

    ... the following graphic details the particulars of my dealing with Insulinitis (my obsessions), but the types of insulin, the glucose monitoring methods, the insulin dosaging method, and the intensity with which individuals attempt to try to stay within normal glucose levels (70 mg/dl to 120 mg/dl) varies from individual to individual; as for outcomes (was a particular insulin guess "right"?, was a particular food or drink ingestion "right"?), the incessant unrelenting constant persisting certainty, regardless of effort or best of intentions, is
    i n s u l i n   &   g l u c o s e   u n p r e d i c t a b i l i t y
    yield probabilistic outcomes,
    only "right" a percentage of the time,
    sometimes resulting in glucose levels too high,
    sometimes resulting in glucose levels too low


Treatment with exogenous insulin is required, with the exception of Latent Autoimmune Insulinitis, which can be treated without exogenous insulin at first, but which must be treated with exogenous insulin eventually as beta cell functionality is lost gradually rather than quickly as occurs in most Insulinitis cases diagnosed in childhood, and in many Insulinitis cases diagnosed in young adulthood.
Insulinitis Treatment Profile
Exogenous Insulin
Required for everyone who has Insulinitis. However, those with Latent Autoimmune Insulinitis, oft-times misdiagnosed as having Cellosis, can be treated without exogenous insulin until that condition advances (over a period of years), at which time exogenous insulin must be used. In almost all Insulinitis diagnosed in childhood, and in many Insulinitis cases diagnosed in young adulthood, exogenous insulin is required upon diagnosis. All exogenous insulin dosages require guessing at the "right" amount of insulin to dose with every insulin dosing decision.

Insulin must be injected (typically, multiple times, with at least 1-2 injections daily to maintain ongoing insulin needs, and additional injections if on an intense insulin regimen - prior to meals or snacks which raise glucose levels, or in response to the glucose going too high) or pumped (with quick-acting insulin, 15 to 20 minutes after pumping, basal for ongoing insulin needs, and additional insulin, bolus, before meals or when glucose rises too high), or injected for basal needs and inhaled (Afrezza) for mealtime bolus needs.

A new type of inhaled insulin (Afrezza) is available to accommodate bolus needs, but the minimal dosage is 4 units, and ongoing insulin needs (basal) must be handled via 1 to 2 daily injections in those who have Insulinitis who use Afrezza. For reasons unknown, not recommended to deal with ketoacidosis. Has been approved for those with Insulinitis, but unknown to what extent those with Insulinitis are using inhaled insulin, so it's most likely that most using this type of insulin are the 15% with Cellosis who use exogenous insulin, typically along with other Cellosis medication.
Other Medications
Everyone with Insulinitis must use probabilistic exogenous insulin guesses. Some with the condition are also prescribed additional medication(s), as follows, based on their risks of developing long-term sequelae and based on how well or poorly their exogenous insulin is keeping their glucose levels lowered to within normal glucose ranges (70 mg/dl to 120 mg/dl):
  • Pramlintide (Symlin), an injection before one eats can slow movement of food to curb a sharp increase in glucose level that can occur if one gives insufficient insulin before non-low-carb meals.
  • High Blood Pressure Medications, such as angiotensin-converting enzyme (ACE) inhibitors or angiotensin II receptor blockers (ARBs), which can also help to keep one's kidneys healthy; recommended for those who have blood pressures above 140/80 millimeters of mercury (mm Hg).
  • Aspirin, (low dose) may be recommended for its purported heart protection.
  • Cholesterol Lowering Drugs (Statins), may  be recommended. Cholesterol guidelines tend to be more aggressive for people with any of the High Glucose Conditions because of the elevated risk of heart disease.

    Low-density lipoprotein (LDL, or "bad") cholesterol should be below 100 mg/dL (2.6 mmol/L), and if you already have heart disease, your LDL goal is below 70 mg/dL (1.8 mmol/L).

    High-density lipoprotein (HDL, or "good") cholesterol is recommended to be over 50 mg/dL (1.3 mmol/L) in women and over 40 mg/dL (1 mmol/L) in men.

    Triglycerides, another type of blood fat, are ideal when they're less than 150 mg/dL (1.7 mmol/L).
A small minority, in addition to exogenous insulin, use one or more of the medications which are not FDA approved for use to treat Insulinitis, but instead are FDA approved for use in those with Cellosis or other High Glucose Conditions.
Insulinitis Risks Overview

Risks of having and dealing with Insulinitis vary over time. The most severe short-term risk is when one first gets the condition. If it's not detected in time, and handled with probabilistic exogenous insulin guesses (doses of insulin that while life-saving, also place one at risk of a severe low glucose event), or if it's misdiagnosed, one can die due to going into a hyperglycemic ketoacidosis coma.

Exogenous Insulin

Exogenous Insulin, a life-saver for everyone who has Insulinitis, ever since it first saved human lives in 1922, after experiments on dogs demonstrated its efficacy in 1921, first widely used to save lives in 1923. However, it's an extremely dangerous substance, required to stay alive for everyone with Insulinitis, -but- also placing one's life at risk with every insulin dosing decision involving danger when the glucose falls too low, the danger increasing as one's glucose falls down to levels which those who have no glucose anomaly never experience.

The following chart includes estimates as to the variations in time of onset, peak, and duration of most of the insulin widely used in America. Combination insulins aren't included. Note that these times are variable, both those displayed at different websites, and in actuality, in the way they work in different individuals, at different times and in differing dosages, and under different metabolic influences (key word: unpredictability). For comparison, comprehensive insulin information from Straight Healthcare.

The blood glucose chart (displayed in mmol/l units, converted to the nearest whole unit of mg/dl which are the units used in American glucose meters, arrived at by multiplying the mmol/l value by 18) shows the way in which the body automatically responds to lowering glucose levels to prevent the glucose level from going too low in those who have no glucose anomaly, as well as the way in which the body responds if the glucose continues to go into hypoglycemic territory, that situation faced by
  • everyone who has Insulinitis, due to our total dependence on probabilistic exogenous insulin guesses

  • everyone who has HUT, Hypoglycemia Uncaused by Treatments for High Glucose,

  • some of those who have Cellosis, those who are on medications which can cause hypoglycemia, though the risk to those with Cellosis who are on medications which can cause hypoglycemia is lessened by the far lower loss of pancreatic beta cells, by the continued but lower insulin release, and by the continued epinephrine and glucagon release which automatically respond to hypoglycemia in those with Cellosis

    and by

  • some of those with Gestational Cellosis, or Diminosis, or Neonatal Diminosis, or other High Glucose Conditions, those who use any hypoglycemia-causing medications, with the nature of the risk similar to the hypoglycemia risks entailed in those with Cellosis who use any medications which can cause hypoglycemia
In those who have a fully functional pancreas with no glucose anomaly, their pancreatic endogenous insulin production from beta cells ceases when their glucose level drops to ...

... 4.6 mmol/l (83 mg/dl)

In those who have a fully functional pancreas with no glucose anomaly, their endogenous glucose-raising hormones glucagon via pancreatic alpha cells and epinephrine from the adrenal medulla are released if their glucose level continues to fall to ...

... 3.8 mmol/l (68 mg/dl).


Exogenous Insulin -- DANGER, DANGER, DANGER !!!

In the Hypoglycemia graphic above, the hypoglycemia defenses and the perfect glucose normalcy of everyone who has no glucose anomaly is displayed, along with the hypoglycemia causes in those who have Insulinitis (highlighted in white with a dark red background).

In those with Insulinitis, endogenous insulin production is totally or near-totally gone, so exogenous insulin must be dosed (guessed at) and it does not cease functioning regardless of what one's glucose level is. So, there is no turning off of insulin at 83 mg/dl. One can clearly see the manner in which both automatic reduced endogenous insulin release -and- automatic increased endogenous glucagon release are critical aspects of preventing hypoglycemia, but are lost in those who have Insulinitis.

Also, one can clearly see the reduction in automatic epinephrine release (which raises glucose levels in those without Insulinitis) and the reduction in being able to sense hypoglycemia (much to all of the time) in those with Insulinitis who have hypoglycemic unawareness while awake (everyone with Insulinitis is hypoglycemic unaware while sleeping).

Glucagon and Epinephrine release in those with Insulinitis?

Excerpts [with inserts, not part of original articles, included in brackets]: 

  • Hypoglycemia in ... [Insulinitis]

    ... within 5 years of ... [Insulinitis] diagnosis, almost all individuals with ... [Insulinitis] fail to generate an adequate glucagon response to hypoglycemia ...

    - - - end excerpts - - -

  • Mechanisms of Hypoglycemia Counterregulation

  • ...

    Intensively Treated Patients With ... [Insulinitis] Have Impaired Glucagon and Epinephrine Responses to Hypoglycemia


    In patients with ... [Insulinitis] of long duration (> 5 years), epinephrine constitutes the main defense against hypoglycemia, because the pancreatic alpha cell glucagon secretory response to hypoglycemia is irreversibly lost. However, clinical studies have shown that the epinephrine response is also impaired in ... [Insulinitis] patients undergoing intensive insulin treatment.

    This "double whammy" (lack of glucagon and epinephrine response) places intensively treated ... [Insulinitis] patients at significant risk for recurrent hypoglycemia. In addition, frequent antecedent hypoglycemia reduces the counterregulatory responses to future hypoglycemia by 50% - creating a vicious cycle ... where hypoglycemia induces further hypoglycemia.

    ...

    - - - end excerpts - - -



    What Happens When Hypoglycemia Causes Glucose
    Levels to go below 60 mg/dl in those who have Insulinitis?

    Per the blood glucose chart, the following glucose readings when one is suffering hypoglycemia are associated with the following events (however, from experiencing the following innumerable times over the more than 54 years that I've had Insulinitis, I can add that the particular events and glucose levels displayed reflect general rules, but vary from individual to individual, and may occur at glucose levels differing from those displayed in the following):


When the glucose falls into the dangerous territory iterated above, despite all the efforts to guess right on insulin dosages and to respond with the right level of glucose to prevent the glucose from plunging dangerously low, one can fall into an Insulinitis Nightmare, that perilous / helpless / out of control / life-risking territory of severe low glucose in which loss of cognizance, seizure, loss of consciousness, self-recovery after many hours of unconsciousness, outside intervention provided recovery, or death can occur.


