An Easier Diabetes Primer

This is intended to be a rather superficial overview of diabetes for those totally unfamiliar with the disease. Consider it the cliff-notes to the rather large wikipedia page or various other “primers” available on the web (the American Diabetes Association page for example, which seems more readable than wikipedia’s). I present this information in terms of what the non-diabetic probably doesn’t know – but might want to (and should). And in part, I’m writing this to better clarify it for myself. I’m bolding the first instances of important terms.

What is It?

Diabetes mellitus is a condition wherein a person’s ability to adequately control blood sugar (BS) levels in their blood is compromised.

Basic Physiology Lesson:

Most of the food we eat is turned into glucose (sugar) by the body via digestion, to be burned as energy.

Meanwhile, beta cells in the pancreas create insulin, a hormone which helps muscles and other cells to use glucose (insulin allows glucose to enter the cells). The proportion between glucose and insulin is important here, but fortunately the non-diabetic pancreas is very adept at producing just the right amount of insulin in proportion to the amount of glucose currently in our bodies. Glucose concentrations in our blood increase when we eat; the pancreas releases insulin in response to bring down glucose levels.

So it’s a balancing act. Not enough insulin, and the amount of glucose in the blood (our BS levels) increases (hyperglycemia). Too much insulin, and glucose levels decrease (hypoglycemia).

Diabetes is commonly divided into three main types: type 1, type 2, and gestational. (Recently there have been more subdivisions: type 1.5, pre-diabetes, and so on, but for our purposes these types can often be grouped under type 2.)

Type 1 diabetes is an autoimmune disease, meaning that the diabetic’s body attacks and destroys the insulin-producing cells in the pancreas. The reason(s) behind this are not clearly understood. The result, however, is that type 1 diabetics produce very little to no insulin, and must inject insulin daily from diagnosis till death. Before the early 20th-century (when injectable insulin was first introduced), type 1 diabetes was a death sentence. The Greeks described diabetes as “a melting down of the flesh and limbs,” as without enough insulin, cells burn themselves for energy.

Type 1 diabetes has at various times been referred to as juvenile diabetes or insulin-dependent diabetes mellitus (IDDM). Juvenile, because onset is often early on in a person’s life.

Type 2 diabetes is probably not an autoimmune disease. Instead, type 2 diabetics have, for a variety of reasons, insulin resistance (IR). They can produce as much – or even more – insulin than a non-diabetic. The insulin produced simply doesn’t work as well.

Type 2 diabetics may also not produce as much insulin. This can be the result of an as-yet unknown reason, or because of years of increased insulin production burning out their pancreas’ beta cells. (Type 2 diabetes might not be diagnosed for years. During this time, the pancreas will attempt to overcome the IR by producing a lot of insulin. This wears out the beta cells in the pancreas.)

Type 2 diabetes has been called adult- or maturity-onset diabetes, or non-insulin-dependent diabetes mellitus (NIDDM). These terms are increasingly irrelevant, however, as type 2 diabetes diagnoses increase rapidly in younger and younger patients, and as many with type 2 require insulin shots.

Gestational diabetes is often temporary, and a condition in pregnant women. Like type 2, this means IR and high BS levels. This can result in complications with the birth. Gestational diabetes affects between 3-10% of births, and the women are typically at a much higher risk for developing type 2 at a later date. It’s screened for during pregnancy.

In a sentence, diabetes is a disease where you do not have enough insulin (either in quantity or effectiveness) to normalize the BS levels in your body.

Why does It happen?

Type 1 diabetes is most times a product of genetics, but in some instances can be the product of virus infections (Coxsackie virus, german measles). The causes of type 2 are less clearly understood, but there are several risk factors which include obesity, a sedentary lifestyle, and a large intake of calories or carbohydrates, depending on who you talk to (adoption of the “western diet.” What is eaten might not be as important as how much and whether it leads to obesity). There is also necessarily a genetic component to type 2. Some people will always be obese and sedentary and never get diabetes. Others will. Some diabetics aren’t obese or sedentary at all. About 80% of type 2s are overweight however, which seems to lead to IR and the slippery slope of diabetes and decreased pancreas function.

