Insulin (part 6): You have been in the dark

What if you have completely minimized oxidative stress and inflammation, and your sleep is amazing and restorative, yet you still struggle with insulin resistance? You wind up at the endocrinologist’s office and they ruled out MODY (Maturity Onset Diabetes of the Young). Your pocket suffers a hole from paying for extensive gene testing, which all comes back normal or of uncertain significance. You don’t drink alcohol, nor have you had a scorpion bite to cause your pancreas to shut down. You have excluded all the rare textbook causes of insulin resistance, blood glucose dysregulation, pancreatic insufficiency, and diabetes. Can you have insulin resistance or diabetes just from bad luck?

Well, before you consider bad luck as a cause, let’s look into bad decisions first. You may realise that, looking back into the past decades, you have decided to go out into the sun in the morning or late afternoon only, stay indoors at midday, work behind glass panes, avoid direct sunlight at midday as it is too hot, apply sunscreen when you do go out, lose track of time whilst working outdoors until you get sunburn, and not bother to check your vitamin D levels. Not to mention that even when you did check your level, your practitioner used the laboratory-provided ranges and advised you that your vitamin D level was absolutely normal.

We’ll unpack that paragraph another day. Today, though, our focus is on how the unsuspecting vitamin D has any role in regulating your body’s response to insulin. The science here is not new; most people know that vitamin D is the main driver for moving calcium in the body. That’s why we were told that low vitamin D causes rickets, which doctors hardly diagnose anymore. Its twin, osteomalacia, is commonly diagnosed in GP consulting rooms, yet no one associates it with vitamin D—a scary reflection of our practitioners' knowledge of the human body in health and in disease. Are you ready for a truth bomb? Osteomalacia is rickets; they are the same medical condition. The only difference between the two is the time of diagnosis. In a child, it’s called rickets; in an adult, you get a fancier name: osteomalacia. The bottom line is that the only way we can absorb calcium from our diet is with the help of vitamin D. No vitamin D means no calcium absorption. Some vitamin D means some calcium absorption, but the question is: is your ‘some’ enough?

That is up to the body to decide. Your delicately made body maintains a super-tight balance on blood calcium levels. It won’t easily give in to the slack in your diet and vitamin D production by letting the calcium concentration go beyond or under a certain level. That is because calcium influences the body’s functioning on a millisecond timescale. Your nerve synapses depend on it, as do your heart muscle contractions, to name just two. If your body doesn’t guard it like a hawk, you’ll end up with cramps everywhere. Yes, your mysterious leg cramps, for which you take Sifrol or Valium, have a known, established medical cause. Magnesium is a favorite band-aid because it modulates calcium.

So, when you slack on getting sunlight, or have been in the dark for sometime, the body must look for calcium sources elsewhere. Fortunately, it doesn’t have to go very far, as our bones are a massive calcium reservoir. A gland in the body, called the parathyroid (embedded in the thyroid gland but not the thyroid gland itself), puts out a signal—parathyroid hormone (PTH)—which allows the body to harvest calcium from the bones, making up for the deficiency. Very neat, isn’t it? This fallback mechanism is beautiful and will keep us going for a while, but it’s not perfect. Bones are not bottomless; one day they will end up brittle (osteoporotic) or at least lose their hardness (rickets or osteomalacia).

The bigger issue is that when PTH stimulates bone resorption (the medical word for mining), the process is not as finely regulated as when calcium is absorbed from the gut with the help of vitamin D. Most of the time, we wind up with an influx of calcium—like a major migration into the blood vessels—and now the body has another problem to solve. Too much calcium kills us just as quickly, if not sooner, as too little. Worry not; we have another fallback plan. Our cells absorb the excess calcium to bring the blood level down into the tight range it needs to be in.

Fallbacks are fallbacks; they always come with a price tag. In the insulin case, when cells are filled with calcium, there is more resistance. Think about it like limescale: if your hot water dispenser's tiny nozzle is covered in limescale, you won’t get a good flow of hot water. The fat cells simply can’t take in more stuff (fat or sugar energy) once they’ve taken up more calcium than their normal share. They will have to say no to insulin. As if that’s not bad enough, vitamin D deficiency—the original reason for the extra calcium in the cells—also stimulates IKKβ, which affects IRS-1 phosphorylation (if you remember this from the last posts). It’s coming at you from all angles to pull you away from optimal.

We summarise all these complex processes in the term insulin resistance. The problem is that we forget what causes it in the first place. We don’t like to admit it, of course, because we have our more important pride to look after. I’ve done it myself. Pharmaceuticals are a quick cover up to this issue, as people will judge me knowledgeable while my ignorance and amnesia are never going to be noticed, let alone brought up by the suffering patients in front of me.