   
Insulinitis Risk Profile
Severe Low Glucose
Total dependence on probabilistic exogenous insulin guesses (injected or pumped in or inhaled for meal-time needs and injected for ongoing needs) causes high risk of hypoglycemia, which in its most severe form includes risk of loss of cognizance, seizure, unconsciousness, and at its worst, death (in an estimated 5% to 11% of those who have Insulinitis).
 
A significant percentage of those who have Insulinitis experience daytime hypoglycemic unawareness, making it much more difficult to avoid hypoglycemia unless one is using a continuous glucose monitor. Of course, everyone who has Insulinitis experiences hypoglycemic unawareness while sleeping, so once again, a continuous glucose monitor or a hypoglycemic sensing dog or waking up multiple times each night (by setting alarms, like I do) are the only options to try to battle hypoglycemia (and hyperglycemic excursions) while sleeping.

Hyperglycemia / Ketoacidosis
Insulinitis is typically first diagnosed due to hyperglycemia causing involuntary weight loss, tiredness, thirst, hunger, increased urination. When ketoacidosis occurs, the condition causes death if not diagnosed in time to counter it with exogenous insulin. 

Ongoing usage of exogenous insulin minimizes one's hyperglycemia risk, but does not eliminate it, and over the long term, many deal with the long-term sequelae which transpire, the risk of those higher the higher one's HbA1c levels (average glucose levels) are.

Long-Term Sequelae
  • A high chance of reduced life expectancy

  • Increased risk of
    • stroke
    • coronary artery disease
    • atherosclerosis (hardening of the arteries)
    • neuropathy (damage to the nerves)
    • amputation
    • eye problems including blindness
    • kidney damage including kidney failure
    • many types of malignant cancer (not all types)
    • sexual problems (in both men and women)
    • pregnancy risks to pregnant women with Insulinitis and to their unborn babies

  • Those risks increase over time and are higher when one's HbA1c levels (average glucose levels over a recent one to two month period) are higher.
    However, the chance of having a severe low glucose event increases when one's HbA1c levels are lower, although some claim that with lower carb ingestion matched with lower insulin dosing, they are able to minimize the frequency of having a severe low glucose event.

    Note - alzheimer's disease is shown to have an increased risk of occurring in those with Cellosis, but unclear / controversial if Insulinitis does or does not increase the risk of alzheimer's disease.
Other Conditions
People with the Insulitis-caused type of Insulinitis are at increased risk of other autoimmune conditions:

  • Thyroid disorders (in up to 33% of those who have Insulinitis)
  • Celiac disease (in up to 5% of those who have Insulinitis)
  • Addison's disease  (in an unknown percent of those who have Insulinitis)

Insulinitis is diagnosed in an estimated 5% of Americans who have one of the High Glucose Conditions, but since the rate of Cellosis diagnoses is rising rapidly, the percent of High Glucose Conditions diagnosed as Insulinitis is declining. Both Insulinitis and Diminosis are currently unpreventable, unlike Cellosis, which is estimated to have been preventable in at least 90% of those diagnosed with Cellosis.

About 50% of Insulinitis is diagnosed in childhood and 50% is diagnosed in adulthood. About 85% of those living with Insulinitis are adults. Lifestyle, weight, and diet do *not* contribute to the risk of getting Insulinitis. Inherited genes do contribute to the risk, and if one has a relative who has it, one's risk is increased, but some get it even though they have no known relatives with Insulinitis.

The following two videos, inspiration from the JDRF (Juvenile Diabetes Research Foundation) regarding efforts to find a cure and dramatic improvements in the treatments for Insulinitis (Islit), using the old "type 1 diabetes (T1D)" words.

"Turning Type One Into Type None" Video (JDRF : Believe)

"Turning Type One Into Type None" Video (JDRF: Plan for the Future)
The overall risk of getting Insulinitis in childhood is less than one-half of 1% in America, and the overall risk of getting Insulinitis at any time in one's life is less than 1% in America. As noted in the Insulinitis Causality Profile, the risk in America is moderate, and depending where one is born, the risk may be significantly higher or lower than in America.
 
Some famous people who have Insulinitis:


"A Little Bit Longer" Video (Jonas Brothers : August 13, 2013)

   
Got the news today doctor said I had to stay
 A little bit longer and I'll be fine
 When I thought it'd all been done
 When I thought it'd all been said
 A little bit longer and I'll be fine

But you don't know what you got until it's gone
 And you don't know what it's like to feel so low
 And every time you smile, you laugh, you glow
 You don't even know, know, know
 You don't even know

All this time goes by, still no reason why
 A little bit longer and I'll be fine
 Waiting on a cure but I can tell you
 None of them are sure

 A little bit longer and I'll be fine

But you don't know what you got until it's gone
 And you don't know what it's like to feel so low
 And every time you smile, you laugh, you glow
 You don't even know, know, know

 
So I'll wait 'til kingdom come
 All the highs and lows are gone
 A little bit longer and I'll be fine

 


 
Latent Autoimmune Insulinitis (LaIslit)

(formerly called
latent autoimmune diabetes
or type 1 diabetes or,
confusingly,
when used without clarifier, diabetes)


Insulinitis typically occurring in adults when Insulinitis is diagnosed past age 30, with at first, reduced insulin production, but eventually, due to the autoimmune cause of the condition, all insulin production is lost. Initially, many with this condition are misdiagnosed as having Cellosis.
Latent Autoimmune Insulinitis
Causality / Treatment / Risk Profile

Causality
Follows the same predominance of Insulitis causality as present in the overwhelming majority of those with Insulinitis. See Insulinitis Causality Profile for details. The slower onset of Insulitis / Insulinitis in Latent Autoimmune Insulinitis, thus far unexplained -- this type of Insulinitis was first documented in the 1990s. Age of onset, typically past age 30, and difficult to find documentation on the number diagnosed with Latent Autoimmune Insulinitis in ages younger than 30.
Treatment
Prior to the total or near-total loss of insulin production, many with this condition are misdiagnosed as having Cellosis, and are treated as if they had Cellosis. Once the condition worsens over a period of years and the total or near-total loss of insulin production transpires, probabilistic exogenous insulin guesses become a required treatment just like it does upon diagnosis of rapid-onset Insulinitis immediately upon diagnosis. For complete information on treatment, refer to the Insulinitis Treatment Profile.
Risk
The same as presented in the Insulinitis Risk Profile, the only exception being that since the onset is slower, the risks are presented later, and similar to Cellosis, one is more likely to go a long period of time without being diagnosed than one is when Insulinitis onset is rapid, so that extended period with high glucose levels increases the risk of long-term sequelae. However, since insulin is typically not used to deal with the condition in the first few years, the severe low risks that accompany the use of probabilistic exogenous insulin guessing are removed from the picture until exogenous insulin is required.
As their condition fails to respond to standard Cellosis treatments, eventually the diagnosis is switched to Insulinitis. The condition, once insulin production is severely reduced over time, is identical to the Insulinitis which has rapid onset.



 
Cellosis (Clos)

(formerly called type 2 diabetes or adult diabetes
or non-insulin dependent diabetes or confusingly,
when used without clarifier, diabetes),

preceded by PreCellosis (PreClos) (formerly called prediabetes)
 
The insulin production of persons with Cellosis continues at a less than effective basis (i.e., at a reduced but continuing level) which is caused by insulin resistance resulting in beta cell reduction over time.

PreCellosis refers to slightly elevated glucose levels (HbA1c levels of 5.7 to 6.4) which may be countered with diet & exercise to delay or forestall the onset of Cellosis (HbA1c levels of 6.5 and higher).

The osis (dictionary definition) part of the PreCellosis, Cellosis, and Diminosis words:

a suffix occurring in nouns that denote actions, conditions, or states, esp. disorders or abnormal states.

PreCellosis / Cellosis Causality Profile
Timing / Preventability / Reversibility
Cellosis, like Latent Autoimmune Insulinitis, is typically a slow onset condition, taking many years to advance to Cellosis, preceded by PreCellosis.  Prior to and during PreCellosis, Cellosis has a high degree of preventability if diagnosed in time, with lifestyle changes, primarily involving diet and exercise. It's estimated that Cellosis was preventable in over 90% of those who get it.

Reversibility? Diet and exercise have been shown to reverse the condition in a small percent, but typically the reversal is only partial, and not long-lasting. Gastric bypass surgery, especially among those who don't use exogenous insulin, has been shown to reverse Cellosis in many, the reversal lasting a considerable period of time among many.

Insulin Resistance

In the overwhelming majority of those with Cellosis, the condition is preceded by insulin resistance.

Weight
Cellosis can occur at any weight, but the risk of getting it increases as one's weight increases: the risk of getting it is lowest when one is underweight, second-lowest when one is normal weight, third highest when one is overweight, second highest when one is obese, and highest when one is severely obese.

Age

One's risk of getting it is lowest before age 5, rare from age 5 to 10, associated with increased weight in most who get it above age 10, moderate at ages 10 to 45, increased in ages 45 to 65, and significantly increased above age 65.

Lifestyle
One's risk of getting Cellosis is increased when one is sedentary, when one's exercise level is inadequate, when one's diet is unhealthy, when one gets too little or too much sleep, and when one smokes (the more one smokes, the higher the risk).

Pregnancy
Women are at risk of Gestational Cellosis while pregnant, but for the overwhelming majority who have Gestational Cellosis, it ends upon the end of the pregnancy; however, Cellosis continues in a minority of those women even after the end of the pregnancy, and the overwhelming majority are at increased risk of getting Cellosis later in life, and also are at increased risk if their baby weighs over 9 pounds at birth.

Genetics / Geography

One's risk of Cellosis increases when one parent has Cellosis, and dramatically increases when both parents have Cellosis. However, one is at a lower risk of Cellosis when neither parent has it. The risk of Cellosis varies based on one's ethnicity and location; unclear whether that differentiation is attributable mostly to genetics or mostly to differences in lifestyle apart from inherited genetic differences.

