Karmel Allison - Where is My Robot Pancreas?

Karmel was born in Southern California, diagnosed with Type 1 Diabetes at the age of nine, and educated at UC Berkeley. Karmel now lives in San Diego with her husband, where she is loving the sunshine, working in computational biology at the University of California, San Diego, and learning to use the active voice when talking about her diabetes. Read full bio

Eyeballs out

Karmel Allison | April 02, 2013

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Cataract surgery.

Child
I have been
diabetic longer
than you are old
long i chiiiild
a gentle gnawing
a slow abrasion
and now you say
you say let’s
pluck out her eye
now there’s the long i
and so they will
vacuum it out
a routine plucking
throooop like that
thousands thousands
a year and I think
of all the eyeballs
cohabitating
in their vacuum
lovers watching
a primordial soup
plastics plastics
are the future
I trust him
what’s his name the Jew
plastic lens
unfolds telescopes
like an umbrella
and then I will
cycloptic stare
one eye in a vacuum
darling darling
will you do me
a favor I need
a right eye
can you please
be my eyeball see
for me tell me
what do you see
a child chiiiild
a diabetic child
veins slowly abraded
from inside out
eyeballs out.

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They cured diabetes in dogs?

Karmel Allison | March 24, 2013

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Last month, the news started circling: they cured diabetes in dogs! Mice we hear about often– but dogs is new and exciting. So what’s the story there?

The publication in question is “Treatment of Diabetes and Long-term Survival Following Insulin and Glucokinase Gene Therapy,” [1] published out of Spain in the journal Diabetes. Unlike many of the recent therapies that have made it to clinical trials, this study doesn’t try to reset the diabetic immune system or prevent the development of autoimmunity. Instead, the authors demonstrate successful treatment of diabetes in dogs using a gene therapy approach they had previously used in mice.

What exactly is their gene therapy approach? First, a quick primer on gene therapy (and here I insert my disclaimer: gene therapy is outside of my area of expertise, and so I read and comment on this paper only as an observer, and not as an informed expert. Take it all with a grain of salt!). Gene therapy is the therapeutic application of techniques that have been used in labs for many years to insert particular strings of DNA into cells such that the machinery of the cell takes the DNA, transcribes it into RNA, and then makes the protein that is encoded in the DNA. This extremely powerful technique allows us to force cells to make proteins that they might not otherwise make, and in the last decade it has started to see success in small trials to treat a number of diseases. For example, in 2006, scientists used gene therapy to generate T cells that made a receptor that recognized specific cancer cells, allowing the T cells to kill the cancer cells [2]. Another example is the use of gene therapy in 2010 to make a patient’s bone marrow cells produce the beta-globin gene that they lacked due to a genetic defect [3].

These and other similar successes are leading many research groups to study gene therapy and the ways we might use it to treat disease. However, in addition to demonstrating the power of gene therapy, these success stories implicitly demonstrate some of the difficulties; the ability to arbitrarily express any protein in any cell would be incredible, so why don’t we just use gene therapy to treat everything? As it turns out, designing and targeting a string of DNA at a cell is not easy. Currently, we use what are called viral vectors to get the DNA inside cells– basically, we make a virus that contains the DNA we want to insert, and infect cells with the virus. The virus enters the cell, and can integrate its DNA segment into the chromosomes of the host cell, or can leave the DNA separate, floating around as if it were a separate chromosome. There are a number of different virus types that are used, with a variety of advantages and disadvantages, but I’m sure you can imagine what makes people nervous about gene therapy– we’re leveraging the existing natural ability of viruses to invade cells to our advantage, but our knowledge of how exactly to direct and control the virus is still developing. Sometimes there are off-target effects, where the viral vector ends up affecting a gene we didn’t intend to affect. And it’s not easy to hit every type of cell– what do you do if the target cell is not sitting somewhere easy to reach? Further, any time you introduce a foreign gene into the body, you risk the immune system deciding to attack. And even if it doesn’t, the cells that do take up the DNA and make the target protein might only do so for a little while before dividing, dying, or otherwise changing. In other words, gene therapy is incredibly powerful and full of promise– but it’s still nascent, and there’s lots of work to be done, one study and one trial at a time.

And the paper published in Diabetes was one such study– a step forward in using gene therapy. The authors in this paper discuss an approach to curing hyperglycemia using two viral vectors that force the expression of two genes in skeletal muscle (that is, the muscles you use to move around that are connected to your bones). Skeletal muscle is not a standard target in treating type 1 diabetes, where we more often hear about T cells and beta cells. However, skeletal muscle plays an important role in glucose control because it is the end destination of much of the body’s circulating glucose. Normally, in cells in the muscle, special proteins called glucose transporters take glucose into the cell and allow it to be converted into energy for the cell’s use. Insulin binding to the outside of the cell is what turns the glucose transport system on, so, under normal circumstances, a person eats food, which gets processed in the gut, releasing glucose into the blood stream. At the same time, a delicate concert of signals causes the pancreas to release insulin, which travels through the body and makes cells present glucose transporters on their outsides such that they can take glucose in from the blood, and blood sugar levels remain steady. In a diabetic, with no beta cells to make and release insulin, the sugar stays in the blood unless insulin is injected directly.

