This website has an insulin and blood-sugar simulator. It illustrates the connection between eating and the rise in blood sugar and insulin (and of course the later fall of both levels). But why is insulin part of it?

Quite simply: Pancreatic hormone that signals cells to absorb glucose from the blood. Central regulatory hormone of energy metabolism. is a hormone with many jobs and effects in the body, and in each chapter I look at a few of them.

Today it’s about diabetes mellitus, or rather Type 1 diabetes (T1D). After Type 2 in the previous chapter, perhaps a slightly odd order - but I chose it based on how common the two variants are.

The diagnosis

T1D is an autoimmune disease. The body attacks tissue in its own pancreas - the tissue that would normally produce the insulin the body needs to process (among other things) dietary carbohydrates correctly. As a result the body produces little or no insulin of its own. That makes T1D (too little insulin) essentially the opposite of T2D (too much insulin). The end effect is the same (blood sugar too high), but for diametrically opposite reasons.

T1D is a genuinely life-threatening condition, because insulin is vital, and in its absence blood sugar rises to extremes.

T1D usually appears early in life, often in childhood. But, more rarely, also later in adults as “LADA” (Latent Autoimmune Diabetes in Adults).

Before insulin was discovered and made medically usable - by Banting and Best in 1921/22 - T1D was treated partly by extremely low food intake (essentially a starvation cure) - but that only bought an extension of life on the order of a month. (1)

Hypo Hyper

With T1D there are two completely different danger situations: hyperglycemia and hypoglycemia. Hyperglycemia means: blood sugar is too high. Hypoglycemia is the opposite: blood sugar is too low. As we know from this article, the body needs a certain amount of carbohydrate to operate. In a hypo, there isn’t enough. That happens occasionally when insulin is overdosed, for example because the food doesn’t contain the expected amount of carbohydrate.

On a site that mostly deals with low-carb nutrition, one term from the T1D context can’t be missing - along with the proper context:

Ketoacidosis vs ketosis

Dangerous Metabolic state in which both very high blood sugar and very high ketone level appear at the same time. Typically observed only with type 1 diabetes. Not to be confused with ketosis. โ†’ more is a state that can occur during hyperglycemia - that is, excessively high blood sugar: blood sugar climbs enormously, but the body can’t reach the energy. The liver starts producing ketone bodies - but in excessive amounts. Ketone bodies are acidic (“acid”), and too many of them can lead to over-acidification of the body (acidosis).

In the context of a diet-induced Metabolic state in which the body burns fat rather than glucose for fuel. Characterised by a measurable level of ketone bodies in the blood. โ†’ more, these ketone bodies are present in relatively small numbers, and are quite positive. In the context of ketoacidosis they are far too numerous and life-threatening.

I keep hearing reports that these two terms are held to be identical even by medical staff - that’s not correct. Both do have to do with the presence of ketone bodies, but in ketosis blood sugar is always normal to low, in ketoacidosis markedly elevated. And the amount of circulating ketones is dramatically different between the two states.

Therapy

The classic medical approach is: since we can add insulin artificially, that’s what we do. The patient’s life can carry on exactly as before. Only the correct amount of insulin has to be injected at every meal.

New technology like continuous glucose monitoring supports this superbly: those affected have an overview of their blood sugar across 24 hours. Combined with an insulin pump, that really is a comfortable option.

Anyone who has to dose manually, though, and doesn’t have these continuous measurements, has to estimate what’s needed themselves. Another reason to dose yourself is when you know better than the algorithm in the device: because hypoglycemia is genuinely dangerous, the devices dose insulin rather cautiously, they tend to under-correct, so that in the end blood sugar can stay permanently slightly elevated.

And anyone who also knows that the body’s own insulin, in its mode of action, is not so much tuned to carbohydrates as to proteins, will be interested to learn that there are very different insulin preparations: long-acting insulin variants are injected as a “basal” once a day - or even less often. Fast-acting insulin (the artificial variant is actually geared more toward carbohydrate metabolism) always at mealtimes.

Simulating the therapy

Anyone who tries the simulation on this site will see that the body’s insulin response to identical meals is not identical: it also depends heavily on the composition and the order of the food. The same amount of carbohydrate behaves differently in the body depending on whether it’s eaten with protein and fat, or without. It also behaves differently depending on what you eat first (just try it: simulate an entrecote 10 minutes before white rice and fruit juice, then the other way round)

Someone who knows their prepared food well can calculate the amount of carbohydrate correctly, but when order and other ingredients make such a big difference, dosing insulin is always a bit of a gamble too.

