Injected Insulin and Type-2

   Insulin has a bad reputation!  People are afraid of it (and not just because of the needles), A lot of people think of it as “the final frontier” the last resort when nothing else works!

 Many people wonder why they should use insulin if their body already makes too much insulin and they have insulin resistance.  For others, especially type-1 diabetics insulin is a life saver.  Before the discovery of insulin a painful death was imminent.  Doctors have also been guilty of threatening T2 patients with if they don’t comply to their current program they’ll have to start using insulin!

An article in Diabetes Forecast Magazine also states: “There’s even a name for this conundrum: psychological insulin resistance (PIR), which researchers say is endemic in diabetes care. PIR manifests itself in the myriad reasons people say they want to avoid insulin therapy, including the weight gain associated with insulin use, the pain and inconvenience of injections, risk of hypoglycemia, and concerns about efficacy. Then there are the straight-out errors, like the comments about ED and insulin. “People associate it with bad outcomes,” says Richard Rubin, PhD, a professor of medicine at Johns Hopkins University—for example, the idea that “your grandmother had worse diabetes complications after the insulin started.” Of course, those complications were the result of damage done before or in spite of starting insulin treatment—which, for all the reasons just listed, people tend to hold off on until things get desperate.

Most people with type 2 diabetes suffer from two major defects:insulin resistance and insulin deficiency or beta cell “burnout.”  Insulin resistance can start years before outright diabetes develops, but beta cell disfunction can start even sooner.  An article In BetaCell Science states:  In the classic longitudinal study of normally glucose-tolerant Pima Indians, obese, insulin-resistant subjects who did not progress to T2DM followed the normal disposition curve over time because of normal β-cell compensation while those who progressed to diabetes (“progressors”) started below the curve and declined further as a manifestation of β-cell failure. In this study, progressors exhibited evidence of β-cell dysfunction even before reaching the range of impaired glucose tolerance (IGT), and by the study’s end their insulin secretion had decreased by 78%, with only a 14% decrease in insulin sensitivity.  So their beta cell function declined by 78% while their insulin resistance only increased by 14%.  And yet most of the treatments are geared toward reducing insulin resistance in T2 currently while defects in beta cell function are basically ignored.  Considering these early first line changes any future cure would have to begin at the beta cell level.

When food is ingested, insulin is secreted by the beta cells into the bloodstream. The insulin travels to the liver or muscles, where it attaches to receptors on the surface of the cells like a key in a lock. In non-diabetic people, this process allows individual glucose molecules to enter the cells of muscles, liver, and other organs. However, the cells of people with insulin resistance are “turned off” to the insulin key, so much of the glucose cannot enter the cells.

The pancreatic beta cells respond to this resistance by making extra insulin, (this can also cause a condition known as Hyperinsulimia or high circulating levels of insulin) which for a time keeps glucose in the normal range. If people with insulin resistance do not manage to control the condition their beta cells may lose the ability to produce enough extra insulin to overcome their insulin resistance. That is the second defect in type 2 diabetes: a relative deficiency of insulin.

When the pancreatic beta cells can no longer overcome the insulin resistance, blood sugars begin to rise. It has been stated by some sources that when persons are first diagnosed with type 2 diabetes, they have already lost over fifty percent of their beta cell function. Hopefully in the future this will be less so as diagnosis criteria and methods improve.

Some people can control their diabetes for years with a good diet and exercise routine plus one, two, or even three different medications. However, there are many conditions that may render these drugs either ineffective or no longer safe for the patient. These include:

Acute infections or other serious illnesses
Pregnancy
Major surgery
Congestive heart failure
Kidney disease
Liver disease
Use of other drugs (prednisone and some psychiatric medications)
Excessive weight gain
Antibodies that destroy beta cells (in people with type 1, misdiagnosed as type 2)
Progressive loss of beta cell function

Unfortunately, many people with type 2 diabetes experience progressive loss of beta cell function. Their overworked beta cells seem to burn out, and drugs that were once effective can no longer hold their A1c’s below 7%.

Starting Insulin

The overwhelming majority of type 2′s eventually require insulin to obtain or preserve satisfactory glucose control. Research clearly shows that achieving good control early on prevents diabetic complications, including nerve, kidney, eye and heart disease, up to twenty years later.

Patients’ misguided fears about needles, hypoglycemia, and weight gain often lead to reluctance and physician inertia. A recent survey found that fewer than half of all physicians made any change in diabetes therapy even for patients with A1c’s of over 9%.

A similar study at Johns Hopkins found that it took an average of 240 days before doctors added insulin or another drug for patients who could not achieve good control. By the time they finally took action, two-thirds of their patients had A1c levels approaching 10%.

Table 1 lists the indications for initiating insulin therapy in patients with diabetes. Even when initiation of insulin is clearly indicated, however, both patients and their physicians are often reluctant to do it. Some patients are needle-phobic, not realizing that modern insulin syringes and insulin pens are virtually painless.

Table 1: Indications for Starting Insulin

All patients with type 1 diabetes
Ketoacidosis or severe hyperglycemia (blood sugars over 500)
Presence of serious infection (for example, pneumonia)
Concurrent illness (such as heart attack)
During and after major surgery
During pregnancy
Failure to achieve ideal glycemic control with two or three oral agents
A1c over 10%
A1c over 7.5 % plus fasting glucose over 250
Patients who are underweight or losing weight without dieting
Patients who have symptoms from blood sugars over 200
Any patient who is hospitalized
Patients requiring steroids (such as prednisone) for other disorders
Onset of diabetes prior to age thirty, or a duration over fifteen years
Complications such as painful diabetic neuropathy

In order to understand insulin therapy, it is important to understand how the body uses the insulin it produces naturally.  Insulin released from the pancreas helps move glucose from the bloodstream into the cells of the body, which then use the sugar for energy. Because the cells need energy all the time, the body must have not only a constant supply of glucose, but also enough insulin to deliver this sugar to the cells.

