Diabetes: More Than Just Diet And Doughnuts.
The people who know these things calculate that by 2050, 30% of us will be living with and quite possibly, dying from, some form of diabetes.
And if the heightened risk of gangrene, strokes and kidney failure that come with a diabetes diagnosis aren’t terrifying enough, the cost to governments (even those in countries with a private healthcare system) has the potential to bankrupt whole nations.
(Gulp, these are US figures for 2017 and are in billions of dollars! Click here to go the original research article.)
A disease with such dreadful health and financial implications has to be worth learning a little more about, and perhaps over a cup of coffee?
(A study of more than 100, 000 people showed woo-hoo, regular coffee drinkers were less likely to be diagnosed with diabetes.)
Diabetes mellitus (its full, official name) acquired the first part of its title from the Greek for siphon - people with undiagnosed diabetes mellitus need way more pee breaks than those of us without this disease.
The “credit” for the mellitus part probably goes to a long dead British physician with the practice of sipping his patients’ urine and noticing, “yum, that tastes sweet”.
And the Latin word for sugary/honeyed is ….mellitus!
(I mentioned this in a recent class and a student reported working for an older veterinarian still employing this technique with his canine patients! I suppose it has the advantage of being free?)
There are two types of diabetes mellitus, type 1 (DMT1) and type 2 (DMT2)and although copious amounts of sugary pee happen with both forms (at least before diagnosis and proper management), they differ in a very important way – in the roughly 10% of diabetes mellitus patients with type 1, the body doesn’t produce (enough) insulin whereas in patients with type 2 diabetes, the body often over produces insulin, but is unable to respond to that hormone.
Which begs the question, what does insulin do for us?
I hear “something to do with sugar” and that’s a great place to start – making sure we know what sugar is …
….which is not as simple as as this image suggests!
Noticed things like evaporated cane juice, corn syrup, and molasses on the ingredients lists on jars of pasta sauce, cereal boxes and tubs of coleslaw? These (and about thirty others) are sugar pseudonyms, almost all of them made up of the same two sugars, fructose and glucose, just in different proportions.
For instance, the white sucrose crystals we sprinkle over our porridge are equal parts fructose and glucose but the agave syrup in our iced tea is three parts fructose for every one part glucose.
And the dextrose in our shop-bought bread?
That’s just glucose by another name!
Confusing isn’t it?
Leaving aside the fact that the use of these opaque terms leads to consumers frequently not realizing quite how much “sugar” is in their food….
(In this typically perceived “healthy” food, a yoghurt, I counted 7 different types of sugar, can you find them?)
… it matters because it’s glucose molecules that we really care about.
Many cells can use almost anything from our diet to power their needs but our super picky neurons, the specialized cells in our brain, spinal cord and nerves, generally have to use glucose to keep themselves ticking over.
Unfortunately, the qualities of glucose molecules that make them brilliant energy parcels, also prevent them from moving easily out of our blood and into our cells (it’s a chemistry thing!).
Cue insulin!
It’s insulin’s most important role to travel in our circulation, poking many of our cells into allowing glucose entry.
Just as we have to have our photo I.D in hand for homeland security to allow us to journey from one country to the next, many of our cells require insulin to be in contact with them before they’ll permit glucose to cross their membrane (border!).
In type 1 diabetes mellitus, the pancreas starts producing less and less insulin, glucose molecules can’t cross the “border’ from the blood into cells and blood glucose rises.
(The pancreas is tucked up underneath the liver and weighs around 3oz normally.)
Our blood-filtering kidneys are always performing a delicate balancing act, ensuring that waste products are transferred from blood into urine whilst preventing precious glucose from moving into that same urine. If blood glucose gets too high, such as in the undiagnosed/untreated person with DMT1, the kidneys become overloaded and some glucose ends up in the urine.
Hence the sweet tasting pee!
Why would a pancreas reject its destiny and abandon its career in insulin production?
Most often, it’s probably a combination of inherited genes and a viral infection – after obliterating the invading virus, the immune system in genetically susceptible individuals gets carried away with its protective role and mistakenly embarks on the destruction of a healthy pancreas.
In diabetes mellitus type 2, the problem starts not with the pancreas, but with cells and specifically, the insulin receptors on their outer surface.
Normally, it’s the docking of insulin with these receptors that “unlocks” the entryways for glucose to move from the blood into a cell - type 2 diabetes develops when cells lose their insulin receptors. Early on, people with DMT2 will often be unaware of the looming disaster as their pancreas will actually increase its insulin output to compensate for their cells’ reduced ability to respond.
Kind of like when older people counteract their declining taste sensitivity by adding twice as much salt to everything!
That extra insulin will help some glucose to move into cells but blood glucose will still be too high and as in people with DMT1, the overloaded kidneys will let glucose through into the urine.
Ultimately, even a formula 1 pancreas won’t be able to produce enough insulin to overcome the increasing loss of receptors and the consequent cellular indifference to insulin, and symptoms will start to appear.
The risk factors for DMT2 include family history (i.e genes) but also obesity, lack of exercise, and too much refined food.
But before we rush to judgement about those who develop this seemingly, largely avoidable form of diabetes, consider for example, the more than 11 million low-income Americans who live in “food deserts” – for them, owning a car for supermarket runs to load up with fresh produce is nearly impossible.
And the food banks, invaluable for low-income families, are almost always stocked with shelf-stable, ultra-processed foods, exactly the ones known to both increase the risk of developing type 2 diabetes as well as worsening the disease in those already diagnosed.
But people at risk of type 2 diabetes could at least exercise because even if they can’t afford a gym membership, running in the park’s free, right?
Except who would be comfortable exercising when their next meal’s not a certainty?
As always, I’m not a medical doctor and learning how to reduce your personal risk factors or understand your treatment options is a conversation to have with your health care provider.
Hopefully, our post’s given you at least some of the tools to start that conversation.
Stay curious,
Doctor P
(Interested in the very rare and completely different disease, diabetes insipidus? Sign up for our monthly newsletter to find out all about that)