Age is also a factor. Pancreas function (like many things) decreases as we age. Racial minorities are statistically more prone to the disease than those of white European descent.

Because of the role genetics play and our still hazy understanding of the disease, most times it’s irrational and counter-productive to “blame” the diabetic for being overweight or having a poor diet. (Contrary to popular belief, sugar consumption itself has nothing to do with causing diabetes, unless it leads to weight gain.) Much of today’s research suggests the common trait of a “thifty” gene(s) among diabetics, which was great to have during times of famine, but today during times of plenty causes weight gain and IR.

About 10% of the diabetic population is type 1; the rest are type 2 and its various subtypes.

What happens?

The primary result of diabetes is out of control blood sugar (BS) levels (usually – high or hyperglycemia). Unchecked, this can result in a huge variety of illnesses.

The early warning signs are frequent urination (coupled with increased thirst), blurry or quickly failing vision, fatigue, and recurrent yeast infections. After years, the undiagnosed diabetic will begin to have more severe symptoms such as sores that won’t heal, numbness or tingling in extremities, kidney or cardiovascular problems, and further (more permanent) damage to the eyes. Weight loss occurs in type 1s.

The problem is that onset (of type 2) is slow and the disease is degenerative when left undiagnosed, so noticing these symptoms is difficult for someone who may otherwise feel healthy.

The primary goal when diagnosed is normalized BS levels. It is thought that increased or wildly fluctuating BS levels lead to most of the complications associated with diabetes.

A Word About Blood Sugar (BS) Levels And Testing:

Blood sugar, in the US, is measured in mg/dL – milligrams per deciliter. (Internationally, it’s mmol/L – millimoles per liter.) Normal fasting levels – when you haven’t been eating – for the non-diabetic are usually in the 70-100 mg/dL range (to be more precise, usually 80-90 mg/dL). In the hour or two after eating, a non-diabetic might see a spike to 120 or 140 mg/dL if they ate a lot of sugar or fast-acting starches.

For comparison, diabetic BS levels, out of control, might reach as high as 400, 500, or even higher. At these levels, a hospital stay is often warranted. The diabetic struggling with control might see numbers peak into the 200 mg/dL range weekly. All of the complications related to diabetes increase substantially as sustained BS levels increase. Even a non-diabetic with average numbers in the low 80s will have a smaller risk for associated complications than a non-diabetic in the 90s, statistically-speaking.

Naturally, there’s a whole host of diabetes-related lab-work beyond the scope of this post which tells a lot more about BS control and other important issues. But home testing of BS is critical to getting and maintaining good levels, especially in the first few months or years of living with the disease.

Testing a person’s blood sugar involves pricking a finger, getting a drop of blood onto a test strip, which is inserted into a small blood glucose monitor which “reads” the level of glucose in the blood. This reading tells the amount of glucose in the blood at that very moment. It’s relatively painless, easy, and the biggest cost is the test strip. (About $1 if you’re paying out of pocket, usually about 5 cents with insurance.) You’ve probably seen Wilford Brimley hawk testing supplies on TV.

Acute (short term) complications of diabetes include:

• Ketoacidosis: increased amounts of ketones in the blood decrease the blood’s pH level, resulting in loss of consciousness, death
• Nonketotic hyperosmolar coma: essentially, extreme dehydration in the cells, also requiring immediate hospitalization
• Hypoglycemia: extremely low BS, which again results in loss of consciousness, coma, and death if not treated

Chronic (long-term) complications include:

Microvascular (damage to small blood vessels, or nerve damage)

• retinopathy: extreme / total loss of vision
• neuropathy: decreased sensitivity in extremities, in many cases leading to amputation and / or amyotrophy (muscle weakness)
• nephropathy: kidney damage, eventually requiring dialysis if left untreated

Macrovascular (damage to large cells, or arteries. Atherosclerosis plays a large role.)

