The Truth About Fat and Proteins

Blood sugar goes up when the sugar going into the bloodstream is greater than the amount of sugar being taken out of the bloodstream.

The reasons that the body has trouble taking sugar out of the bloodstream are, essentially, the reasons that people have diabetes.

Some treatments of diabetes, however, focus on the rate at which sugar is added to the blood stream. This is done in two ways: with medications that change the speed at which the body releases sugar after meals (these medications include metformin and symlin, among others), and with dietary means. Dietary means typically focus on changing what types of foods are eaten to consume those foods that are converted to sugars the slowest.

Generally, there is a ranking in terms of how fast it takes the body to go from eating a food to adding sugar to the blood stream. Most people believe that some foods do not add sugar to the blood stream. This is a lot less true than is widely supposed.

Here are five general sources of energy for the body:
Alcohol (which this post will not deal with), fats, proteins/amino acids, complex carbohydrates, and simple carbohydrates.

I don't actually know how the body gets energy from alcohol so I'm gonna leave it alone for now. Complex carbohydrates and some simple carbohdrates require some breakdown before turning into glucose (some simple carbohydrates are glucose to begin with) but I think that's pretty straight forward.

So this post is about how the body turns proteins and fats into glucose. The process of turning something that's not a carb into sugar is called gluconeogenesis. Gluconeogenesis takes place in the liver and occurs more when the body is under starvation conditions or is eating a diet low in carbohydrates. Gluconeogenesis is driven by glucagon. Glucagon production in type 1 diabetics is often abnormally high (because in the normal pancreas, insulin kinda tells the alpha cells to slow production of glucagon), but may also be normal or low (such as in diabetes where the entire pancreas or islet cells have been damaged or are missing).

When the body breaks down fat for energy, it separates the fat into two parts to start with. One part is a fatty acid, (whether this can be turned into glucose in humans is debatable), and the other part is glycerol.
Glycerol is considered a complex carbohdyrate if you eat glycerol as is. It takes some work for your body to convert it into glucose, but it happens.

The things your nutrition label calls proteins may be amino acids actually together in a chain (in which case they are proteins) or they may be plain amino acids. If you eat them as proteins, your body nonetheless breaks them down into their component amino acids. Your body can then use the amino acids to build the proteins it needs. If there are extra amino acids left over, the body may store them as fat or turn them into glucose. Most (I have seen this number at 12, 13, and 14) of the amino acids are typically turned into glucose; another four or five can be turned into glucose if needed. Two amino acids never turn into glucose in human beings (those two are leucine and lysine and they are called the ketogenic amino acids because they are ketogenic).

So, the body gets from food to glucose at different speeds (and at different percentages of the food) depending on what is consumed. Typically, when people take insulin in a basal-bolus pattern, they take bolus insulin based only off of the carbohydrates they eat, because the carbohydrates are absorbed most quickly and because it's easier to just count carbs. Some people also count proteins and inject for a smaller portion of the protein (I do not do this because I have trouble figuring out just how much to inject for the proteins and because counting just carbohydrates seems to work reasonably well for me).
Proteins and fats and even some of the carbohydrates are converted to sugar slower and are often covered by basal insulin. In people whose bodies make some insulin, often that insulin can prevent rises in blood sugar when the sugar is going into the blood stream at slower rates.

In the DCCT, the large scale trial often used as evidence that more intense blood sguar control prevents, delays, and reverses complications in type 1 diabetics, higher fat diets were not associated with lower insulin needs or lower A1cs. Other studies have had had other results, but it is safe to say that if you take, for instance, 70% of your insulin as bolus and 30% as basal while on a high carbohydrate diet, if you do not make insulin, going to a low carb diet will not drop your insulin needs to your current basal needs.
Here is the DCCT authors' analysis.

And just for fun, the glucose song:

While You Sleep

There's been more research on type 2 diabetes and sleep than on type 1 diabetes and sleep because sleep deprivation causes insulin resistance (and so it's hoped that correcting sleep deprivation will prevent type 2 diabetes).
The research on type 1 diabetics and sleep is generally not about the sleep per se; it's about what happens to us while we're asleep. Why, what happens to us to us when we're asleep? Weellll....

All people have less ability to respond to hypoglycemia while asleep- the body does not like to handle it. Furthermore, people who've had type 1 diabetes long enough will not wake up from hypoglycemia, and we're not any easier to wake up while we're hypo (tested by people who woke up diabetics while they were at blood sugars of 99 and blood sugars of 50 to see how easy it was).

Despite this, at least a third of type 1 diabetics frequently are hypoglycemic while asleep without ever knowing about it. Studies with CGMs suggest that 7% people with type 1 diabetes are hypoglycemic on any given night.

Blood pressure is supposed to go down during sleep. In type 1 diabetics, early autonomic neuropathy causes blood pressure to not change as much as it's supposed to and not having blood pressure fall during sleep is a strong predictor of who will develop kidney problems (stronger predictors are age at diagnosis and A1c). The American Heart Association is recommending Ambulatory Blood Pressure Monitoring for children and adolescents with type 1 diabetes to screen for this issue.

The genetic basis for narcolepsy indicates that a gene protective against type 1 diabetes is high risk for narcolepsy; this might mean that narcoleptics (who are at an astronomical risk for type 2 diabetes) are less likely to have type 1 diabetes; flipped it means that type 1 diabetics are at lower risk of narcolepsy.

Adults with New Beta Cells

Fact: Many human adults have young beta cells.

When the body needs to be able to make more insulin than it is making, it will sometimes produce new beta cells. Guess what it makes the new beta cells out of?! Alpha cells, usually (alpha cells being neighbors to beta cells, and being responsible for making glucagon).
The human pancreas is generally done growing by the time it's about two years old (two years after birth, that is). Beta and alpha cells may continue to be generated anew until about age thirty, and in unusual circumstances, even later.

The beta cells do not turn into alpha cells in the event that the alpha cells are mostly destroyed source, at least not in mice.

There is currently a debate in medical/scientific/research communities about how much beta cell regeneration in type 1 diabetics matters. The question is: if we can stop the body from killing off new beta cells, can the body make enough new beta cells for it to make a significant difference for the diabetes (or perhaps ex-diabetic)? It seems to me that the answer is a pretty definite no for a lot of type 1 diabetics- the ones in which there is no real evidence of any ongoing beta cell production. It might be yes for others.

Santa Gave Him Diabetes

If you've spent much time looking for diabetes song and/or diabetes humor, you've probably run accross this gem:


Andy Stuckey and Jon Murray are a comedic duo; they write and perform funny songs (for adolescents/ adults), such as the one above. They also write ads. In a totally different development, they developed the fuxedo (fake tuxedo- something that looks like more pieces of clothes than it is). They wrote and performed this song about diabetes because Andy Stuckey has it.

Andy Stuckey grew up around diabetes; his younger brother was diagnosed at the age of five, when Andy was about eleven. A few years later, he participated in a screening test for family members and he and his family were told that he was at a higher risk of developing diabetes down the road. More than ten years went by before, at the age of 28, he saw in himself symptoms of diabetes. He was thirsty, he was tired. And so on Christmas, he checked his blood sugar on his younger brother's meter. His blood sugar was 240 mg/dl; Santa had brought him diabetes.

Andy Stuckey has a diabetes blog that was last updated in 2007. His band with Murray (stuckeyandmurray.com) is not about him (but it is a fun website). Googling him didn't get me much further, although it should have- he is the head writer of the tv show Guy Code (on MTV2 on Tuesdays at 11- some parts viewable online). Since I didn't want to write something about him that would be inaccurate because of being out of date, I sent him an email asking if I could write about him- and he wrote back to say that I could call and talk to him. So I did. I didn't do a great job of typing while talking, but here're the most interesting questions and answers:

Jonah Diabetic: What are you most proud of? What do you want to be remembered for?

Andy Stuckey: My kids, definitely. I have two kids, right now they're three years old, and two months- really new.
The show I'm working on right now had the highest premier in MTV2's history.
[note from J: I don't understand ratings- here's an article that's impressed though: http://www.thefutoncritic.com/ratings/2011/11/17/mtv2s-guy-code-delivers-most-watched-p12-34-series-premiere-in-networks-15-year-history-787005/20111117mtv01/]

JD: With your songs, shows, the stuff you write- what's your goal? What do you hope people will get from it?

AS: I want to make people laugh.

JD: There was some talk online about you putting together a diabeetles group- is anything happening in that direction?

AS: We have a whole lot of ideas, but we still need another person- it's not going to happen really soon. It'll probably be just one album, spoofs of Beetles songs with a diabetic twist. When we do it, we'll probably perform for JDRF, try to reach the maximum number of diabetics.

JD: Well, I think the ADA is bigger if you want to include type 2s.

AS: Yeah, type 2s are family too.

JD: In the years that you've been around diabetes, what do you think has changed the most?

AS: How easy it is to check your blood sugar and give insulin. With my brother, we used to have to measure the sugar in his pee, and that only told us what his blood sugar was about four hours earlier.

JD: How are you managing your diabetes? What do you think you'll do differently in the future?

AS: I take Lantus and Novolog and I use the glucose buddy app. [Glucose Buddy] I was just talking to my doc about a continuous monitor- might make things easier. I get in a routine with my foods, it gets kinda monotonous. How many times do you want to eat eggs for breakfast, y'know?

JD: From reading your blog, seeing how your A1cs were [the two A1c measurements there were 5.5% and 4.9%] , I was like, "Whoa, this guy must be honeymooning!" Were you?

AS: Could be. But my blood sugars aren't really higher- my A1cs are still five eight, five nine.

JD: How'd your family react when you were diagnosed?

AS: They were sad. But, y'know, by the time they're thirty (Stuckey was diagnosed at age 28), everybody's got something- a bad back, bum knee, diabetes. For me it was diabetes.

JD: Thanks!