Scientists look at this glucose-insulin signaling system and see several places to intervene: what if we could make other cells produce insulin? Then we would have insulin in the diabetic. The trick here, though, is that too much insulin is bad, too. The usual approach, therefore, is to try to make new beta cells or to make cells that can specifically respond to glucose. The authors of this paper, though, take a less traveled path: instead of trying to manufacture cells that respond to glucose and produce insulin, they say, let’s just force the cells that need the glucose, like those in the skeletal muscle, to take up all the extra sugar that’s in the blood, even if there’s not enough insulin.

How do they do this? That’s where gene therapy comes in. The researchers thought to use viral vectors to force skeletal muscle cells to make the insulin protein. Not enough that the host animal becomes hypoglycemic, but just a little bit, so that cells throughout the body are stimulated to put glucose transporters on the surface of the cell, waiting for glucose. At the same time, a second viral vector forces the expression of a protein called glucokinase (Gck). Gck is normally only expressed in the liver, and it functions downstream of the glucose transporter to help bring glucose in and ready it for processing. Skeletal muscle cells express a similar kinase, but it is less effective at processing the glucose. More importantly, the researchers in previous studies had found that if they forced skeletal muscle to express Gck, it only started working when glucose levels were high, helping to pick up the slack left by the version of the protein naturally in skeletal muscle cells.

So to put all the pieces together: in order to allow glucose to get into cells in the absence of beta cells, the scientists force skeletal muscle cells to make a little bit of insulin, and also to make a protein in the glucose processing pipeline that works very quickly when extra glucose is present. Thus, skeletal muscle cells are able to take up lots of extra glucose, and hyperglycemia is avoided, even without beta cells.

Does this actually work? The authors previously showed that this dual-gene treatment worked with mice [4], but in this study, they moved up to large animals– namely, dogs whose beta cells had been killed with a selective toxin, streptozotocin. The treated dogs thus lost all beta cell function and became hyperglycemic, making them a useful model for type 1 diabetes. After becoming diabetic, the dogs were treated with on of:an injected insulin regimen; the Gsk gene alone; the insulin gene alone; or both the insulin and the Gsk genes. Not surprisingly, without treatment, the dogs were hyperglycemic, and with regular injected insulin, the dogs were better but not great. (For those of you who are diabetics or parents of diabetics, it should come as no surprise that multiple daily injections doesn’t really cut it!)

The dogs given an insulin vector alone failed the glucose tolerance test

 

The dogs treated with both insulin and Gck vectors passed the glucose tolerance test.

And the gene therapy treatments? Expression of Gsk alone did not ameliorate hyperglycemia; without any insulin, the skeletal muscle presumably did not have any glucose transporters on the surface of cells to even begin to let glucose in to reach the Gsk protein. Expression of low levels of insulin alone on the other hand was an improvement over no treatment at all– the dogs regained some of the weight lost upon induction of diabetes, and fasting glucose levels were near normal. However, the dogs were unable to properly process glucose after meals, and, like the untreated dogs, spiked up to 500 mg/dL and remained elevated for hours.

To test both the insulin and Gsk vectors together, the researchers injected five dogs with one or two doses of the viral vectors. The dogs quickly regained normoglycemia, and even the higher doses were tolerated well by the animals, not causing any toxicity or side effects. Unlike the dogs given insulin alone, the dogs given both genes together responded much better to an oral glucose tolerance test, spiking slightly up to between 200 and 300 mg/dL, but stayed well below the levels seen with the diabetic dogs and returned to normal within three hours. (Healthy, non-diabetic controls peaked around 150 mg/dL.) And the really impressive part: the dogs have remained normoglycemic, with continuing expression of insulin and Gsk in the skeletal muscle, for four years and counting.

So what does this all mean? Have the researchers cured diabetes, and if so, how quickly can we move this sort of treatment into humans?

First, my personal soapbox: the researchers here have cured hyperglycemia in the dogs, not diabetes; type 1 diabetes is a complex autoimmune disorder, and the immune aspect was not addressed in this paper. That’s just semantics, though, and as a diabetic, I would be more than happy with a cure for hyperglycemia!

But, that brings me to a problem I see; the researchers have essentially done two things: (1) They enforce low basal levels of insulin, and then (2) they make skeletal muscle cells very insulin sensitive by making them take up glucose faster than normal.

