Your Doctor is Rated on Your Health

Through the Affordable Care Act, physicians will be publicly ranked for how well their patients are doing, especially if the patient is being paid for through medicare and the physician is in a relevant field.

For diabetics age 18-75, the physicians will be ranked on-

Whether or not your A1c is below 9%

Whether your blood pressure is high or not

Whether or not your LDL is low enough (<100 dl="" mg="" p="">
Whether or not you been examined for retinopathy in the past year.

Whether or not you have had a urine test for kidney disease in the past year.

Whether or not you've had an exam of your feet and ankles for neuropathy in the past year (it's unclear to me exactly how extensive they intend the exam to be).

Whether or not the doctor has looked at your shoes or other footwear to decide if it's safe or not.

Whether or not you have been tested for high blood pressure in the past 3 years (this one applies to adults up to 90 and not merely to 75).

Whether or not you meet ALL of the measures of a perfect diabetes patient: A1c below 8% PLUS blood pressure below 140/90 PLUS LDL below 100 mg/dl PLUS no smoking PLUS if you have heard disease, you're on aspirin

Whether or not you've had lipid testing in the past year.

If you have another doctor because of another disease, whether or not there is communication between the two doctors.

If you have a diagnosis of diabetic retinopathy and are any age, then whether or not the doctor has received proof of an eye exam in the past year.

If you have both a diagnosis of certain types of heart disease AND diabetes, then whether or not you have been prescribed a medication in the ARB or ACE inhibitor drug classes.

If you are 5-17 years old and have diabetes, whether or not your A1c has been tested in the past year.

And for all patients, the physician will be ranked based on things like what portion of patients have received a flu vaccine.

This ranking is theoretically intended to allow us to choose better doctors. But you can find even on the government website a list of reasons why this might not be a good idea- namely, your doctor will suddenly have an incentive to stop accepting or stop seeing patients that he has reason to believe will not look good for him. Also, this provides doctors with a reason to do unnecessary testing. For instance, there is really no good reason to test my lipids. Yet because my insurance company rates the doctor on these same things, my lipids have been tested annually for years. And guess what? Every year my TOTAL lipids is under 110 mg/dl and my LDL is under 50 mg/dl. That there is no point in testing the lipids of a person whose lipids were well below normal the previous year is not something that they take into consideration- as far as the writers of these standards are concerned, if I have diabetes, I must be at high risk of high cholesterol levels. Whereas I believe that previous lipid levels are a much better predictor, and that if the one test is not only not high, but below normal, there is no point in testing for high levels for another decade (or longer, probably).

Anyways. You can read or scan or search within the 1,369 page document here:
https://s3.amazonaws.com/public-inspection.federalregister.gov/2013-28696.pdf

Not My Idea- One Way Long-Term CGM Sensors Might Work

Dexcom years ago tried to develop a sensor that would be implanted for six months or a year- a long term sensor- which is why their sensors- the generation before the Dexcom 7, the Dexcom STS- was called Dexcom Short Term Sensors.

So obviously, making and marketing the Dexcom LTS hasn't gone much of anywhere so far.

But people are still working on developing long term sensors and playing with ideas that might make them work. One that I just read that seems sort of far out to me is the idea of using things to cause local growth of blood and lymph vessels near the placement of the sensor!
http://www.ncbi.nlm.nih.gov/pubmed/24243850

Intern/Volunteer Wanted by Pancreum for Artificial Pancreas Project

Not much of a fact, but if you know a mechanical engineer....
http://pancreum.com/car.html


Some facts about glucagon...

#1 Most type 1 diabetics have abnormally high glucagon levels all the time. The local high levels of insulin in people whose pancreata make insulin tell the alpha cells to keep it down. In type 1 diabetics whose alpha cells are not too damaged, the alpha cells make a lot of glucagon.

#2 Injecting glucagon causes nausea in some people, even when used at low doses. This is one of the barriers to using an artificial pancreas; about 1 in 7 people who has gotten glucagon as a treatment for mild hypoglycemia by an artificial pancreas program has reported feeling nauseous. It's not clear why glucagon makes some people nauseous and not others.

#3  Although plans for glucagon pens have been around for quite a while, right now you can only get glucagon in the US as glucagon kits or glucagen kits. The glucagon kit from Eli Lilly is red. The GlucaGen kit is made by Novo Nordisk and it's orange. Both can be stored at room temperature.

