This is an interesting little study.  (I haven’t ranked Diabetologia in the journal heirarchy, however).

Apparently the protective genes for Type 1 diabetes are not as protective as they used to be…………Also, the high risk genes for Type 1 diabetes are not as necessary– all while the incidence of Type 1 diabetes has increased 2.5 times in Finland in the last 40 years.

They theorize environmental pressure as the cause.  Impossible as it is for some here to believe, the Finns must be way ahead of the USA  since Type 1 diabetes is *not* a reportable disease here, and we have no incidence statistics, only things like “this town has not gotten any bigger than it used to be but we never had a pediatric endocrinologist in the past, and now we have two and you can’t get appointments with them they are so busy” and “When I was a teacher I never remember any kids with Type 1 diabetes and now I am a principal and it seems like there are a lot.”

Temporal changes in the frequencies of HLA genotypes in patients with Type 1 diabetes-indication of an increased environmental pressure?

The incidence of Type 1 diabetes has increased 2.5 times during the time period from 1966 to 2000 in Finland-a general trend seen in almost all developed countries that can only be explained by environmental
factors. The aim of this study was to test the possible effect of a changing environment on distribution of genotypes associated with disease susceptibility.

METHODS. HLA DRB1-DQA1-DQB1 genes and two diabetes-associated polymorphisms at IDDM2 and IDDM12 were analyzed. The frequencies of genotypes were compared between cases diagnosed with childhood-onset Type 1 diabetes during the period of 1939-1965 ( n=367) and those diagnosed between 1990 and 2001 ( n=736).

Chi-square statistics or the Fisher’s Exact test were used for the comparison of frequencies of analyzed haplotypes and genotypes in the two groups.

RESULTS. The frequencies of ( DR3) -DQA1*05-DQB1*02 and ( DR4)

-DQB1*0302 risk haplotypes and the high risk ( DR3)

-DQA1*05-DQB1*02/DRB1*0401-DQB1*0302 genotype were higher while proportion of patients carrying protective haplotypes-( DR15) -DQB1*0602 and ( DR1301)

-DQB1*0603-or protective genotypes was lower in patients diagnosed before 1965 as compared to those who developed disease after 1990.

No temporal variation was found in the frequencies of genotypes at IDDM2 and IDDM12.

CONCLUSION/INTERPRETATION.

Our data suggest that the need for genetic susceptibility to develop Type 1 diabetes has decreased over time due to an increasing environmental pressure and this results in a higher disease progression rate especially in subjects with protective HLA genotypes.

Sleep is a mystery. Although no one knows exactly why, it’s required for good health. But now, scientists have found a surprisingly clear connection between sleep and a healthy body: the regulation of sugar levels in the blood.

The new studies, all online December 7 in Nature Genetics, describe the first genetic link between sleep and type 2 diabetes, a disease marked by high blood sugar levels.

In the United States, the number of people with type 2 diabetes is increasing, according to a 2006 paper in the journal Circulation; while the average amount people sleep is dwindling, according to a sleep survey by the Centers for Disease Control and Prevention.

The investigations by three international teams of researchers suggest the trends of rising diabetes and falling sleep are linked via a protein that senses the sleep-inducing hormone melatonin. The research places bodily rhythms, including the clock that sets human sleep cycles, squarely in the blood sugar business.

The idea that diabetes is caused by weight is really toxic.  Yes, 80% of people with type 2 are overweight, but 20% aren’t. Just ask the guy I just heard about who just went on dialysis after experiencing diabetic kidney
failure because no one ever suspected he had type 2 diabetes since he wasn’t fat.

The kidney failure was the first symptom of his diabetes. No one ever tested him for it until it happened. Now his siblings are all testing diabetic too–even the skinny ones–so they can’t donate. None of them had a clue they had a problem because they weren’t fat.

The real problem here is that doctors define “diabetes” with numbers so high that you can be so-called “normal” by many doctors if you have a fasting blood sugar of 124 mg/dl, are spiking up to 199 mg/dl after each meal, and have an hba1c of 6.9%.  You can delude yourself that is normal, but your beta cells know different.