In this dog model, those two things are sufficient to keep the dogs in range. However, if I extrapolate to humans, this seems to be similar to (1) taking a long-acting basal insulin, and (2) taking an insulin sensitizer such as Metformin to make cells particularly responsive to the low levels of insulin. Now, at this point, if you’re a type 1 diabetic, you’re saying, “Yeah, right, like that would work.” I, as a type 1 diabetic, think there may be a lot of value in incorporating Metformin into treatment, and I know there’s a lot of value in long-acting basal insulins. But the two together do not a cure make– there’s bound to still be too much up and down!

So why would this work in dogs? I see two primary possibilities: (A) I am incorrect in my equating the gene therapy to low basal insulin plus Metformin, and really there is something more intricate and responsive going on, or (B) the metabolism and lifestyle of humans is sufficiently different from even large mammals like dogs that what works in the latter is not necessarily sufficient for the former.

I won’t choose between those here, because I am not an expert and do not understand the details of the paper well enough to rule out (A). Plus, I hope (A) is true, and the treatment does work in humans. That would be amazing. Incredible. If (B) is the case, though, this study perhaps serves to reinforce the value of a combined Metformin and insulin treatment for type 1 diabetics, but does not offer a be-all-end-all cure or even a practically preferable path to insulin sensitization given the relative cost and risk of Metformin.

That said, regardless of what they find with this particular application of gene therapy, I do commend the researchers for a unique approach to treating diabetes (we need those!), and also for taking one more step forward with gene therapy. Gene therapy as a field is very exciting, and I look forward to seeing more applications reach the clinic. (The child in me says, “Gene therapy! The future is now!”)

Anyone out there with more knowledge than me? Is the answer happily (A) or unfortunately (B)?

1. http://www.ncbi.nlm.nih.gov/pubmed/23378612
2. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2267026/
3. http://www.ncbi.nlm.nih.gov/pubmed/20844535
4. http://www.ncbi.nlm.nih.gov/pubmed/16731816

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Thinking about Diabetes Complications: Eyeballs and Knees

Karmel Allison | November 20, 2012

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I’ve been thinking about complications a lot lately.

It started with one of my NOD mice– the little guy developed hyperglycemia, as expected. Her blood glucose was above 250 mg/dL, so I separated her from her siblings and came back the next day. (The blood glucose values vary a fair amount, so I ensure the mouse comes up above 200 mg/dL at least three times, each at least 24 hours apart.)

I didn’t end up getting to the third measurement until about 6 days later just because life got in the way. Under normal circumstances, that’s not a big deal; the mice seem to tolerate hyperglycemia for weeks before starting to get visibly ill.

Not this one, though. “This mouse looks pretty sick,” said the tech. And indeed she did– stiff and shivering, wasting away, skin on bones. Poor little thing.

My heart dropped. “I’m sorry, little guy! I didn’t mean for you to suffer!” I said to her in my head. I marked the cage for sacrifice and recited a quick eulogy to myself: “You died for science! We appreciate it!”

Later that night, I kept seeing the little shaking mouse in my mind’s eye. I felt guilty for having left her for that week, but also I felt afraid: diabetes did that. Please, God, don’t let that happen to me!

I went in to the optometrist at Kaiser today to get fitted for monovision contacts– one eye farsighted, one eye nearsighted. You see, I have cataracts because of my poor glucose control during adolescence, and so I have to get my lenses replaced soon. The good news is that cataract surgery is routine, outpatient: just pop in plastic lenses, and you’re good to go. The bad news is that plastic lenses are a sad imitation of the real ones, since they are not attached to the eye muscles, and thus I will lose the ability to focus at different distances. To mitigate this problem, the surgeons will put in one lens designed for distance vision, and one designed for close vision, and I will learn to focus with one eye at a time. The contacts are to practice this.

Osmotic pressure.

High levels of glucose change the osmotic pressure of blood as it flows through the body. The mere thought of that creeps me out.

But there is progress, always progress. The ease of achieving glycemic balance increases over time. Several weeks ago, my Minimed CGM transmitter started to give out. It doesn’t hold its charge very well now, and I have to recharge it for days at a time to make it work again. The Minimed rep told me that because the transmitter is more than two years old, she was surprised it was still working at all.

So I wrote to my doctor and said I wanted a Dexcom.

That was a Friday. The following Monday, the new Dexcom G4 approval was announced. And I thought to myself: am I lucky or what?

I went back and forth between Kaiser and Dexcom for a bit, and then today I got a call, right after the contact lens appointment, while a phlebotomist was setting up to draw my blood for an A1c. It was a local number, and I answered. It was Sean, from Dexcom, letting me know the order had come in from Kaiser, and my new CGM would ship out that day. “Ow!” I thought, because the phlebotomist had just inserted the needle. Then, “Yay!” because I was getting a Dexcom G4. (Like a G6, like a G6.) 

As I left the Kaiser lab, arm taped up, I saw a man in a wheelchair. Big guy, leg amputated at the knee. “Probably diabetes,” I thought to myself. And then: Please, God, let my A1c be good.

Good, bad, those are moral terms we apply to medical assays. I shouldn’t do that.

