Yes, your right. What I think makes skiing so tricky is that its a random combination or aerobic (which definitely probably is leading to lows in me 2 and 48 hours later) and anaerobic (which spikes it almost immediately…sometimes.) Imagine somebody put your blood sugars into a cocktail shaker and just shakes them all up. Some years are more unsettling than others. But, your right, maybe the wind is just gonna blow in the direction that it blows and that’s it. Employ risk mitigation strategies and hope for the best.
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@katers87, thanks for information about alpha cells. I’m gonna read about those. That’s really interesting. I’ve discussed this with my Doc because I thought my liver might be outputting glucagon or sugar. She said that didn’t happen because I was a diabetic, so I forgot about it. I have also considered that cold weather might slow insulin absorption, or intense exercise might make my body absorb insulin faster, or adrenaline might be making BG higher. Your suggestion seems worthy of study. Is that something they can test for? Overactivity of pancreatic alpha cells? Or, we just assume that might happen across the board? Is it a characteristic of type 1 diabetes? This link shows up ‘Not Secure’ in my web browser, so I wont post it, but the article I found was “Alpha cell function in type 1 diabetes” by David Simon Hughes, Parth Narendran.
Unfortunately, I’m not the best resource for alpha cell function. I’ve simply heard that in type 1 diabetics it can be compromised. From the little I’ve read on the subject, I’ve gathered that alpha cells may also be attacked in addition to the beta cells in the pancreas. When I suggested this, I thought that perhaps you were having a harder time recovering from lows and that might be attributable to decreased alpha cell function. It sounds like the recovery is less of a problem than your sensitivity to/perception of lows.
For your reference I’ve listed an article that might give more information on alpha cells, but I doubt this is the problem for the reasons I just stated. Unfortunately, I’m unable to access the full article, but I’ve pasted the relevant pieces of the abstract below.
http://diabetes.diabetesjournals.org/content/47/7/995
“In the first section, we briefly review the importance of the alpha-cell response in recovery from hypoglycemia under both physiologic conditions and pathophysiologic conditions, such as type 1 diabetes…Because the glucagon response to hypoglycemia is often impaired in patients with type 1 diabetes, in the third section, we examine the possibility that autonomic impairment contributes to the impairment of the glucagon response in these patients…We propose that both types of autonomic dysfunction can contribute to the impaired glucagon responses in patients with type 1 diabetes. In the fourth section, we relate restoration of these glucagon responses to restoration of the autonomic responses to hypoglycemia. Finally, in the fifth section, we summarize the concepts underlying the autonomic hypothesis, the evidence for it, and the implications of the autonomic hypothesis for the treatment of type 1 diabetes.”
Also, I’m not sure why your doctor said that your liver is not outputting glucose. Even as diabetics, our liver will output this regularly and this is why we need a basal insulin all the time. Because our liver outputs glucose regularly, we take lantus/tresiba/etc or a basal dose in our pump. She may have misunderstood your question.
You’re right about insulin absorption varying with temperature and intense exercise though (as well as the effect of adrenaline). Intense exercise definitely increases absorption. Cold temperatures tends to have the opposite effect for me, but I think this may vary a bit from person to person.
Thanks a bunch. Thats really interesting. I’ve been curious about things like this.
I’m not sure why the Doc said that either, we may not have been communicating well.
I suspect that I have the same effect as you for cold weather and intense exercise, but that’s hard to measure. Thanks for the article. Much appreciation.
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That’s a marvelous metaphor. Describes the observable results perfectly. 
Alpha cells produce glucagon which signals the liver to dump glucose. In someone non-diabetic as they go low the body quickly reduces insulin levels and the alpha cells increase glucagon and the liver responds keeping the blood sugar tightly controlled and avoiding hypos. But those with diabetes have difficulty. Glucagon is technically the anti-hormone to insulin. Insulin suppresses the liver glucose response, so even if you release glucagon normally it may not work properly to result in a release of glucose. There is even some thought that insulin can suppress the response of alpha cells. More information can be found in this article.
So the upshot is if you use insulin and you have too much insulin circulating and you go low, your body may not respond properly with glucagon and glucose release and you are at higher risk of severe hypos.
