Diabetes Prediabetes Obesity

By Kelly Gregg MD

It is now common knowledge that we know there is an obesity epidemic.  We have about 40% of the adults in the world who are eating the modern Western diet diagnosed with obesity.  As a result, we have more prediabetes and more type 2 diabetes with corresponding complications from this condition.  There are numerous medications used to try to lower your blood sugar. but these are not curing anything, and the condition slowly progresses.
Type 2 diabetes is preceded by prediabetes, at which type we still have a chance to prevent progression.  Prediabetes is preceded by obesity, which is usually present for several years before.
Unfortunately, we now have about a third of the kids with some level of obesity.  Many of these go on to be obese adults, adults with prediabetes, and finally adults with Type 2 diabetes.

I will teach you about obesity and how to prevent it, if you have prediabetes you may be able to prevent progression.  If you have diabetes, you may not be able to cure it, but you can improve your treatment.

 

• Language: English
• Publisher: Kelly Gregg
• Release date: Oct 6, 2023
• ISBN: 9798223190783

Book preview

CHAPTER 1

TYPE 1 DIABETES

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The first step in type 1 or juvenile diabetes is conception.  I say this because this disease appears to have a strong genetic component.  Identical twins have a 50% concordance rate, meaning that if one twin has it the other has a 50% chance of getting it.  Non-identical twins have a 10% chance of concordance.  Normally we would expect about a .3% chance of getting T1DM (Type 1 Diabetes Mellitus).  You can see, genetics has something to do with it.  Exactly what it has to do with it is unknown.  It appears that something initiates an autoimmune response that damages the insulin-producing cells of the pancreas.  We know that autoimmune disease incidence varies around the world, and it ends up so does Type 1 Diabetes Mellitus (T1DM).

We have the twins in which one develops T1DM but not the other, despite both having the same environment.  I think we can all agree that genetics has something to do with it, but probably not a mutation in one gene.  Like a lot of disease and cancer, more than one gene is probably involved.  Similarly, it appears the environment has something to do with it, just as it does with other autoimmune diseases.  Is this a virus or bacteria, an environmental toxin, some factor in the diet, or perhaps a change in the gut microbiome that precipitates the immune reaction?  The answer is still not known but speculation (including mine) abounds.  We can detect autoantibodies in many T1DM patients, but not all, so the etiology is still somewhat blurry to me.  The etiology may be important to determine the cause of the disease, but not the effective treatment.  We do not need to know what caused it; we do know that we need insulin to treat it.

In any case, we have an elevated glucose level which is the definition of diabetes.  The basic etiology is a defect in insulin.  In this case, the problem is a lack of insulin.

Throughout history, this was treated with diet, mainly a low carb diet to reduce the need for insulin.  Today the treatment is insulin: however, diet is still required.  If you are going to artificially replace the correct amount of insulin, you need to pay attention to how many carbs you are eating.  As these mainly young people grow up, they still will have the problem of elevated insulin levels if they eat a high carb diet since they will be taking more insulin, with all the problems associated with higher insulin levels as we will discover later.  If anything, closer monitoring, and limitation of carbohydrates in the diet is going to be required to replicate a more normal metabolic life.

Although there are two peak age ranges where the diagnosis is made (4-7 years and 10-14 years), it can appear later in life whereby an apparent normal adult who is not obese and exercises often, suddenly has some type of immune destruction of the insulin-producing cells and has no insulin.  Again, the etiology is unknown, but the treatment is the same.

I said the treatment was the same but sometimes in the late-onset diabetics, you can nurse the remaining insulin-producing cells along by other medications and reduce carbs to lower the insulin requirement, and thus prolong the time needed to have to begin administering insulin.  Sometimes immune blocking medications can extend the life of the remaining insulin-producing cells.

To review:

Step 1:  You were born with the genetic disposition for T1DM.  Nothing you can do about that.  Regardless of your diet, you may get the disease, I think.  Since the rate of development is lower in some parts of the world than others, it possibly could be related to the early diet.  Right now, I am going to say that there is nothing you can do about it.