Maybe. But on the other hand, dysregulated growth factors and increased osmotic pressure? Bad. Keeping my legs? Good.

I should think less about complications.

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Type 1 and Type 2 Diabetes at the Same Time?

Karmel Allison | November 12, 2012

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One thing I hear occasionally among type 1 diabetics is, “Well, at least I can’t get type 2 diabetes!” This reasoning makes sense if you think only about the two diabetes as two points along a single spectrum, with type 2 diabetes being a metabolic disease that is “the less severe” type 1 diabetes.

I felt compelled to answer: Yes, yes you can. You absolutely can. Yes you can have type 1 and type 2 diabetes at the same time. You’re unlikely to get diagnosed with type 2 diabetes if you already have type 1, because it’s hard to measure the difference in blood sugar values, but you can still suffer from both types of diabetes simultaneously.

Consider: type 1 diabetes is an autoimmune disorder characterized by the T cell mediated destruction of the insulin-producing beta cells. In other words, no beta cells.

Type 2 diabetes is a metabolic disorder characterized by insulin resistance in many of the cells in the body, and can progress to stress-induced (we think) death of the beta cells.

So, if your beta cells are already gone as a result of type 1 diabetes, they can’t die again because of type 2. But you can definitely become insulin resistant, due to obesity, genetic predisposition, and/or hyperinsulinemia.

As if type 1 diabetes weren’t hard enough– consider doing it while your body is insulin resistant as well. Ugh. Don’t do it, people– watch your weight, stay active, eat well. Avoid type 2 diabetes, especially if you’re a type 1 diabetic.

I am thinking about all of this in the wake of having watched the HBO miniseries/documentary, The Weight of the Nation. I highly recommend it– it was made in conjunction with the NIH, and hits a nice balance of being understandable and compelling, and being scientifically based. Plus, Francis Collins makes several appearances. I love that guy. It’s free, with four core episodes and a number of vignettes that go slightly deeper into detail, so check it out: http://theweightofthenation.hbo.com

Because, really, diabetes sucks, so let’s do what we can to avoid it when we can.

YouTube Preview Image

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TCOYD San Diego, in pictures

Karmel Allison | October 29, 2012

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This weekend was the annual Taking Care of Your Diabetes (TCOYD) conference and faire, put on by the illustrious Dr. Steve Edelman. I was there to talk about online resources and social media with the fun and fabulous Kelly Close and Manny Hernandez, and also to volunteer at the booth for our San Diego JDRF chapter.

I had a great time– getting a chance to hang out with Kelly and Manny was a blast, and it’s always fun to see familiar diabetes faces from all around. I was especially pleased to catch up with all the super-cool people at Insulindependence, and to meet David Lim of Diabetic Lifestyle, which makes pump-friendly compression shorts.

And, extra-special bonus: I got to meet our very own Mollie Busby, representing Riding on Insulin!

Pics, or it didn’t happen!

Kelly Close and Manny Hernandez at TCOYD San Diego

Me, Kelly Close and Manny Hernandez at TCOYD San Diego

TCOYD San Diego

JDRF at TCOYD San Diego

Riding on Insulin at TCOYD San Diego

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Pills, pills, pills: Can a diabetic take too many vitamins?

Karmel Allison | October 14, 2012

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Growing up with type 1 diabetes, one of the sticking points (pun intended!) was always that it couldn’t be managed with oral medication. Nope– “Shots, shots, shots!”  it was, and not in a fun, drinky way. And then in 2005, I graduated to an insulin pump, but that’s just a more mechanically complex syringe. Treatment, for me, is about blood and tissue and infusion.

So it’s a little disorienting to find myself popping handfuls of pills every day now that I’ve entered adulthood. Granted, most of them are over-the-counter vitamins, but still– I count nine caps a day:

  • Synthroid (for autoimmune thyroiditis)
  • Estrogen (to keep hormone levels in balance)
  • A salt cap (my blood pressure runs low, and this seems to help)
  • A multivitamin (from GNC; two pills, each of which is pretty big as is, so I’m glad it’s not combined into one)
  • A Vitamin D/Calcium supplement (from Costco; two pills, to meet the 1000mg/day bone health recommendation from my doctor)
  • Fish oil supplement (from Costco; I hate taking this one, because I can taste the fish oil)
  • Low-dose aspirin (from CVS, a sugar-free, safe for diabetics version)

 

Looking at this list, I get slightly worried. Should I be taking so many vitamins? Doesn’t that seem like maybe it could have unforeseen negative effects? Is it too much? Should I go all natural?

Then my more rational side kicks in and reasons, well, everything I eat and breathe all day is full of synthetic everything; these vitamins and medications were carefully selected (I read reviews and Consumer Reports, and I read the FDA statement on lead content in women’s vitamins), so really the question is not nothing versus a set of supplements, but rather tons of engineered input versus some additional engineered input that is specially selected to be helpful. But, still. Nine pills a day? That’s weird, right?