Cellosis is caused by polygenetic + lifestyle (in Preventable Cellosis) factors, differing from the non-lifestyle polygenetic causality of Insulitis Insulinitis, the non-lifestyle polygenetic causality of Unpreventable Cellosis, and differing from the monogenetic causalities (a different single gene causing each different type) of Diminosis.
Other Conditions
The following conditions or drugs increase the risk of getting Cellosis, as documented in the provided links
  • Acromegaly, oversecretion of growth hormone from the anterior pituitary gland, causes glucose intolerance in 40% and Cellosis in about 20% of those with the condition (affects 60 in a million people); Acromegaly entails oversecretion of growth hormone from the anterior pituitary gland, leading to a growth of all bones resulting in gigantism; when involved in causing Cellosis, it leads to insulin resistance & reduced beta cell function

  • Aldosterenoma, adrenal gland tumor that overproduces aldosterone, produces metabolic dysfuntion that can result in insulin resistance, gaining weight, and Cellosis

  • Alstrom Syndrome, associated with obesity and early-onset Cellosis in ages as young as 3.

  • Antipsychotics, increased risk of Cellosis due to weight gain in some antipsychotics: highest risk with Clorazil (clozapine), Zyprexa (olanzipine), medium risk with Seroquel (quetiapine), Risperdal (risperidone)

  • Bardet-Biedl Syndrome, with Laurence-Moon Syndrome either separate or a part of Bardet-Biedl Syndrome, leads to obesity, blindness, and other severe disorders,  usually starts in childhood and continues throughout one's life, with obesity increasing the risk of Cellosis; also, the non-glucose anomaly Insipidus sometimes is associated with Bardet-Biedl Syndrome

  • Beta-Adrenergic Agonists, older beta-blockers increase risk of Cellosis by more than 25 percent

  • Cytomegalovirus infection, a type of herpes infection found in 50 to 80 percent  of those over age 40, doubled risk of Cellosis in those who are at least 85 years old relative to the risk present in those over 85 who don't have the infection (also, regarding Insulinitis, maybe)

  • Friedreich's Ataxia, an inherited neurodegenerative disease, is a disorder associated with mitochondrial iron accumulation and is associated with a high incidence of Cellosis, suggesting a possible relation between mitochondrial iron accumulation leading to mitochondrial DNA damage and Cellosis

  • Highly Active Antiretroviral Therapy (HAART) drugs, used to treat individuals who have HIV/AIDS, studies have shown that it substantially increases risk of Cellosis (also, it caused Insulinitis in 3 Japanese men in 1 study)

  • HMG CoA reductase inhibitors - statins, a nearly 50 percent increased risk of Cellosis to people taking the cholesterol-lowering drugs in a large Finnish study

  • Hypothyroidism, low and low-normal thyroid function are associated with an increased risk of developing Cellosis and progression from PreCellosis to Cellosis in a large Dutch study

  • Klinefelter Syndrome, affects 0.1% (1 in 1,000) to 0.2% (1 in 500) of male infants at birth, males who are born with at least one extra X chromosome; as many as 2/3rds to 3/4ths of men with this condition are undiagnosed during their lifetimes, increases risk of Cellosis and many other adverse conditions

  • Mitochondrial DNA, a growing body of evidence now demonstrates a link between various disturbances in mitochondrial functioning and Cellosis

  • Myotonic Dystrophy, increased insensitivity to insulin increases the likelihood of  Cellosis

  • Polycystic Ovary Syndrome or Hyperandrogenic Anovulation or Stein-Leventhal Syndrome, affects 5% to 10% of women aged 18 to 44 and increases the risk of getting Cellosis

  • Prader-Willi Syndrome, a congenital (present from birth) disease resulting in obesity and increased risk of Cellosis, reduced muscle tone and mental ability, and sex glands that produce little or no hormones.

  • Thiazides, drugs used to reduce the risk of death, stroke, heart attack, and heart failure due to hypertension, may increase the risk of Cellosis by up to 50 percent

  • Turner Syndrome, a substantially increased risk of Cellosis by adulthood (also, women have a moderately increased risk of Insulinitis in childhood)

  • Werner Syndrome, characterized by premature aging and increased risk of Cellosis, occurs in 1 in 100,000 births
Cellosis causality is different than Insulinitis causality: lifestyle, weight, diet, and aging are frequently implicated in Cellosis causality, but do not cause Insulinitis; one's risk of Cellosis increases as one gets older, but one's risk of Insulinitis is highest in youth and decreases with age


PreCellosis / Cellosis Type Profile
(derived from PreCellosis / Cellosis Causality Profile)
When all Cellosis is being referred to, a clarifying Cellosis Type isn't necessary. However, when a specific type of Cellosis is being referred to, an additional word or words helps to clarify exactly which one is being referred to.

In the overwhelming majority of Cellosis, polygenetic causality combined with insulin resistance resulting from dietary and sedentary factors and/or smoking and/or sleeping too much or too little (i.e., lifestyle factors) are involved, and in most of that overwhelming majority who have Cellosis, overweight (the more one is overweight, the greater the risk) is involved, and age increases one's risk after age 45. I've finally determined (this being my third effort to do so in the last two days) that the overwhelming majority of Cellosis falls into the following two types:

Preventable Cellosis
It's estimated that 90% of Cellosis can be prevented (the lifestyle factors mentioned above) per an article in the New England Journal of Medicine: "if people exercised more, ate better, stopped smoking and adopted other healthy behaviors", plus polygenetic factors differing from those which cause Unpreventable Cellosis and differing from the non-lifestyle polygenetic factors which cause Insulitis Insulinitis.

Unpreventable Cellosis

Unpreventable Cellosis factors in the overwhelming majority of the remaining 10% of those with Cellosis:
  • Polygenetic causality which is unrelated to lifestyle, and differing from the polygenetic factors + lifestyle factors (mentioned above) that cause Preventable Cellosis and differing from the non-lifestyle polygenetic factors which cause Insulitis Insulinitis
  • In some, it results from a reduction in insulin production which is unrelated to insulin resistance or lifestyle
  • In some, the causality is primarily related to older age, not lifestyle

The Cellosis related to Other Conditions (causalities) are detailed below.

Cellosis related to Other Conditions
When one of the following conditions or drugs causes Cellosis, the following Cellosis Type results (see the table above for details):
  • Acromegaly Cellosis
  • Aldosterenoma Cellosis 
  • Alstrom Syndrome Cellosis 
  • Antipsychotics Cellosis
  • Bardet-Biedl Syndrome Cellosis
  • Beta-Adrenergic Agonists Cellosis
  • Cytomegalovirus Cellosis
  • Friedreich's Ataxia Cellosis
  • Highly Active Antiretroviral Therapy Cellosis
  • HMG CoA reductase inhibitors - statins Cellosis
  • Hypothyroidism Cellosis
  • Klinefelter Syndrome Cellosis
  • Mitochondrial DNA Cellosis
  • Myotonic Dystrophy Cellosis
  • Polycystic Ovary Syndrome Cellosis
    or Hyperandrogenic Anovulation Cellosis
    or Stein-Leventhal Syndrome Cellosis
  • Prader-Willi Syndrome Cellosis
  • Thiazides Cellosis
  • Turner Syndrome Cellosis
  • Werner Syndrome Cellosis

PreCellosis and Cellosis are treated with diet & exercise, weight loss (in individuals who are overweight), oral and/or injected medications apart from insulin, and in an estimated 15% of cases (typically many years after getting Cellosis), exogenous insulin (injected or pumped in or inhaled) may be used along with the other Cellosis treatments.

The Cell being referred to is the small mass of protoplasm bounded by semipermeable membrane, capable of performing fundamental functions of life.

Insulin Resistance

In persons with Cellosis, the body's cells do not respond correctly to insulin. This is called insulin resistance, and typically, this is how PreCellosis and Cellosis begin. Insulin resistance means that fat, liver, and muscle cells do not respond normally to insulin. As a result, glucose does not get into cells to be stored for energy as it did prior to the onset of PreCellosis and Cellosis.

In the following video, the old term "type 2 diabetes" is used in most of the video to explain the causality of PreCellosis and Cellosis which entails the insulin resistance condition. The video begins with an explanation of how insulin normally allows glucose to be transported into cells, followed by an explanation of how insulin resistance causes Cellosis.

Unfortunately, the video ends with the use of the old "diabetes" term, misleading / confusing in that the entire video is solely about Cellosis, and has nothing whatsoever to do with Insulinitis or Diminosis or any of the other High Glucose Conditions, yet another (in an almost inexhaustible list) of examples supporting changing the old diabetes / diabetic names to the new names promoted in this article:

"Insulin Resistance in Cellosis" Video




Cellosis Treatment Profile
Diet and Exercise
Everyone with Cellosis is well-advised to use diet and exercise to try to prevent, reverse, and deal with Cellosis if prevention doesn't work. A significant percentage (estimated at over 90%) could've prevented Cellosis prior to or during the PreCellosis phase, had they known they had PreCellosis or had they engaged in lifestyle prevention methods (diet and exercise).

Those with Cellosis, diet and exercise are all that's used to deal with glucose levels in an estimated 20% of those with diagnosed Cellosis. However, due to the slow onset of the condition, it's estimated that up to 33% of those with Cellosis have not yet been diagnosed with the condition, and due to their unawareness, their high glucose condition is not treated.

Oral Cellosis Medications
Oral medications of the Sulfonylureas type started being used to treat Cellosis late in the 1950s, but most of the oral medications to deal with Cellosis began to be used in the 1990s. None of these medications are FDA approved to treat Insulinitis, and many (not all) of these medications are specifically warned against being used by anyone with Insulinitis. The medications that work to increase insulin production in those with Cellosis have no impact on those with Insulinitis.

If multiple Cellosis medications are used (either in separate medications or in combined medications which aren't included below), the impacts and side effects of each medication are combined. The following list only includes some of the notable side effects; consult detailed medication profiles for a complete list of all potential side effects.