• Coronary artery disease: heart attack
• Cerebrovascular disease: stroke, or blood clot in the brain
• Peripheral vascular disease: obstructions in major arteries outside the heart

Random Statistics:

Most diabetics die of heart disease or stroke, most have high blood pressure, and diabetes is the leading cause of new cases of blindness among adults (12,000 to 24,000 cases each year). More than 60% of non-traumatic lower-limb amputations occur on diabetics – that’s about 82,000 amputations in 2002.

Statistics courtesy of the National Diabetes Information Clearinghouse.

The World Health Organization estimates at least 171 million people around the world are diabetic, a number expected to double by 2030. In the US, the National Diabetes Information Clearinghouse estimates that 20.8 million Americans (about 7% of the population) have diabetes, with 6.2m of those undiagnosed. Furthermore, the Centers for Disease Control and Prevention estimate that 1 in 3 Americans born after 2000 will develop diabetes in their lifetime.

All of this can be depressing and frightening for those recently diagnosed or families of. Skip to the “it’s really not all bad” section if you want the good news.

So what do You do?

Type 1 diabetes has no cure, type 2 diabetics can receive pancreas transplants. (Good luck finding a spare pancreas.) New cures and solutions are in the pipeline, but for today’s diabetic, controlling BS levels and diabetes boils down to two or three things (depending on the severity):

Diet – “Opinions are like assholes: everyone’s got one.”

The proper diabetic diet runs along similar lines. Sugar is drastically limited: that’s all anyone can agree on. The American Diabetic Association prescribes a fairly high-carbohydrate, low-fat diet similar to the traditional food pyramid. Many people adopt a “low” carbohydrate diet. This is because large amounts of carbs, especially starches, can spike BS levels drastically – even more so than table sugar in some cases. (Protein and fats do not increase blood sugar nearly as much or as quickly.) For the purpose of understanding diabetes, simply realize that the “proper” diet is a hotly contested issue.

Exercise

Exercise, both aerobic (ie. running) and anaerobic (ie. weightlifting) is essential for good blood glucose control. This is because it can both stimulate the beta cells of the pancreas (increasing insulin production) and decrease insulin resistance. Weight loss (a byproduct of exercise) also leads to decreased IR, so it’s a positive feedback loop. Exercise also builds muscle, which uses (and stores) glucose at a much higher rate than other cells. The benefits of exercise (and weight loss) are well-documented.

Medication

A few decades ago, there were really only two options: sulfonylureas (developed shortly after World War II), and shooting insulin. Today, in addition to these, we have meglitinides and phenylalanine derivatives, biguanides, alpha-glucosidase inhibitors, thiazolidinediones – “just to name a few.” Most are oral, some are injected similar to insulin.

When insulin was first developed, it was modified from cows and pigs. Today, only human insulin is approved for use in the US. Most are analogs (lab-grown). There is a huge variety in insulin, both basal (for when you’re fasting) and bosol (injecting before meals), of varying lengths and rates of absorption.

Medications for diabetes work either by reducing insulin resistance, increasing insulin production (or quantity, in the case of injecting insulin), or reducing glucagon (a hormone, made by alpha cells in the pancreas, which increases glucose in the blood). Determining what medication works and in what quantities is really decided on a case-by-case process.

It’s really not all bad

Diabetes is a chronic condition and care is full-time for the rest of the diabetic’s life. The good news is, that with normalizing BS levels, the risks and complications can be minimized, and the diabetic can lead an entirely normal life free of amputations or blindness. Sometimes, being diagnosed with a terminal disease can be the best thing that happens to a person. It puts things into perspective: the impermanence of life, the renewed desire of living every day to the fullest, and the importance of good health which includes diet and exercise.

Post-script: If you’re still bummed out, go back and read the post again – pronouncing diabetes like Wilford Brimley – “dia-bee-TUS.”

For more Information

David Mendosa created one of the first and still best resources on the internet at www.mendosa.com. Inside you’ll find links to practically every other significant page on diabetes on the internet. Other resources have already been linked to, including the ADA and NDIC.