The aspirin is the most recent addition. I feel like I’m young to begin worrying about cardiovascular health and cancer, but, then again, I’m a diabetic, and I seem to aim for high-intensity life rather than carefree, stress-free living, so heart disease and cancer are real risks. And the scientific pendulum has swung back in favor of daily low-dose aspirin as a “We don’t understand why it works, but it seems to help,” long term preventative for cancer (see, for example, the recent piece in Science Magazine on the controversy over aspirin).

However, if we don’t really understand the mechanism behind things like aspirin, but we theorize that somehow over the long term they have measurable effects that we think right now are positive, then it is easy to imagine that over the long term these seemingly innocuous pills could be having measurable negative consequences as well. How can I know? To paraphrase Milan Kundera, if I only live once, I cannot test both scenarios– taking these vitamins every day versus not, all else being equal. I can read studies and consider the aggregate statistics, but without understanding how exactly they work, I can only guess what the exact effect will be on me, for my body. Maybe taking Vitamin D will make me 1% less likely to get a bone fracture down the line. But maybe the molecular formulation of the capsules interacts with some errant cells lodged in my bones somewhere, and day after day helps those cells get stronger, and actually I’m 1% more likely to get bone cancer in sixty years.

And then I pause this stream of thought and I consider: sixty years! Think of how far we have come, that I, a diabetic, think nothing of forecasting my life sixty years out.

Besides, statistically speaking, my worrying about the outcomes of taking so many pills is more likely to cause long term damage than just taking the pills.

Put more poetically (and to make up for the fact that I began this post with a reference to LMFAO), consider the passage from one of my most favorite books, Kundera’s Unbearable Lightness of Being:

“There is no means of testing which decision is better, because there is no basis for comparison. We live everything as it comes, without warning, like an actor going on cold. And what can life be worth if the first rehearsal for life is life itself? That is why life is always like a sketch. No, ‘sketch’ is not quite the word, because a sketch is an outline of something, the groundwork for a picture, whereas the sketch that is our life is a sketch for nothing, an outline with no picture.

Einmal ist keinmal, says Tomas to himself. What happens but once, says the German adage, might as well not have happened at all. If we have only one life to live, we might as well not have lived at all.”

Which brings me to the most reasonable conclusion I see possible: que sera, sera. And with that, it’s 78F and sunny in October in San Diego, so I’m going to go outside and enjoy that– the threat of skin cancer be damned!

 

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If a Diabetic Runs a Half-Marathon in the Woods…

Karmel Allison | September 02, 2012

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Somewhere around kilometer 18, I think.

Hey, so, guys? I ran a half-marathon. Really!

I didn’t really plan on it– on Wednesday, my roommate here in Kuopio, Finland, mentioned that there was a marathon that Saturday, which was coincidentally my last weekend here in Finland. I was interested, as a half-marathon seemed like a really nice way to close out my stay here in Kuopio, but I had never run that far in my life, and I had a lot to do in those final days.

But I did like the idea of being able to tell everyone I had run a half-marathon. Forget personal achievement; I am a child of the “If no one’s there to hear the tree fall, it didn’t happen” generation. That said, I am also the kind of person who sometimes doesn’t try things for fear of failure– what if I tried to run the marathon and couldn’t make it?

And in my consideration of the possibility of failure, I wasn’t so much worried about muscle fatigue as blood sugar mayhem. Normally I run in the early mornings; how would I change my schedule to start a really long run at 11:00? Would I need more insulin because of the adrenaline, or less because of the activity? If I got high, would I regret having done this twenty years down the line? What if I go really high because I misjudge how much insulin I need and have one of those awful I’m-300-for-hours experiences? What if I try to prevent that by taking more insulin and end up low? Will I know it? Will my CGM warn me? I’m in the middle of a foreign country– what if I go so low I pass out? Who would take me to the hospital?

Ah, yes, diabetes. Where any physical activity comes with fear of death. Lovely.

My strategy to reconcile these two emotions– the desire to finish a half-marathon and the fear of premature death induced by glycemic excursions– was to register for the race (the 50 euro fee served as a nice commitment device), but tell only a handful of people that I was running so that if I chickened out, or if I started the race and had to bail because of uncontrolled blood sugar, I wouldn’t have to publicly admit failure.

Ah, yes, mild neurosis. Where any experience comes with intense internal debate. Better than fear of death.

Given that I decided to do this only a few days before the actual race, I didn’t have time to train. The farthest I had run before the race was somewhere in the 13km range, about two-thirds of the 21.1km I would be running. I did, however, have enough time to fret about how I would do this, and what-was-I-thinking. My plan was to take sugar, my meter, and 20 euros with me in some sort of sport pack I would buy, and then try to run pretending that it was just a normal, morning run. Eat right before, bolus some insulin but not much, and then watch my CGM during and adjust accordingly. Based on my morning runs, I was expecting the beginning of the run to cause my blood sugar to drop (hence eating beforehand), followed by a gradual climb starting around the 45 minute mark.