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I guess I should have also mentioned that the alpha cells are not attacked by the autoimmune process behind autoimmune T1. It is only the beta cells that are attacked.
Thats a great article, Brian_BSC. Its surprisingly ‘readable,’ and FREE! Its amazing that they are testing individual system variables. I wouldn’t of thought they had any way of doing that.
I found kater’s article, and it says that “…most patients who have had type 1 diabetes for 1-2 decades have totally lost their glucagon response to IIH and have blunted epinephrine responses, these studies helped to explain the impairment of glucose recovery observed in patients with long-term type 1 diabetes.” (Gerald J. Taborsky, Jr., Bo Ahren and Peter J. Havel) They describe it as an ‘acute complication’ of ‘intensive insulin therapy.’ “Because it now appears that autonomic mediation is an important determinant of the glucagon response to hypoglycemia in humans, we propose here that autonomic impairment, together with [Beta]-cell destruction, contributes to the loss of this glucagon response in type 1 diabetes.” “The acute autonomic dysfunction should be fully reversible, while the subclinical autonomic neuropathy may only be partially reversible, particularly if there are structural defects in autonomic nerves induced by either long-term hyperglycemia or total [Beta]-cell destruction. Indeed, successful pancreas transplantation, which can restore euglycemia without inducing hypoglycemia, only partially corrects defects in nerve conduction velocity in patients with long-term type 1 diabetes (114). Finally, it is appropriate to reemphasize that the role of autonomic impairment in the deficient glucagon response in patients with type 1 diabetes remains speculative.”
So, I think its saying that we get nerve damage as an inevitable course of ‘diabetic aging,’ that is very likely to inhibit some of our body’s innate ability to autocorrect lows with glucagon/epi/lipolysis/etc. ??? Darn. David_dns might score a point for possible “blind-side”: I was hoping it wasn’t that.
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Thanks for clearing things up Brian 
Glad we have an alpha cell expert here!
The alpha cells are not attacked, but are slowly degraded over time. ??? “These data suggested that type 1 diabetes per se does not abolish the glucagon response to hypoglycemia, but rather that a time-dependent factor associated with this disease leads first to impairment and then to eventual loss of this [Alpha]-cell response” (Gerald J. Taborsky, Jr., Bo Ahren and Peter J. Havel, para 22, section “GLUCAGON RESPONSE TO HYPOGLYCEMIA IN TYPE 1 DIABETES”) That’s not much fun.
The subtle point is what does “glucagon response” mean. It could mean any of three things:
- The signaling to the alpha cells
- The actual response of the alpha cells
- The response in our liver to glucagon
My understanding is that certain autonomic hormone signals (like adrenaline and cortisol) signal the alpha cells to release glucagon. Over time, if you become hypounaware you won’t generate these signals as strongly. Then it is known that insulin can suppress the alpha cell response to hypos and suppress the liver from releasing glucose in response to glucagon. All of these probably factor in to the “glucagon reponse.”
And most of what I know about this subject is what I have read. I’m not a healthcare professional.
So, you might say that if I interpreting this wrong if I am thinking that there is decreased glucagon release into the bloodstream to help counteract hypos ?
Yes, but the key thing is that I am not at all clear it has anything to do with the alpha cells themselves degrading.
But, effectively, one might expect decreased resilience towards hypos as one ages? Or, no? This might be an aging thing, as opposed to a side effect of BG stability?
Seems like there might be too many factors. Based on the article, it’s likely more due to duration of type 1 diabetes than age. However, there’s no way to know if this is contributing to your recent problems.
It also seems that you’re struggling more with “feeling” the lows than recovering from lows, and I’m not sure that alpha cells/glucagon response would impact that.
I think the answer, is yes. But my mental model is not just “age” it’s more sort of wearing out the parts of the body because they got overused so much responding to hypos.
Note that my mental model is different than many others here, who blame it on a kind of neuropathy that hinders response. I can’t tell you that’s wrong, just that it doesn’t feel right. It just feels like I had too many hypos.
To me it honestly feels like so many repeated hypos over so many decades just wore some of the response mechanisms out.
