Managing and Understanding Diabetes

Millions of people have diabetes and almost all of them first had a condition known as pre-diabetes.

Now, federal medical researchers have discovered a simple tool to alert doctors that a patient is at risk for pre-diabetes and on the path to the full disease.

The tool is simple and costs nothing. A patient is administered an oral glucose tolerance test and the time it takes to reach maximum sugar level is recorded. Those who take longer to reach that maximum threshold are at greater risk of pre-diabetes, the researchers found.

“Our research may help clinicians and public health officials guide patients to better and more cost-effective decisions about risk for pre-diabetes” said Stephanie Chung, M.B.B.S., the study’s first author and an assistant clinical investigator at the National Institute of Diabetes and Digestive and Kidney Diseases, which is part of the National Institutes of Health (NIH).

The implications

The implications are fairly clear. By giving the glucose test and noting the time to reach maximum levels, doctors can get a heads-up that the patient is at risk for developing pre-diabetes, placing them at even greater risk of developing type-2 diabetes.

Simply put, having pre-diabetes means your blood sugar level is higher than normal but not yet high enough to be type-2 diabetes. It's not a given that pre-diabetes turns into full-blown type-2 diabetes, but it happens a lot.

However, with significant lifestyle changes – eating a nutritious diet and getting plenty of exercise – a patient can return his or her blood glucose levels to normal. In fact, there have been cases where people with type-2 diabetes have actually reversed the disease with radical lifestyle changes.

Early damage

However, the Mayo Clinic warns that if you have developed pre-diabetes, you may already be suffering the long-term damage of diabetes.

Unfortunately, pre-diabetes has no obvious symptoms. However, Mayo Clinic doctors say subtle signs include darkening skin in certain parts of the body. You may be at risk for pre-diabetes if you are overweight, eat an unhealthy diet, and get little exercise.

Type-2 diabetes is a serious condition. It's triggered when your body starts having trouble using insulin, which transports glucose into cells. When that happens you are at risk of building up too much glucose in your blood.

There's a lot of talk about the high cost of health care, but do you know which conditions contribute most to health care spending?

If you said diabetes, you're right -- a new study finds diabetes costs $101 billion annually in diagnosis and treatment and is growing 36 times faster than the cost of heart disease, the leading cause of death and the second most-expensive condition. 

"While it is well known that the US spends more than any other nation on health care, very little is known about what diseases drive that spending." said Dr. Joseph Dieleman, lead author of a paper published in JAMA and Assistant Professor at the Institute for Health Metrics and Evaluation (IHME) at the University of Washington. "IHME is trying to fill the information gap so that decision-makers in the public and private sectors can understand the spending landscape, and plan and allocate health resources more effectively."

In fact, the study found that just 20 conditions make up more than half of all spending on health care in the United States.

While diabetes and heart disease primarily affected consumers 65 and over, lower back and neck pain, the third-most-expensive condition, primarily strikes adults of working age.

These three top spending categories, along with hypertension and injuries from falls, comprise 18% of all personal health spending and totaled $437 billion in 2013.

This study distinguishes between spending on public health programs from personal health spending, including both individual out-of-pocket costs and spending by private and government insurance programs. It covers 155 conditions.

$2.4 trillion

In addition to the $2.1 trillion spent on the 155 conditions examined in the study, Dr. Dieleman estimates that approximately $300 billion in costs, such as those of over-the-counter medications and privately funded home health care, remain unaccounted for, indicating total personal health care costs in the US reached $2.4 trillion in 2013.

Other expensive conditions among the top 20 include musculoskeletal disorders, such as tendinitis, carpal tunnel syndrome, and rheumatoid arthritis; well-care associated with dental visits; and pregnancy and postpartum care.

