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  • Writer's pictureRyan Allen

Updates and insights from living with T1D

It’s been around nine months since I was formally diagnosed as a type 1 diabetic, and while it can definitely still be hectic at times to manage my glucose levels, I feel I’m starting to finally get in a position where things are at least more predictable. Along with this, I’ve made some key observations from my continuous glucose monitoring (CGM) which I think are definitely worth sharing with everyone, regardless of whether one has diabetes or not. While blood glucose is not the be-all end-all measurement for health, it can be a decent approximation of one’s physiological state at any given moment.


Figure 1: Recent examples of my 7-day, 14-day, 30-day, and 90-day reports from Dexcom G6 continuous glucose monitoring. Over the last few months, my glucose control has improved significantly, largely as a result of refining my insulin regimen and optimizing my routine.


As many can probably guess, I have started insulin therapy for my type 1 diabetes (T1D). For those who don’t know, this is because the mechanism of T1D is an autoimmune reaction that kills the pancreatic beta-islet cells, which produce insulin. Without insulin, the body lacks a consistent, efficient system to transport glucose from the bloodstream into cells, and blood glucose levels can skyrocket, causing all sorts of downstream issues. However, type 1 diabetics pose several interesting metabolic experiments, given their unique condition of knowing exactly how much insulin is circulating in their system at any time. For example, much debate exists around whether a lot of the harms of type 2 diabetes, or insulin resistance, results from high blood glucose (hyperglycemia) or high insulin (hyperinsulinemia), both of which appear to be problematic in different ways. Of course, for those with T1D, the problem is mainly going to be the high glucose, so one can use them to differentiate the effects of high glucose with and without the high insulin.


In my own experience, it’s been fascinating to experiment with which scenarios are most conducive to high glucose levels, independent of carbohydrate intake which would obviously spike it. Since I am taking a constant dose of insulin, and am quite aware at this point of its typical effect on me when all variables are held constant, I can observe what happens to my blood glucose when any one factor changes from my baseline state. Virtually all backed up in the scientific literature as well, these anecdotal phenomena fall into a couple categories, namely those that decrease insulin sensitivity (reduce insulin receptor-mediated uptake of glucose into cells from the blood, usually due to the body triggering some form of protective mechanism) or those that upregulate gluconeogenesis (production of glucose anew in the body).


When it comes to the former, exercise is a clear factor in mediating insulin sensitivity. Not only does exercise (particularly low-end aerobic exercise) increase non-insulin dependent glucose uptake into muscle cells, but it also enhances sensitivity to insulin signaling, perhaps due to increased energetic demand for metabolism within the cells. During periods where I am unable to exercise much, I not only notice a higher average blood glucose, but higher spikes from foods that normally would not give me as much trouble. The same sort of thing happens when I am sleep-deprived. Anyone who knows me that closely knows how much I value sleep in one’s health, and seeing how it impacts my blood glucose has been a big reason why. In fact, Nick has seen this too. Occasionally taking his static blood sugar with a finger-prick glucometer, he told me recently that he saw his highest-ever glucose (110 mg/dL, which makes me jealous) following a high-carbohydrate meal after he had been sleep deprived. Our observations seem to be legitimate. There have been several studies demonstrating that poor sleep impairs insulin sensitivity, and while mechanisms are unclear, it may have to do with fundamental benefits sleep has with regards to things as basic as our cellular metabolism or epigenetic modifications.


Moreover, cortisol–both a sleep-wake controlling and “stress” hormone–increases with a lack of sleep and generally upregulates gluconeogenesis as well, bringing us to the latter category of situations that raise blood glucose. It is situations like this where I have seen my glucose shoot up even in a fasted state, since my liver is producing it endogenously (itself, inside the body, without outside intake). I see the effects of cortisol not only with sleep, but perhaps most obviously with stressful situations. Even if I do not consciously feel nervous or anxious, I have noticed that when I have been in high-stakes scenarios or engaged in public speaking, my blood glucose takes off, likely due to cortisol. Sometimes stressful situations are inevitable, but this is a clear sign to me to avoid chronic exposure to environments that will exacerbate unease or anxiety. Finally, I have also found any infection or level of inflammation to trigger increases in glucose levels, potentially via both transient insulin resistance and gluconeogenic mechanisms. The immune response does appear to upregulate transcription of gluconeogenic genes, and is generally considered a stressor in itself. As the body shifts into a desperate, protective mode, that also tends to be a cue for insulin resistance.


Why are all of these observations relevant? Well, it seems that, while amplified ten-fold in a type 1 diabetic, the impacts of each can be extrapolated to the average person, showing why so many of the habits we preach are so beneficial to overall health: regularity of exercise, consistency of sleep, avoiding illness, reducing stress, limiting processed foods and refined carbohydrates. Even if the effects of bad habits aren’t as visible in your blood glucose, they’re being felt elsewhere in your metabolism. It could be high insulin and early signs of insulin resistance, it could be mitochondrial damage or hyperactivity. No matter what it may be, it is safest to mitigate all-around disease risk by taking these established lifestyle measures to improve overall health.





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