#4 The instructions inside the kit are for extreme low blood sugar, where a person has passed out, and you might as well give a full dose intramuscularly. Some folks use a "mini dose" with a regular insulin syringe subcutateously, taking 0.15 mL (1mg/mL) for hard to treat but not quite as bad hypoglycemia, the full dose being 1 mL (- 1 mg) for adults and 0.5 mg for young children. My doctor recommends the mini dose but I never have tried it yet.

#5 Glucagon acts on the glycogen stores of the liver. In people with liver disease, or who are drunk, or whose glycogen stores are depleted due to fasting, illness, or previous use of glucagon, the glucagon will not raise blood sugar.

Islet Cell Composition

The islets of the pancreas contain five types of cells, named after the first five greek letters.
Alpha cells make glucagon, which stimulates the liver to release glycogen and produce sugars.
Beta cells (which make up 85% of the islets) make pro-insulin (which splits into insulin and cpeptide) and pro-amylin (which becomes amylin).
Gamma cells are often called PP cells; they make a  "pancreatic polypeptide". I find this a really silly name given that insulin is also a panceatic polypeptide.
Delta cells make somatostatin (we have other places in the body were somatostatin is made).
Epsilon cells make ghrelin, which is mostly made elsewhere in the body, and which is a hormone that has a lot to do with controlling hunger.

In embryonic development, the pancreas begins in two pieces.

The pancreas develops from two buds growing from the proto-duodenum, and they merge towards the end of the first trimester.
Human embryos begin making insulin around the beginning of the fifth month of gestation; during the second trimester.

Reactive Hypoglycemia

The most common form of hypoglycemia in people who are not on medications causing hypoglycemia is reactive hypoglycemia.

In the average person's postprandial blood sugar curve, the blood sugar rises during and after the meal, then falls to slightly below the starting blood sugar, and then rises back to the starting blood sugar.

In many people whose pancreata are struggling to make enough insulin, or whose initial insulin response to meals is blunted (ie not making enough incretins or not responding to incretins), after the initial blood sugar rise, there is a drop in blood sugar that is much more dramatic than the normal drop that results in hypoglycemia. It is called reactive hypoglycemia because the hypoglycemia is caused by an over reaction to food.

It should be treated by a diet with no big meals, and snacks through the day. An extreme low carbohydrate diet is usually fairly good at preventing lows, but it isn't necessary; a diet in which a person eats a roughly consistent number of carbs every couple of hours during the day works as well (meals should get smaller in the evening). For milder cases, simply avoiding big meals- and especially avoiding big meals that are followed by exercise (a classical bad move would be a wedding banquet followed by energetic dancing)- is sufficient.

Shoulder pain and reduced range of motion is more common in diabetics

I only found one decent study looking at age and length of diabetes in people with frozen shoulder. It claimed the risk did not go up for type 1 diabetics until they had been diagnosed 20 years.

None of the studies I found on type 1 or type 2 diabetes on frozen shoulder showed a strong statistical link of gHbA1c and frozen shoulder; some found a weak link.

When comparing the risk to nondiabetics, the studies I found had a range of risk of 33% increase compared to nondiabetics (a large large Chinese one year study where a large group of shoulder complaints was lumped together), up to 860% (a small Scottish study that looked specifically at confirmed frozen shoulder).

Mitochondrial Mutations Can Cause Diabetes

Most of the cells in our bodies have two sets of DNA. One set is our genes as we usually think of them- 23 pairs of chromosomes that determine the proteins that our bodies make. These genes come equally from our mothers and our fathers, although each of us has some new mutations- changes in the genes- of our own.

But the mitochondria within each cell have their own set of DNA. This set comes from our mothers, with no contribution at all from our fathers. But like our other DNA, this DNA sometimes has mutations, and mutations may be passed down maternally.

Some of the mutations in mitochondrial DNA cause diabetes. Diabetes caused by the most common mitochondrial mutation tends to be caused by gradual deterioration of beta cells and therefore a gradual inability to make insulin. It is not autoimmune, and it is not usually accompanied by insulin resistance. The diabetes is most often diagnosed in teens, young adults, or middle aged adults; less often in the elderly and rarely in young children. Of people with the mutation, half are diagnosed with diabetes by the age of 38, and 80% are diagnosed by the age of 60. 