A hiccup: the store I went to the day before the race only had giant, hiking fanny packs. Plan B: I got a money belt that I was able to tie a few extra knot into so that it fit tightly around my waist. Crisis averted.

On race day, I spent the morning stretching a little and video chatting with my husband, who assured me that he would of course still love me if I didn’t finish the race. Good– I felt much more comfortable knowing that I had “permission” to fail. Not that anyone except me would view not finishing as failure, but, well, like I said– mild neurosis.

At 9:00 AM, I caught the bus over to the race start site. It was darn cold outside for this San Diego girl. When I left the house, it was 48F, and windy. By 11:00 when the race started, it had warmed up to somewhere between 50 and 60F, which was bearable and preferable to heat, but still biting cold.

After getting my race bib, wandering around for a while, and going to the bathroom twice because I was so nervous, I queued up with the runners a few minutes before 11:00. Blood sugar was 83 mg/dL; I ate a protein bar and took .3 units of insulin.

It was sort of strange to not know what exactly was going on, since all the signs and announcements were in Finnish, but it was easy enough to just start going when everyone else did. Incidentally, about 80% of the contestants were wearing Asics. They must market well in Finland. And very few people had music players; this being my first race, I was unsure if that was a race thing or a Finnish thing. I had my iPod, full of Tiesto. Nice running music.

And I was off. Everyone started out really fast! I was being passed by children and overweight old women alike. “There’s no way I can keep up that pace!” I thought. Within the first kilometer, though, everyone thinned out, and I was able to find some people to follow. My strategy was to pick out the full-marathoners who were running a little faster than me, and follow them. That way, I figured, I was trailing someone who was normally way out of my league, but because the routes were overlapping, was accessible to me.

By kilometer 2, my CGM was complaining that I was low. Bullocks, I thought. I ate right before this, and I can tell when I might be low because my limbs feel heavy. Looking at the trace, it was obvious my CGM had just gone kaput on me. I suspect this happens during exercise sometimes because my body redistributes glucose to the areas that need it, leaving my abdomen looking curiously low to the sensor stuck inside. Just a theory. But in any case, the CGM was dead to me. That’s okay, I thought, I can do this.

I felt a little like Luke Skywalker– close your eyes, and feel the force. Am I high? Am I low? Feel the glucose…

The first 3km were easy. And so were the next eight. It was a pretty run, a nice tour of the forests and the city. The air was cold and sharp, but clean. Finland is so green; it’s incredible.

At 11km, I was feeling pretty good– halfway there! I didn’t have a watch (whoops), so I had no idea what my time looked like, but I was keeping up with my chosen rabbits, so I figured that was good enough. Kuopio is very hilly, which was nice, because the hills make it easy to pass a bunch of people in one go. My competitive nature came out, and I found myself pushing to pass certain people.

At 13km, I was excited– this is the farthest I’ve ever run! Anything past here is gravy. I kept trying to maintain pace, telling myself that now was when I was at risk of getting tired and having to walk the rest.

I could tell that I wasn’t low, and that meant I was probably inching upwards. I bolused insulin, a few tenths of a unit at a time, every four or so kilometers.

The kilometer markers kept going by. Between 14 and 16, I thought maybe the race would never end. But by 17, I was still feeling good, with plenty of power left, and so I knew that barring unforeseen disaster, I totally had this.

The last five kilometers or so were mostly uphill, which seemed like a cruel trick at first, but was actually kind of nice, because pushing up hills kept me from slowing down too much. Eighteen, nineteen– I was speeding up realizing I was almost there. Twenty and twenty-one, and race around the corner and I was there! I made it! A friendly face there cheering me on, to boot.

What I told everyone was that I just wanted to finish. What I told myself was that I wanted to do it in less than three hours. Final time? Two hours and four minutes and change. Of course, being who I am, my first thought was that I totally could have done it in less than two had I known I was so close. Next time…

And blood sugar at the end? A healthy 151. Started climbing as soon as I was done, so I bolused and began walking with my friend towards her home.

So, I ran my first ever half-marathon. In just over two hours! Did I mention I’m a diabetic? And a girl? And not a runner? Yippee! I’m pretty proud of myself. And I’ve shared now, so this tree makes a sound.

6 comments

An Open Letter to Tim Gunn: I am a real woman!

Karmel Allison | August 25, 2012

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First things first: I am a big Project Runway fan, and you play no small role in that. You appear to be one of those rare people who is infinitely likable. Everyone should have a little Tim Gunn sitting on their shoulder. Thanks!

And now to the meat of the matter: I just watched the “real women” episode of Project Runway, Season 10. Every season there is one such episode– where the designers have to design and fit a client who is not a professional model, and is instead a woman proportioned more like the rest of the country. The “real women” challenges are particularly interesting; they highlight some of the assumptions made by the designers, separate the versatile wheat from the one-size-only chaff, and also allow us viewers to connect more closely to the whole process.