Medication
Type
Description
Notable Side
Effects

Alpha-glucosidase
Inhibitors

(Acarbose: Precose)

(Miglitol: Glyset)

Oral medication taken with first bite at each meal
Glucosidase inhibitor which works by slowing down the enzyme that turns carbohydrates into glucose, slows gastric emptying, not used to treat Insulinitis
Flatulence in a large percent,  and diarrhea,  abdominal pain, or skin rash in a small percent
Biguanides

(Metformin: Glucophage),

(Metformin liquid: Riomet),

(Metformin Extended Release: Fortamet,
Glucophage XR, Glumetza)
Oral medication, taken twice a day with breakfast & evening meal

Extended release usually taken once a day in the morning
FDA approved in 1994, increases insulin sensitivity (i.e., reduces insulin resistance), reduces the amount of glucose produced by the liver, not used to treat Insulinitis, may be used to treat PreCellosis, may reduce one's risk of getting Cellosis
Lactic acidosis (rare, but serious & potentially fatal side effect)
Bile Acid Sequestrants

(Colesevelam: Welchol)

Oral medication taken one or two times daily with a meal
FDA approved in January of 2008, lowers bad cholesterol, may be used with a statin to lower bad cholesterol further, per the Welchol website it only lowers glucose levels when used with metformin, sulfonylureas, or exogenous insulin; it is not used to treat Insulinitis
May cause constipation, upset stomach, indigestion, headache, stomach pain, or diarrhea
Dopamine Elevators

(Cycloset: bromocriptine mesylate)
Oral medication taken daily with food within two hours after waking up
FDA approved in May of 2009, lowers glucose levels via unknown means, but a Cycloset graphic indicates the means is reduced insulin resistance, not used to treat Insulinitis
May cause nausea, constipation, headache or dizziness, seizures, and/or strokes
D-Phenylalinine Derivatives

(
Nateglinide: Starlix)

Meglitinides

(Repaglinide: Prandin)
Oral medication taken with meals
FDA approvals - Nateglinide: 2000, Repaglinide: 1997,
these meds stimulate the pancreas to quickly produce more insulin, not used to treat Insulinitis

Low glucose, small weight gain
DPP-4 Inhibitors

(Alogliptin: Nesina)

(Linagliptin: Tradjenta)

(Saxagliptin: Onglyza)

(Sitagliptin: Januvia)

Oral medication taken once daily
FDA approvals -
Nesina: January 2013, Tradjenta: May 2011,
Onglyza: July 2009,
Januvia: October 2006, inhibits dipeptidyl peptidase 4 enzyme, increases activity of incretins which suppresses pancreatic glucagon secretion, increases pancreatic insulin secretion, reduces glucose output from the liver, & decreases gastric emptying, not used to treat Insulinitis

May cause acute pancreatitis; in August of 2015, FDA issued a warning that DPP-4 Inhibitors may cause joint pain that can be severe and disabling; in April of 2016, FDA issued a warning that saxagliptin and alogliptin containing medicines may increase the risk of heart failure, particularly in patients  who already have heart or kidney disease
SGLT-2 Inhibitors

(Dapagliflozin: Farxiga)

(Canagliflozin: Invokana)

(Empagliflozin: Jardiance)
Oral medication taken once daily
FDA approvals -
Farxiga: January 2014,
Invokana: April 2013,
Jardiance: August 2014, lowers glucose levels by helping kidneys get rid of glucose, not used to treat Insulinitis; in August, 2015, Jardiance was shown to reduce  risk of heart attack in a long-term clinical trial
May cause frequent urination; In May of 2015, FDA issued a warning that SGLT-2 inhibitors can trigger ketoacidosis; in September of 2015, FDA strengthened warning that Canagliflozin increases risk of bone fractures & decreases bone mineral density; in May of 2017, FDA warned Canigliflozin doubles amputation risk
Sulfonylureas

(Chlorpropamide: Diabines)

(Glimepiride: Amaryl), 

(Glyburide: Diabeta, Micronase),

(Glipizide: Glucotrol, Glucotrol XL),

(Micronased Glyburide: Glynase)

(Tolbutamide: Orinase)
Oral medication taken once or twice a day with a meal
First used in the 1950s, stimulates the pancreas to release more insulin, both right after a meal & then over several hours, not used to treat Insulinitis
Low glucose, may occasionally cause skin rash, irritability, upset stomach
Thiazolidinediones

(Pioglitazone: Actos)

(Rosiglitazone: Avandia)
Oral medication taken at the same time daily
First used in the late 1990s, decreases insulin resistance, reduces glucose output by the liver, decreases lipotoxicity, not used to treat Insulinitis
May increase risk of serious heart problems; pioglitazone may be linked to increased risk of bladder cancer

Injected Non-Insulin Cellosis Medications
Five non-insulin Cellosis injectables have been FDA approved since 2005, and one of them (Pramlintide) is the only Cellosis medication with FDA approval to be used by a small minority of those with Insulinitis (along with required exogenous insulin) who aren't achieving desired glucose levels solely with required exogenous insulin.

Medication
Type
Description
Notable Side
Effects

Albiglutide (Tanzeum)
Weekly injection (glucagon-like peptid, GLP-1, receptor agonist)
FDA approved in April of 2014, augments glucose dependent insulin secretion, suppresses inappropriate glucagon secretion, & slows gastric emptying, not used to treat Insulinitis
May cause upper respiratory tract infection, diarrhea, nausea
Exenatide (Byetta)
Injected twice daily 60 minutes before breakfast & dinner (incretin mimetic)
FDA approved in April of 2005, enhances insulin secretion when glucose is high while decreasing glucose secretion & decreasing liver's glucose output; slows digestion keeping one feeling fuller longer, decreases appetite, not used to treat Insulinitis
Low glucose when used with a sulfonylurea, may cause acute pancreatitis
Exenatide Extended Release (Bydureon)
Weekly Injection (incretin mimetic)
Same as listed above for Byetta, with the exception that it was FDA approved in January of 2012
Same as listed above for Byetta
Dulaglutide (Trulicity)
Weekly injection (glucagon-like peptid, GLP-1, receptor agonist)
FDA approved in December of 2014, increases glucose-dependent insulin release, decreases glucagon secretion, slows gastric emptying, not used to treat Insulinitis
In over 10%, may cause nausea or diarrhea or vomiting
Liraglutide (Victoza)
Injected once per day (incretin mimetic)
FDA approved in January of 2010, stimulates insulin production, decreases glucagon secretion while suppressing liver's glucose output, slows gastric emptying, not used to treat Insulinitis
May cause weight loss; may cause low glucose if used with insulin or other drugs that stimulate insulin production
Lixisenatide
(Adlixin, Lyxumia)
Injected once per day (GLP-1 receptor agonist)
FDA approved in July of 2016, Adlixin, attaches to GLP-1 receptors, activates them, & causes insulin release, not used to treat Insulinitis
May cause hypoglycemia, nausea, vomiting, diarrhea, headache
Pramlintide (Symlin)
Injected before meals (amylin analog)
FDA approved in March of 2005, slows food moving through stomach, reduces glucose production by the liver, helps keep post-meal glucose levels from going too high; the only FDA approved drug that may also be used (along with required exogenous insulin) to treat Insulinitis
May suppress appetite and cause weight loss; may cause nausea; may cause severe low glucose


Exogenous Insulin Used by 15% of Those Diagnosed with Cellosis

Unlike Insulinitis, in which 100% must use exogenous insulin to stay alive, Cellosis is dealt with via exogenous insulin (in addition to other treatments detailed above) in only 15% of those with Cellosis.

Other Treatments
  • High Blood Pressure Medications, such as angiotensin-converting enzyme (ACE) inhibitors or angiotensin II receptor blockers (ARBs), which can also help to keep one's kidneys healthy; recommended for those who have blood pressures above 140/80 millimeters of mercury (mm Hg).
  • Aspirin, (low dose) may be recommended for its purported heart protection.
  • Cholesterol Lowering Drugs (Statins, which can also be used by those with Insulinitis, or Welchol, solely used by those with Cellosis for its glucose-lowering - if used with metformin, sulfonylureas, or exogenous insulin - and cholesterol lowering properties) may be recommended. Cholesterol guidelines tend to be more aggressive for people with any of the High Glucose Conditions because of the elevated risk of heart disease.

    Low-density lipoprotein (LDL, or "bad") cholesterol should be below 100 mg/dL (2.6 mmol/L), and if you already have heart disease,  your LDL goal is below 70 mg/dL (1.8 mmol/L).

    High-density lipoprotein (HDL, or "good") cholesterol is recommended to be over 50 mg/dL (1.3 mmol/L) in women and over 40 mg/dL (1 mmol/L) in men.

    Triglycerides, another type of blood fat, are ideal when they're less than 150 mg/dL (1.7 mmol/L).
Reversibility via Gastric Bypass Surgery?
27% of individuals with Cellosis who underwent gastric bypass surgery had complete remission as of 5 years after surgery, with remission defined as an HbA1c level of  6% or less, normal fasting glucose < 100 mg/dl, and completely off of all medication which lowers glucose levels for one year. Short-term remission rates are reported to be as high as 80%, but are often not sustained over the long-term.


   
Reversability via a Very Low Calorie Diet?
A study by Professor Roy Taylor, Newcastle University, of 30 volunteers, 12 who've had Cellosis for up to 10 years used a 600 to 700 calories per day diet to reverse their Cellosis and remained Cellosis-free 6 months later. Average weight loss? 31 pounds. Roy Taylor mentions removal of pancreas fat as the key to Cellosis reversal, and claims that if they keep the weight off, they'll remain Cellosis-free. Another claim, that glucose levels will be lowered with the diet even in those whose Cellosis isn't reversed.

Doubtful that this diet could be used by peope who are slightly overweight, normal weight, or underweight, and that area wasn't addressed in any articles I've found about the study. Also at issue, will the people who lost the weight be able to maintain the weight loss as time passes? A larger study of 300 people with Cellosis is underway.

