Damping Down Diabetes

PrevalenceSRxA’s Word on Health was very excited to learn of some amazing new research coming out of UC San Francisco.  Scientists there have identified a new way to manipulate the immune system and keep it from attacking the body’s own molecules in autoimmune diseases such as type 1 diabetes, rheumatoid arthritis and multiple sclerosis.

More than 100 different autoimmune diseases have been discovered and they disproportionately affect women.  Of the 50 million Americans living and coping with autoimmune disease  more than 75% are women.  Autoimmune diseases are one of the top 10 leading causes of death of women under the age of 65 and are responsible for more than $100 billion in direct health care costs annually.   Crohn’s disease, ulcerative colitis, lupus, multiple sclerosis, rheumatoid arthritis, psoriasis and scleroderma by themselves account for > $50 billion.

eTACBut now, researchers, led by immunologist Mark Anderson, MD, PhD, a professor with the UCSF Diabetes Center, have discovered a type of immune cell called an extrathymic Aire-expressing cell (eTAC), which puts a damper on immune responses.  eTAC’s are a type of  dendritic cell – which make up less than 3% of the cells in the immune system. And, eTAC cells themselves account for a small fraction of all dendritic cells. eTACs reside in lymph nodes and spleen in both humans and mice.

In this study, Anderson’s team determined that eTAC’s can counteract the overactive immune response in autoimmune diseases and, in a mouse model of diabetes, can be manipulated to stop the destruction of the pancreas.

By displaying “self” molecules to T cells that target them, and permanently turning off these T cells, eTACs help the immune system tolerate the molecules naturally present within us.  “The mouse model we are working with involves using T cells that normally attack the islet cells of the pancreas, specifically by recognizing a molecule called chromagranin A that is present on islet cells,” Anderson said. “But if the eTACs can get to the T cells first and display chromagranin A, they can prevent T cells from attacking the islets.”

mouse diabetesAnderson aims to exploit eTACs therapeutically by finding out how to grow them in large numbers outside the body. “We need to figure out how to grow a lot of these cells, to load them up with whatever molecule it is that we want to induce tolerance to, and then to load them back into a patient,” he said. “Such a strategy could help selectively shut down an unwanted immune response, such as the anti-islet immune response in type 1 diabetes.”

Dendritic cells work with T cells a bit like a sheriff working with a bloodhound.  But instead of presenting an article of clothing, dendritic cells present a specific molecule. If the molecule displayed by the dendritic cell matches the one the T cell was born to target, then that T cell would be activated to expand its numbers and to attack cells or tissues where the molecule is present.

When the interaction is between eTACs and T cells, however, the targeted T cell instead is turned off forever, and never seeks its molecular prey.

Diabetes wordcloudGiven that the prevalence and incidence of and type 1 diabetes and other autoimmune diseases, such as Crohn’s, lupus and celiac disease are on the rise, this new research is extremely important, both from a public health and economic perspective.  With as many as three million Americans having type one diabetes and the incidence growing by more than 3% per year a cure is desperately needed.

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Lift Weights to Lower Blood Sugar?

Red-White_muscleSRxA’s Word on Health was interested to read that researchers in the Life Sciences Institute at the University of Michigan have overturned a long-held belief that whitening of skeletal muscle in diabetes is harmful.  Instead, they found that the white muscle that increases with resistance training, age and diabetes actually helps to keep blood sugar in check.

The insights identified in the study may point the way to potential drug targets for obesity and metabolic disease.

We wanted to figure out the relationship between muscle types and body metabolism, how the muscles were made, and also what kind of influence they have on diseases like type 2 diabetes,” said Jiandie Lin, Life Sciences Institute faculty member.

Much like poultry has light and dark meat, mammals have a range of muscles: red, white and those in between. Red muscle, which gets its color in part from mitochondria, prevails in people who engage in endurance training, such as marathon runners. White muscle dominates in the bodies of weightlifters and sprinters – people who require short, intense bursts of energy.

lifting-weightsWhen you exercise, nerves signal your muscles to contract, and the muscle needs energy. In response to a signal to lift a heavy weight, white muscles use glycogen to generate adenosine triphosphate (ATP) – energy the cells can use to complete the task. While this process can produce a lot of power for a short time, the glycogen fuel soon depletes.

