Before reading this chapter please start with chapters:
First Concepts.
WOB is Optimal

Type 1 diabetes mellitus is a deficiency of insulin production by beta cells manifested by hyperglycemia and glycosuria. Medicine therefore proposes that treatment ought to correct the deficiency  by supplying the missing hormone. The aim being to restore blood glucose to its normal level, i.e. to reestablish normoglycemia.  Does this approach consider also the WOB demands? Our  doubts are discussed in the chapter ‘What is normoglycemia? While medicine regards type-2 diabetes  as an evolving hyperglycemia it ought to be regarded as an evolving normoglycemia, and since type-1 diabetes is manifested by a rising blood sugar, the notion of an evolving normoglycemia may apply here as well.

The disease proceeds through the following stages:

1. Chronic beta cell infection (insulitis) accompanied by normoglycemia.
2. Pre-clinical (undiagnosed) hyperglycemia.
3. Clinical diabetes mellitus manifested by hyperglycemia, glycosuria, and secondary manifestations, e.g. keto-acidosis and glucose toxicity

Type-1 diabetes is driven by an ongoing latent virus  infection of Langerhans islet cells (insulitis) which impedes insulin production. Insulitis is manifested by autoimmune markers, e.g. Insulin  antibodies. The three stages may thus be rephrased as follows:

1. Normal insulin production.
2. Compensated hypo-insulinism.
3. Decompensated hypo-insulinism ending in beta cell aplasia.

Stage-1 is manifested solely by autoimmune markers. Only in retrospect it may be  regarded as a forerunner of diabetes since in some patients with autoimmune markers insulin production may remain normal. The same is true for patients in stage-2. Some may remain compensated for years and  diagnosed in advanced age. For this reason the term ‘juvenile diabetes’ was renamed as type-1 diabetes.


How strong is the argument that type-1 diabetes is an auto immune disease? This statement  is based on observations, e., g.,  beta cell death, beta cell  and insulin antibodies, which  also accompany viral infections. Insulin antibodies appear also in type-2 diabetes patients  receiving insulin.  The notion of autoimmunity is an interpretation  and not a fact. Here this view is unacceptable since WOB is optimal  and does not commit suicide.(v. "Self and non-self"). In order to limit the spread of virus WOB may kill infected beta cells by mobilizing T-cells, which is a protective measure and not a suicide. The  so called auto-antibodies are markers of a virus driven beta cell necrosis, initiated either by the virus or T-cells.


When planting our therapeutic strategy we ought to consider the fate of  patients with pre-clinical hypo-insulinism  who are healthy, since their WOB is silent.  WOB manages to control their disease for years.  Recently their condition received a new name: Latent Autoimmune Diabetes in the Adult or, LADA which refers to  autoimmune forms of diabetes not requiring insulin initially.  It is also  called   slow-progressing type 1 diabetes. These patients are called here Insulin-yogis. The yogi-suffix highlights their capability to live in peace despite insulin deficiency.

Since diabetes is generally incurable,  the therapeutic objective is to slow down disease progression which depends on the balance between host (WOB) and driver (virus). It  may be slowed down either by eliminating the virus or strengthening WOB. Since the first cannot be realized, insulin-yogis somehow improve their WOB control. What is their secret? Applying it to other patients might save many from decompensation and beta cell aplasia.

It is striking that they can manage with less insulin. Only in an emergency, e., g., infection, followed by keto-acidosis, they need insulin, which marks also the onset of the clinical stage of diabetes. After recovery some patients may  resume their pre-clinical hypo-insulinism  and do not need external insulin. Nevertheless they  will receive it.


Throughout the pre-clinical stage  WOB is silent  and operates well with less   insulin. Nevertheless doctors are uneasy and search for these healthy patients with hyperglycemia since over the years elevated blood sugar might cause glucose toxicity. For this reason they recommend that even healthy compensated diabetics should receive insulin. After all there seems to be no harm in treating these patients with insulin.


When WOB faces a beta cell deficiency it adjusts all processes to this new condition. As diabetes progresses WOB maintains an equilibrium called here a solution. Diabetes proceeds from solution to solution and since the patient feels healthy these solutions are optimal. When receiving  external insulin WOB creates a new equilibrium (solution) which may be less optimal than that in the untreated hypo-insulinism.  Simply because insulin level is only one component of this balance. 


Actually the virus destroys more than just beta cells. Diabetes is driven by an infection of the entire islet, or insulitis which destroys also other hormone producing cells,  e., g., glucagon. It seems reasonable thattype-1 diabetes is a multi-endocrine deficiency. Glucagon may not be as vital as insulin and does not affect the overall clinical picture particularly since other hormones like epinephrine may take over.

External insulin interferes with this delicate balance.  In response WOB gradually cuts down internal insulin production making the patient more and more dependent on external insulin. Like in type-2 diabetes , which  in the beginning is manifested by insulin resistance, and later on turns into  insulin  deficiency.

The fine tuning of homeostasis

At any instant WOB maintains an equilibrium. Even if an ingredient oscillates all the time it  maintains a balance with other processes in the body.  Actually all processes in the body participate in this oscillation and so maintain an equilibrium. External insulin perturbs this delicate balance. Even the most sophisticated insulin pump cannot match the efficiency of internal insulin, and WOB objects to it, sending signals such as, dizziness, vertigo, malaise and sugar craving. This is the price for getting external insulin.


The physician has to work out a compromise between WOB objection to external insulin and  the necessity to avoid a possible glucose toxicity in the future. Is the risk of glucose toxicity  so serious as to make the patient insulin dependent?


Paolo Pozzilli, and Umberto Di Mario
Autoimmune Diabetes Not Requiring Insulin at Diagnosis (Latent Autoimmune Diabetes of the Adult)  Definition, characterization, and potential prevention

Marian Rewers and Georgeanna J. Klingensmith
Prevention of Type 1 Diabetes

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