The following graphic displays Cellosis Treatments apart from Gastric Bypass Surgery, all of which utilize that most critical treatment angle which oft-times is unmentioned, the human brain which must make critical daily decisions in every aspect of the treatments, whether using diet and exercise alone, or using diet and exercise along with oral medications and/or injected medications:


Some famous people who have Cellosis:



Cellosis Risk Profile
Low Glucose
The primary short-term sequelae of Cellosis has a risk of mild and severe hypoglycemia which is much lower than it is in those who deal with Insulinitis, all of whom are at a high risk of both mild and severe hypoglycemia:
  • If Cellosis is treated solely with diet and exercise, mild and severe hypoglycemia are absent, and varying degrees of remission are possible though unlikely to last for a long period of time

  • If Cellosis is treated with gastric bypass surgery, a high degree of remission is possible, and many have shown that their remission lasts for a significant period of time; when no hypoglycemic-causing oral or injected medication is used after gastric bypass surgery, mild and severe hypoglycemia are absent

  • Injections of Exogenous Insulin or Pramlintide, and some oral medications (D-Phenylalinine Derivatives, Meglitinides, & Sulfonylureas) raise the risk of mild and severe hypoglycemia; however, most Cellosis medications do not cause hypoglycemia when used alone, but note, combining any medication that can cause hypoglycemia with any medication that doesn't cause hypoglycemia (either individually or in a combined medication not listed below), hypoglycemia can result
    Medications which don't cause hypoglycemia when used alone Medications which can cause hypoglycemia when used alone or when used in combination with any of the other medications in this table
    Albiglutide (Injected)
    Alpha-glucosidase Inhibitors
    Biguanides
    Bile Acid Sequestrants
    Dopamine Elevators
    DPP-4 Inhibitors
    Dulaglutide (Injected)
    Exenatide (Injected)
    Liraglutide (Injected)
    SGLT-2 Inhibitors
    Thiazolidinediones
    D-Phenylalinine Derivatives (Nateglinide)
    Exogenous Insulin (Inhaled, Injected, or Pumped)
    Lixisenatide (Injected)
    Meglitinides (Repaglinide)
    Pramlintide (Injected)
    Sulfonylureas


  • In the 15% of those with Cellosis who use exogenous insulin as part of their treatment profile, risk of mild and severe hypoglycemia increases the longer one is on an exogenous insulin treatment. However, per most reports, when compared to those with Insulinitis: its frequency is less, hypoglycemic unawareness is less, and its severity is usually less

Lactic Acidosis

Metformin includes the risk of lactic acidosis, which is potentially fatal. Therefore, if one has Cellosis and a kidney disorder, lung disease, or liver disease, one should not take Metformin, as taking Metformin in anyone with any of those conditions increases one's risk of lactic acidosis.

Ketoacidosis
In May of 2015, the FDA issued a warning that SGLT-2 inhibitors can trigger ketoacidosis.

Acute Pancreatitis

The following Cellosis medications may cause acute pancreatitis: DPP-4 Inhibitors or Incretin Mimetics (injected Byetta or Bydureon, injected Victoza).

Multiple Side Effects
Oral and injected medications have extensive side effects unique to each type of drug. Consult detailed information on the Cellosis drug(s) one is using or interested in for a complete list of all potential side effects.
Hyperglycemia
Cellosis is typically first diagnosed after many years due to the presence of long-term hyperglycemia causing any of the following symptoms (though notably, sometimes people get Cellosis without exhibiting any symptoms): tiredness, thirst, sudden unexplained weight loss, hunger, increased urination, skin problems, slow wound healing, fatigue and irritability, blurry vision, tingling or numbness in hands or feet. If not diagnosed and treated in time, death can occur.

An array of treatments are available for those with Cellosis, enabling one to reduce one's hyperglycemia risk, but those treatments do not eliminate hyperglycemia, and over the long term, many deal with the long-term sequelae which transpire, the risk of those higher the higher one's HbA1c levels (average glucose levels) are.

Long-Term Sequelae
    The long-term sequelae of Cellosis has a similar risk to the long-term sequelae of Insulinitis (with one possible exception - see below), though since Cellosis is often undiagnosed for many years, significant damage due to persisting unknown high glucose levels typically occurs prior to Cellosis diagnosis and treatment.

  • A high chance of reduced life expectancy

  • Increased risk of
    • alzheimer's disease (shown to increase the risk in those with Cellosis, unclear / controversial if Insulinitis does or does not increase the risk of alzheimer's disease)
    • stroke
    • coronary artery disease
    • atherosclerosis (hardening of the arteries)
    • neuropathy (damage to the nerves)
    • amputation
    • eye problems including blindness
    • kidney damage including kidney failure
    • many types of malignant cancer (not all types)
    • sexual problems (in both men and women)
    • pregnancy risks to pregnant women with Cellosis and to their unborn babies
Those risks increase over time and are higher when one's HbA1c levels (average glucose levels over a recent one to two month period) are higher. However, the chance of having a low glucose event increases when one's HbA1c levels are lower if using any of the drugs which cause hypoglycemia (see above).

Other Conditions
People with the Cellosis are at increased risk of contracting the following other conditions:
  • Cushing's Syndrome (people who are obese, have Cellosis, and have high glucose levels and high blood pressure are at increased risk of developing Cushing's Syndrome)
  • Hypothyroidism and Hyperthyroidism (12% of those with Cellosis have a thyroid condition compared to 7% of the general population)

  • Pancreatitis (a 2.8 times greater risk for getting pancreatitis than the risk for those who don't have Cellosis; also, some medications used to treat Cellosis, Byetta - Januvia - Onglyza - Victoza, increase one's risk of getting acute pancreatitis)
Unfortunately, a large number of persons with PreCellosis become individuals with Cellosis, and aren't diagnosed until they have had Cellosis for a considerable period of time.

Cellosis is diagnosed in an estimated 90% to 95% of all persons who have one of the High Glucose Conditions. Unlike Insulinitis and Diminosis, which are unpreventable, it's estimated that Cellosis was preventable in at least 90% of those diagnosed with Cellosis.





Gestational Cellosis (GesClos)

(formerly called
gestational diabetes or confusingly,
when used without clarifier, diabetes)


Gestational Cellosis is overwhelmingly a temporary condition which ends within 4 to 6 weeks after birth. However, Cellosis continues in a minority of those women even after the end of the pregnancy, and the overwhelming majority are at increased risk of getting Cellosis later in life, and also are at increased risk if their baby weighs over 9 pounds at birth.

Gestational Cellosis
Causality / Treatment / Risk Profile

Causality
Develops in the last half of the pregnancy. Women over age 25, women who have PreCellosis, women who have a close relative with Cellosis, women who had Gestational Cellosis during a previous pregnancy, women who are obese, women with excessive weight gain during pregnancy, and women who've previously birthed a baby over 9 pounds are at highest risk for developing Gestational Cellosis.

Hormones produced by the placenta and other pregnancy-related factors contribute to insulin resistance, which occurs in all women during late pregnancy. Insulin resistance increases the amount of insulin needed to keep blood glucose levels normalized. If the pancreas can’t produce enough insulin to adequately deal with the insulin resistance, Gestational Cellosis occurs.
Treatment
About 85% treat their Gestational Cellosis with diet and exercise. Of the 15% who are put on medications, most start with Cellosis oral medications, with an unknown percentage put on exogenous insulin injections at some point.
Risk
As many as one-third of women who've had Gestational Cellosis will have PreCellosis after giving birth. About one-third to one-half of women who've had Gestational Cellosis will have it again in a later pregnancy. About one-half of women who've had Gestational Cellosis will develop Cellosis at some point in the future.

In from 2% to 10% of pregnancies, Gestational Cellosis is present.





Diminosis (Dios)

(formerly called maturity onset diabetes of the young or confusingly,
when used without clarifier, diabetes,

often misdiagnosed as type 1 diabetes or as type 2 diabetes)

Diminished insulin production occurring in mostly young people due to a single gene inherited from one parent or the other. Initially, depending on the type of gene causing the condition, it may be treated with diet or sulfonylureas. Some types require exogenous insulin early on, others may require it later. The condition is caused by a single gene (monogenetic) rather than
  • multiple genes + environmental trigger(s) (i.e., non-lifestyle factors) which cause Insulitis Insulinitis

  • differing multiple genes + lifestyle factors which cause Preventable Cellosis (in 90% of those with Cellosis)

  • differing mulitiple genes (and non-lifestyle factors) which cause Unpreventable Cellosis (in 10% of those with Cellosis)
If one parent has Diminosis, their children have a 50% risk of Diminosis. It predominantly occurs before age 25.
Diminosis
Causality / Treatment / Risk Profile

Causality / Treatment
Diminosis should be suspected when a High Glucose Condition is detected in a nonoverweight individual under age 25 who isn't experiencing ketoacidosis. However, it may occur in individuals who are overweight. Unfortunately, Diminosis is misdiagnosed as Insulinitis or Cellosis initially, in a large percentage of Diminosis occurrences.

The treatment is based on the specific gene causing the condition, as depicted in the following table.

* GCK and IPF1 (PDX1) also listed in the Neonatal Diminosis area as they rarely occur one week after birth; INS also listed in the Neonatal Diminosis area as it occurs in 20% of Permanent Neonatal Diminosis cases - within 6 months after birth

Gene
Affected
Protein

How
Common

Usual Age
of Onset

Treatment
HNF4A
hepatocyte nuclear
factor 4ɑ (alpha)
up to 10% of Diminosis
adolescence or
early adulthood
sulfonylureas for most, some may need exogenous insulin
GCK *
glucokinase
2nd most common Diminosis
most commonly in early childhood
diet modification and physical activity; medications usually not required; some patients do not require any treatment during childhood
TCF1
hepatic nuclear factor 1ɑ (alpha) or HNF1ɑ (alpha) or HNF1A
most common Diminosis
adolescence or
early adulthood
initially - diet, some may later need sulfonylureas, some may later need exogenous insulin
IPF1 * ; also known as PDX1
insulin promoter factor 1
rare
early adulthood; can occur later
sulfonylureas for most, some may need exogenous insulin
TCF2
hepatic nuclear factor 1β (beta) or HNF1B
up to 10% of Diminosis
adolescence or
early adulthood
exogenous insulin
NeuroD1, or BETA2
neurogenic differentiation factor 1
rare
in the 4th decade of life
exogenous insulin
KLF11
kruppel-like
factor 11
rare
adolescence or
early adulthood
sulfonylureas or exogenous insulin
CEL
bile salt
dependent lipase
very rare
adolescence or
early adulthood
sulfonylureas or exogenous insulin
PAX4
paired domain gene 4
very rare
adolescence or early adulthood
sulfonylureas or exogenous insulin
INS *
insulin
rare
adolescence or
early adulthood
sulfonylureas or exogenous insulin
BLK
tyrosine kinase, b-lymphocyte specific
very rare
adolescence or
early adulthood
sulfonylureas or exogenous insulin

Risk
The risk profile of Diminosis is similar to the risk profile for Cellosis, with the exception being that medications other than sulfonylureas or exogenous insulin are rarely used to treat Diminosis. Also, the amount of medications required to deal with Diminosis are most often significantly less than the amount required to deal with Cellosis.