Each season, the women selected for the challenge are thematically linked. This season, we saw women whose friends had nominated them as desperately needing a makeover. In years past, we have seen brides-to-be, women who lost a lot of weight, daughters going to the prom, mothers of the contestants, and so on.

And so I would like to propose the theme for next season: women with fashion challenges imposed by medical need.

Yeah, that’s right. I’m talking about me, here. Chicks with insulin pumps. And Continuous Glucose Monitors and a bunch of other junk taped to their bodies.

Most of the time, I wear my pump like a pager, clipped on to my waistband. Really hip. When I got married, I strapped my insulin pump to my leg with a piece of velcro that I then hooked on to my underwear with a safety pin and string. When I wear a bikini, I have so many tubes and wires and puncture wounds all over the place that I have had to carefully cultivate an attitude of “Screw it,” and just deal with it. I rarely wear dresses because figuring out how to attach my medical devices to myself and still be able to see and use them is a headache.

I would love to have a Project Runway designer make me a fabulous outfit that takes into account my particular medical needs. Please? I nominate myself as the diabetic client, and then there are the women missing limbs; in wheelchairs; on dialysis; with dermatological sensitivities; and the list goes on.

Think of the possibilities! And the stories that can be told! Educational for the audience, and also heartwarming. This is a perfect idea, you must agree. 

C’mon, Mr. Gunn– what do you think?

Yours truly,
The chick with the insulin pump

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Heisenbugs and the Diabetes Observer Effect

Karmel Allison | July 23, 2012

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Warner Heisenberg

Night 1: wake up in the night with my continuous glucose monitor (CGM) barking at me. Measure my blood sugar– 189. Ugh. Too tired. I take 1 unit of insulin, and go back to sleep, only to be woken up several hours later by my CGM again. Measure my blood sugar. 57. Ugh. Eight grams of carbohydrates to correct. Brush my teeth again. Sleep again.

Night 2: wake up in the night with my CGM barking at me. Measure my blood sugar– 205. Ugh. Take .7 units of insulin, knowing the 1 unit from last night was too much. Above 200 mg/dL, I try to stay awake to make sure my blood sugar goes back down. It takes an hour. A long, tired hour of checking every few minutes only to see I’m still above 200. Finally, a 180. Back to sleep. Wake up an hour later, my CGM barking again. Still high. Take another .4 units of insulin. Sleep. Another hour. Barking. High. Measure. 191. Seriously? Another .7 units. Wake up in the morning at 75 mg/dL.

Night 3: expecting to go up again at night, I take extra insulin with dinner. Hanging around with the hubby, and bam, I’m 47 before I feel it. Eat 12 grams of carbs, suspend my basal insulin. Wait. Go back up to 72. Reenable my insulin, continue about my business. I’m 75 before going to bed. I leave it be. Wake up in the night with my CGM barking. 181. Ugh. Last night took more than a unit and a half to get back down; I hedge, and take 1.1 units. Wake up several hours later with my CGM barking again. 60. It’s only an hour until I wake up for real, and I don’t want to eat and brush again. Suspend my basal for half an hour, and wake up an hour later at 59. Close enough.

But what’s going on here? Besides the fact that all of the sudden I’m going straight up at night (that happens for a week at a time occasionally. Hormones?), my required correction bolus is all over the map. I needed way more insulin on night 2 than nights 1 and 3, clearly. Why? What makes this night different than all other nights? (Yes, that is a Passover shout-out.)

And then it occurs to me: it looks like a heisenbug.

A what? A heisenbug. The word heisenbug comes from software engineering, where it was coined to name a bug (or error) in software that can’t be easily debugged because the act of trying to observe the bug changes its behavior. The term is a pun derived from the name of Werner Heisenberg, who described the “observer effect” in quantum mechanics, in which the act of observing a process fundamentally changes the process.

With computers, heisenbugs are rare occurrences; software is designed to execute a series of operations, and doesn’t care about who’s watching it. There are peculiar cases, though, where trying to add code to debug a problem seems to change or even fix the problem. Consider a case where two processes are failing because they compete for the same resources on the computer. You don’t know why the processes are failing, so you add some code to print out status messages as the processes run. The act of printing out messages, though, causes the programs to run at slightly different rates, and so both are able to finish without ever running into each other. Magically, trying to observe the two processes seems to make the problem go away, even though it does not address any actual functioning of the processes. A heisenbug.

But people are not like computers, and it occurred to me after these three nights that we are full of heisenbugs, diabetics especially so. Any process that involves hormones or emotions, it seems, is necessarily at risk of introducing heisenbugs. For example, imagine that you are feeling arbitrarily sad, so you start recording the events in your life at the end of the day, to try to track down what is causing this malaise. Lo and behold, the act of reflecting on your day proves to be a clarifying habit, and after a week you feel much more optimistic and happy, without ever having found a single “cause” for your feelings. A heisenbug.