Play, sport and stress, which can massively affect blood sugar on their own, aren’t even factored in yet.

It’s especially hard for parents who have to dose for their freshly diagnosed children - who therefore can’t even bring their own bodily sense into the dosing. I think that the sheer necessity of regularly giving children an injection leads to a great deal of caution, respect and fear. And reports from parents confirm it.

The Law of Small Numbers

Anyone who actually tries dosing insulin should play through different ways of eating. The simulation can be paused in between or slowed down, to take the time pressure out of it.

There are various things to compare:

The simulation lets you compare your own T1D metabolism with another profile that simulates a working pancreas. The comparison profile is set in the “Parameters” section.

Ideally the glucose and insulin lines of your own simulation and the comparison profile lie on top of each other - in practice that never happens, but it is the actual goal of the insulin injections.

One lesson: Dr. Bernstein, a Type 1 diabetic diagnosed as a child who was still practising as a physician at over 85, formulated the “Law of Small Numbers”:

Eat in a way that requires only a little insulin to be dosed, and you’ll have a far easier time keeping blood sugar under control. (3)

Low-carb, or even a ketogenic diet, doesn’t necessarily make the task trivial, but it does make it considerably easier: suppose you make a 10% error in dosing insulin (because of the biological variables you can’t gauge): someone who, due to a high carbohydrate load, injects 20 units may be off by 2 units. Someone who skips the carbohydrates and needs only 2 units deviates by maybe 0.2 units. That’s still not correct, but comparatively easy to handle.

The completely unnecessary combination

Low-carb may not yet have arrived as an option with much of the medical staff

  • but for many patients or parents it’s a welcome way to help with the problem themselves. Quite apart from the fact that a high insulin dose over a long time can sooner or later also lead to insulin resistance. Yes - it’s possible, as a T1D patient, to saddle yourself with T2D on top. But absolutely unnecessary.

Fortunately, with injection you have a precise overview of the amount of insulin you’re giving your body - and a markedly increased amount is a clear sign of developing insulin resistance. A luxury you don’t have in ordinary (T2D) prediabetic life.

There’s no need to yank the wheel around…

… if instead you make small course corrections now and then. It makes a big difference whether you suppress high blood sugar with a massive deployment of insulin, or simply never let it arise in the first place.

And if you’re worried that this runs so strongly counter to the usual dietary guidelines: They explicitly do not apply to T1D patients!

Related articles

Blood glucose meter with test strips
Insulin, Chapter 3

Even though Type 2 diabetes is often called a ‘sugar disease’: the real elephant in the room is insulin. The good news: patients can help themselves - if they want to.

Blood glucose meter with test strips
Insulin, Chapter 2

Insulin is in the center of many noncommunicable diseases. In this chapter we’re looking at the various types of Diabetes. โ˜๏ธ๐Ÿค“: More than 2!

Blood glucose meter with test strips
Insulin, Chapter 1

A closer look at some of insulin’s key roles: regulating blood sugar, driving fat storage, and ultimately influencing body weight

  1. Wikipedia: History of diabetology (German)
  2. Further explanations in the side text on the profile page, reachable via the question mark at the top right edge of the page
  3. Dr. Richard K. Bernstein’s Diabetes Solution, plus the website
    In psychology and statistics, the “Law of Small Numbers” diabetes-book.com/laws-small-numbers/ (*) actually describes a fallacy (people wrongly infer from small samples to the whole). Dr. Bernstein, however, hijacked the term and defined it purely mechanically for diabetic metabolism.
    His law can be summed up in a single sentence: “Big inputs make big mistakes; small inputs make small mistakes.”
  4. Wikipedia: Richard K. Bernstein - I couldn’t find the exact end of his time as a practising physician, but he held “teleseminars” until shortly before his death and published them on YouTube

(*) Note: As I write this, diabetes-book.com is offline for a while. I’m not sure if, when and in what state it comes back online. The book stands - I link my local bookshop around the corner, with no affiliate code, and trust that everyone knows where to get books - and that this can also be the little shop on the corner that doesn’t block footpaths and bike lanes every day.