I think there are shorter -term “wear-out” effects too. e.g. having a couple medium-to-large hypos over just a few days further hinders my ability to feel a hypo. But normalizing my blood sugars or even running them just a little high helps bring the ability back within a few days. The fact that I have observed this cycle so many times, is what causes me to think in terms of the “worn out used up” model with at least a little resiliency.
Not to go on and on about it. But, these Mystical Forces always fascinate me!!! I love the mystical forces that increase system complexity because they are so tricky to identify and implement controls for. It makes for fun experiments. Thanks, you guys, for the articles. I’ve been needing articles about things like this for a while. Now, I know where to start reading about them. Even if I know know ‘why’ things happen, I like to know what variables might be at play.
Yes, time spent as a diabetic is identified as a critical factor. No way to know, for certain, about the mechanism…as always. I will call them ‘mystical diabetic forces.’ And Brian’s right that ‘glucose recovery,’ is hard to interpret. But, the most surprising part of the article was that the innate mechanisms (although they can’t say, specifically, what they are) that help counter balance hypos deteriorate with ‘diabetic age’ or duration of the disease.
I guess I am struggling with an increase in diabetic symptomatology associated with hypos, or perhaps, “an increase in severity of hypo.” I would think that could be a result of my body putting out less glucagon or epi, or performing less breakdown of fat into simple sugar (mystical forces). I have always blamed sugar output from one of these mystical variables for bumping me high when I exercise. Seems feasible that a decrease in them might impact the experience/severity of lows. I’m not sure if going blind represents a decreased ability to recover from lows or an instance of ‘severe hypoglycemia,’ but it might. This is my 20th anniversary of being type one, so I maybe I’m just a late bloomer on some of those impaired functioning they speak of. If they have demonstrated that the rate of change decreases during recovery time, might there also be an analogous increased rate of change during the drop, increasing symptoms?
“Because most patients who have had type 1 diabetes for 1-2 decades have totally lost their glucagon response to IIH and have blunted epinephrine responses, these studies helped to explain the impairment of glucose recovery observed in patients with long-term type 1 diabetes (10-14). In many patients with newly diagnosed type 1 diabetes, both glucagon and epinephrine responses to hypoglycemia are quantitatively normal, as is the rate of glucose recovery from hypoglycemia (15). In contrast, many patients who have had type 1 diabetes for less than a decade have blunted glucagon responses with normal epinephrine responses, but a delayed glucose recovery (15). From these studies, the concept emerged that the glucagon response is critical for normal glucose recovery and that impairment of the glucagon response is a major factor in the susceptibility of patients with type 1 diabetes to episodes of prolonged and severe hypoglycemia (5).”
I think they are more concerned with the ‘prolonged’ part of recovery (rate of increase shown in red) and I am more concerned with ‘severity’ (rate of decrease on the way down). Not at all a bad article for starting to think about this problem.
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Yea, they say neuropathy. I am definitely developing a much wider definition for ‘neuropathy’ this year. It encompasses more than I thought. But, I’m like you - I just sorta view it as normal aging or ‘wearing out,’ because it’s inevitable that we are always having increased duration of diabetes as we age. It just feels ‘healthier’ to view it as a thing that happens as we age, as opposed to the effect of inevitable, destructive complications. Your comments are useful.
Just to clarify with everybody, I’m totally not perceiving this as a hypo-unawareness issue (although you could probably challenge me on that). Because I crashed a car and lost vision (strong physiological symptoms of brain malfunction) during only a moderate low, I would term this an issue with hypo ‘severity.’ It feels like the pattern that has developed is one of increased severity/symptoms of hypos.
I think there’s many ways to classify what you’re experiencing, and it sounds like you’ve had a chance to review a lot of helpful possibilities.
However, when you experienced the strong symptoms you described, your low was not moderate. A blood glucose level of 40 is a severe low blood sugar. If my blood sugar drops to that range, I am severely compromised and generally cannot even remember what occurs. Your description of “increased symptoms of hypos” is very fitting though as you have previously had different experiences in the past in that range. I personally would not rule out a change in hypo-awareness because, as the title of this post states, you’ve recently experienced an increased stability and are now experiencing increased hypo symptoms.
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