Hormones are the body's mechanisms
for adapting its functions to changes in the environment.
Insulin is a hormone. Only the body itself, when in balance, can
properly determine the correct amount of hormones to release. One should note the controversies in recent
years concerning other hormone replacements.
Insulin does two things:
1. Lowers blood glucose.
2. Promotes fat storage.
Although these two functions are
related, it is better to view them as independent and separate, for the sake of
understanding diabetes.
When exogenous (bottled) insulin
is used in type 1 diabetics it promotes fat storage. When endogenous (human source) insulin is released from the
pancreas, through the action of an oral medicine used by type 2 diabetics to
stimulate extra insulin release, it promotes fat storage. When endogenous insulin is released due to
an increase in blood glucose concentrations from a food intake in normal
non-diabetic persons, it promotes fat storage.
The more insulin in the system, the more fat is stored. The more fat is stored, the more insulin
resistance there is. The more insulin
resistance there is, the more insulin is required to lower blood glucose
concentration. This is also a vicious
self-compounding circle.
I have only been overweight while
on insulin. I wonder if overweight
people don't have too much insulin in their bodies, which is a sign of a heavy
glucose load, the cause of which has not been properly identified yet.
The only reason that the pancreas
releases insulin is in response to a glucose (sugar) load, or an increase, or a
sudden increase in the amount of glucose (sugar) in the system. Glucose stimulates insulin release. The goal should be to use the least amount
of insulin that will keep blood sugar normal.
Therefore, in order to control the
amount of insulin released, one needs to control the glucose entering the
system, which stimulates insulin release.
A long fast should stop most glucose concentration increases in the
blood, as well as most insulin release from the pancreas. Fasting may be difficult if not impossible
for some bottled insulin users because of insulin peaks (period of time when
insulin is more active). Insulin peaks
necessitate food intake. Ketosis will
occur when fasting, increasing blood glucose levels slightly. Then the cause of hyperglycemia can be
narrowed down to other things such as infections.
Frequent fasting to control blood
glucose levels is not recommended because it messes up the digestive system and
basically makes one sick. Instead, a
low glycemic (low sugar content) diet over the long term is a better goal. Always keep blood glucose in the normal
range. If necessary gradually decrease
the dose of insulin, or oral agent that promotes insulin release,
accordingly. When using an oral agent
that promotes insulin release, think of it as taking insulin.
If an insulin user stops using
insulin suddenly, the absence of that insulin will result in ketosis (breakdown
of fat to glucose), then increasing blood glucose levels, resulting in diabetic
ketoacidosis, a life threatening condition.
The glucose lowering function of
endogenous insulin and of exogenous insulin may or may not lower blood glucose
levels efficiently or effectively due to the multiple compounding factors
causing blood glucose levels to rise, as listed above. The main factors are sugars, carbohydrates,
and infectious diseases, but these are not all inclusive.
What this means is that for a
given glucose concentration load, the amount of insulin that is needed to
control that blood glucose load to normal levels (80-120 mg/dl) may be either
small, large, fixed, variable, routine, or ever-changing, due to the blood
sugar raising factors listed above.
Most diabetics on insulin that I
have met have reported having had a cold-like infection, and losing a lot of
weight prior to diagnosis for diabetes.
I will explain this:
An infection causes the blood
glucose concentration to rise above the capacity of the pancreas to produce
enough insulin to lower it. This sends
the body into a condition of ketosis, which is the breakdown of fat into
glucose. This is why weight loss occurs. This glucose (from fat) increases blood
glucose levels even further, resulting in diabetic ketoacidosis.
One factor that should be
considered in Juvenile Diabetes is growth.
A child is growing all the time, the body is always changing, and the
amount of fat stored in the body is changing.
Think of an older person, who has a poor diet, doesn’t exercise, and
gains weight: that person becomes a type 2 diabetic. This is because of insulin resistance and perhaps disease. Some pregnant women temporarily get type 2
diabetes. This is attributable to the
changes in weight. Stress is also known
to be a cause of temporary type 2 diabetes.
Why should a child be any
different? The insulin producing
capacity of the pancreas in relation to the size and fat content of a child's
body is always changing. At certain
points in the growth development of the child, the system may be taxed to the
limit. Sugars, carbohydrates, inactivity,
and particularly infections trigger diabetes.
Just as in an adult, if a child is started on insulin at a young age,
the child's body will develop and adapt itself to the extra insulin in the
body. Not all diabetics on insulin are
obese, but I would attribute this to diet and to demeanor. A person using insulin who is calm, who is
not emotional, who eats conscientiously, routinely, and with moderation will
probably have excellent blood glucose control and be a thin diabetic. Insulin use and growth may be the reason why
the true nature of type 1 diabetes has eluded doctors and researchers for so
long.
The main problem I have had using
insulin over the years was that I took two shots of NPH insulin a day. This insulin starts to peak 2˝ - 3 hours
after injection; the peak lasts up to 8 hours, and then drops off somewhat but
lasts up to 23 hours. By taking two
shots a day, the tail end of activity of this insulin overlapped with the next
shot of NPH insulin. I also used
Regular insulin for meals, which begins to peak 1 hour after injection and
lasts 6-8 hours. Because of this overlapping,
slight daily changes in timing of when I took the injections, unforeseeable
varied physical activity, changing work load, and ever-changing meal menus, it
made the whole scheme unpredictable and therefore unmanageable. It also served to conceal the true nature of
my condition.
Every single day of my life for the last 21 years has been a guessing game of how much insulin to take. I have learned how to be right most of the time, but when I was wrong, the cure was either to eat when hypoglycemic or to suffer when hyperglycemic. In the first case, I loved to eat so it was easy. Hypoglycemia causes an instinctive knee-jerk reaction to want to eat more than is necessary to correct the problem, resulting in increased blood glucose. I recall having had hypoglycemia often in the first few years of the condition.
I have rarely had severe hypoglycemia (low blood glucose
levels) due to insulin reactions but the few that I had have filled me with
vigilance and fear about passing out. I
intentionally ran my blood glucose on the high side so as to avoid any chance
of public embarrassment. Also low blood
glucose makes me feel light-headed and so I ended up saying dumb things. I trained myself to bite my tongue when I
suspected hypoglycemia. Occasionally, I
have said things that I still regret due to hypoglycemia and also to
hyperglycemia.