Other key findings include:

• Women ages 85 and older spent the most per person in 2013, at more than $31,000 per person. More than half of this spending (58%) occurred in nursing facilities, while 40% was expended on cardiovascular diseases, Alzheimer's disease, and falls.
• Men ages 85 and older spent $24,000 per person in 2013, with only 37% on nursing facilities, largely because women live longer and men more often have a spouse at home to provide care.
• Less than 10% of personal health care spending is on nursing care facilities, and less than 5% of spending is on emergency department care. The conditions leading to the most spending in nursing care facilities are Alzheimer's and stroke, while the condition leading to the most spending in emergency departments is falls.
• Public health education and advocacy initiatives, such as anti-tobacco and cancer awareness campaigns, totaled an estimated $77.9 billion in 2013, less than 3% of total health spending.

Top 10 diseases

The top 10 most costly health expenses in 2013 were:

1. Diabetes - $101.4 billion

2. Ischemic heart disease - $88.1 billion

3. Low back and neck pain - $87.6 billion

4. Hypertension - $83.9 billion

5. Injuries from falls - $76.3 billion

6. Depressive disorders - $71.1 billion

7. Oral-related problems - $66.4 billion

8. Vision and hearing problems - $59 billion

9. Skin-related problems, such as cellulitis and acne - $55.7 billion

10. Pregnancy and postpartum care - $55.6 billion

Oftentimes, scientists and medical experts need to look at the most minute details in order to understand the human body and the diseases that affect it. And since technology in the field is advancing all the time, they are able to do it to a greater degree.

In that vein, new research on how the body produces insulin may allow future therapies to evolve that better treat diabetes. Dr. Markus Grompe, who is best known for his work with stem cells, has found that there are at least four subtypes of insulin-producing beta cells in humans. It is the first study of its kind that has identified multiple types of such cells, and the information could mean a lot.

“Further understanding of cell characteristics could be the key to uncovering new treatment options, as well as the reason why some people are diabetic and others are not,” explained Grompe.

Identifying new cell types

Diabetes currently affects over 29 million people in the U.S. alone, and it occurs when a person’s insulin-producing beta cells are disrupted or cease to function. Without these cells doing their job, a person loses their ability to regulate their blood sugar levels, which can result in extreme fatigue, weight loss, vision ailments, pain in the extremities, and nerve damage, to name a few.

Up until this point, the medical community had thought that only one type of beta cell existed, but Grompe and his colleagues were able to isolate beta cells and classify three additional types.

Additionally, they found that there are hundreds of genes that differently express cell types, which leads to varying production of insulin in the body. The differences between these genes and cells could explain the differences between the types of diabetes and why certain people are susceptible to them.

“Some of the cells are better at releasing insulin than others, whereas others may regenerate quicker. Therefore, it is possible that people with different percentages of the subtypes are more prone to diabetes,” Grompe explains.

The next step for the researchers will be to attempt to understand how different cell subtypes are created so that they can create an approach for medical treatment. The full study has been published in the journal Nature Communications. 

Over 29 million people in the U.S. have diabetes, and over eight million who have it are undiagnosed, according to a 2014 statistical analysis. Although the disease affects so many, it has been hard for scientists and researchers to nail down a cure. This is due, in part, to the fact that the disease can take different forms, and there are still some things that researchers do not know about them.

However, a recent study conducted at the University of Pennsylvania has shed some light on type 2 diabetes. Researchers at the Perelman School of Medicine believe that they have finally found the cause of insulin resistance, which is characteristic of this particular type of the disease.

Excess fat

Many people attribute insulin resistance to fluctuating sugar levels in the body, but researchers say that it also has to do with the amount of fat in the body. In particular, too much fat inside of skeletal muscle is one main cause of insulin resistance.

With this in mind, scientists went about trying to find out how excess fat could be removed from skeletal muscle. If this fat could be removed, they reasoned, then it would also be possible to prevent insulin resistance from occurring. But in order to do that, there were some questions that had to be answered first.

“This research sought to answer a few large questions. . . How does fat get into skeletal muscle? And how is the elevation of certain amino acids in people with diabetes related to insulin resistance?” asked Dr. Zoltan Arany, senior author of the study. “We have appreciated for over ten years that diabetes is accompanied by elevations in the blood of branched-chain amino acids, which humans can only obtain in their diet. However, we didn’t understand how this could cause insulin resistance and diabetes. How is elevated blood sugar related to these amino acids?”