Zinc and Insulin

In the last thirty years, the antibodies associated in medical minds with type 1 diabetes have changed considerably. I wrote about, a while back, a person who'd written a book about health care, whose daughter had been diagnosed with diabetes and tested for antibodies at the same hospital that I was, Children's Memorial Hospital in Chicago, some twenty years before me. At the time of his daughter's diagnosis, just like at the time of my diagnosis, it was standard practice to test for antibodies- but the antibodies being tested for were different. Different antibodies have continually been added and subtracted from the diabetes antibody tests because the newer antibody tests are found to have better specificity and sensititivity.
His daughter was tested for bovine milk antibodies, which are certainly found in the type 1 diabetes population at higher levels than in the general population, but not in a very dramatic way; it nonetheless pointed to a possible cause of diabetes, to know that those antibodies are more common. I was tested for insulin antibodies (why those would cause diabetes is pretty straightforward), Glutamic Acid Decarboxylase antibodies (GAD coats the islet cells), and Islet Cell Antibody 512 (another easy name). I was positive for the latter two.

I was diagnosed only five years ago, but there's already been a change to the classic antibody panel done for type 1 diabetes. The new antibody tested for has a descriptive name: it is ZnT8, which stands for Zinc (Zn) Transporter (T) 8 (the 8th type of zinc transporter, the one responsible for insulin- see wiki blurb. The name does indeed point to something that is found in abundance in the pancreas and in the islet cells.

Zinc has been known to be a part of insulin for more than eighty years. I just read a very informative article on the state of knowledge of the relation of zinc and diabetes written in 1936. The article is an evaluation of certain insulin addititives, particularly zinc and protamine, and analyzes the amount of zinc in various insulins for sale at that time.

Anyways, as it happens, zinc is important to everybody, and its functions matter to the development of most cases of diabetes. Zinc deficiencies, which affect between a third and a fourth of all people worldwide (a smaller portion in the food secure part of the world) causes insulin resistance, probably because the body needs zinc to make insulin. Mutations of the zinc transporter gene can result in various forms of diabetes. Autoimmune attacks on the zinc transporters is a better predicter of the development of type 1 diabetes than any other antibody currently known.

All of us who inject insulin are also injected zinc and one thing I found myself wondering when I was fairly newly diagnosed was, do we inject a significant amount of zinc? Can we overdose on the zinc in our insulin? Studies seem to suggest that diabetics, including type 1s, generally don't have enough zinc, so the answer clinically is probably not. But here's another way to look at it.

The recommended daily allowance of zinc for adult men and women are 11 mg and 8 mg per day respectively. The amount required for toxicity is between 20 mg and 40 mg per day.

Let's pretend you inject 100 units of insulin per day. How much zinc are you injecting?
100 units of insulin with nothing added contains roughly 0.015 mg zinc- maybe a little more, but definitely nowhere near your daily requirement of zinc.
But most of the insulins on the market have a little zinc added. If you took 100 units of Lantus, you'd be getting 0.045 mg zinc from the Lantus. With Levemir, 100 units would get you 0.08 mg of zinc, and 100 units of Novolog of Novolog would get you roughly 0.03 mg of zinc. With NPH you'd be getting about 0.035 mg zinc. Apidra and Regular have no zinc added at all, so all you'd be getting is the endogenous 0.015 mg of zinc.
So, even if all of your insulin was Levemir, and you were a woman taking 100 units of Levemir per day, you'd be getting just under 1% of your daily zinc requirement from your insulin.

You'd have to have some really heavy duty insulin resistance to be getting a significant percentage of the RDA of zinc through insulin injections- unless! injected zinc does more than oral zinc. I know of no evidence of this though.

How Common Is Diabetes?

That depends on how you define it!
According to current definitions, half of American adults over 65 are diabetic or prediabetic.

More interestingly, according to extrapolations from the SEARCH study, roughly 1 in 400 people under the age of 20 in the United Stateshas diabetes (including all types of diabetes), for an estimated 215,000 youths. The estimate they were putting out last year, based on 2007 data of how old people in the US are plus data on diabetes prevalence from about ten years ago, was 186,300 youths, which was a little more than 1 in 500.
Frankly, the data is not exact enough to get a good guess. But it is likely that between 1 in 300 and 1 in 500 Americans is or was diagnosed with type 1 diabetes by the age of 20.

In other countries, the risk is fairly different. Prevalence in Finland is greater than 1 in 200, while prevalence in some parts of Asia is less than 1 in 1000.

Interesting Resources

Even if you don't know much about diabetes, chances are you've heard of two diabetes organizations: The American Diabetes Association (ADA) and JDRF. And you probably know how to google. This is a rundown of some resources I think you ought to know about.

I don't think the JDRF is much of a resource, but it does have a penpal service for kids and if you want to fundraise for them, it'll let you. In some areas it provides kits and connections for the newly diagnosed. Website: jdrf.org

The ADA, American Diabetes Association, has the website diabetes.org, which tells you what a big name they are. They have multiple interesting publications, most prominently the Diabetes Forcast (intended for diabetics and our families). They publish guidelines on diabetes care (such as how often your A1c should be checked) and diagnosis that are followed by most of the world, and that influence your insurance company. They also run diabetes camps, fundraising shindigs, expos, and support groups.

Children With Diabetes, childrenwithdiabetes.org, was founded by a parent of a kid with diabetes, dx at age 2 and now older than I am (well, I guess she was older than me all along). It was bought and is owned by Johnson and Johnson (maker of bandaids, among other things). CWD has newsletter, email lists, chats, a forum, surveys, and an extensive website. Unfortunately, a lot of what's on there, particularly products, are seriously out of date. The website is type 1 focused and is intended especially for parents but has been more open in recent years to adults with type 1 diabetes. CWD has various educational seminars and conferences; the biggest one is the Friends For Life conference that happens annually in Florida.

tudiabetes.org is currently the largest social networking site for diabetics and SOFFAs (significant others friends family and allies). It offers some very minor other services. You can find me on there as JonahD.

If you are uninsured, it is worth knowing about programs that will provide you with free insulin, such as Lilly Cares(which will provide humalog, nph, regular and glucagon for free if you are uninsured and not making too much money) and Novo Nordisk's Patient Assistance Program, which will cover Novolog, NPH, Regular, Levemir, Glucagen, and metformin. Sanofi Aventis also has a Patient Assistance Program that covers Apidra and Lantus. These programs all require you to have a doctor who prescribes the medications and is willing to have your medications shipped to xem, and then you pick them up for free. They have different levels of poverty requirements.

The National Institute of Diabetes and Digestive and Kidney disease has a diabetes clearinghouse website. It is most interesting for its statistics. Whoever writes the website has a dramatic writing style that grates on me.

If you are at all interested in the idea of being in a clinical trial, or if you simply want to know what's going on in your area, you should know about clinicialtrials.gov. All clinical trials in the US are required to post here,and some studies being conducted elsewhere are also posted here. However, you shouldn't have your hopes too high when looking for a study. At the moment, there are 279 trials related to type 1 diabetes and many more related to other diabetes posted on the site that are currently looking for volunteers or will be looking soon. The search brings up studies on complications, treatments, prevention of development of diabetes, prevention of development of complications, extension of the honeymoon, and more.
Although there are other websites with clinical trials, and others with non-clinical trials, this is the most complete site for trials that have a real chance of accomplishing anything.
I am eligible for one study in my area- I am eligible for an islet cell transplant. A lot of transplant related stuff comes up in my search- clinicaltrials.gov is how I know that they're doing bone marrow transplants on recently diagnosed (less than five months) diabetics at my hospital.
You can also find study results of many trials- if you want to see what Exubera did to A1c or body weight or anything like that, you can find it on this website.

Pubmed is my favorite place to just browse journal articles about diabetes (and everything else). Pubmed provides a listing of most medical articles published. If you are looking for very specific information, it may be hard to find, and some things will only let you see a title. But that doesn't mean it's not worth looking through. If you spend much time reading there, you'll learn a lot. I suggest sometime looking at the very earliest things published on a topic- that often provides more basic information.

Speaking of places you'll learn a lot, I've always been a library fan (I have been a library volunteer for more than half of my life). Books about diabetes are a real mixed bag, unfortunately. The library of congress areas for diabetes are RC660 to 662 (diabetes) and RJ420.D5 (pediatric diabetes). You will also find books about diabetes in other parts of the library.

Hopefully, your doctor and CDE are good resources too. And you can make an appointment to talk to a diabetes educator or a nutritionist who might have something to teach you if you want.

Online websites may allow you to buy diabetes supplies cheaper than elsewhere; at least they let you compare prices. Your insurance company's website should be familiar to you and probably lets you look at the formulary and compare prices of drugs (if slowly and arduously). You may need to create an account to do this.

There are a wide variety of interesting diabetes blogs out there. I am not going to make a list (at least not today). Fortunately, lots of bloggers make their own lists of diabetes blogs they like. Here is Kerri's list.

Happy hunting.

What Can I Donate?

Note: This post is specific to US policy.

Type 1 Diabetics who are alive are allowed to donate blood if they've never received bovine insulin from the UK and meet other blood donor requirements (I miss the requirements because I'm too small). Diabetics are more likely than the general population to be excluded for answering that that they do not feel healthy, or taking aspirin, or having kidney disease, etc.

Living type 1 diabetics are generally barred from donating anything else. I believe type 2s are as well but the policies I found were somewhat vague as to a person with
well controlled type 2 diabetes not on insulin might be eligible.

People with all autoimmune diseases are barred from donating bone marrow (at least on paper- my mother was accepted for the bone marrow registry and she has rheumatoid arthritis) and people who take medications to control diabetes are also barred.

Dead diabetics, on the other hand, can be organ donors. There has been some discussion in the medical literature about how healthy a dead person has to have been to make a good enough organ donor, particularly in regards to organs for which their is a shortage, such as kidneys. In 1995, the net of potential donors was expanded to accept cadaver donors who had had diabetes or hypertension or who had been dead a little longer.
People waiting for organs in the United States are allowed to indicate whether or not they are willing to accept an organ from an "Expanded Criteria Donor"; such donors would include dead diabetics. The pancreas would likely not be viable, but kidneys (even if you have microalbuminuria), liver, heart, and lungs,
not to mention corneas- these could extend somebodies life.