Two important sources of glucose are carbohydrates from foods and glucose made in the liver. The liver supplies the body with glucose primarily during times when a person does not eat, both by breaking down complex sugars stored in the form of glycogen and by creating new sugar from proteins and fats in a process called gluconeogenesis. The combination of glucose from eating and glucose made by the liver provides a supply of sugar 24 hours a day. To move this sugar into the cells that need it for energy, insulin must be present 24 hours a day as well.

Although the body produces glucose continuously, the amount of blood sugar varies throughout the day. More glucose is present after eating meals, particularly meals containing sugar and other carbohydrates. Smaller, relatively constant amounts are present during the times when only the liver is producing sugar. The pancreas typically produces insulin in a similar pattern. In other words, a relatively small amount of insulin is present all day long to deal with the sugar that the liver is producing. Increased amounts are produced in response to eating, and even more is produced after a meal laden with carbohydrates and sugars.

Thus, the insulin produced by the body has essentially two roles: basal and bolus. The insulin produced for the “basal role” addresses the glucose that the liver is making throughout the entire day and night. This is a fairly constant background/baseline amount and is present whether or not a person eats. The “bolus role” is the quick burst of insulin that the pancreas makes to address the sudden appearance of extra glucose caused, for example, by eating. Bolus insulin may therefore be thought of as mealtime insulin and basal insulin as all-day background insulin.

In type 2 diabetes, there is not enough insulin available to perform these tasks, allowing blood sugar to run high. It may be that insulin is actually elevated, but that, due to insulin resistance, it is not able to do its job. Insulin therapy provides extra insulin to augment that which the body is failing to produce or properly use. For patients with type 2 diabetes, insulin dosing needs to ”make up the difference” between what the body needs and the inadequate amount it has available.

Insulin dosing may be categorized in terms of whether it fills the basal role or the bolus role. There are different types of insulin to generally fit one role better than the other.

Basal-bolus insulin is one of the most advanced approaches to diabetes care, offering a way to closely simulate natural insulin delivery. The basal insulin addresses the glucose the liver makes, while the bolus insulin addresses the sugar in the foods that are eaten. Because some people need more basal insulin and others need more bolus insulin, this regimen can be custom fit to the needs of each individual.

In addition to lowing the numbers efficiently by by-passing the body processes and going straight to the cells, muscles and organs affected, injected insulin also allows the beta cells and liver processes to “rest” by not needing to continuously produce higher levels of insulin. This also reduces the high circulating insulin levels (Hyperinsulimia) which has been proven to cause other conditions such as heart disease over time.

Often newly diagnosed people with very high numbers are put directly on insulin therapy to reduce the numbers quickly and give the body a “rest”.  It’s often the case that after a time they can then be switched to oral medications once the body has adjusted from this rest period.

For others with significant beta cell loss the insulin therapy is long-term, but extremely effective in controlling the numbers and reducing further complications. It also serves to help retain some beta cell function by not overworking the ones that remain.

Injected insulin lowers BS levels without the need of the beta cells producing (in this case overproducing) insulin to lower the levels. If the insulin is dosed properly there isn’t a higher amount of it because what’s injected is used and/or stored in a short period of time.. That’s one function. When the beta cells aren’t forced to over-produce they “rest”, thereby not burning out the way they do when overworked.

If you don’t reduce the carbs you will need higher levels of injected insulin, but it’s not coming from the beta cells. If you eat high amounts of carbs but don’t overdose on insulin you won’t necessarily increase your “circulating” insulin levels as long as it’s being utilized. There’s a difference between high amounts of insulin used and high circulating levels in the system, I think that might be where the confusion lies for so many people. You might very well gain weight with this type of activity, which might lead to more insulin resistance.

It’s not my purpose in the scope of this post to outline all of the factors to reduce insulin resistance, only to explain the insulin function. I already wrote a huge link on insulin resistance  click here

It also isn’t my purpose in this post to defend diet and exercise or any of the other steps that can be taken. Of course there are many other factors to consider and steps that can be taken. But this only explains the role of injected insulin.

There is no question that diet and lifestyle changes can produced major results in delaying the onset of T2 and much is discussed about the recent studies to that effect.  In many cases these changes produced greater results percentage-wise than many of the popular medications.  But as BetaCell Science states:  The Finnish Diabetes Prevention Study and the US Diabetes Prevention Program, both showed a 58% reduction in diabetes less incidence among individuals with IGT treated with diet and exercise for ∼3 years (46, 47). Also, diabetes rates in pre-diabetic patients treated with metformin for the same period declined by 31% (46), and, in high-risk patients treated with acarbose in the STOP-NIDDM randomized trial, by 25% (48). Although these findings are consistent with the concept that early intervention to lower glucose levels may check disease progression, they may reflect delays in, rather than prevention of, progression, because cumulative incidence rates of diabetes rose at the end of these studies in both treatment and control groups.

So it appears that an even earlier intervention on a beta cell level is our most promising option at this time.  Research is currently in it’s earliest stages.  Perhaps by expanding the current research in beta cell development a cure will be found for ALL types of diabetes.

Maybe when I publish my book “What Dr. Oz Didn’t Tell You” I’ll explain the rest.

Sources: 

Basal/bolus Therapy

Embracing Insulin

Targeting Beta Cells Early

 Lizzy

 © LO 11/1/10

 
Knowledge is Power