This is the hong kong-iest thing I’ve ever seen: the entire series of Gossip Girl on the stores of a bookshelf, filed under religion.
Monthly archives for February, 2011
your vomitus smears the carriage
This sign is from one of the light buses that drives people around hong kong after the subway closes. It read:
“Your vomitus smears the carriage,
cleaning charge HK$300.”
Don’t smear the carriage!
Gazing into the pool
Well, I’m not going to pretend I’m not a narcissist. I like staring at myself as much as the next guy. It’s just that normally, I try to refrain from shmearing my buttery love for myself all over the internet with a butter knife, but to hell with that. In the past week, friends took two good-lookin pictures of me, and I’m gonna share ‘em with the world.
photos by Anya and Keting
Oh, 1916
I found a cute little book called “The Starvation Treatment of Diabetes.” It was written in 1916 by doctors at Mass. General, and it’s pretty neat to see what the scientific wisdom was before the discovery of insulin in 1922.
It gets off to a good start. Here’s the beginning of the treatment:
“For forty-eight hours after admission to the hospital the patient is kept on ordinary diet, to determine the severity of his diabetes. Then he is starved, and no food allowed save whiskey and black coffee. The whiskey is given in the coffee: 1 ounce of whiskey every two hours, from 7 a.m. until 7 p.m. This furnishes roughly about 800 calories. The whiskey is not an essential part of the treatment; it merely furnishes a few calories and keeps the patient more comfortable while he is being starved.“
In 1916, the authors make no distinction between type 1 and type 2 diabetics, and apply the same treatment to both sets of patients. Doctors understood that sugar in the urine (which occurs at a blood sugar higher than 180 mg/dl) was unhealthy, and so put their patients on a starvation diet until the sugars dropped, and then switched to a low-carb diet afterwards. They monitored “diacetic acid” and acetone in the urine, so they had some knowledge of ketosis. The case report is interesting:
The adult, clearly type 2 diabetics get a very effective reduction in their blood sugar from the starvation and low-carb diet. This makes sense–the treatment is almost identical to what’s used today, except we now have drugs like Glucophage that make our cells more sensitive to insulin, and doctors don’t treat with whiskey (bummer, man). The children, on the other hand, who present with hyperglycemia and ketosis, don’t do so well. 50% of them die as an immediate result of the treatment, which makes sense, as starvation would only encourage a body with very low insulin production to switch entirely to fat as an energy source, producing more ketones and aggravating the patient’s ketoacidosis. At any rate, if a type 1 diabetic is in diabetic ketoacidosis, and there’s no insulin around, there’s not really much anyone can do for the patient–he has basically no insulin production, and it’s only a matter of time before the increasing acidity of his blood due to the ketoacidosis starts to mess with ion transport and wreak havoc all over his body, and then it’s over.
All I can say is that I, for one, am a fan of insulin.
…And we roll our eyes and secrete amylin and insulin in unison
A couple days ago, I signed up to give a talk at the Chinese University in Hong Kong, and I was wicked nervous. I’ve only spoken in public a few times since I’ve been diabetic, I noticed that in my previous talks, I was much shakier than normal, my thoughts were muddled, my emotions out of control, and my self-confidence was completely trashed. What was weird was that I’d measured relatively high blood sugars just before my previous talks, and I didn’t feel like I could blame hypoglycemia for my behavior.
Well, this time around, I wore a continuous glucose monitor, and I kept several rolls of Mentos handy, in case I needed to boost my sugar. An hour before the talk, I cut my basal rate to 25% of my usual rate, down to 0.20 units/hr. Reading through my notes on the way to the talk, I noticed that I was very focused and engaged, and my glucose monitor showed that my blood sugar was dropping, despite the low basal rate. I ate about 30g of mentos-carbs to bring my sugar up from 80mg/dL to 140 mg/dL. My target glucose is 100mg/dL, but I hypothesized that public speaking is a very glucose-intensive activity for me, and I wanted a buffer of glucose. My version of pre-gaming before the talk.