If we count things you are allowed do donate dead or alive, then just about the only things diabetes stops you from donating are your pancreas (which you might be able to donate to a research study) and your bone marrow.

That means that being diabetic is no excuse not to register as an organ donor.

X-Linked

Last November I wrote that type 1 diabetes, unlike the vast majority of autoimmune diseases, is more common in men than in women. As it turns out, that is only true in populations where type 1 diabetes is more prevalent generally.
A few months ago I was browsing through OMIM (the Online Mendelian Inheritence in Man project). There are lots and lots of genes associated with type 1 diabetes. Two of those genes are located on the x chromosome. In combination with other genes- and ONLY in combination with those genes- one of the x chromosome genes increases susceptibility to type 1 diabetes in people who carry the DR3 marker (commonly found in type 1 diabetics of European descent).

The other one is the FOX regulator gene that I have heard lots about but never in terms that I really understand; it is linked to a whole bunch of complex immune disorders.

So, in populations where the DR3 diabetes genes are common, type 1 diabetes is more common in guys because it is a bit x-linked, and in other populations it is more common in women, because it is an autoimmune disorder.

In case you need a reminder of how X-linked disorders work: everybody has at least one X chromosome (fetuses without x chromosomes are miscarried), and people can have various numbers of x chromosomes. However, most men have one x chromosome and most women have two x chromosomes. Most x-linked disorders are recessive; if a person has one normal allele and one allele for a disorder, the person does not have the disorder. Therefore, having multiple x chromosomes protects you against having the disorder.
For instance, red-green color blindness, which is easily the most common x-linked disorder, occurs in roughly (ROUGHLY) 1 in 8 men, and 1 in 64 women.
That's because it works like this (pretending all sons are XY and all daughters XX):

If the father and mother have all normal color sight genes, none of the kids have this type of colorblindness, no matter the kids' sex.
If the father is colorblind and the mother has two normal color sight genes, none of the kids has this type of colorblindness, no matter the kids' sex.
If the father is colorblind and the mother is a carrier, half the kids are colorblind, no matter the kids' sex.
If the father is colorblind and the mother is colorblind, all the kids are colorblind, no matter the kids' sex.
If the father is not colorblind, and the mother is not colorblind but is a carrier (and roughly 1 in 6 women is), then half of the sons and none of the daughters are colorblind.
If the father is not color blind, and the mother is, all of the sons are color blind and none of the daughters are.

Ten Best Reasons (Excuses) For an Unexpectedly High Blood Sugar Reading:

10. The lancing device had sugar on it.

9. Somogyi effect.

8. You injected slow acting insulin instead of fast acting.

7. You're holding the meter upside down (there is a down side to a mini meter, get it?).

6. You injected air instead of insulin.

5. Somebody changed the key code on your meter without telling you!

4. The restaurant gave you soda with high fructose corn syrup even though you ordered diet soda.

3. You spilled some of the soda on your hands.

2. Your maltose levels are high.

1. You have diabetes.

Kidney Donations and Diabetes

I just came from a memorial service for a mentor of mine. I met her six years ago, when I was seventeen and she was about twice my age at that time. She was facilitating an advocacy/support/education group for transgender youth. It met every Wednesday and once I started going, I was there every week (except for movie nights).

Ten months later, I was diagnosed with diabetes. As I've probably said before, I had a lot of different emotions around my diagnosis. But on the night that I went back, I was giddy with fear, and the nervous excitement of being out on my own (no nurse present) with diabetes. And I said that I had just been diagnosed with diabetes (I didn't say type 1 because the type wasn't confirmed until three weeks after my diagnosis). I said I was going to be carrying insulin and syringes and doing things that might make it look like I was breaking the rules, though I wasn't.

Lois (that was her name) did something with that that I didn't see coming. She used me as a (good) example about how we should take care of our selves and of our health, and then she talked about her health. I had known her for ten months; I had spent at least 60 hours with her by that point. I had not known that her kidneys had failed and that she had spent seven years on hemodialysis. She said that, after seven years, when her doctor told her that he had a kidney for her, at first she thought he was joking. Lois told us what it took to take care of herself on dialysis and to keep going. She showed us the big bumps on her arms that they had used. She told us about calling dialysis centers when she traveled. She told us about what it meant to be responsible.

About two months later, Lois said, "Guess what Jonah?" and she pulled out a blood sugar meter. She had been diagnosed with diabetes, too. Her diabetes was probably secondary to her transplant medications- transplant medications are known to cause insulin resistance.
There's even a name for diabetes caused by transplants: NODAT. The acronym stands for New Onset Diabetes After Transplant. Estimates for prevalence of NODAT among transplant recipients varies by a lot. I think 15% is a fairly good estimate.
Lois's diabetes was treatable by oral medications. NODAT inorporates elements of both type 1 and type 2 diabetes in that it features insulin resitance but often damage to the pancreas as well. But most of the time, it is treatable as if it were any other type 2 diabetes.
Unfortunately, NODAT is something that also develops in pancreas recipients. Sometimes you can trade type 1 diabetes for type 2. (Insert sigh)

Lois's body eventually rejected the new kidney, and it was removed, and she went back on dialysis. Unlike a lot of people on dialysis, Lois went on working. When I last saw her, in September, she was busy at work. Lois died last week at the age of 41 years. It had been thirteen years since her kidneys had failed. In those thirteen years, Lois accomplished more than most people accomplish in a life time.

I went to her memorial service this evening. Today is the transgender day of remembrance. For the past many years, we in Chicago have had a memorial service for the dead (killed by transphobia) followed by a celebration of living transgender people. Our celebration has taken the form of a talent show (I've performed a couple of times), and the master of ceremonies was Lois.
Tonight we did not have a talent show. We had a memorial for Lois instead. Her mother and sisters were there. Her church family was there, and the transgender community showed up in droves. The room in which we met has 156 seats. Every seat was filled, dozens of people sat on the floors, and a small crowd stood near the doors.
People were there for more than one reason. Those of us who spoke mentioned three. Lois was a mentor to hundreds (if not more) members of Chicago's TGLB community. She founded and ran groups. She inspired people. She made us want to be the people she said we could be (reason one). Lois was also community to a lot of people. She was a faithful churchgoer, and she still knew the people she had known in high school. She drew people into all of her communities- her faith community, the queer communities (which she kinda created), and communities of activism (reason two). She was also a vibrant, funny, fun, humble, righeous person that people just liked (reason three).

One of the things I found myself thinking about during and after the memorial service (though I was mostly thinking about Lois and about what I wanted to say about Lois in my speech) was that if Lois had given up when her kidneys failed- if Lois had lived the typical (for Americans) two years on dialysis or if her spirit had failed her then- then most of us there wouldn't have known her. Lois's huge accomplishments happened while she was sick, while she was making two or three appointments per week for dialysis, or dealing with a transplant, which had its own problems. Renal failure is not the end of life.

Lois died fairly young, but she got done a whole lot that wouldn't have happened had she died younger. I can only hope that I get as much done in my life, whether I die at 40 or 80 or 120.

Causes of Vision Impairment in Diabetics

The CDC just released a report saying that the percentage of adult, non-institutionalized, civilian, diabetics who answer yes to the question "Do you have any difficulty seeing even with glasses" has declined, from almost a fourth, to a sixth.

Here's a fact you probably didn't know: Diabetes increases risk of multiple eye diseases.

Although the eye disease most associated with diabetes is diabetic retinopathy (the majority of people who have had any type of diabetes for at least twenty years have some retinopathy, although only a minority will actually go blind from it), diabetes also significantly increases risk of the other two major causes of eye diseases of adulthood: cataracts and glaucoma. Diabetics are also over represented among people who go blind from strokes or traumatic brain injuries.

There are also syndromes that cause both blindness and diabetes. For example, Wolfram Syndrome. Wolfram Syndrome is a recessive genetic disorder that causes a non-autoimmune type 1 diabetes, with onset in childhood (average age of diabetes onset in Wolfram Syndrome is 6 years). Roughly 1 in a 1000 people with childhood onset type 1 diabetes has Wolfram Syndrome; roughly 1 in 400,000 people is born with Wolfram Syndrome. The gene for Wolfram Syndrome was the first gene found that always causes type 1 diabetes. People with Wolfram's develop type 1 diabetes, but also a whole lot of other things including diabetes insipidus, hearing loss, weakness, atrophy of the eyes, and in adulthood, neurological degeneration that often leads to death. Wolfram Syndrome is probably under diagnosed.
Note: I am referring to the diabetes of Wolfram's as type 1 diabetes because it is caused by an inability to make insulin- the pancreas is the target of the disease, and it does not cause insulinn resistance. Some people prefer to see it as a different sort of diabetes.
Diabetes is also associated more strongly with autoimmune diseases that cause visual impairment, such as Graves' and MS.
Premature babies (who may develop retinopathy of prematurity) are slightly more likely to go on to develop diabetes later, although I don't think it's a very significantly increased risk.

There are some really rare syndromes that increase risk of diabetes and retinitis pigmentosa, but they're not generally related.

Macular degeneration, which is extremely common in old people, is associated with some lifestyle issues that are also associated with type 2 diabetes; despite that, I am not aware of any statistical correlation between the two diseases.

So What if It's Autoimmune?

Roughly 80% of cases of type 1 diabetes are autoimmune (where type 1 diabetes refers to diabetes caused by an absolute lack of insulin).
Additionally, at least 15% of cases of type 2 diabetes have an autoimmune component.