There was quite a bit of research in the 1970s which suggested that low carbing could push up insulin resistance. There never was a consensus on why. However, that is why if you are low carbing and are scheduled for a Glucose Tolerance Test, you have to go off the low carb diet for a few days. Otherwise the results will be artificially high.

My insulin resistance turned out to be very high after 15 months of serious low carbing. Since I had not had it tested before, it  is unknown whether it had increased after a long stint of low carbing or not.  But I am open to the possibility that it might be.

I have twice now low carbed for significant amounts of time (3 years and 15 months) and then suddenly experienced intense physiological burn out. This past time testing revealed extremely high fasting insulin despite a very low carb intake (and a 5.4 hba1c).

Unfortunately, most of the 1970s research is not available on line except for abstracts so the details of the studies can be very tough to track down.

I would not worry about low carbing increasing IR as long as you are feeling good and not running into weight problems.  For me the sign of increasing IR was that I started to gain weight at the food intake level where I’d been maintaining for a long time, that I started to feel exhausted all the time, and that I was suddenly feeling hungry all the time with normal blood sugar levels while low carbing.  Metformin cleared all these symptoms up even though I ended up eating more, rather than less, carbs with it.

I had cut way back on my Diovan this winter, which may have hastened the process this time since Diovan apparently lowered my insulin resistance. But when I burnt out on low carbing a few years ago after 2.5 years of a tight low carb regimen I wasn’t on any drugs and experienced the identical symptoms.

This seems to be yet another area where it can be a problem for some people and not for others. It is certainly not a reason to avoid low carbing. But if you low carb and start feeling rotten, it’s worth investigation.

There is no better source of information regarding the complications that can accompany medications you take, than your own pharmacist.

Your own physician can direct you to information regarding the diabetes prevention study and whether you can participate. Do be aware that it’s a study – in order to be meaningful, they have to have an equal number of subjects who DO NOT recieve the kind of care they’re studying – and for the subject to know WHICH group they were in – the study group or the control group – would invalidate the study.

That has happened with a number of such studies – patients managed to find out, or simply guessed (often as not, guessed wrong) that they were in the control group, and they refused to continue in the study, or began swapping medications amongst themselves, in an understandable effort to ensure that they at least got “some” of the “good stuff”.

There’ve been instances of researchers accepting bribes of money, property and/or sex for information that should’ve remained confidential. Their research was deemed worthless, and a number of them not only lost their jobs, a few were accused of fraud.  Bottom line: If you are in hopes of being admitted as a test subject, you must not expect to be allowed to choose which study group you’re inserted into.

There have been a couple of studies done, or are currently being done, where they give a person with potential for diabetes small doses of insulin.  The theory being that this will help prevent the disease from kicking in.  I looked into to one of these a while back, with the thought of possibly voluteering my children.  But for a variety of reasons it didn’t happen.

There is a large multi-center research study currently going on to see if diabetes can be prevented.  This study is sponsored by an agency of the federal government.  In San Antonio, Texas,  the program is located at the UT Sch of Medicine.

The study has four arms:  (1) intensive interventions into lifestyle including wt loss and increased exercise with (2) glucophage and a placebo of rezulin plus general advice about wt loss and increased exercise, (3) rezulin and glucophage placebo with the same advice, and finally (4) placebos of both glucophage and rezulin and general advice about wt loss and increased exercise.

The research is expected to continue until about 2002.  This program is actively seeking volunteer  research subjects who are at risk for diabetes, as determined by a family history of diabetes, being overweight, or abnormal glucose tolerance test.

There is a home page about this study.  I don’t have the exact citation but you can locate it using any internet  search engine to look up the words DIABETES PREVENTION PROJECT.  There are many centers of this project throughout the United States.

They are actively recruiting volunteer research subjects who are NOT diabetic but at risk for developing the illness.

To my way of thinking,  using small doses of insulin to prevent diabetes (at least type II diabetes) makes no sense at all to me because many type II diabetes have an EXCESS of natural  insulin already. The problem is that many type II diabetics  can’t use the insulin for some reason or another.  The two medications being used in this research (rezulin and glucophage) make the body better able to utilize the natural insulin that the body already has.