Step 2:  You develop symptoms and have high glucose levels.  High glucose levels are generally not good for the body.  High glucose levels with no insulin is deadly to the body.

Step 3:  You start insulin and monitor your blood sugar to avoid too high or too low glucose level.  You count carbs and dose appropriately.  Since you will be doing this for over fifty years, you might as well try to keep the insulin level as low as possible while maintaining a normal glucose level.  To do this you will need a low carb diet. 

How low depends somewhat on your age, but as an adult, you may be able to go low.  Exercise can increase the amount of glucose absorbed by muscles through a mechanism that does not require insulin.  In addition to low carb, this may also allow you to decrease your total insulin burden.  All these statements apply primarily to adults.

Step 4:  Someday we may be able to give pancreas cell transplants or provide immune therapy when we first see a decrease in insulin production that may extend the time where insulin is not required.  Someday we may be giving children a vaccine to prevent the development of T1DM.  Regardless, diet will always be a part of the treatment.

I recently have added a recommendation to those who have a family history of Type 1 diabetes.  I advise the mothers to breast feed if possible, and then to use A2 milk for the diet.  For more information see last chapter.

Everyone with T1DM has a health care provider.  Take their advice, not mine.

CHAPTER 2

METABOLISM

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It seems like every book I write must include this chapter and possibly the next, so if you have read any of my books, you may have already read something like this.  I originally did not want to cut and paste this portion of the book from my other books, but there are only so many ways to say the same thing.  Also, I have continuously refined the information so that I think it now is pretty good and difficult for me to improve upon.  Therefore, you may feel cheated if you have read some of my other books. 

Of course, if you have read them, you probably don't need to read this chapter anyway.  If you only know the basics of nutrition, say the metabolic equivalent of long division, you need to read it.  If you know the metabolic equivalent of calculus, just read the first and last sentence of every paragraph.  If you know the metabolic equivalent of solving quantum wave equations, skip this chapter.

Your food is divided up into fats, carbohydrates, and protein.  About 99% of what you eat goes into one of these categories.  In this book, I am not going to care about vitamins and minerals.  It is rare in this country that anyone suffers from a real vitamin deficiency disease such as rickets or scurvy. In the United States, in one day we probably urinated out enough vitamins to satisfy the requirements of the rest of the world for a week.  Someday I will write about vitamins but then I will have to go into witness protection from everyone getting mad at me.

Let's start with fats.  Fats come in two basic forms.  One is a chain of carbon atoms of varying lengths which are termed a fatty acid.  These usually have between 4 and 28 carbon atoms.  Sometimes the carbon atoms are linked together in what is called a double bond.  Saturated fatty acids mean no double bonds, unsaturated means one or more double bonds.  Saturated fatty acids are more likely to be solid at normal temperatures, unsaturated more likely to be liquid. 

When someone says something like omega 3 fatty acid that means the double bond is at the third carbon from the omega end.  An omega 6 fatty acid means double at the 6 carbon.  The number 1 carbon is the first carbon opposite the COOH (Carboxyl) end.  There is a lot of misunderstanding among both professionals and laypeople about the role of saturated versus unsaturated fatty acids.  My view, saturated fats are not bad for you.  This may be another chapter.

For the most part that is all the biochemistry you need to know.  You will hear these terms used and now at least you kind of know what they are talking about.  In real life, you don’t eat fatty acids. You take three fatty acids, hook them up to a glycerol molecule, and you get a triglyceride.  This is what you are eating with a piece of bacon.  It is a much more compact way to store fat and does not use up as many water molecules, so this is the way nature works. 

When you eat fat, your stomach acids and digestive enzymes break down the triglycerides into component fatty acids which can be different in the same triglyceride.  This is what is absorbed into the body, not the triglyceride.  Unlike carbohydrates and proteins, fatty acids are absorbed through the