What does this mean?
Antibodies are produced by cells made in the bone marrow (the immune system is mostly made of cells made in the bone marrow, thymus, and spleen). In order for a person to develop an autoimmune disease, xe needs to have a semi-functional immune system, which means xe needs to have bone marrow.
The only medically likely transmission of type 1 diabetes has occurred through a bone marrow transplant in which the donor was a type 1 diabetic. In the most published case, the recipient was the sister of the donor. She received the transplant at the age of 25, when antibody negative, and was diagnosed with diabetes at age 29, at which time she was antibody positive. http://www.ncbi.nlm.nih.gov/pubmed/8098394
A longer summary of all cases of bone marrow donation by type 1 diabetes is here; the short story is that most recipients do not develop type 1 diabetes but a lot more than could be randomly expected to, do.
The role of the bone marrow in creating autoimmunity means that bone marrow transplants have the possibility of causing auotimmunity- but they also mean that bone marrow transplants have the possibility of curing autoimmunity. What happens to a person's autoimmune disease when you kill off the person's bone marrow, and then give xem a bone marrow transplant?
Answer: Just about anything. In a fairly famous series of clinical trials, doctors removed and radiated bone marrow,killed off the bone marrow left in the body, and then replaced the bone marrow in the patients, who were newly diagnosed type 1 diabetics. Some of them no longer had diabetes. In some, the autoimmunity and diabetes reoccurred. In some, it didn't go away in the first place.
Currently, if you are a newly diagnosed adult type 1 diabetic (antibody positive and never been in DKA), you are eligible to participate in such a trial at the hospital I go to.

Autoimmunity also means that immunosuppressants have some chance of preventing, treating, or even reversing the disease. Type 1 diabetics who go on immunosuppressants rarely have a full remission but are more likely to make more of their own insulin. In some type 1 diabetics, the autoimmune process seems to have been a one time deal- the antibodies came, they marked the territory, the macrophages came and gobbled up the beta cells, end of story. In other cases, it seems to be more of an ongoing battle- the antibodies came, they marked the territory, the body went and made more beta cells, the macropaghes came and ate the marked beta cells, repeat ad infinitum. In the latter case, immunosuppression may be more likely to make a difference.

Another reason to care if it's autoimmune: the more autoimmune diseases you have, the more you're likely to develop.

Today I was out and about and ran into a Deaf (capital D signifies person is culturally as well as physiologically deaf) friend. We spent a couple of hours chatting. My signing skills are not fluent (I was flattered when she said I was going too fast at one point- mostly my signing is sloooow) and her English is not fluent (although, her written English is definitely better than my sign). So we were chatting in a less than fluent manner. And, not for the first time, we got to talking a bit about diabetes (Dexcom alarmed high while we were talking). She didn't know the sign for diabetes so she accepted the sign I used- a d backed a closed mouth. But the most common sign for diabetes is just the sign for sugar (which I find problematic because that word means too many things and the little context things, I don't pick up on). Various variations of a d handsign near the neck or mouth are also used sometimes in ASL.
In other words, there is no standard sign for diabetes.

So here's my question for you. If you were making up a gesture to mean diabetes, or something about diabetes, what would it look like?
There are standard signs for things like injection, btw- we actually were talking about injections too.

How Much Insulin Do Other People Take?

I was trying to write a post on partial diabetes remissions (honeymoons) when I came across the following problem:
Type 1 diabetics need insulin, right. In full blown type 1 diabetes, our bodies make very little insulin, so we need to inject enough for all of our needs. If a person needs a very small amount of insulin, or no insulin, and still gets decent blood sugars, we can assume that a person is making insulin. Also, if a person needs an unusually large amount of insulin, we can assume that the person has insulin resistance.
So the question is, what is a normal amount of insulin for a type 1 diabetic who isn't making any to need? Generally in studies on people with type 1 diabetes that are looking for people still making some insulin, a lower cut off is used based on insulin use plus bodyweight. The most common lower cut off is 0.5 u/kg/day, although sometimes cut offs of 0.4 u/kg/day or even 0.3 u/kg/day. Below 0.3 u/kg/day, it is very clear: you're making insulin.

I looked further at two large scale studies. One of them was a Polish study of over 22,000 children and adolescents with type 1 diabetes who were at least two years post-diagnosis (which probably means that a very few were still making insulin). Normal insulin use varied by age, sex, andwhether the person used shots or a pump. Puberty clearly caused an increase in insulin need. The difference between insulin needs in injectors and pumpers most probably had to do with different ways of calculating insulin use- in fact I think the pumpers' insulin usages should probably be used for computing everybody's normal. If you are under 25, you may want to click over to take a look at the graphs for yourself. In people my age, they find that the the 95th percentile of insulin usage was roughly 1.2 u/kg day; the 75th percentile was roughly 0.9 u/kg/day, the 50th percentile was roughly 0.75 u/kg/day, the 25th percentile is roughly 0.55 u/kg/day, and the 5th percentile is roughly 0.4 u/kg/day.
http://eje-online.org/content/158/4/543.long

The other study I looked at was a Japanese study including all adults diagnosed with type 1 diabetes under Japanese criteria, which almost certainly includes a large number of people with what we'd call LADA and other who are making a large amount of their own insulin. In the group of 400 people dx'd under the age of 20, the average insulin use was 0.9 u/kg/day; in the group as a whole, average insulin use was 0.7 u/kg/day.
http://www.jstage.jst.go.jp/article/endocrj/55/6/1025/_pdf

By the way, to compute your insulin use in this form, you first have to figure out how many units of insulin you use on the average day, which may or may not be easy depending on if you use a pump (which will figure this out for you) or, if on MDI, how consistant you are about how much insulin you use. Anyway, once you have that figure, you can divide by your weight in kilograms. Alternately, you could multiply the number of units you use per day by 2.2, then divide by your weight in pounds.
For instance, I use roughly 35 units of insulin per day. To the nearest kilogram, I weigh 45 kilo. That makes my insulin use 0.78 u/kg/day, which makes my insulin needs well within the normal range for a person my age.

What does this mean for you? If you take less than the 5th percentile of insulin usage without taking oral medications, it means you might want to see if you really have a form of diabetes in which treatment with oral medications is possible.

Postcard Exchange

For World Diabetes Day I participted in a postcard exchange. I was sent a name and address and I sent the postcard above. It's impossible to read in the picture; on the actual postcard I realized the contrast wasn't so great on the circle itself where I put a timeline, but I pressed hard so the letters were readable by me and my parents (they have old people vision). I wrote a bit about me on the sides (including the address of this blog), and I mailed the postcard to David.
In return, I recieved the layered, detailed, artsy postcard above (that's the front of it). The postcard he sent has two layers- two white cards, with a blue card in the middle. The blue circle was created by cutting a hole on the paper so you can see the blue below, and The back said it was from David, who has had type 1 diabetes longer than I've been alive (he was diagnosed in 1986- I was born in 1988). His one word about diabetes is fight, which he exemplifies with advocacy and with continuing on, even though he is legally blind. There is no excuse to give up, he says.
I do sometimes think that people with other disabilities are under represented on the diabetes online community, and I'm glad to see more of that presence. I also do find some hope in people with complications getting along with their lives because it makes my future less scary, because retinopathy had already occurred in 86% of the Wisconsin Diabetes cohort, 20 years post diagnosis.

David, I hope you were able to magnify my card to readability or found somebody to read it to you. Thanks for the card!

Uh-oh, I have about two minutes to stick in a fact for today.

How's this: Early versions of the oral glucose tolerance test were done with blood from the earlobe.

You can test blood sugar from a wide variety of spots but will get the wrong mix of serum (which has more sugar) and whole blood (which has more protein and therefore less sugar) to compare. However, the most commonly used spots are: fingers (includes thumbs), base of thumb, forearm, toes, heels (in babies that don't walk yet), and yes, earlobes. Toes are not recommended for anybody with neuropathy.
Dr. Bernstein recommends the part of the fingers that are between the knuckles but I couldn't get enough blood there when I tried it myself.

Ketoacodis - Some Strange Cases

If you have type 1 diabetes, you have probably been warned about diabetic ketoacidosis- and if you haven't been, I'm warning you now.

Diabetic ketoacidosis is an acute complication of lack of insulin, relative or absolute, usually from type 1 diabetes. Here's what the term refers to:

Acidosis: arterial blood has a pH level that it likes- the normal range is 7.35 to 7.45 (slightly basic) Generally speaking, the diagnostic criteria for acidosis requires pH level to be equal to or less than 7.30, although sometimes acidosis is diagnosed or treated between 7.30 and 7.34

Keto: related to ketones. Ketoacidosis is acidosis caused by the presence of ketones, which for diagnostic purposes may be found in the blood or urine; in ketoacidosis there are usually ketones in both the urine and blood

Diabetic: having to do with diabetes. A person may be diagnosed with diabetic ketoacidosis by ADA standards if blood sugar on admission is over 200. Some places use a blood sugar cut-off of 250 or 300, and some places will diagnose "diabetic" ketoacidosis with blood sugars below 200 if the patient is known to have diabetes.

Diabetic ketoacidosis can develop in hours or it can take some time (maybe a month). It is a medical emergency and you can depend on being hospitalized if you are diagnosed with it. Severity ratings for ketoacidosis depend on pH levels (7.25-7.3 is mild, 7.00 to 7.25 is moderate, below 7 is severe) and/or symptoms. Death from ketoacidosis that is treated occurs at very different rates at different hospitals, but depends a lot on the severity of the ketoacidosis when treatment starts. Death rates for mild ketoacidosis may be below 1 in 200; death rates for severe ketoacidosis are as high as 1 in 5 when treated (untreated, all cases of severe ketoacidosis would likely lead to death).

Diabetic ketoacidosis risk factors include: being sick, especially when throwing up, pregnancy, not taking insulin, severe insulin resistance, insulin pump failure, eating disorders, being undiagnosed.

Now for some things you didn't know:

1. Diabetics go into ketoacidosis without high blood sugar more commonly than non-diabetics.

This article describes cases "euglycemic diabetic ketoacidosis". It is one of the first articles to describe the idea; a lot of diabetics with ketoacidosis who did not have very high blood sugars. The author suggests a blood sugar of below 300 as euglycemic, which has some obvious flaws (299 is a high blood sugar) but to be fair, he has 16 cases with blood sugars below 200, and 7 are below 100 (lowest blood sugar with a DKA diagnosis? 36!) All but one patient was already diagnosed with type 1 diabetes, hence the "diabetic" label. On what grounds ketoacidosis was diagnosed, I am not certain, given that he doesn't seem to have measured blood pH levels at all. Patients were symptomatic of ketoacidosis and had ketones.