Immune-mediated diabetes (formerly called insulin-dependent diabetes) is a disease that affects the way your body uses food. Immune-mediated diabetes is also called type 1 diabetes.

In type 1 diabetes, your body destroys the cells in the pancreas that produce insulin, usually leading to a total failure to produce insulin. It typically starts in children or young adults who are slim, but can start at any age.

Without insulin, your body cannot control blood levels of sugar. And without insulin, you would die. So people with type 1 diabetes give themselves at least one shot of insulin every day.

An estimated 500,000 to 1 million Americans have this type of diabetes today.

Type 2 diabetes is a disease that affects the way your body uses food.

Type 2 diabetes used to be called non-insulin-dependent diabetes. The most common type of diabetes, it affects about 15 million Americans. Nine out of ten cases of diabetes are type 2.

It usually occurs in people over 45 and overweight, among other factors.

When you have type 2 diabetes, your body does not make enough insulin. Or, your body still makes insulin but can’t properly use it. Without enough insulin, your body cannot move blood sugar into the cells. Sugar builds up in the bloodstream. High blood levels of sugar can cause problems.

Diet has long been believed to be an important risk factor for non-insulin-dependent diabetes. Animal studies generally support a relation between high-fat diets and development of insulin resistance.

However, conclusive epidemiologic evidence is lacking. To further investigate the role of dietary fat and carbohydrate as potential risk factors for the onset of non-insulin-dependent diabetes mellitus, current diet was assessed among a geographically based group of 1,317 subjects without a prior diagnosis of diabetes who were seen in the period from 1984 to 1988 in two countries in southern Colorado.

In this study, 24-hour diet recalls were reported prior to an oral glucose tolerance test. Persons with previously undiagnosed diabetes (n = 70) and impaired glucose tolerance (n = 171) were each compared with confirmed normal controls (n = 1,076). The adjusted odds ratios relating a 40-g/day increase in fat intake to non-insulin-dependent diabetes mellitus and impaired glucose tolerance were 1.51 (95% confidence interval 0.85-2.67) and 1.62 (95% confidence interval 1.09-2.41), respectively.

Restricting cases to diabetic persons with fasting glucose greater than 140 mg/dl and persons with impaired glucose tolerance confirmed on follow-up, the odds ratios increased to 3.03 (95% confidence interval 1.07-8.62) and 2.67 (95% confidence interval 1.33-5.36), respectively. The findings support the hypothesis that high-fat, low-carbohydrate diets are associated with the onset of non-insulin-dependent diabetes mellitus in humans.

Diabetes is defined as having certain levels of blood sugar, either fasting or postprandial.

The underlying process for diabetes is decline in capacity to properly metabolize carbs. This capacity declines with age in persons with propensity towards diabetes, until finally they are unable to handle carbs that they eat and show high levels of BG, at which point a diabetes diagnosis is made.

Now, consider two pre-diabetic twin brothers, Abraham and Benjamin, whose carb handling capacity declines exactly the same over time.

Then, Abraham decides to “go on a diet, eat less and exercise”, and Benjamin does not go on a diet.

Then, as Abraham and Benjamin’s carb capacity declines, Benjamin finally shows diabetic blood sugars. Abraham is now slimmer, is “eating less” than Benjamin, so, even though he has same capacity as Benjamin, he is not straining that capacity as much. So, Benjamin is declared diabetic and Abraham celebrates that he has “prevented diabetes”.

In reality, Abraham has not prevented anything and is postponing his high blood sugar until such time as his loss of carb capacity catches up with his lower weight and lower calorie needs. That’s good for him, as he is able to enjoy slim life and postpone diabetic complications. What I want to say is that there is no genuine “diabetes prevention” here.

Does it make sense?

If so, then, the three year diabetes prevention trial does not really show that diabetes prevention is possible, as it claimed. It is a valuable study, but perhaps it makes too far reaching conclusions.

Possibly, all that weight loss and exercise does, is buy us a few valuable years. People who are doing Atkins for life, can probably even find that out numerically, by tracking the change in the level of carbs that they can eat without regaining weight and without blood sugar swings. If this level needs to be adjusted downward periodically, then can extrapolate the trend and see when it gets low enough.