I presented for twenty minutes, and started feeling hypoglycemic fifteen minutes into the talk. My meter confirmed it, showing that I was down to 60mg/dL. I ate 60g of carbs while I finished the talk, and then went into an hour and a half of question and answer. I dipped hypoglycemic regularly during that period, and ate 120g of additional carbs to maintain my blood sugar, marveling as I did so. I ate a total of 210g of carbs over two hours, giving myself a total of .4 units of insulin via my basal drip. My blood sugar immediately after the talk was 94.
I’ve never done anything–ANYTHING–that consumes glucose at this rate. Extreme exertion, sex, deep thought–all of these consume glucose at higher than normal rates, but public speaking appears to require about twice as much glucose as even the toughest exercise. During this talk, I felt pretty good, too–none of the shakiness or muddled thoughts I’d felt during previous talks. Maybe all I needed was a giant pile of sugar to get me through.
Half an hour after I finished, I was on the train back home and I noticed my blood sugar skyrocketing. I quickly switched back to my original basal rate and gave myself a corrective dose. Whatever glucose-intensive state I was in had worn off, and the remainder of the glucose I’d consumed was getting released into my bloodstream without a hyperactive brain to gobble it up.
I’ve heard a number of people mention that glucose is the brain’s primary fuel. I’ve also heard that the glucose transport mechanisms in the brain are GLUT1, GLUT3 and GLUT5, not GLUT2, which is the insulin-promoted transporter in adipose and muscle cells (**). I don’t really know the truth behind these statements, and a quick googling, followed by an in-depth googling, didn’t do anything to clarify. I want to get a better understanding of the physiology here, but the implication is that my brain is capable of consuming glucose without any insulin, and the harder I think, the more my brain chows down on my glucose. That’s very interesting, and definitely worth some more in-depth research. If it’s true, I could potentially lower my blood sugar, without insulin, simply by increasing brain activity. It wouldn’t get any glucose into my muscle and fat cells, which are depending on glucose to promote the GLUT2 transporter that primarily brings glucose into those cells, but any method of controlling my sugar without insulin is a pretty neat notion, and worth some more reading. Stay tuned!
*Also, I’ve been reading the Four-Hour Body, by Tim Ferris, and I saw mentions of a glucose transporter that isn’t insulin promoted but moves glucose into muscle cells. This is also pretty interesting to me. Are there other glucose transport mechanisms that don’t require insulin, and could it be possible to incorporate those into a differently-structured glucose regulation system? It’s the future, man. Time to hit up pubmed!
** After a bit more reading, I can say that that sentence is completely wrong. GLUT4 is the insulin-promoted transporter in fat and muscle, and GLUT1 and GLUT3 are the particularly exciting transporters en la cabeza. In my budding understanding of the brain’s glucose uptake mechanisms, GLUT1 gets glucose across the blood-brain barrier, and GLUT3 gets it into neurons.
Two tail stocks and a steel toolpost
Neat top, right? Here’s where it was made:
It was made in a little village in Kutch, India, on a makeshift, human powered lathe, by a machinist who held the cutting tools with his feet. Crazy! It’s the most out-there way I’ve ever seen anyone make a product.
Cutting the wood
Adding the color. The paint is a hard, waxy material that melts onto the wood.
Gorgeous finished products, made by a bow, two tree stumps, and some dude’s feet
The reset button on my pancreas
About a month ago, I had a really active day. I biked 13 miles over some mountains, went spelunking and rappelling, and then biked back. At the end of the day, I was completely pooped, sweaty, and generally beat. And one more thing–I was barely using any insulin at all.
Every type 1 diabetic has two numbers that determine how much insulin they need: their basal rate and their insulin to carb ratio. Whenever a I eat a meal, I estimate the carbohydrates in the meal and give myself a proportional dose of insulin. My body turns the carbohydrates into glucose, and the insulin signals my cells to gobble up the glucose and use it for whatever the cells want to do (produce ATP, store excess glucose as fat or glycogen, etc). My insulin to carb ratio is one unit of insulin for every 15mg of carbohydrates. Later, when I’m walking home after dinner, my body takes some of the excess glucose that it squirreled away (as glycogen) after my meal and slowly releases it back into my bloodstream. This is a nifty regulatory mechanism that allows everyone–diabetics and non-diabetics alike, are able to walk around in between meals without keeling over once their body has scarfed up all the glucose from the meal. Being a diabetic, however, I can’t make insulin on my own, and so I need a basal rate of insulin to match the rate my body releases glucose into my bloodstream. My body releases glucose at varying rates throughout the day, as well as dumping all kinds of other hormones into my blood that affect my body’s response to insulin, so my basal rate of insulin also varies during the day, from .8 units/hour in the morning to .45 units/hour at night.