Abstract of study comparing rates of DKA in women with type 1 diabetes who were or weren't pregnant, and, when they did go into DKA, how high their blood sugars were. The pregnant women went into DKA more often and at lower blood sugars. Average blood sugar in DKA for pregnant women was 293 mg/dl and for non-pregnant women the average blood sugar in DKA was 495 mg/dl. There was also one case of ketoacidosis in a pregnant woman without high blood sugar.

2. Starvation can cause ketoacidosis, with or without diabetes.

Case of euglycemic ketoacidosis in a type 1 diabetic who had stopped eating for two or three weeks. His blood sugar was 105 mg/dl, pH was 7.3 (mild ketoacidosis), ketones large, A1c 11.5%.

Starvation ketoacidosis in a man eating a fruit-only diet (BMI 16). His venous pH was 7.08, which means he was in moderate/severe ketoacidosis. His blood sugar was normal on admission, went into the upper 500s when he was fed, went down with insulin, stayed down without insulin. Source

Case report described as ketoacidosis in which a man eating a low carb (15grams of carbs per day) diet for three weeks was admitted to the hospital with a high blood sugar (267 mg/dl) and very slightly low pH 7.34 with ketones. He was treated for diabetic ketoacidosis. His blood sugar went normal and stayed there without more insulin. He does not meet true criteria for DKA because his pH was 7.34, and while that is low, it's not low enough to meet diagnostic criteria. His only symptom was abdominal pain.

Type 1 Diabetics are way more likely to be diagnosed with DKA, but between 5 and 20 percent of cases occur in type 2 diabetics.

Case report of ketoacidosis in a pregnant woman with type 2 diabetes. She was admitted with a pH level that was a little low (7.32) and a blood sugar of 77, but her pH level dropped to 7.23 (moderate acidosis) with a blood sugar still below 100. She had ketones.

Having blood ketones and urine ketones doesn't mean you have ketoacidosis, but a blood ketone level above 1.5 is a good reason to get it checked out

This study looked at all people coming to the ER with a blood sugar above 250, comparing those who were and weren't diagnosed with DKA, and suggesting using a blood ketone meter is better than using urine ketones for finding DKA- although DKA patients are equally likely to have high urine ketones and high blood ketones (that is, they have both urine blood ketones and high urine ketones) way more people who do not have ketoacidosis have high urine ketones, whereas most of the people who came to the emergency room with high blood ketones (about three fourths of them) had ketoacidosis. This study also makes the interesting statement that one fourth of people in the ER have diabetes. Out of the patients in the study who did have DKA, at least 10 out of the 56 had type 2 and not type 1 diabetes.

The second most common cause of ketoacidosis in the United States is alcoholic ketoacidosis, a form of alcohol withdrawal experienced by alcoholics.

My advice is that if you have diabetes, you should check your ketone levels more often if you start a new diet, are sick and vomitting, or pregnant. Especially pregnant! And if you care about somebody alcoholic or are trying to help an alcoholic sober up, encourage the person to eat something.

And now for a song (written by a medical student)

How Big Is Your Needle?

If you inject your insulin using an insulin pen, you use needles.

If you inject your insulin with a syringe, you probably use needles.

If you have pump sites, you use needles.

It is possible to have diabetes without using needles- you could use a jet injector that uses intense force to push the insulin through your skin, and you could poke your finger to get it bleed with laser lights (or you could probably get away without checking your blood sugar). But I think it's pretty safe to say that if you've had type 1 diabetes in the last eighty years, you've used needles- many many times.

Your needle generally comes with two measurements- the length of the needle, and the gauge of the needle. For an insulin pen, you can use needles as short as 4mm or as long as 12.7mm. Neither of these are very long- 12.7mm is half an inch. If you use syringes, the shortest needle you'll get is 8mm and although really long needles are not meant for injecting insulin, you can use a longer needle if you chose to. Insertion set needles match cannula lengths and are typically 6mm or 9mm, although I'm not really sure what the range is. Sensors for Dexcom and Minimed are inserted with half inch needles.
The gauge of the needle is a nonlinear indication of the width or diameter of the needle. Confusingly enough, a bigger gauge indicates a thinner needle. Needles associated with diabetic use have gauges ranging from 32 (BD's nano pen needle) to 21G (Navigator sensor's inserter needles).

Why would you want a big needle? Well, to insert a sensor probe or a cannula, the needle clearly needs to be as wide as the sensor or cannula. I am not aware of any reason for insulin to need to pass through any large width of needle, but thinner needles may be more likely to break, especially if you reuse them, and they might be more expensive to make.
As for length of needle- for most of diabetes history, the goal has been to inject insulin into the fat tissue, although sometimes people aim at muscle or veins. You certainly do not want to inject the skin. And sometimes doctors don't want to worry about how thick your skin might be, so they inject long needles. If you inject very close to the skin but in the fat tissue, it's possible that if you inject a large volume of insulin, some of it will irritate the skin (where the pain receptors are) and that will make your shots hurt more. If you use a needle that's on syringe, the needle has to be capable of penetrating the top of the vial of insulin as well as going into you correctly, unless you are using luer lock syringes and changing the needle between filling the syringe and doing your shot.
However, many many studies have shown that having skin that's more than 4mm deep in any of the places people commonly inject insulin is rare, even in people who are morbidly obese. You can find those studies elsewhere on this blog.
For comparison- if you donate blood, your blood will be drawn with a 16G or 17G needle (OUCH) so that the blood cells don't get squished coming out of you.
Blood draws are typically done with 21G to 23G needles, and IV lines are typically 20G to 22G. You can see a chart showing gauge differences on wikipedia: http://en.wikipedia.org/wiki/Needle_gauge

Using the math you learned in middle school, you can figure therefore that a 32G pen needle that is 4mm long has a volume (not subtracting inner air) of .173 cubic millimeters.
A large end insulin needle is about 12mm long and 28G, which gives a volume of 1.235 cubic millimeters.
The Navigator sensor probe, at roughly 13mm long and 21G, has a volume of 6.686 cubic millimeters.
The Navigator sensor probe is roughly the size of needles used for blood draw.
If you have a doctor (or nurse!) express surprise that you or your child takes shots every day without much complaint but hates blood draws or IVs, please tell them this fact:

The needles used for blood draw are typically 5 to 30 times as large as the needles used for injecting insulin.

Are New Insulins Better?

Insulin was first usefully injected into a diabetic in 1922.
By 1923, insulin was being produced and sold commercially for Eli Lilly and by Haegdorn Nordisk as a nonprofit. But the insulin they were producing was worlds away from the insulin that you and I inject today. For one thing, they got it from cows and pigs; for another, it contained significant impurities and was not at all concentrated. It took a little while to standardize strengths, so that a person didn't know how much ze was getting, and there weren't any options between insulin types.

In 1936, protamine zinc insulin was released from Nordisk. This insulin had been formulated to act more slowly, to reduce the number of daily injections needed. The protamine came from the semen of trout.

In 1946, Neutral Protamine Hagedorn insulin was developed, and it began to be sold in 1950. This was called neutral because it has a pH of 7.0 like water, protamine because it contained protamine, Hagedorn after Hans Christian Hagedorn (cofounder of Nordisk), and insulin because it contained insulin (from pigs). NPH Insulin is still sold today although it currently contains synthetic insulin and synthetic protamine.
NPH had and continues to have, two points in its favor. Point one is that it last a fairly long time- two or sometimes even just one, shot of it per day will provide some insulin coverage all day. Point two is that it can be mixed with other insulins. Mixing NPH with regular insulin (or, later, Novolog, Humalog, or Apidra) allows a person to, in just two shots per day, inject for breakfast (covered by morning regular), lunch/daytime basal (covered by morning NPH), supper (covered by evening regular), and bedtime snack/nighttime basal/dawn phenomenon (covered by NPH). Some people still wanted fewer injections, a smoother basal, and an insulin with less reputation for being inconsistant- which it was.

Of the insulins developed prior to 1990, NPH and regular are the only ones that are in any sense their same selves and modern insulins, proving that they work in FDA trials, have to show non-inferiority to NPH and regular. However, a number of other insulins were around in the latter half of the 20th century, and some were probably better than NPH as far as basal insulins go.

Anyways. Time went by. Pork insulin began being molecularly altered so that it was molecularly the same as human insuln instead of being off by a molecule. In the 1980s, insulin began being produced by genetically engineered bacteria. In 1983, Lilly started selling the stuff as Humulin (Humulin N, Humulin R, Humulin L, etc) and Nordisk followed suit five years later with the Novolins. Ironically, the new insulins were less pure. Also in the 1980s, the use of insulin pumps got really going. In the 1990s, the first insulin analogs appeared, claiming to have shorter durations of action and to therefore be more appropriate for mealtime injections as well as for pump wearers. These were Humalog and Novolog. In the first decade of the twenty first century, four new insulins- Lantus and Levemir for basal, Apidra and Exubera for bolus (Apidra claiming to be super fast and Exubera being inhaled) hit the US market. The last of the pork based insulins (and Exubera) left the market.
Currently, NPH and Regular sell for considerably less than Lantus, Levemir, Humalog, Novolog, or Apidra (oddly, Apidra is the cheapest and least often covered by insurance of the newer insulins). Most diabetics are started on the newer insulins.

So when I really read the package inserts for my insulins, looking to see how much people's A1cs had improved, I was in for a shock.

None of the newer insulins have shown themselves to improve A1cs by a significant amount in any study (I would consider it significant if it represented an A1c difference of 0.4 or greater, although none really did any better than 0.2 at the most), when compared to NPH and Regular. Many of them make the claim (some more convincingly than others) that they reduce significant episodes of hypoglycemia and/or that they improve after meal excursions. But they don't do it enough to alter the A1c or fructosamine scores in large studies of patients. I will include some links at the bottom, but here is my overall impression after reading studies looking at these insulins:

Novolog (insulin aspart). Some studies comparing Novolog to Regular found slightly improved A1cs in the Novolog group versus Regular; others found no difference. After looking at a lot of studies, it seems to me that Novolog wins- by a teeny tiny margin. Novolog users have A1cs about 0.1 lower than Regular users (difference between an A1c of 7.8% and 7.9%). I suspect this has something to do with the clearer need for Regular users to inject with time to spare before meals. Novolog users in open label trials consistantly preferred Novolog, probably because getting Novolog generally meant being told to inject right before eating instead of half an hour earlier. Novolog is associated with more stomach aches. Results on whether Novolog reduces hypoglycemic events are mixed but the overall answer seems to be that Novolog users have fewer really major hypoglycemic events- probably because they don't inject and then lose track of time and forget to eat.

