Quote:
Originally Posted by LexusLover
It's real simple. Change your diet, and restrict your sugar intake.
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Lots of things to do
unless he doesnt understand, which is likely the case, since his A1c is still above a 7, which means although his Blood glucose might be currently normal, for the most part it is high.
He needs to eat low carb(veggies/fruit) and exercise and maybe take bromocriptine as Lyle Donald talks about below:
About the Book
Bromocriptine is a dopamine agonist drug (meaning that it acts like dopamine in the brain) that has been used for over three decades for the treatment of a number of conditions such as Parkinson’s disease, acromegaly (the disease Andre “The Giant” had), and overproduction of the hormone prolactin. You may be wondering what this has to do with the topic of body composition.
As I discuss in many of my articles and other books, the body regulates factors such as body weight, composition and appetite through a variety of hormones such as insulin and leptin. It turns out that those hormones exert at least part of their effect through dopamine levels in the brain. When people diet, dopamine levels drop in the brain and this is responsible for many of the effects (such as lowered metabolic rate, increased hunger, etc.) that occur.
My book
Bromocriptine starts by outlining the systems that regulate body weight and fat levels before explaining how the drug bromocriptine can ‘trick’ the body into thinking that it’s not dieting so that metabolic rate doesn’t slow, hunger is decreased, etc. Side effects, dosing and everything else related to the drug and how it can be used for various purposes related to body composition are outlined in detail in the book.
which is available online
ie
http://freeweb.siol.net/mikelus/Lyle...mocriptine.pdf
Insulin, insulin resistance and diabetes
To understand the next batch of data, I have to make a quick tangent and give
you a very rough overview of insulin resistance, what it is and what it causes to
happen in the body. Please realize that this is a topic on which endless chapters
could be written, but I’m going to spare you the details and just sketch out the basics.
Maybe I’ll write the Insulin Resistance Handbook some day; for now you only get the
short course.
Insulin is a peptide (protein) based hormone that is released from the
pancreas primarily in response to changes in blood glucose levels. Although insulin
has numerous effects in the human body, its primary role is in the maintenance of
proper blood glucose levels. Although there are occasional exceptions, generally
insulin goes up as blood glucose goes up, and down as it goes down.
As insulin goes up (in response to increasing blood glucose levels), it tries to
bring blood glucose back down by pushing glucose into muscle and fat cells; as
insulin goes down (in response to decreasing blood glucose levels), it allows blood
glucose to come back up again. Kind of like a thermostat, insulin acts as a very basic
feedback loop (although I should mention that other hormones are also involved in
blood glucose regulation as well) to try to keep blood glucose levels within ’normal’
ranges.
Along with its primary role of regulating blood glucose, insulin also acts as a
general storage hormone in the body, shifting the body from a state of nutrient
mobilization (pulling calories out of cells for use) to one of nutrient storage (putting
calories into cells to be used later or using them right then and there). So when you
eat a meal, insulin levels will go up depending on a host of factors including the
amounts of each nutrient (protein, carbohydrates, fat, fiber), the form of the meal
(liquid or solid), and the types of each nutrient in the meal.
As with other hormones, when insulin levels go up, that insulin floats around
until it runs into an insulin receptor where it binds and causes stuff to happen. What
happens depends on what tissue you’re talking about (41). In the liver, insulin
promotes liver glycogen storage, increases protein synthesis, and increases fat
storage. In the muscle, its effects are similar: insulin increases glucose uptake and
glycogen storage, increases protein synthesis, and increases the storage of fat as
intramuscular triglycerides. In fat cells, insulin acts to increase glucose uptake and to
increase both fat synthesis and storage.
Now, knowing that insulin’s main role is to move nutrients out of the
bloodstream and into liver, muscle or fat cells, let’s think about what happens when
those cells become resistant to the effects of insulin. That is, if insulin’s main job is to
move nutrients out of the bloodstream, and insulin resistance prevents it from doing
its main job, what happens? If you guessed that nutrients would accumulate in the
bloodstream, you guessed right.
Since blood glucose can’t be cleared effectively, due to insulin resistance,
blood glucose levels rise and the person develops hyperglycemia (above normal
blood glucose). Since the body is still trying to bring blood glucose back down, it
continues to release more and more insulin (which can eventually cause the
pancreas to shut down completely) causing hyperinsulinemia (above normal insulin
levels).
Since fat can’t be moved out of the bloodstream either, the person develops
hyperlipdemia or hypertriglyceridemia (depending on which technical sounding word
you prefer, both mean above normal fat levels in the bloodstream). Because of other
changes, mainly in liver metabolism, folks who are insulin resistant also have above
normal cholesterol levels, called hypercholesterolemia. There are myriad other
effects that occur in insulin resistance as well, but this should be sufficient to give you
a basic idea of what’s going on. To put it as bluntly as possible, insulin resistance is
pretty much one big metabolic clusterfuck.
One final effect I want to mention is that severe insulin resistance causes a
negative partitioning of calories away from muscle cells and towards fat cells. The
basic cause is that muscle cells become insulin resistant before fat cells under most
circumstances. That is, typically muscle cells become insulin resistant first, causing
calories to be shuttled more rapidly into fat cells. Eventually the fat cells become
insulin resistant too, and the effects described above (an accumultion of nutrients in
the bloodstream) occurs.
Without going into too much detail, just realize that being able to drive nutrients
(glucose and amino acids) into muscle tissue is critical to maintaining normal
muscle growth and function. If insulin can’t do its job, because of insulin resistance in
the muscle cell, muscle will essentially ’starve’ and shrink. At the same time, since
calories can’t be stored in muscle cells, they get put into fat cells instead (at least until
the fat cells become insulin resistant as well).
The take home message is that insulin resistance in the muscle, which is
where it typically occurs first, causes a negative partitioning effect, causing muscle
loss and fat gain, even with no real change in caloric intake. I should note that this
same phenomenon occurs in other conditions such as cancer wasting, which just
happen to induce severe insulin resistance.
The other take home message is that reversing of fixing insulin resistance,
through whatever means would tend to reverse all of the above described effects. Fat
loss would occur, frequently with a simultaneous gain in muscle mass, and blood
levels of glucose, insulin, triglycerides, and cholesterol would go down. Keep that in
mind as I discuss the other effects of bromocriptine below.
I should also mention that insulin resistance and one type of diabetes, called
Type II diabetes, are inter-related. So don’t get freaked when I move from talking
about insulin resistance to diabetes in the next section. Insulin resistance (also
called the Insulin Resistance Syndrome, the Metabolic Syndrome, or Syndrome X) is
essentially a pre-diabetic state. Left unchecked, insulin resistance will develop into
full blown Type II diabetes.
Now, there are many different factors which determine the degree of insulin
resistance. Genetics play a key role, of course, as does total calorie intake, type of
food intake, and activity levels. A high-calorie, high-carbohydrate (especially refined
carbohydrates), high-fat diet coupled with low levels of activity causes muscle and fat
cells (again, muscle cells before fat cells in general) to become insulin resistant
through a variety of mechanisms. Some of these mechanisms are purely local, that is
occurring from changes directly in the muscle or fat cells but I don’t want to get too far
into the details.
As it turns out, the brain is also playing a controlling hand in inducing insulin
resistance and calorie partitioning by controlling hormone and neurotransmitter levels
(remember from an earlier chapter that the brain is not only getting signals from the
rest of the body, but sending signals back out).
So that’s the overview of insulin resistance/Type II diabetes, what it is and what
it causes to happen in the body. Now let’s reconnect that information with
bromocriptine with a short segue.
The long range Obamacare plan...