Roughly 1% of all cases of diabetes are believed to be caused by mitochondrial mutations. Because hearing loss is often caused by the same mitochondrial mutations that cause diabetes, hearing loss that comes before a diabetes diagnosis, hearing loss and diabetes in a young adult is a good reason to suspect mitochondrial diabetes. Another good reason to suspect mitochondrial diabetes is a family in which there is a mitochondrial pattern of inheritance- all or most of the siblings born to the same mother developing diabetes and/or hearing loss, the mother and her siblings, the maternal grandmother and her siblings. Macular disease in the eye is usually mild enough that it doesn't cause problems, but if it is there at all, it should also raise a red flag.

Mitochondrial mutation related diabetes is associated with a lot of health issues that a person might want to know he was at risk for; it's also NOT associated with some of the health issues associated with type 2 diabetes (ie hypertension) or type 1 diabetes (autoimmune thyroid disease). 

Some Things About Insulin Glargine

Lantus is the brand name of the insulin glargine sold by Sanofi worldwide. Profits are shared with Novo Nordisk because of a lawsuit Novo Nordisk filed some years ago saying that the patent belongs to them.
In India, insulin glargine is also available under the name Basalog, sold by Biocon.
In India, the price of insulin glargine has therefore dropped in the last few years, but in the US the price increased about 10% over the last year (the company's reasoning seems to be that they can get away with it).

Sanofi advertises Lantus as lasting 24 hours for a flat basal profile. This is not much backed up by their own data, which shows that:
-in the person that it lasted the least amount of time for, there was no glargine detectable in the person's blood 10 hours after injection
-they did not measure levels of glargine in the blood MORE than 24 hours after injection, only up to 24 hours. In most people, there was still glargine active at 24 hours. The half life of Lantus injected subcutaneously in lab animals is about 30 hours and there is some evidence that it is about that length in humans as well. In this study where glargine was made radioactive and injected into type 2 diabetics, the time it took for half the glargine to leave the body was 26.3 hours. http://www.ncbi.nlm.nih.gov/pubmed/12931275

Lantus does not reduce A1cs in any studies by any statistically significant amount as compared to NPH or Levemir. Its strongest point is that it reduces the risk of hypoglycemia at night compared to NPH- and that it does pretty dramatically. It also lends itself to allowing a basal bolus system of injection when used with a fast acting insulin.

Lantus is currently the most prescribed insulin in the United States. Personally, I don't think it deserves the honor, given that most of the prescriptions are in people with type 2 diabetes who do not use any other insulin and would probably get as good or better control with once daily injections of NPH.

One large and well publicized study of Lantus users showed a higher risk of breast cancer in Lantus users as compared to users of other insulins (the risk was only in people using Lantus without another insulin). No other study has found the same results.

Glargine insulin is made by genetically modified escherichia coli bacteria for Sanofi, and by a genetically modified pichia pastoris yeast for Biocon.

Cancer Risk in Diabetics

My mother has a theory about why genes that pose higher type 1 diabetes risk are as common as they are. She thinks they lower the risk of cancer. This makes a little bit of theoretical sense, because a strong immune is more likely to kill off cancer cells. Does it hold up to the evidence?
I am not aware of a study of cancer rates in relatives of diabetics, and having diabetes doesn't tend to extend people's lives. The evidence does suggest, however, that type 1 diabetics are less likely to develop and die from cancers.

Type 2 diabetes (or maybe the insulin resistance) almost certainly is a cancer risk:
Japanese study on cancer death risk and impaired fasting glucose
Meta Analysis of studies with a total of over a million men concluding that diabetes is a risk factor for prostate cancer
Strangely enough, right after that I found this article about the reasons diabetes is protective against prostate cancer- go figure.
Australian study concludes higher breast cancer risk for people with type 2 diabetes

But type 1 diabetes, if anything, is protective.


Although type 1 is a risk factor for a handful of specific cancers.
Acute Lymphoblastic Leukemia is often diagnosed within a year of type 1 diabetes. Although I'll admit to wondering if the diabetes in these kids is misdiagnosed as being type 1.


Most studies on cancer rates and diabetes has shown that type 1 diabetics have about 95% of the cancer risk of non-diabetics. That is, we are 5% less likely to develop cancer than other people our age, which is not a huge difference, but which is considerably more interesting when you figure that type 2 diabetics have a cancer risk that is higher than that of age matched non-diabetics. And, this is also despite the fact that type 1 diabetics are at increased risk of a few specific cancers (stomach cancer because of celiac, pancreatic cancer because things that don't work right are more likely to become cancerous, ovarian cancer probably because of the increased PCOS, leukemia probably because its a white blood cell thing).