Only one study comparing Humalog to Regular found that Humalog reduced A1cs compared to Regular; that one was a small (30 people, 19 on Humalog and 11 on Regular) study of adult pumpers that found a difference of 0.34 (difference in average A1c was 7.66 v 8.0). Many large studies found no difference whatsoever; the one study is either a fluke or it takes a pump to see a difference (I vote for fluke- that one study didn't look well done).

Lantus does not lower A1c compared to NPH in any studies, not even studies where NPH is being given only once per day, and people know they're trying Lantus. Lantus also doesn't have the 24 hour duration it's advertised to have (it lasts longer than 24 hours in most people) and it has more site reactions- it's not neutral, it's acidic, and it stings. It does seem to cause less hypoglycemia, probably because it doesn't have that middle of the night peak. It also is associated with lower wake up numbers- I am not sure I see the value in that.

Apidra is mostly compared to Humalog and Novolog instead of to Regular. It doesn't produce lower A1cs. Nuff said.

Levemir has been tried in twice a day shots compared to NPH twice per day and sometimes did a little better, sometimes not. Overall, a meta analysis seems to say that Levemir improves A1c by 0.05 percentage points- meaning that if the A1c tests were totally accurate to the degree of the reading (that is, an A1c of 6.5 always meant your A1c was betwee 6.45 and 6.54) then half of all A1cs would go down by the last number- say, from 7.9 to 7.8. Not a huge difference.

All of the insulins mentioned had the benefit that in some cases where a person was having weird reactions to another insulin, they were able to switch to another insulin and did better.

The major differences between the insulins were ease of use- one shot of Lantus per day vs two of NPH, injecting right before eating vs half an hour earlier- and price.

Sources:

Blurb of study comparing Novolog to Regular, claiming Novolog is better with unchanged fructosamine scores. http://www.ncbi.nlm.nih.gov/pubmed/10332685
Abstract of study of 29 patients on pumps comparing Novolog and Regular. Fructosamine scores were better with regular: http://www.ncbi.nlm.nih.gov/pubmed/11194244
Abstract of large (n=1070) open label study comparing Novolog and Regular; difference in A1c between Novolog and Regular was 0.12, in favor of Novolog- confidence interval 0.03 to 0.22
Large (n=882) open label study comparing Novolog and Regular; difference in A1c was 0.15 in favor of Novolog. Novolog was injected right before eating and Regular was injected half an hour before eating. http://care.diabetesjournals.org/content/23/5/583.long
Study (n=294) comparing premixed Novolog with NPH to premixed Regular with NPH; difference in A1c was 0.10 with a confidence interval that making it statistically insignificant .http://www.ncbi.nlm.nih.gov/pubmed/12027927
Small study comparing Apidra to Novolog and Humalog used in pumps. No difference in A1cs :http://www.ncbi.nlm.nih.gov/pubmed/21457066
Small open label cross over study (n=107) comparing Regular and Humalog- Humalog made no difference in A1c http://www.ncbi.nlm.nih.gov/pubmed/8750567
Small double blind study of pumpers (n=30) on Regular or Humalog- Humalog users had A1cs .34 lower: http://www.ncbi.nlm.nih.gov/pubmed/9032100
The abstract to this large (n=1008) three month study of Regular users and Humalog users indicates that A1cs were taken but does not report changes in A1c in conclusion, suggesting that Humalog did not perform better than Regular. http://www.ncbi.nlm.nih.gov/pubmed/9000704
In another paper on the same group, they say that the A1c decreased in both the Regular and Humalog users over the study period, by the same amount: http://www.ncbi.nlm.nih.gov/pubmed/9183237
Another paper written by people who took part in a part of the above study, they note that after the big study ended, the A1cs of the people on Humalog rebounded- to higher than before the study, despite staying on Humalog: http://www.ncbi.nlm.nih.gov/pubmed/9418839
The abstract to this study of roughly 500 type 1 and type 2 diabetics says that insulin lispro users averaged A1cs of 8.1 compard to 8.3 in Regular users: http://www.ncbi.nlm.nih.gov/pubmed/9083709
This meta-analysis did not find Humalog to be better than Regular in terms of long term blood sugar control: http://www.ncbi.nlm.nih.gov/pubmed/9377611
This study of kids with type 1 showed an insignificant difference in A1c between Humalog and Apidra users. http://www.ncbi.nlm.nih.gov/pubmed/21291333
This exchange of letters includes a good summary of studies comparing Humalog and Regular, showing that only one- the one with 30 people on pumps- showed a statistically significant difference in A1c and arguing that Humalog didn't really improve hypoglycemia either: http://www.cmaj.ca/content/159/11/1353.reprint
Study (n=534 type 1s) comparing NPH and Lantus showed non-significantly better A1cs in NPH users. http://www.ncbi.nlm.nih.gov/pubmed/10834423
Study (n=518) of type 2 diabetics using NPH or Lantus showed non-significantly better A1cs in NPH users (although Lantus users didn't gain quite as much weight): http://www.ncbi.nlm.nih.gov/pubmed/11315821
Study (n=619) of type 1 NPH users who did or didn't switch to once daily Lantus. Switchers had a statistically insignificant decrease in A1c. http://care.diabetesjournals.org/content/23/11/1666.long
Study (n=349) of kids with type 1 who had been taking NPH once or sometimes twice a day who did or didn't switch to Lantus once daily. Those who switched had insignificantly higher A1cs: http://care.diabetesjournals.org/content/24/11/2005.long
Very small (n=19) study comparing Levemir and NPH. No difference.
Review of large numbers of studies comparing NPH and Levemir finds Levemir reduces A1c by statistically significant amounts- 0.05. That is, about half of people with an A1c reading of 7.7 would get a 7.6 instead. http://www.ncbi.nlm.nih.gov/pubmed/22046606
Insulin was first usefully injected into a diabetic in 1922.
By 1923, insulin was being produced and sold commercially for Eli Lilly and by Haegdorn Nordisk as a nonprofit. But the insulin they were producing was worlds away from the insulin that you and I inject today. For one thing, they got it from cows and pigs; for another, it contained significant impurities and was not at all concentrated. It took a little while to standardize strengths, so that a person didn't know how much ze was getting, and there weren't any options between insulin types.
In 1936, protamine zinc insulin was released from Nordisk. This insulin had been formulated to act more slowly, to reduce the number of daily injections needed. The protamine came from the semen of trout.
In 1946, Neutral Protamine Hagedorn insulin was developed, and it began to be sold in 1950. This was called neutral because it has a pH of 7.0 like water, protamine because it contained protamine, Hagedorn after Hans Christian Hagedorn (cofounder of Nordisk), and insulin because it contained insulin (from pigs). NPH Insulin is still sold today although it currently contains synthetic insulin and synthetic protamine.
NPH had and continues to have, two points in its favor. Point one is that it last a fairly long time- two or sometimes even just one, shot of it per day will provide some insulin coverage all day. Point two is that it can be mixed with other insulins. Mixing NPH with regular insulin (or, later, Novolog, Humalog, or Apidra) allows a person to, in just two shots per day, inject for breakfast (covered by morning regular), lunch/daytime basal (covered by morning NPH), supper (covered by evening regular), and bedtime snack/nighttime basal/dawn phenomenon (covered by NPH). Some people still wanted fewer injections, a smoother basal, and an insulin with less reputation for being inconsistant- which it was.
Of the insulins developed prior to 1990, NPH and regular are the only ones that are in any sense their same selves and modern insulins, proving that they work in FDA trials, have to show non-inferiority to NPH and regular. However, a number of other insulins were around in the latter half of the 20th century, and some were probably better than NPH as far as bolus insulins go.
Anyways. Time went by. Pork insulin began being molecularly altered so that it was molecularly the same as human insuln instead of being off by a molecule. In the 1980s, insulin began being produced by genetically engineered bacteria. In 1983, Lilly started selling the stuff as Humulin (Humulin N, Humulin R, Humulin L, etc) and Nordisk followed suit five years later with the Novolins. Ironically, the new insulins were less pure. Also in the 1980s, the use of insulin pumps got really going. In the 1990s, the first insulin analogs appeared, claiming to have shorter durations of action and to therefore be more appropriate for mealtime injections as well as for pump wearers. These were Humalog and Novolog. In the first decade of the twenty first century, four new insulins- Lantus and Levemir for basal, Apidra and Exubera for bolus (Apidra claiming to be super fast and Exubera being inhaled) hit the US market. The last of the pork based insulins (and Exubera) left the market.
Currently, NPH and Regular sell for considerably less than Lantus, Levemir, Humalog, Novolog, or Apidra (oddly, Apidra is the cheapest and least often covered by insurance of the newer insulins). Most diabetics are started on the newer insulins. So when I really read the package inserts for my insulins, looking to see how much people's A1cs had improved, I was in for a shock.
None of the newer insulins have shown themselves to improve A1cs by a significant amount in any study (I would consider it significant if it represented an A1c difference of 0.4 or greater, although none really did any better than 0.2 at the most), when compared to NPH and Regular. Many of them make the claim (some more convincingly than others) that they reduce significant episodes of hypoglycemia and/or that they improve after meal excursions. But they don't do it enough to alter the A1c or fructosamine scores in large studies of patients. I will include some links at the bottom, but here is my overall impression after reading studies looking at these insulins:
Novolog (insulin aspart). Some studies comparing Novolog to Regular found slightly improved A1cs in the Novolog group versus Regular; others found no difference. After looking at a lot of studies, it seems to me that Regular wins- by a teeny tiny margin. Novolog users have A1cs about 0.1 lower than Regular users (difference between an A1c of 7.8% and 7.9%). I suspect this has something to do with the clearer need for Regular users to inject with time to spare before meals. Novolog users in open label trials consistantly preferred Novolog, probably because getting Novolog generally meant being told to inject right before eating instead of half an hour earlier. Novolog is associated with more stomach aches. Results on whether Novolog reduces hypoglycemic events are mixed but the overall answer seems to be that Novolog users have fewer really major hypoglycemic events- probably because they don't inject and then lose track of time and forget to eat.
Only one study comparing Humalog to Regular found that Humalog reduced A1cs compared to Regular; that one was a small (30 people, 19 on Humalog and 11 on Regular) study of adult pumpers that found a difference of 0.34 (difference in average A1c was 7.66 v 8.0). Many large studies found no difference whatsoever.
Lantus does not lower A1c compared to NPH in any studies, not even studies where NPH is being given only once per day, and people know they're trying Lantus. Lantus also doesn't have the 24 hour duration it's advertised to have (it lasts longer than 24 hours in most people) and it has more site reactions- it's not neutral, it's acidic, and it stings. It does seem to cause less hypoglycemia, probably because it doesn't have that middle of the night peak. It also is associated with lower wake up numbers- I am not sure I see the value in that.
Apidra is mostly compared to Humalog and Novolog instead of to Regular. It doesn't produce lower A1cs. Nuff said.
Levemir has been tried in twice a day shots compared to NPH twice per day and sometimes did a little better, sometimes not. Overall, a meta analysis seems to say that Levemir improves A1c by 0.05 percentage points- meaning that if the A1c tests were totally accurate to the degree of the reading (that is, an A1c of 6.5 always meant your A1c was betwee 6.45 and 6.54) then half of all A1cs would go down by the last number- say, from 7.9 to 7.8. Not a huge difference.
All of the insulins mentioned had the benefit that in some cases where a person was having weird reactions to another insulin, they were able to switch to another insulin and did better.
The major differences between the insulins were ease of use- one shot of Lantus per day vs two of NPH, injecting right before eating vs half an hour earlier- and price.
Humalog (insulin lispro)
Blurb of study comparing Novolog to Regular, claiming Novolog is better with unchanged fructosamine scores. http://www.ncbi.nlm.nih.gov/pubmed/10332685
Abstract of study of 29 patients on pumps comparing Novolog and Regular. Fructosamine scores were better with regular: http://www.ncbi.nlm.nih.gov/pubmed/11194244
Abstract of large (n=1070) open label study comparing Novolog and Regular; difference in A1c between Novolog and Regular was 0.12, in favor of Novolog- confidence interval 0.03 to 0.22
Large (n=882) open label study comparing Novolog and Regular; difference in A1c was 0.15 in favor of Novolog. Novolog was injected right before eating and Regular was injected half an hour before eating. http://care.diabetesjournals.org/content/23/5/583.long
Study (n=294) comparing premixed Novolog with NPH to premixed Regular with NPH; difference in A1c was 0.10 with a confidence interval that making it statistically insignificant .http://www.ncbi.nlm.nih.gov/pubmed/12027927
Small study comparing Apidra to Novolog and Humalog used in pumps. No difference in A1cs :http://www.ncbi.nlm.nih.gov/pubmed/21457066
Small open label cross over study (n=107) comparing Regular and Humalog- Humalog made no difference in A1c http://www.ncbi.nlm.nih.gov/pubmed/8750567
Small double blind study of pumpers (n=30) on Regular or Humalog- Humalog users had A1cs .34 lower: http://www.ncbi.nlm.nih.gov/pubmed/9032100
The abstract to this large (n=1008) three month study of Regular users and Humalog users indicates that A1cs were taken but does not report changes in A1c in conclusion, suggesting that Humalog did not perform better than Regular. http://www.ncbi.nlm.nih.gov/pubmed/9000704
In another paper on the same group, they say that the A1c decreased in both the Regular and Humalog users over the study period, by the same amount: http://www.ncbi.nlm.nih.gov/pubmed/9183237
Another paper written by people who took part in a part of the above study, they note that after the big study ended, the A1cs of the people on Humalog rebounded- to higher than before the study, despite staying on Humalog: http://www.ncbi.nlm.nih.gov/pubmed/9418839
The abstract to this study of roughly 500 type 1 and type 2 diabetics says that insulin lispro users averaged A1cs of 8.1 compard to 8.3 in Regular users: http://www.ncbi.nlm.nih.gov/pubmed/9083709
This meta-analysis did not find Humalog to be better than Regular in terms of long term blood sugar control: http://www.ncbi.nlm.nih.gov/pubmed/9377611
This study of kids with type 1 showed an insignificant difference in A1c between Humalog and Apidra users. http://www.ncbi.nlm.nih.gov/pubmed/21291333
This exchange of letters includes a good summary of studies comparing Humalog and Regular, showing that only one- the one with 30 people on pumps- showed a statistically significant difference in A1c and arguing that Humalog didn't really improve hypoglycemia either: http://www.cmaj.ca/content/159/11/1353.reprint
Study (n=534 type 1s) comparing NPH and Lantus showed non-significantly better A1cs in NPH users. http://www.ncbi.nlm.nih.gov/pubmed/10834423
Study (n=518) of type 2 diabetics using NPH or Lantus showed non-significantly better A1cs in NPH users (although Lantus users didn't gain quite as much weight): http://www.ncbi.nlm.nih.gov/pubmed/11315821
Study (n=619) of type 1 NPH users who did or didn't switch to once daily Lantus. Switchers had a statistically insignificant decrease in A1c. http://care.diabetesjournals.org/content/23/11/1666.long
Study (n=349) of kids with type 1 who had been taking NPH once or sometimes twice a day who did or didn't switch to Lantus once daily. Those who switched had insignificantly higher A1cs: http://care.diabetesjournals.org/content/24/11/2005.long
Very small (n=19) study comparing Levemir and NPH. No difference.
Review of large numbers of studies comparing NPH and Levemir finds Levemir reduces A1c by statistically significant amounts- 0.05. That is, about half of people with an A1c reading of 7.7 would get a 7.6 instead. http://www.ncbi.nlm.nih.gov/pubmed/22046606