Diminosis Type Profile
(derived from Diminosis Causality / Treatment / Risk Profile)
When all Diminosis is being referred to, a clarifying Diminosis Type isn't necessary. However, when a specific type of Diminosis is being referred to, the exact monogenetic cause helps to clarify exactly which one is being referred to.

The monogenetic cause of Diminosis varies based on the exact gene which causes the condition (a different gene in each type, as detailed below). When a specific gene cause is being referred to, the following Diminosis Type results (see the table above for details):
  • HNF4A Diminosis
  • GCK Diminosis
  • TCF1 Diminosis
  • IPF1 Diminosis or PDX1 Diminosis
  • TCF2 Diminosis
  • NeuroD1 Diminosis or BETA2 Diminosis
  • KLF11 Diminosis
  • CEL Diminosis
  • PAX4 Diminosis
  • INS Diminosis
  • BLK Diminosis

It's estimated that up to 5% of diagnoses of Cellosis or Insulinitis may actually be Diminosis, but Diminosis is only diagnosed in 1% to 2% of the total number diagnosed as having one of the High Glucose Conditions. Both Insulinitis and Diminosis are currently unpreventable, unlike Cellosis, which is estimated to have been preventable in at least 90% of those diagnosed with Cellosis.

References for the information in this section and in the Neonatal Diminosis section:





Neonatal Diminosis (NeoDios)

(formerly called neonatal diabetes, or one of the
types of maturity onset diabetes of the young,
or confusingly,
when used without clarifier, diabetes
)

High Glucose Condition (which isn't Insulinitis) with diminished insulin production occurring in the first 6 months after birth, caused by a single gene. 
Some types (see below) are transient, but if transient, it may recur later.

Neonatal Diminosis
Causality / Treatment / Risk Profile

Causality / Treatment
Neonatal Diminosis should be suspected when a High Glucose Condition is detected in the first 6 months after birth. 50% of Neonatal Diminosis is permanent and 50% is transient, going away within the first 18 months of age.

The treatment is based on the specific gene causing the condition, as depicted in the following tables.

* GCK is also the 2nd most common form of Diminosis and IPF1 (PDX1) is also a rare form of Diminosis also listed in the Diminosis area with characteristics differing from those involved in Neonatal Diminosis;
INS also listed in the Diminosis area as it sometimes occurs more than 6 months after birth

Permanent Neonatal Diminosis (PND)

Gene
Affected
Protein

How
Common

Usual Age
of Onset

Treatment
KCNJ11
kir6.2
Most common Permanent Neonatal Diminosis (30%)
3 to 6 months
sulfonylureas for most, some may need exogenous insulin; this gene can also cause Transient Neonatal Diminosis
ABCC8
sur1 - sulfonylurea receptor 1
tied for 2nd most common Permanent Neonatal Diminosis (20%)
1 to 3 months
sulfonylureas for most, some may need exogenous insulin; this gene can also cause Transient Neonatal Diminosis
INS *
insulin
tied for 2nd most common Permanent Neonatal Diminosis (20%)
birth to
6 months
sulfonylureas or exogenous insulin
GCK *
glucokinase
rare
1 week
exogenous insulin
IPF1 * ; also known as PDX1
insulin promoter factor 1
rare
1 week
unknown as source says "treat to replace endocrine & exocrine pancreas functions"
PTF1A
pancreas transcription factor 1A
rare
at birth
unknown as source says "treat to replace endocrine & exocrine pancreas functions"
FOXP3, IPEX syndrome
forkhead box P3
rare
sometimes present at birth
exogenous insulin
EIF2AK3, Wolcott-Rallison syndrome
eukaryotic translation initiation factor 2-alpha kinase 3
rare
3 months
exogenous insulin and treatment for associated conditions

Transient Neonatal Diminosis (TND)

Gene
Affected
Protein

How
Common

Usual Age
of Onset

Treatment
ZAC/HYMAI
ZAC: pleomorphic adenoma gene-like 1 or PLAG1

HYMAI: hydatiform mole-associated and imprinted transcript
Most common Transient Neonatal Diminosis
birth to
3 months
initially, exogenous insulin; reduce dosage as needed; if it recurs, treat with diet and physical activity; may also require exogenous insulin
KCNJ11
kir6.2
uncommon cause of Transient Neonatal Diminosis; most common Permanent Neonatal Diminosis (30%)
birth to
6 months
sulfonylureas
ABCC8
sur1 - sulfonylurea receptor 1
rare cause of Transient Neonatal Diminosis; tied for 2nd most common  Permanent Neonatal Diminosis (20%)
birth to
6 months
sulfonylureas
HNF1 β (beta); also known as HNF1B
hepatocyte nuclear factor 1B
rare
birth to
6 months
exogenous insulin

Risk
The risk profile of Permanent Neonatal Diminosis is similar to the risk profile for Diminosis, with the additional risk of slow growth before birth; however, the risk profile of Transient Neonatal Diminosis is unique, as the condition goes away in a relatively short time period after it occurs, but can recur. Its transient nature, similar to Gestational Cellosis, the only High Glucose Conditions which, by their very nature, are intrinsically self-curing. However, Transient Neonatal Diminosis increases the risk of getting Cellosis.

Neonatal Diminosis Type Profile
(derived from Neonatal Diminosis Causality / Treatment / Risk Profile)
When all Neonatal Diminosis is being referred to, a clarifying Neonatal Diminosis Type isn't necessary. However, when a specific type of Neonatal Diminosis is being referred to, the exact monogenetic cause helps to clarify exactly which one is being referred to.

The monogenetic cause of Neonatal Diminosis varies based on the exact gene which causes the condition (a different gene in each type, as detailed below) and based on whether the Neonatal Diminosis is Permanent or Transient. 
Permanent Neonatal Diminosis (PND)
When a specific type of Permanent Neonatal Diminosis is being referred to, the exact monogenetic cause helps to clarify exactly which one is being referred to (see the table above for details):
  • KCNJ11 Permanent Neonatal Diminosis
  • ABCC8 Permanent Neonatal Diminosis
  • INS Permanent Neonatal Diminosis
  • GCK Permanent Neonatal Diminosis
  • IPF1 Permanent Neonatal Diminosis
    or PDX1 Permanent Neonatal Diminosis
  • PTF1A Permanent Neonatal Diminosis
  • FOXP3, IPEX syndrome Permanent Neonatal Diminosis
  • EIF2AK3, Wolcott-Rallison syndrome Permanent Neonatal Diminosis
Transient Neonatal Diminosis (TND)
When a specific type of Transient Neonatal Diminosis is being referred to, the exact monogenetic cause helps to clarify exactly which one is being referred to (see Transient Neonatal Diminosis Causality / Treatment area above for details):
  • ZAC/HYMAI Transient Neonatal Diminosis
  • KCNJ11 Transient Neonatal Diminosis
  • ABCC8 Transient Neonatal Diminosis
  • HNF1B Transient Neonatal Diminosis

It occurs in from 1 in 100,000 to 1 in 500,000 births. The permanent forms of Neonatal Diminosis are similar to other Diminosis conditions (the exception being their occurrence within 6 months after birth), but the transient forms are unique in that, like Gestational Cellosis, they go away but can recur. It may be treated with sulfonylureas, although exogenous insulin may be required.


 


Other High Glucose Conditions (Ohiglucons)

(formerly called other diabetes mellitus or confusingly,
when used without clarifier, diabetes
)

The following website, the primary source for the Other High Glucose Conditions listed in this section. That website fails to note that one of the conditions (Wolfram Syndrome) also causes Insipidus, and one of the conditions (Bardet-Biedl Syndrome) sometimes is associated with Insipidus, in addition to what I've found regarding their disparate causal relationships listed above for 55 of the Other High Glucose Conditions:
  • Insulinitis, 10 + 3 maybe yes/maybe no

  • Cellosis, 19

  • Diminosis, 11

  • Permanent Neonatal Diminosis, 8

    and

  • Transient Neonatal Diminosis, 4
Etiologic (assigning or seeking to assign a cause) Classification of Diabetes Mellitus (old name for High Glucose Conditions)

At that website, there is a category called "others" in each of the 8 major areas listed. While researching the listed conditions, I found 4 unlisted conditions that should be added:

Alstrom Syndrome, Werner Syndrome,
Polycystic Ovary Syndrome, and Hypothyroidism

The 24 Other High Glucose Conditions not documented above (as they're either unique High Glucose Conditions or their involvement in causing Insulinitis or Cellosis is unknown or unclear) are included in the following area, along with brief summaries in each of the 8 major areas on the 55 conditions which cause either Insulinitis, Cellosis, Diminosis, or Neonatal Diminosis.

Other High Glucose Conditions
Causality / Treatment / Risk Profile

Causality

Beta Cell Function Genetic Defects

These conditions cause Diminosis or Neonatal Diminosis or for Mitochondrial DNA, cause Cellosis

Drug or Chemical-Induced

Pentamidine & Vacor - Pyrinuron - Pyriminil can cause Insulinitis, Alpha Interferon & Highly Active Antiretroviral Therapy (HAART) may or may not cause Insulinitis; Antipsychotics, Beta-Adrenergic Agonists, Highly Active Antiretroviral Therapy (HAART), HMG CoA reductase inhibitors - statins, & Thiazides can cause Cellosis         

Diazoxide (unique or unknown or unclear)

Dilantin (unique, doesn't appear related to causing High Glucose conditions in a drug used to control epileptic seizures; does, however, raise glucose levels in those who already have any of the High Glucose Conditions)

Glucocorticoids (unique, but can cause Cellosis; when Cellosis is caused by glucocorticoids, it is transient unless the use of glucocorticoids coincidentally coincided with getting Cellosis caused by some other condition)


Nicotinic Acid (unique or unknown or unclear, with some articles supporting using this when one has Cellosis, and some articles cautioning that nicotinic acid use results in higher glucose levels in those who already have Cellosis, but I was unable to find information which conveyed that any High Glucose Condition resulted from nicotinic acid)

Thyroid Hormone
(unique, used to treat Hypothyroidism - see Hypothyroidism and Hyperthyroidism in Endocrinopathies area)

Endocrinopathies

Acromegaly, Aldosteronoma, Hypothyroidism, & Polycystic Ovary Syndrome can cause Cellosis

