Insulin, Chapter 2
This site has an insulin and blood sugar simulator. It illustrates the relationship between eating, blood sugar, and the rise of insulin — and, of course, the subsequent fall of both. But why is insulin part of the picture at all?
Simple enough: Pancreatic hormone that signals cells to absorb glucose from the blood. Central regulatory hormone of energy metabolism. is a hormone with many roles and effects in the body, and each chapter I look at a few of them.
Chapter 2 covers a selection of what are called “non-communicable diseases” — elsewhere known as “diseases of civilisation”. Specifically the most obvious ones: the various types of diabetes. Later chapters will also look at conditions not primarily attributed to insulin.
Since I’m not a doctor and treat no one, I take the liberty of naming connections that current medical consensus doesn’t necessarily trace back to insulin yet, but for which there are plausible hypotheses or case studies. When I list something, that doesn’t mean insulin is the decisive factor — only that it plausibly plays a part. But let’s start with the obvious:
Too Little Insulin
The body absolutely requires insulin. When it’s absent, that’s a serious matter.
Type 1 Diabetes
Type 1 Diabetes (T1D) is an autoimmune disease: the immune system attacks and permanently destroys the insulin-producing beta cells of the pancreas. The body then produces no or almost no insulin — and without insulin it has no way to shuttle blood glucose into cells. Administering Exogenous substances are those supplied from outside ('eaten') — opposite of 'endogenous': substances present within the body. insulin is a matter of survival.
A dangerous condition that can arise in T1D is 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. → more — not to be confused with Metabolic state in which the body burns fat rather than glucose for fuel. Characterised by a measurable level of ketone bodies in the blood. → more, which features in many articles on this site.
If you’d like to model T1D in the simulator: simply create a personal profile, enable “I inject insulin”, and enter the relevant values.
Too Much Insulin
More common — and in its own way more dangerous for its slow, creeping course — is the opposite: too much insulin. The technical term is hyperinsulinaemia. It’s rarely mentioned, which may itself be partly down to the terminology. The conditions it can give rise to are all the more familiar (just the diabetes variants for now; more later).
Type 2 Diabetes
Type 2 Diabetes (T2D) is typically diagnosed when fasting blood glucose is persistently elevated and HbA1c — a three-month average of blood glucose levels — exceeds a threshold.
The underlying mechanism is insulin resistance: cells respond less and less to the insulin signal (more on this in Chapter 1), so the body produces ever more insulin in response. Blood glucose is the last thing to go wrong — by the time it becomes a concern, insulin resistance has often been running for years.
An earlier diagnosis would be possible: fasting insulin rises measurably long before blood glucose sounds the alarm. It’s a separate parameter in the simulator on this site — a good reason to ask for it at your next blood test.
Type 2 Diabetes is commonly considered chronic and progressive — which is at least true as long as nothing changes about the underlying cause. That remission through dietary change is possible and documented is something Chapter 3 examines in detail.
Insulin, Chapter 1
T2D is the best-known manifestation of insulin resistance, but far from the only one. Insulin resistance appears in the research literature as a factor in a surprisingly long list of conditions. Later chapters will look at more of them, including hypertension. For now, just two examples from across the spectrum — ones that fit neatly under the diabetes umbrella by name:
Type 3
The label “Type 3 Diabetes” for Alzheimer’s disease goes back to research by Suzanne de la Monte (Brown University) (1). The mechanism: insulin resistance of the brain. Neurons that respond less and less to insulin can no longer efficiently take up glucose. A rather uncomfortable situation for cognition.
An alternative fuel would be helpful. How fitting that the brain can derive roughly two-thirds of its energy from ketone bodies — the fuel the body makes available when insulin is low and fat metabolism is active.
Who still remembers which fuel the body prefers to burn?
The Preferred Fuel
Type 4
The link between PCOS (polycystic ovary syndrome) and insulin resistance is well established (2). The “Type 4” label is not medically established — but handy enough as a structural aid for this series to borrow.
T2, T3, T4: A Common Thread
What all three share: insulin resistance as the underlying mechanism. And with that, a shared implication: it’s well worth having fasting insulin measured — not only to catch T2D early, but to keep the full spectrum of potential consequences in view.
(For T1D this is of course relevant too — though it’s typically discovered through acute symptoms rather than values that creep upward over years.)
Insulin Resistance — Just the Beginning
The longer I read the relevant research, the more often insulin resistance turns up as a factor in diseases of civilisation — sometimes as a contributing cause, sometimes as a suspected or confirmed primary driver. For those who’d rather not wait for the next chapters, here’s a list — not exhaustive, and without citations for now:
- Hypertension — insulin influences sodium retention and vascular tone
- Non-alcoholic fatty liver disease (NAFLD/NASH) — the liver is the first organ to convert excess glucose into fat
- Certain cancers (including breast, colorectal, and endometrial) — insulin and Insulin-like Growth Factor 1 - a hormone structurally similar to insulin that promotes cell growth and division. Produced mainly in the liver, partly in response to insulin. Chronically elevated insulin levels typically correlate with elevated IGF-1. Relevant because IGF-1 as a growth factor can also promote the growth of cancer cells. → more act as growth factors
- Gout — hyperinsulinaemia impairs the kidneys’ excretion of uric acid
- Depression and other mental health conditions — a growing field of research; overlap with metabolic syndrome
- Excess weight — as we already have come across in Chapter 1.
…and that, again, was only part of the picture.