A List of Interesting Blood Sugar Monitors

The Accu Chek Voicemate-this discontinued meter currently sells for over a thousand dollars (originally it sold for about five hundred dollars). In addition to talking, it had the unusual feature of reading off and identifying insulin types! It was intended for blind users and incorporated the Accu Chek
It used 4 microliters of blood and couldn't operate in cool (less than 50 degrees Fahrenheit) weather or in very hot (over 104 degrees Fahrenheit) weather.
The newer model of this meter, the Accu Chek Voicemate plus takes 1.5 microliters of blood but still can't deal with bad weather. The Accu Chek Voicemate Plus is not available in the US.

The Nova Max- this underrated meter uses two kinds of test strips- one for measuring blood sugar, one for measuring blood ketones. As a blood sugar meter, it uses the smallest blood sample of any meter- 0.3 microliters- but is not known for being especially accurate (although it meets FDA standards). As a blood ketone meter, it uses 0.6 microliters of blood. The Novamax is for sale currently (I use it as a ketone meter only). Insertion of strips into the meter is somewhat more difficult than standard.

The Accu Chek Aviva- my current meter. This is a larger clunkier version of the Accu Chek Nano- they both use Accu Chek Aviva test strips, which use 0.6 microliters of blood. The Nano is smaller and has a backlight but is not available in the United States. These strips incorporate numerous filters and checks and are known for being more accurate than most.

One Touch- the one touch line of meters includes the One Touch, One Toucher 2, One Touch Ultra Mini (in many colors), and One Touch Ultra. The use either of two different types of test strips- currenly one with blue stripes which advertises that it double checks its own results. They use 1 microliter of blood. The One Touch Ultra communicates with Dexcom and Minimed CGMs for automatic calibrations (which may or may not be desired).

The Accu Chek Compact is an all in one meter that stores a drum of test strips inside the meter, and has a detachable lancing device on the side. I don't like it because it uses 1.2 microliters of blood and the lancing device is a softclix and I prefer a multiclix.

The Glucowatch was the major precursor to CGMs. In fact, it was a continuous glucose monitor. Launched in 2002, the glucowatch was worn like a wristwatch and included two electrodes. It was moderately accurate- roughly as accurate as modern CGMs, which is to say that it had problems but was pretty good. Unfortunately, it caused skin problems for most users- including burns- and it cost a lot. Like the modern CGMs, it needed calibrations, incorporated a warm up period, and needed replacement sensors. Although three different models were released- the original Glucowatch, Glucowatch Biographer, and Glucowatch Biographer II- it was discontinued in 2007 and sales of sensors stopped in 2008.

There are many blood sugar meters for sale currently, because it is a high profit industry. I am aware of dozens of companies making meters- most of the companies that make meters make more than one. The things to look for in a meter, in my opinion, are test strip cost, accuracy, and blood sample size requirements (0.3 microliters is the smallest you can currently get and 0.3 to 1.5 is about the range. It matters more for some people than others). Extras that some people like are memory and averaging features, communication with a pump or CGMS, backlight, incorporated lancing devices or test strips, size, color and skins (stickers that go over the meter), display, and talking.

Diabetes on Mt Everest

My CDE in the hospital where I went in the weeks following my diagnosis had a poster on her wall (or maybe it was on the door) of a guy climbing a mountain. She pointed it out to me to have a little discussion about how to deal with diabetes in extreme temperatures, because if insulin freezes, it's not good anymore. And as you may know, it's kinda cold on a mountain. According to my CDE, this type 1 guy climbed Mount Everest with his insulin taped to his skin to keep it warm.

I was sitting out in the cold today, getting ready to do a shot. My insulin was plenty warm, but I wasn't. And it occurred to me that the real question is, how did he safely bare his skin for the shot?

So, today's post is about the Everest climbers I can find who've climbed with diabetes.

