Diabetes mellitus type 2, also known as non-insulin-dependent
diabetes mellitus (NIDDM) used to be mainly a condition of middle
and old age, common in people over 60. Modern dietary changes
have now caused the condition to be found in younger people including
children. Diabetes type 2 is associated with hyperglycaemia and
obesity. Diabetics are at higher risk for hypertension, retinopathy,
nephropathy, and atherosclerotic coronary and peripheral vascular
disease.
In diabetes type 2 the pancreas continues to produce insulin
but the insulin has decreased effectiveness in its normal function
of stimulating glucose uptake by muscle, and in restraining glucose
output by the liver. This syndrome is known as "insulin resistance",
with the result is that blood glucose remains high. Most people
with the condition are treated by diet, exercise and oral drugs,
but a few may need insulin to maintain control.
Let us see what is really happening in this condition. Although
the pancreas responds to high blood glucose by releasing the peptide
hormone insulin, the base or lowest level of circulating blood
glucose is set by the liver. Blood glucose rises considerably
in the hours after a meal, but then the level starts to fall.
The level falls faster if the individual is physically active and using
the glucose to fuel muscle action. As the level falls below the
set point, the liver supplies more glucose to raise the glucose
to the set point again.
In persons consuming a high carbohydrate diet in excess of the
amount needed to produce just sufficient glucose for their normal
level of physical exercise, the liver set point rises over time.
If this pushing-up of the set point continues over a long time
then the liver habituates to a higher level set point. The set
point is found by a standard test called the plasma fasting glucose
(FPG) test, which measures blood glucose after an overnight fast
of ten hours. During the ten hour fast the only consumption can
be plain water. Electronic meters with a blood drop test strip
are available at low cost to measure FPG at home.
There are slight variations between individuals, but two consecutive
FPG readings of over 5.6 mmol/L (100 mg/dL) now officially classsifies
a person as pre-diabetic, indicating the need for attention to
diet and exercise if diabetes is to be avoided. Over 7.0 mmol/L
(126 mg/dL) is now recommended to be the level indicating full
diabetes type 2.
However the FPG level for blood glucose likely to trigger or
maintain miliaria class conditions is two out of three readings
greater than 5.0 mmol/l, (90 mg/dL) a level not previously thought
important.
Now we know that when the blood glucose set point is habituated
at a higher level the pancreas produces more insulin, but this
higher output insulin is not as effective as normal insulin. The
higher the output, the less effective the insulin becomes.
The pancreas has both exocrine outputs of hormones and also endocrine
outputs. The insulin output is endocrine, being output into circulation,
but to reach circulation the insulin travels in ducts which
behave like exocrine ducts, and are havards. Thus, when high blood
glucose stimulates a higher insulin output speed, the final insulin
product output is modified and the insulin is not effective. This
action of pancreatic havards is the cause of so-called "insulin
resistance".
The group of drugs known as sulfonylureas stimulate the output
of insulin from the pancreas without reference to the actual level
of blood glucose. They prompt the production of glucose at the
slower basal level. This insulin is fully effective in reducing
blood glucose before mealtimes when the pancreas would not normally
be producing insulin. The temporary reduction in blood glucose
by these drugs is useful in partially rehabituating the liver
to a lower set point level of blood glucose. However, following
ingestion of carbohydrate, blood glucose rises sharply, the insulin
output speeds up and so the insulin again becomes ineffective.
It follows that treatment of diabetes type 2 needs to be aimed
firstly at preventing the pancreatic insulin ducts from modifying
the insulin in passage through the ducts. Essential hypertension
is doubly dangerous for diabetics and needs to be treated. Both
treatments can be effected by the use of ActivSignalTM
Sodium, which signals to both the pancreatic ducts and the sweat
ducts to switch off their reaction to increased speed, treating
both diseases. The first commercial ActivSignal product is now under development.
The second and simultaneous aim of treatment is to reduce the
habituated liver set point for the release of glucose. This is
normally effected by diet and exercise and also the use of anti-diabetes drugs.
Diabetes type 2 illustrates for us why some miliaria class conditions
are more prevalent among certain groups of people. The much studied
Pima people had a settled way of life by the Gila River of Southern
Arizona, starting 30,000 years ago. They were expert agriculturalists,
irrigating the desert, and athletes in their society were highly
regarded. The daytime heat and frequent use of sweat lodges kept
their sweat ducts in original habituation, and so their blood
sodium was maintained. The Pima were well known for their ability
to run long distances.
Manual agricultural work has a pattern of usage of blood glucose
by muscle for long periods, and food consumption of just sufficient
an amount to maintain bodily condition. As a result, over centuries,
the liver habituates to a low set point for the release of blood
glucose, because traditionally blood glucose has been low and
correspondingly sodium has been high.
During the last century, the day-long manual work of the Pima
has ended, and instead the Pima spend their days in the shade
probably eating an amount of food which is slightly in excess
of muscle energy requirement. So their blood glucose easily rises
above that low original habituation set point, and because it
was low, then they are much more likely to be susceptible to miliaria
class conditions than groups with a higher set point.
It will also be appreciated that for those doing manual work
all day long, and whose blood glucose is being fully used by muscle,
a high carbohydrate diet is appropriate and healthy. This changes
entirely when, in following generations, the day-long manual work
is no longer necessary.
We are all susceptible to miliaria class conditions, but those
groups who are more susceptible will be those who, a few generations
ago, traditionally did manual work in hot climates, and who therefore
have inherited a lower liver glucose release set point, as indicated
by their original habituation basal FPG level.
Fortunately, the invention of signalling products means that
we can change the adverse habituation causing miliaria class conditions,
to innate healthy original habituation. This means that adverse
habituation does not have to pass on to future generations.