New way to treat diabetes

In order to answer these questions, Dr. Arany and his team began examining amino acids and what happened when they broke down. They found that when these compounds broke down, a byproduct called 3-HIB was created. After being secreted by muscle cells, 3-HIB activated certain cells which resulted in more fat being stored in skeletal muscle tissue.

Researchers observed this phenomenon in mice and saw that when it happened it led to insulin resistance. By blocking 3-HIB from synthesizing, researchers were able to keep excess fat from going to the skeletal muscle and insulin resistance was no longer a problem.

Dr. Arany is quick to note that 3-HIB byproducts are also plentiful in humans who have type-2 diabetes, so although there will need to be more research to prove that there is a link, he is confident that one may be discovered in the future.

“The discovery of this novel pathway – the way the body breaks down these amino acids that drives more fat into the muscles – opens new avenues for future research on insulin resistance, and introduces a conceptually entirely new way to target treatment for diabetes,” he said.

The full study has been published in Nature Medicine. 

Smartphones may soon be able to add one more entry to their rolodex of skills: the ability to act as a tool to measure blood glucose levels for those suffering from Type 1 diabetes.

After 20 years of research, University of Virginia School of Medicine researchers are in the final testing phases of a system that can automatically measure and monitor blood sugar levels. Early testing produced promising results. Now, researchers say actual patient testing is going well, and the system is circling the landing towards completion.

The app—called “InControl”—can control everything people with diabetes need, eliminating the need for finger pricks and manual insulin injections. This ease of the system could prove to be a game-changer in the lives of 1.25 million people who suffer from the disease.

Effortlessly manages levels

The so-called “artificial pancreas” has been in the works since 2006, says lead researcher Boris Kovatchev, director of the Centre for Diabetes Technology in the US. 

Kovatchev’s own father suffered from diabetes, so he saw firsthand the need for an easier way to live with the disease. “We show that it is not only possible, but it can run on a smartphone,” says Kovatchev.

Every five minutes, the system will report blood glucose level results to the app on a nearby android smartphone. It will analyze the data, and if necessary, adjust insulin levels on a small, wearable insulin pump.

Wirelessly controls pump

The app works by controlling an insulin pump: a device which is already used by approximately 350,000 diabetes sufferers in the US. The pump works by delivering user-adjusted doses of insulin to the bloodstream through a very fine needle; it can be worn discreetly under an article of clothing or hooked to a belt.

The wireless monitor, which talks to the pump, is as tiny as a flash drive and can be worn anywhere on the body. Together, the two devices create a digital treatment ecosystem of sorts that can handle the burden of the disease.

"It runs on a five-minute cycle and takes information from these devices and calculates the next best option for the patient pretty much any point in time,” said Chad Rogers, the CEO of TypeZero Technologies, which has licensed and refined the technology.

Final phases of testing 

The ultimate goal is to make managing Type 1 diabetes automatic and effortless.

“If it is working, you do not know that it is there,” says Francis Doyle III, dean of Harvard’s Paulson School of Engineering and Applied Sciences, who is collaborating with Kovatchev on the system

UVA researchers have brought the system to nine locations across the U.S. and Europe to try it on 240 patients. Researchers hope to have the trials complete and the system perfected in four years.

In the last decade there has been an explosion in the number of type 2 diabetes cases, coinciding with a massive rise in obesity.

The disease is a long-term condition caused by too much glucose, a type of sugar, in the blood.

Now, researchers at Newcastle University in the UK say they have found a simple way to reverse it; lose weight.

After a small trial, the scientists have concluded that reducing the amount of fat around the pancreas in type 2 diabetes patients returns organ functions to normal. They say this shows that the excess fat in the diabetic pancreas is specific to type 2 diabetes and important in preventing insulin from being made.

When that excess fat is removed, insulin secretion increases to normal levels. In other words, they were diabetes free.