First, the guy on my CDE's poster was probably Will Cross. As if being a high school principal wasn't enough adventure, Will Cross has attempted to climb Mount Everest numerous times. He didn't go all the way in 2004 or 2005; in 2007 he made it to the top. Will Cross was diagnosed with diabetes when he was nine; it was about thirty years later that he climbed Everest. He was sponsored by Novo-Nordisk, and was using Novolog and described as using Novolin-N (the NPH made by Novo-Nordisk) on his first couple climbs. He is described in the 2007 articles as wearing an insulin pump as well as using a NovoFlexPen. Some of the articles about his climb claim that he couldn't check his blood sugar, but he clearly says he did check his blood sugar- my guess is that the meter didn't always work when he wanted it to. He has a wife and six kids. He is an American.

Geri Winkler, also a teacher, was diagnosed with diabetes when he was 28 years old, in 1984. In 2006, he became the first diabetic to get to the top of Mount Everest. He was sponsored by Bayer, which makes a blood sugar meter and A1c now kits. He is from Austria.

Sébastien Sasseville first got to the summit of Everest in the year before he was diagnosed with type 1 diabetes. He climbed it again seven years later. He raised money for JDRF on the second climb. He is also affiliated with CWD and triabetes. He is Canadian.

There are a number of posts from John Jackson claiming that he and his son, Dan Jackson, were going to climb Everest earlier this year. His son is 17 and was diagnosed with diabetes + celiac aged 2. But I don't know what happened with that. They are British, and Dan uses a minimed pump. They were trying to raise money.

I thought it was interesting that all three (or four) diabetic Everest climbers used diabetes to help fund their expeditions. Also, that there are three or four type 1s climbing Everest- I think that means that, statistically and humorously speaking, being a type 1 diabetic is a risk factor for climbing Mount Everest!

Smoking and Diabetes

It was getting late and I was short on ideas that interested me. Fortunately, I just so happened to pick up a trivia book my brother left around. The book is called Your Pinkie is More Powerful than Your Thumb: And 388 Other Surprising Facts That Will Make You Wealthier, Healthier, and Smarter Than Everyone Else and the author is Mark Di Vincenzo. The "facts" in the book seem to be hypotheses based on a studies. But one (on page 23) gave me an idea.
The book says: In the diabetes study, researchers followed 10,892 middle aged smokers who did not have diabetes from 1987 to 1989. Those who quit increased increased by 70 percent their risk of developing diabetes for the first six years after they quit [compared to people who'd never smoked]. Those who continued to smoke also increase their risk for developing diabetes- but by only 30 percent.

I looked for this study. I don't see it, but I did find another study (a Japanese one), of thirty thousand people, roughly 900 of whom reported quiting smoking between the first measurement and the second, who did not report resumed smoking. It followed all of these people for a few years. The fasting blood sugar of those who quit was significantly higher the next year, and the year after that, but then it began to go down. http://www.jstage.jst.go.jp/article/jea/21/6/21_431/_article

So: smoking increases diabetes risk and quitting smoking will, at least temporarily, make the risk a little worse.

If you already have diabetes, there are plenty of reasons to quit smoking, even if you are convinced you will die too young to worry about lung cancer.
Smoking messes with circulation; so does diabetes. Diabetic smokers have higher risks for a variety of complications compared to nonsmoking diabetics.

For instance, in the Wisconsin Epidemiology Study, which has been following 943 people diagnosed in a particular part of Wisconsin with type 1 diabetes under the age of 30, for about thirty years, the risk of having a toe, foot, or leg amputated after 25 years with diabetes was roughly 10%. Not exactly a small risk, IMHO, but the majority of participants had A1cs above 9%. The biggest risk factor for an amputation (in this group) was being a guy (triple the risk compared to women). The next biggest risk factor was smoking. People who had quit smoking had an intermediate risk. A1c was a significant risk; the people writing this up did not rank it as a higher risk factor than smoking and sex because they were looking at how much a difference in A1c mattered if you had an A1c of 8% vs 11%, which didn't matter as much as the difference between 11% and 15%. Running a crazy high A1c like 15% will run you into all kinds of trouble.The Article
BTW, not so fun fact (cited in article above) if you compare type 1 and type 2 diabetes with the same diabetes duration, the type 2 diabetics are at higher risk of having something amputated.
In the same population, smokers were two and a half times more likely than non smokers to have had severe hypoglycemic episodes in the previous year- either because smokers don't take care of themselves generally, or because smoking makes your hypoglycemia awareness worse. Severe hypoglycemia was hypoglycemia that made them pass out or have an overnight hospital stay (or both).

Who Pays For Diabetes Research?

It's hard to look at the shifting trends in topics about diabetes being studied without wondering what drives them. Who does diabetes research? Who pays for it? Who approves it? Why?

I can only begin to answer those questions. Some diabetes research is, clearly, paid for entirely by drug companies who are hoping that the results will help them sell their product or improve their odds of getting the product past the FDA or other regulatory bodies. Some small research is done by individual physicians who simply wish to share their observations or to study something that makes them curious, or by graduate students looking to write papers. Some research is funded and driven by well known diabetes names- the JDRF, the ADA, or the Iaccoca Foundation- that get money from donations from individuals, corporations, and sometimes governments. The ADA and JDRF often fund research done by drug companies (if you look up research by grant type on the ADA website, you'll notice that four of the grants are named after drug companies- Novo Nordisk, Takeda, and Merck).

A tremendous amount of diabetes research however is funded by tax monies. The United States Government has pledged $150 million per fiscal year for type 1 diabetes research for the past few and upcoming two years. The money is given to researchers and organizers after approval from the NIDDK. This money has gone to fund well known projects, such as trialnet (which two of my siblings participated in) as well as lesser known projects.
To compare these monies, the American Diabetes Association reported, for the fiscal year ending in 2009, income of $261 million, $141 million of which went to programs, which I think includes research.
The JDRF reported $198 million dollars income for a recent year, $156 million of which was spent on programs, which, again I think includes research. (Source: Charity Navigator)

A search on pubmed brings up 115 articles in which the authors acknowledge receipt of JDRF monies. Of these, 6 were published in the past year. Of these, one was a survey on quality of life in type 1 diabetics. One was about inflammation but otherwise was medical gobbledygook to me. One was a report of laboratory research that might translate into a prevention/treatment of diabetic kidney disease. One was a triggr follow up, which is a study of siblings and offspring of type 1 diabetics looking to find anything that might be responsible for triggering type 1 diabetes. In this case they are looking to see if a hypoallergenic formula might prevent diabetes. Another was a study on preventing kidney disease in diabetic rats. The last was a study looking to see how certain medications used to treat type 2 diabetes affect beta cells.
A search on pubmed brings up 149,792 articles in which the authors acknowledge connection to the NIDDK. Most do not have to do with diabetes. Out of the most recent three hundred articles, all published since this summer, twenty four were about diabetes, nine of the twenty four being clearly relevant to autoimmune type 1 diabetes, one being about HIV related diabetes, one being about the creation of the monogenic diabetes register, and thirteen stating that they were about type 2 diabetes or insulin resistance. A lot of research was done on transplantation.
Searching for ADA funded research is a little harder, because I keep getting articles done by people named Ada. Also, I get articles not funded by the ADA that cite "ADA guidelines"

Diabetes research done outside the United States has a lot in common with US research when it comes to drug industry funded research. However, other countries have other interesting slants and focuses. For instance, researches in various European countries have countrywide health databases to mine data from. Researchers in some places with standardized medicine do research looking to find that it's safe to reuse needles, for instance, or to promote cheaper ways of dealing with diabetes. Certain Asian and South American publications try to compare their populations' diabetes to that of Americans (the Japanese publish quite about about fulminant diabetes in the elderly).

Genetic Drift and Type 1 Diabetes

Almost all types of diabetes have a known genetic component. A very small number of diabetes types are determined by one gene- you got the gene, you got the diabetes. A much larger portion of diabetes types and cases are multifactorial in cause, but also in the specific genetic cause.

Meaning, as a type 1A diabetic, that my likelihood of developing diabetes was strongly impacted by MULTIPLE genes in the region of the genetic code where there is more variability in genetics, but that some factors other than my genetics certainly impacted the fact that I got diabetes- if type 1A diabetes was totally genetic, identical twins would always both have it or both not, and that's not how it goes.

Anyways, one of the interesting things about the genetics of type 1 diabetes is that the highest risk genes are heterozygous. That means that, unlike in straight up genetic diseases where having two parents carrying the same faulty allele (carriers) resulting in an increased chance of the disease, in type 1 diabetes, the highest risk comes for people who have combinations of different high risk alleles, not two of the same high risk allele (an allele makes up one parent's contribution towards a gene). If this paragraph didn't make sense to you, don't worry about it. Do ask me to clarify if you know how to get me to word it better though.

Anyways. One of the more unusual explanations for increases and decreases in disease are based on which genes are becoming more and less common. This is based partly on who has how many kids (that determines allele frequency), but also on who people have their kids with. It should be obvious that certain diseases (like the above mentioned recessive genetic disorders) are less common if people are having their kids with people who are not their fourth cousins, etc. With more complex genetically influenced diseases (including most autoimmune diseases), it's a little harder to predict what population mobility will do to disease patterns.

However, one of the things that seems to be happening is that, more so than in previous generations, people are choosing to have children with partners whose alleles in the areas that code for the immune system are complementary- they are picking to have kids with people whose immune systems are different from their own. This is mostly a good thing (at least according to theory) but it is resulting in more people of my generation and below who have the high risk genes for developing type 1 diabetes.

Unfortunately, this theory is not supported by the American evidence, which says that among those diagnosed with diabetes as kids in the last many years, fewer these days have the high risk immune system genes. I was looking for the article on which I based most of this post, and found instead some studies comparing the frequency of the highest type 1 diabetes risk genes in the US and saying that it's gone down, and now I sort of feel like erasing what I wrote, but I won't. Instead I'll give you a link to this excellent article and count the fact of the day to be as follows:
The portion of children diagnosed with diabetes in the United States whose diabetes can be attributed to high genetic risk declined between 1965 and 2005.