Cushing's Syndrome
(unique, but people who are obese, have Cellosis, and have high glucose levels and high blood pressure are at increased risk of developing Cushing's Syndrome)

Glucagonoma (unique, resulting when a tumor in the alpha cells causes increased production of glucagon; a High Glucose Condition results in 80% to 90% of those who have Glucagonoma; affects fewer than 1 in 20 million)

Hypothyroidism and Hyperthyroidism (unique, associated with, but non-causal in Insulinitis: up to 33% of those with Insulinitis have a thyroid condition; 12% of those with Cellosis have a thyroid condition, and per one large study, hypothroidism is causal in Cellosis; 7% of the general population has a thyroid condition)

Pheochromocytoma (unique, a rare tumor of the adrenal glands that can lead to hyperglycemia)
 

Somatostatinoma (unique and rare neuroendocrine tumor occurring in 1 in 40 million persons, can cause hyperglycemia by inhibiting the normal release of insulin)

Exocrine Pancreas Diseases

Pancreatectomy, Pancreatitis, & Trauma can cause Insulinitis if insulin production is totally or near totally lost
       

Cystic Fibrosis (unique, with some similarities to some aspects of Cellosis, and differing similarities to a few aspects of Insulinitis, it's different enough to list this as a unique High Glucose Condition; 1 in 2500 are born with Cystic Fibrosis; of those with Cystic Fibrosis, a High Glucose Condition is present in 2% of children, 19% of adolescents, and 40% to 50% of adults)

Fibrocalculous Pancreatopathy, also known as Tropical Chronic Pancreatitis (unique, seen only in developing countries, reported from many parts of Africa, South America and South-East Asia, its highest prevalence is in Southern India; high glucose develops 10 years after the condition is first detected due to abdominal pain)

Exocrine Pancreas Diseases (continued)

Hemochromatosis (unique, the most common single-gene disease in Western populations, affecting 1 out of every 200-300 people; without treatment, the disease causes the liver, heart, and pancreas to fail, leading to cirrhosis, heart disease, and a high glucose condition; if treatment occurs early, all of those conditions can be prevented; hemochromatosis can be virtually cured through treatment, blood-letting, but the other conditions, if already present, they reflect the degree of damage which occurred before hemochromatosis was cured)

Neoplasia (unique or unknown or unclear, difficult to ascertain the relationship between neoplasia, which includes the dreaded cancer word, and High Glucose Conditions, but since the area this is under pertains to exocrine pancreas, one would assume that the neoplasia referred to involves the exocrine pancreas)

Pancreatectomy (a unique High Glucose Condition occurring when a pancreatectomy results in continued insulin production which is insufficient to prevent a High Glucose Condition; however, if a total or near-total pancreatectomy results in a total or near-total loss of insulin production, Insulinitis transpires)

Pancreatitis (unique, and two areas -- Causal and Resulting: causal when reduced insulin production causes High Glucose levels; if insulin production is totally or near-totally reduced due to chronic pancreatitis, Insulinitis results; Resulting? can result when one has Cellosis, with a 2.8 times greater risk for getting pancreatitis than the risk for those who don't have Cellosis; also, some medications used to treat Cellosis, Byetta - Januvia - Onglyza - Victoza, increase one's risk of getting chronic pancreatitis)

Trauma (a unique High Glucose Condition occurring when trauma results in insulin production which is insufficient to prevent a High Glucose Condition; however, if a trauma results in a total loss of insulin production, Insulinitis transpires)

Infections

Congenital Rubella can cause Insulinitis, Cytomegalovirus may or may not cause Insulinitis and can cause Cellosis in those over 85

Insulin Action Genetic Defects

Leprechaunism / Donahue Syndrome (Unique, impaired development of organs & tissues throughout the body resulting in death of most with this condition by age 2, impacts less than 1 per million, insulin resistance causes high glucose levels)

Lipoatrophic High Glucose Condition (Unique, with insulin resistance causing high glucose levels; also characterized by severe lipodystrophy)

Rabson-Mendenhall Syndrome (Unique, a severe insulin resistance syndrome causing high glucose levels, with affected individuals usually surviving 'til their teens or twenties, impacts less than 1 in a million)

Type A Insulin Resistance Syndrome (Unique, a milder severe insulin resistance syndrome which is generally not life-threatening, causing high glucose levels, impacts about 1 in 100,000)

Other Genetic Syndromes

Down's Syndrome, Turner Syndrome in females during childhood, & Wolfram Syndrome at ages 6 to 16 can cause Insulinitis; Alstrom Syndrome, Bardet-Biedl Syndrome, Klinefelter Syndrome, Friedreich Ataxia, Myotonic Dystrophy, Prader-Willi Syndrome, Turner Syndrome in adults, & Werner Syndrome can cause Cellosis

Huntington Chorea (unique or unknown or unclear)

Porphyria (unique or unknown or unclear)

Uncommon Forms of Immune-Mediated

Stiff Person Syndrome can cause Insulinitis     

Anti-Insulin Receptor Antibodies
(unique or unknown or unclear)

Treatment
Treatments vary for each condition. As for the nature of dealing with high glucose levels in each condition, the array of medications listed in the Cellosis treatments area are likely candidates, but particular conditions may be more or less likely to be helped by some of the types of medications used to deal with Cellosis.
Risk
The risks vary for each condition, and the high glucose condition risks vary based on the type(s) of medication used and the ability to keep HbA1c levels as close to normal as possible without having an unacceptable increase in hypoglycemic risks. Refer to the Cellosis Risk Profile for treatment risks and long term sequelae from dealing with high glucose levels.

Other High Glucose Conditions Type Profile
(derived from Other High Glucose Conditions Causality / Treatment / Risk Profile)
When all of the Other High Glucose Conditions are being referred to, a clarifying Other High Glucose Conditions Type isn't necessary. However, when a specific type of Other High Glucose Condition is being referred to, the specific type helps to clarify exactly which one is being referred to. 55 Other High Glucose Conditions are causal in either Insulinitis, Cellosis, Diminosis, or Neonatal Diminosis. See the four separate Types Profile areas above for details, and note that those types are also listed in the 8 major areas of the table above.

24 Other High Glucose Conditions are unique or unclear as to their causal relationships to Insulinitis, Cellosis, Diminosis, and Neonatal Diminosis, and are listed below (see the table above for details):

Drug or Chemical-Induced
  • Diazoxide Ohiglucon
  • Dilantin Ohiglucon
  • Glucocorticoids Ohiglucon
  • Nicotinic Acid Ohiglucon
  • Thyroid Hormone Ohiglucon
Endocrinopathies
  • Cushing's Syndrome Ohiglucon
  • Glucagonoma Ohiglucon
  • Hypothyroidism Ohiglucon & Hyperthyroidism Ohiglucon
  • Pheochromocytoma Ohiglucon
  • Somatostatinoma Ohiglucon
Exocrine or Pancreas Diseases
  • Cystic Fibrosis Ohiglucon
  • Fibrocalculous Pancreatopathy Ohiglucon
  • Hemochromatosis Ohiglucon
  • Neoplasia Ohiglucon
  • Pancreatectomy Ohiglucon (if insulin production is totally or near-totally reduced, Pancreatectomy Insulinitis results)
  • Pancreatitis Ohiglucon (if insulin production is totally or near-totally reduced, Pancreatitis Insulinitis results)
  • Trauma Ohiglucon (if insulin production is totally or near-totally reduced, Trauma Insulinitis results)
Insulin Action Genetic Defects
  • Leprechaunism / Donahue Syndrome Ohiglucon
  • Lipoatrophic Ohiglucon
  • Rabson-Mendenhall Syndrome Ohiglucon
  • Type A Insulin Resistance Syndrome Ohiglucon
Other Genetic Syndromes
  • Huntington Chorea Ohiglucon
  • Porphyria Ohiglucon
Uncommon Forms of Immune-Mediated
  • Anti-Insulin Receptor Antibodies Ohiglucon





High Glucose Conditions (Higlucons)

(formerly confusingly called diabetes mellitus
or diabetes without clarifier)


Sometimes, the old diabetes word is used to refer to a condition which is known to exist in all who have any of the High Glucose Conditions; this transpires a minority of the time the old diabetes or diabetic word is used.

Most often, when the old diabetes or diabetic word is used, only one or a subset of all High Glucose Conditions is being referred to, making it difficult or impossible to know which one is actually being discussed.

Someone with ______

(formerly called diabetic, except someone with reactive
hypoglycemia, they were referred to as someone
with reactive hypoglycemia)


Refers to someone who has one of the High Glucose Conditions, most often,  though it may also be used to refer to someone who has the non-glucose anomaly Insipidus, or someone who has the low glucose condition Hut.

Sometimes the old diabetic word is used in conjunction with other conditions or sequelae which result from having one of the High Glucose Conditions or the non-glucose anomaly Insipidus. It's often times difficult or impossible to know which condition is being referred to when the old diabetic word is used.

The ideal solution, do away with the old diabetic word, and replace it by humanizing the description of the individual with a particular glucose anomaly, or with the non-glucose anomaly Insipidus, by simply identifying them as someone with ______ (see following list, [with old names, ideally no longer in use, detailed in brackets to the right of the new names]): 
  • Insulinitis (Islit) [old name: type 1 diabetes]

    Example of this new naming convention with the exact nonconfusing name for the actual condition I got in March of 1961, when I was 5 years old:


-or-
  • Latent Autoimmune Insulinitis (LaIslit) [old name: latent autoimmune diabetes]
-or-
  • PreCellosis (PreClos) [old name: prediabetes]
-or-
  • Cellosis (Clos) [old name: type 2 diabetes]
-or-
  • Gestational Cellosis (GesClos) [old name: gestational diabetes]
-or-
  • Diminosis (Dios) [old name: maturity onset diabetes of the young (MODY)]
-or-
  • Neonatal Diminosis (NeoDios) [old name: neonatal diabetes]
-or-
  • One of the Other High Glucose Conditions (Ohiglucons) [old name: typically, called diabetes, sometimes with a clarifier, oft-times without a clarifier]
-or-
  • Insipidus (Ins) [old name: diabetes insipidus]
-or-
  • Hypoglycemia Uncaused by Treatments for High Glucose (Hut) [old name: reactive hypoglycemia]
Also, in doing away with the old diabetic word, replace it with the exact condition involved (for example, instead of diabetic retinopathy, you'd have Insulinitis Retinopathy if it was caused by Insulinitis, Cellosis Retinopathy if it was caused by Cellosis, etc. (see list above).