Now, what’s neat is that exercise improves the effectivity of insulin. If I’m running really hard, or lifting weights, the same quantity of insulin can metabolize a larger quantity of glucose. For me, during my bike ride, it meant that I kept going hypoglycemic, because my body was much hungrier for glucose than it is when I’m sitting in my office, and I had enough basal insulin in my system that it basically gave my body a free pass to gobble up as much glucose as it possibly could, resulting in my blood sugar taking a swan dive. Throughout the ride, I had to stop several times and eat some candy, bringing my glucose levels back up, and to adjust my basal rate of insulin, reigning in my body and saying, “Whoah, there! Eat a little slower. And close your mouth when you chew!” By the end of the day, my basal rate was 25% of its normal level.
Now, what’s interesting is that somehow, that intense physical activity reset something in my body. For weeks afterwards, my basal rate remained low. I brought it back up from the miniscule amounts I gave myself during the ride, but I found that I could keep my glucose levels steady with only 75% of my previous dose. Somehow, (I hypothesize), that intense physical exercise increased my body’s sensitivity to insulin.
Well, that’s all well and good, but then something else happened last week. Specifically, I was staying up late, working on a robot, and around four in the morning I got a powerful hunger for some cereal. I ate a box and a half of muesli, which is an astounding amount of carbohydrates and requires an equally heroic dose of insulin. That night, my blood sugar kept rising, despite my normal basal rate, and even despite my constant corrective doses of insulin, meant to compensate for the excess concentration of glucose and bring it back down to human levels. In fact, over the next several days, I struggled to keep my blood sugar in line, watching it consistently trend high. I eventually increased my basal rate by about 40%, and found that I was able to maintain my blood sugar levels by wearing, essentially, a beer helmet of insulin.
Now this is fascinating–intense exercise semi-permanently increased my body’s sensitivity to insulin, and a binge of carbohydrates and insulin semi-permanently reduced my sensitivity. After a week of stasis at the high doses of insulin, I decided to try a little experiment to see if I could reset my body’s sensitivity with more intense exercise. So I hopped on my bike, flogged myself all over town, climbed 2.5 kilometers of stone stairs to the top of Lion’s Rock, climbed down, and then biked some more. Lo and behold, I became more sensitive to insulin, and I decreased my insulin usage by about 20%. It’s two days later, and I’m still at the reduced insulin dose.
So what does this mean? Well, unsurprisingly, it means that our bodies aren’t described by simple, constant formulas. Our actions affect our bodies’ internal processes, and our bodies are always working behind the scenes, fine-tuning the guts of the racecar to match the way we drive. One of the things I love about being diabetic (an odd sentiment, to be sure) is that it gives me a glimpse into the intricate web of variables, adjustments and feedback loops that affect just one regulatory process in my body. There are countless mechanisms like this in my body that are whirring along just fine behind the scenes, and as an engineer, a scientist and a tinkerer, I genuinely enjoy popping the cover off a broken mechanism, taking a wrench to the internals, and fixing it up as best I can.
Playing with myself
I want to write about this game I made up for myself. Like all proper games, it’s very simple and incredibly hard. It goes like this:
When you’re walking in a city, wait until the sidewalk ahead of you is completely empty for a while. Close your eyes, keep walking, and count how may seconds you can stand having your eyes closed.
I can only manage 10 seconds, max, before my lids snap open. I’ve been playing this with myself for a couple years, now, trying to push my comfort levels farther and farther. I don’t think the difficulty comes from the lack of sight but rather from the abrupt loss of a sense you rely heavily upon. I think that even if I got comfortable navigating without sight, the sudden transition would continue to throw me off, every time.
You know what kills me about this? A robot would be able to deal with the loss of a redundant sensory channel without blinking a FET. Why is it so damn hard for me?