Similarly, imagine my blood sugar is high in the middle of the night. I administer insulin according to previous experience to try to bring it back down, and, like a good little diabetic, I wait up and observe the downward arc to make sure everything is going to plan. However, it’s the middle of the night, and my body was not ready to be awake. It’s in a bit of a shock, starts releasing some cocktail of hormones and brain-juices to keep me awake. And so my previous hyperglycemic experience is now a fundamentally different experience, as in trying to observe this bout of hyperglycemia, I have changed some number of variables. What I found the other night no longer applies, because I am observing this particular night, and that changes my activity levels and hormones, and that changes my body’s response.

A bloody heisenbug.

So what do I do next time? I can’t just start going to sleep above 200 and assume all will be okay– what if there is a real issue like a blocked set? And I’d rather not stay up for an hour every time I wake up in the night and have to take a correction bolus.

There is a fairly straightforward solution in this particular case– if I plan to stay up, recognize I will likely need more insulin to combat a sort of middle-of-the-night-dawn-phenomenon, but that if I go right back to sleep, I should take less insulin.

But that doesn’t solve the bigger problem– that diabetes is a complicated mess of problems and bug reports that requires an awful set of ad hoc rules and memory space to keep functional.

In conclusion, I would like a cure, please.

Or, a more immediately practical alternate conclusion: keep an eye out for heisenbugs, and adjust your debugging behavior accordingly.

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Shopping for a new insulin pump: Who’s selling?

Karmel Allison | July 18, 2012

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Medipacs ( http://www.medipacs.com/ ) is a start-up making small drug infusion pumps using an expandable polymer, rather than the standard syringe-pump system. Nowhere near market, but I encourage smaller and simpler pump design!

I have long complained about the Medtronic Continuous Glucose Monitor (CGM), but for a little while, I had made peace with the sucker because I had entered some sort of CGM zen in which I could use a single sensor for two weeks, and in a couple of cases, nearly a month. It was amazing. Two boxes lasted so long that the last few actually expired.

With longevity like that, I could overlook the inaccuracies and idiosyncrasies of the Medtronic sensor as compared to the Dexcom. It hurts like hell, but if I only need to harpoon myself once every three weeks, whatever!

But then it stopped. Two boxes of magic sensors, and now I can get maybe 7 days, if I’m lucky. Back to where I started. Shit.

And so, I find my mind wandering. I think of that Omnipod rep I see everywhere in San Diego (John? Josh? I’ve got his business card somewhere…), and his promise of a new Omnipod and a new Dexcom sometime this year. Hmm. And I start searching for images and press releases (sensor porn?).

Looks like the new Dexcom is hoped for sometime this year. More accurate, better, blah blah– what really gets me is that they ditched that stupid egg-shaped sensor, and are going with a slimmer, boxier one. Thank goodness. Who would ever design a giant, black, egg-shaped receiver? Do you know of any popular consumer electronic devices that are egg-shaped?

Medtronic has been promising a new, better sensor for a while now, but, well, I won’t wait forever. My patience has expired.

If I switch to the Dexcom sensor, though, why bother sticking with the Medtronic pump? I have used a Medtronic pump since I started pumping in 2005, when the only choices offered by Kaiser were Medtronic and Animas, and I kept with the Medtronic so I could have the integrated CGM and pump. But the pump itself is very utilitarian. If I get a new CGM– do I want a new pump, too? Which one?

The Tandem t:slim is the hot new kid on the block. But then I’m carrying around two receivers, for the Dexcom and the t:slim, plus a meter. And the slick black screen is cool, and the iPhone-ish design is a big step forward… but it’s still not that small. I mean, neat, yeah, but not like, “Oh wow, I’m going to go through all the trouble of arguing Kaiser should cover this” neat.

I like the Omnipod in theory. A patch pump, with a purse-able receiver is an attractive idea. And I admit I’m a sucker for their marketing approach– “We are the pump of diabetic athletes!” they seem to say, and I find myself thinking, “Well, maybe if I had that pump, I would be a diabetic athlete!” But then when I look at the pump– it’s still kind of big. That’s a big lump to have attached to my arm or torso or whatever. The new one (this summer?) is going to be smaller… but only by a third, which is still not the svelte nubbin I was hoping for.

The real question for me is, given the weight and size of the pod, how much shear stress can it take before it comes off? The Omnipod seems popular among kids, which is promising– kids probably go through way more wear and tear than I do. But I see kids with the pods strapped on or otherwise doubly-adhered. Do I have to? How often am I going to have to deal with a pod that’s fallen off due to jostling and sweating? And, okay, let me just be direct: how much sex does it take to un-adhere an Omnipod?

When I saw the Cellnovo last year at the American Diabetes Association conference, I thought that was a sexy pump. I totally want that. But there’s the whole FDA issue there. Darn.

Recommendations? Advice? Votes? Any insulin pump reps out there want to make a case?

 

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