Outside the High Glucose Area





Non-Glucose Anomaly
       
Insipidus (Ins)


(formerly called diabetes insipidus or confusingly,
when used without clarifier, diabetes
)

Excessive urination and extreme thirst (especially for cold water and sometimes ice or ice water) are typical for this condition. Insipidus causes no hyperglycemia (elevated blood glucose) or hypoglycemia (low blood glucose), the only one of the old diabetes words which does not entail any glucose anomaly.

Signs of dehydration may also appear in some individuals since the body cannot conserve much (if any) of the water it takes in.
Insipidus Causality / Treatment / Risk Profile
Causality
Insipidus results from:
  • a problem with the production of vasopressin in the hypothalamus (Central or Neurogenic Insipidus) due to a range of causes: vascular, autoimmune, infection, sarcoidosis, some drugs, surgery, head trauma, benign or metastatic pituitary-hypothalamic tumor (particularly originating from breast and lung), or unknown causes (in roughly half the cases)

    or

  • the kidney's response with an inability to respond to vasopressin (Nephrogenic Insipidus), and which can also be caused by electrolyte imbalances (eg, hypercalcemia), or drugs (eg, lithium toxicity)

    or

  • excessive intake of fluids (Dipsogenic Insipidus) which may be due to a defect or damage to the thirst mechanism, located in the hypothalamus

    or
  • during pregnancy (Gestational Insipidus), excessive and/or impaired clearance of vassopressinase in the placenta or serious diseases of pregnancy (pre-eclampsia, HELLP syndrome, acute fatty liver of pregnancy)

The incidence of Insipidus in the general population is 3 in 100,000. Genetics play a role in less than 10% of Insipidus diagnoses.

One of the Other High Glucose Conditions, Wolfram Syndrome Insulinitis, also can include Insipidus, and another one of the Other High Glucose Conditions, Bardet-Biedl Syndrome, sometimes is associated with Insipidus.

Treatment
In severe cases of Insipidus, it can be virtually impossible to completely eliminate the extreme thirst or need to urinate frequently. Desmopressin and other medications can make a difference, but sometimes only small changes are achieved. Gestational Insipidus may resolve itself on its own, 4 to 6 weeks after pregnancy ends.
Risk
Dehydration in those who don't have Dipsogenic Insipidus, which can lead to low blood pressure, nerve parasthesias, and irregular and rapid heartbeats which could lead to life-threatening conditions. Rehydration is critical, and emergency medical help is required if one is unable to self-rehydrate. Electrolyte imbalances.

Insipidus Types Profile
(derived from Insipidus Causality / Treatment / Risk Profile)
When all Insipidus is being referred to, a clarifying Insipidus Type isn't necessary. However, when a specific type of Insipidus is being referred to, an additional word or words helps to clarify exactly which one is being referred to.
When one of the following conditions causes Insipidus, the following Insipidus Type results (see the table above for details):
  • Central or Neurogenic Insipidus
  • Dipsogenic Insipidus
  • Gestational Insipidus
  • Nephrogenic Insipidus
One of the Other High Glucose Conditions (Wolfram Syndrome Insulinitis) also can include Insipidus:
  • Wolfram Syndrome Insipidus (in about 70% of those with Wolfram Syndrome)
Another one of the Other High Glucose Conditions sometimes is associated with Insipidus:
  • Bardet-Biedl Syndrome Insipidus




Low Glucose Condition
      
Hypoglycemia Uncaused by Treatments for High Glucose (Hut)


(formerly called reactive hypoglycemia, but also
includes a unique type formerly referred to as
fasting hypoglycemia)


Hypoglycemia (glucose under 70) for persons who are not being treated for any of the High Glucose Conditions with any type of medication. Recommended treatments for Hut include a diet which can reduce the likelihood of the pancreas reacting with too much insulin.

Hut
Causality / Treatment / Risk Profile

Causality
Per the National Institutes of Health, the causes of most cases of Hut are still open to debate.

The exact cause of Hut is still unknown, but there are 21 hypotheses that might explain why it can happen (listed in alphabetical order):

  • Beta Blocker Meds (after strenuous exercise) are sometimes associated with Hut

  • Breast cancer is sometimes associated with Hut

  • Chronic high carbs in a diet can trigger Hut

  • Chronic Mental Stress is sometimes associated with Hut

  • Chronic Physical Stress is sometimes associated with Hut

  • Congenital Enzyme Deficiencies can cause Hut

  • Drugs (including antibiotics), their prolonged use is sometimes associated with Hut

  • Enzyme deficiencies can cause Hut, but these are rare and occur during infancy

  • Epinephrine (a hormone that is released in the body during times of stress), sensitivity to it can cause Hut
  • Fasting Hut sometimes occurs after long periods without food, but it also happens occasionally following strenuous exercise, such as running in a marathon

  • Gestational Hut (pregnancy is sometimes associated with Hut)

  • Heartbeat Arrhythmias are sometimes associated with Hut

  • Helicobacter pylori-induced gastritis can cause Hut

  • High simple carbs in a poor diet are sometimes associated with Hut

  • Hormonal conditions (example: hypothyroidism) can cause Hut
  • Hyperinsulinism (excess insulin production), which sometimes is caused by insulinomas (insulin-secreting tumors of the islets of langerhans), which occur in 1 to 4 in one million persons per year, can cause Hut

  • Insufficient glucagon production. Glucagon is a hormone which raises blood glucose levels normally, a hormone which those who have any of the High Glucose Conditions typically measure with bloodpricks - since Hut typically is accompanied with noticable symptoms, most who have Hut deal with it without using bloodpricks

  • Stomach surgery (15% experience Hut after stomach surgery)
  • Upper Gastrointestinal Tract Surgery is sometimes associated with Hut

  • Weakened Immune System is sometimes associated with Hut
Hut usually occurs about 2-4 hours after eating a high carbohydrate meal or ingesting high carbohydrate drinks or snacks (exceptions to that noted above).

Some think Hut results from excessive amounts of insulin the body releases in response to high carbohydrate meals / snacks /  drinks (exceptions to that noted above). When more insulin is released than needed, without sufficient counter responses via release of glucagon and epinephrine, blood glucose goes too low.

But Hut can also happen if your body burns glucose too rapidly, or if your digestive process is too slow in metabolizing the glucose into the bloodstream.
Treatment
Prevention:
  • Eat several small meals and snacks throughout the day, no more than three hours apart during waking hours
  • Eat a well-balanced diet, including lean and nonmeat sources of protein, and high-fiber foods, including whole grains, fruit and vegetables
  • Avoid or limit sugary foods, especially on an empty stomach
  • Be sure to eat food if you're consuming alcohol and avoid using sugary soft drinks as mixers
  • Exercising regularly; exercise increases sugar uptake which decreases excessive insulin release (however, exercise can also cause hypoglycemia in those with Hut, so caution is well-advised)
  • Eat a variety of foods, including meat, poultry, fish, or nonmeat sources of protein, foods such as whole-grains, fruits, vegetables, and dairy products
In the relatively rare cases of Hut that are caused by hyperinsulinism, some drugs are helpful in treating the condition.

Ironically, prevention is tossed out the window when one's glucose goes too low due to Hut, in which case the same glucose-raising substances must be used as those used to deal with Insulinitis or to deal with other High Glucose Conditions if treatment causes low glucose in those with Diminosis, Neonatal Diminosis, Cellosis, or other High Glucose Conditions.
Risk
Generally, since hypoglycemia is both preventable and easily treatable in Hut, with no hyperglycemic risks, and since hypoglycemia is typically less severe and less frequent in Hut than it is in Insulinitis, the risk is most often much lower.  However, in rare cases when Hut fails to respond to treatment, becoming dangerously recurrent / persistent, in such cases, removal of all or part of the pancreas may be required (which is called a pancreatectomy), in which case the individual, if their loss of insulin production is total or near-total, gets Pancreatectomy Insulinitis (one of the types which are uncaused by Insulitis, the overwhelming cause of Insulinitis).


Hut Type Profile
(derived from Hut Causality / Treatment / Risk Profile)
When all Hut is being referred to, a clarifying Hut Type isn't necessary. However, when a specific type of Hut is being referred to, an additional word or words helps to clarify exactly which one is being referred to.
When one of the following conditions or diet or drugs or strenuous exercise causes Hut, the following Hut Type results (see the table above for details):
  • Beta Blocker Meds After Strenous Exercise Hut
  • Breast Cancer Hut
  • Chronic High Carbs Hut
  • Chronic Mental Stress Hut
  • Chronic Physical Stress Hut
  • Congenital Enzyme Deficiencies Hut
  • Drugs Hut
  • Enzyme Deficiencies Hut
  • Epinephrine Sensitivity Hut
  • Fasting Hut
  • Gestational Hut
  • Heartbeat Arrhythmias Hut
  • Helicobacter Pylori-Induced Gastritis Hut
  • High Simple Carbs Hut
  • Hormonal Hut
  • Hyperinsulinism Hut
  • Insufficient Glucagon Hut
  • Stomach Surgery Hut
  • Strenuous Exercise Hut
  • Upper Gastrointestinal Tract Surgery Hut
  • Weakened Immune System Hut





diabetes / diabetic / reactive hypoglycemia
Name
Problems and Solutions

To conclude this article, the graphic below reiterates the suggested new names for
  • the seven disparate types of High Glucose Conditions which currently are oft-times called diabetes, with persons having any of the conditions oft-times called diabetic (diabetes / diabetic, old outdated names), which confuses and misleads because when those terms are used without a clarifier, they most often only apply to only one of the High Glucose Conditions, and which one is oft-times unknown

  • one non-glucose anomaly, diabetes insipidus, which can also go by the old diabetes name, with persons having this condition oft-times called the old diabetic name, which confuses and misleads because those terms are often used to only apply to one, some, or all of the High Glucose Conditions

  • the one low glucose condition which doesn't have the old diabetes name in its current name, but which has a name (reactive hypoglycemia) which confuses and misleads because it doesn't result from any reaction to any medication used to treat any of the High Glucose Conditions