Previous research

This isn't the first study to suggest weight loss might reverse type 2 diabetes. Last year, researchers at the Cleveland Clinic found that bariatric surgery – reducing the size of the stomach so the patient loses weight – appeared to be effective in reversing diabetes.

Meanwhile, like most chronic diseases, type 2 diabetes is treated with drugs, including the newly approved Jardiance.

Roy Taylor, a professor at Newcastle University, says losing weight simply helps patients with type 2 diabetes drain excess fat out of the pancreas, and that allows function to return to normal.

One gram of pancreas fat

“So if you ask how much weight you need to lose to make your diabetes go away, the answer is one gram. But that gram needs to be fat from the pancreas,” Taylor said. “At present the only way we have to achieve this is by calorie restriction by any means – whether by diet or an operation.”

In the trial, type 2 diabetes patients saw the fat levels in their pancreas decrease by as much as 1.2% over eight weeks. With an average pancreas for a person with Type 2 diabetes having a volume of 50 ml, this is the equivalent of around 0.6 grams of fat.

The patients who had never had diabetes experienced no change in the level of fat in their pancreas. That told the scientists that the increase in fat in the pancreas is specific to people who develop type 2 diabetes.

The fat in the pancreas may, in fact, be a trigger for the disease, and individuals vary in how much fat they can tolerate in the pancreas before type 2 diabetes develops.

What to do

Taylor says the research may transform the thinking about type 2 diabetes and its treatment.

Keep in mind, this is a report of research findings. It should not be used by patients to make unilateral decisions about their care or to start or stop prescribed medications.

If you have concerns about type 2 diabetes treatments, you should discuss them with your doctor, mentioning this study. 

Diabetes comes in a variety of different forms. The most common form of the disease, type 2 diabetes, results from cells in the body not using insulin as well as they should. Type 1 diabetes (T1D), however, is much rarer, and results when the body simply can’t produce its own insulin at all. People who have this condition must take part in insulin therapy and other treatments in order to live a full and healthy life.

Scientists from Uppsala University have investigated the disease thoroughly, and believe that a certain protein found in the body could potentially provide a cure.

The protein in question is called interleukin-35 (IL-35), and it is made of immune cells. Dr. Kailash Singh, who is a PhD student at Uppsala University, began studying this immune cell when she was examining T1D in rat models. In her research, she found that immune regulatory T-cells in the models were producing pro-inflammatory destructive proteins instead of IL-35, which is an anti-inflammatory protein.

This reversal is the exact opposite of what should be happening in a normal body, and Singh believes that it may be something that is prompted by T1D.

“This suggests that the good guys (the anti-inflammatory proteins) have gone bad in early development of Type 1 diabetes and therefore our immune cells destroy the beta cell,” she said.

Crucial protein

As a result of this destructive process, Singh found that the levels of IL-35 that should have been present in the models were much lower than they should be. These low levels indicate that the protein may play a crucial role in stopping T1D.

The research team that Singh was a part of, which was led by Professor Stellan Sandler, set out to find if IL-35 could suppress or reverse T1D, even if the disease was already established. The team utilized mice who had been injected with a chemical that induced symptoms of T1D. After the symptoms had been established for two days, the researchers injected them with IL-35 to see if their blood glucose levels normalized.

Their findings show that the blood glucose levels in the mouse models stabilized after they were given the injections. In addition to this finding, the researchers were also able to test IL-35 injections against a specific model of T1D, called non-obese diabetic mouse (NOD). Even after the IL-35 treatments were stopped, diabetic symptoms did not return in any of the subjects.

Unique insights 

"To the best of our knowledge, we are the first to show that IL-35 can reverse established Type 1 diabetes in two different mouse models and that the concentration of the particular cytokine is lower in Type 1 diabetes patients than in healthy individuals. Also, we are providing an insight into a novel mechanism: how immune regulatory T cells change their fate under autoimmune conditions", said Singh.

The full study has been published in Scientific Reports.