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
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
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?
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