However, if the brain tells the muscle to run a slow and steady long-distance race, the mitochondria in red muscles primarily use fat oxidation instead of glycogen breakdown to generate ATP. The supply of energy lasts much longer but doesn’t provide the burst of strength that comes from Paula_Radciffe_NYC_Marathon_2008_croppedglycolysis.

People with diabetes see whitening of the mix of muscle.

For a long time, the red-to-white shift was thought to make muscle less responsive to insulin, a hormone that lowers blood sugar,” Lin said. “But this idea is far from proven. You lose red muscle when you age or develop diabetes, but is that really the culprit?”

To find out, the team set out to find a protein that drives the formation of white muscle. They identified a list of candidate proteins that were prevalent in white muscle but not in red.

mouse weight liftingFurther studies led the team to focus on a protein called BAF60c, a sort of “zip code” mechanism that tells the cells when and how to express certain genes. The Lin team made a transgenic mouse model to increase BAF60c only in the skeletal muscle. One of the first things they noticed was that mice with more BAF60c had muscles that looked paler.

“That was a good hint that we were going in the white-muscle direction,” said lead author Zhuo-xian Meng, a research fellow in Lin’s lab.

They used electron microscopy to see the abundance of mitochondria within the muscle, and confirmed that muscle from BAF60c transgenic mice had less mitochondria than the normal controls.

We saw predicted changes in molecular markers, but the ultimate test would be seeing how the mouse could run,” Lin said.

treadmill mouseIf the BAF60c mice could run powerfully for short distances but tired quickly, the scientists would be able to confirm that the BAF60c pathway was a key part of the creation of white muscle.

Using mouse treadmills, they compared the endurance of BAF60c mice to a control group of normal mice, and found that the BAF60c transgenic mice could only run about 60% of the time that the control group could before tiring.

“White muscle uses glycogen, and the transgenic mice depleted their muscles’ supplies of glycogen very quickly,” Lin said.

After some follow-up experiments to figure out exactly which molecules were controlled by BAF60c, Lin and his team were confident that they had identified major players responsible for promoting white muscle formation.

Now that they knew how to make more white muscle in animals, they wanted to determine whether white muscle was a deleterious or an adaptive characteristic of diabetes.

obese mouseThe team induced obesity in mice by feeding them a “Super Size Me” mouse diet. On a high-fat diet, a mouse will double its body weight in two to three months. They found that obese mice with BAF60c transgene were much better at controlling blood glucose.

The results are a bit of a surprise to many people,” Lin said. “It really points to the complexity in thinking about muscle metabolism and diabetes.”

In humans, resistance training promotes the growth of white muscle and helps in lowering blood glucose. If future studies in humans determine that the BAF60c pathway is indeed the way in which cells form white muscle and in turn optimize metabolic function, the finding could lead to researching the pathway as a drug target.

We know that this molecular pathway also works in human cells. The real challenge is to find a way to target these factors,” Lin said.

Until we know for sure SRxA’s Word on Health recommends a healthy mix of running and weight training.

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Tick-Tock, Tick-Tock. Understanding your food clock!

food-clock 2If the excesses of holiday eating have sent your system into butter-slathered, alcohol-soaked overload, you are not alone. People with jet-lag, those who work graveyard and 24 hour shifts and even late-night snackers know just how you feel.

Turns out that all these activities upset the body’s “food clock”  – a collection of interacting genes and molecules which keep the human body on a metabolically even keel. Look behind the face of a mechanical clock and you will see a dizzying array of cogs, flywheels, counterbalances and other moving parts.

Biological clocks are equally complex, composed of multiple interacting genes that turn on or off in an orchestrated way to keep time during the day. In most organisms, biological clockworks are governed by a master clock, referred to as the ‘circadian oscillator,’ which keeps track of time and coordinates our biological processes with the rhythm of a 24-hour cycle of day and night.

Scientists also know that in addition to the master clock, our bodies have other clocks operating in parallel throughout the day. food clock 1One of these is the food clock, which is not tied to one specific spot in the brain but rather multiple sites throughout the body. The food clock is there to help our bodies make the most of our nutritional intake. It controls genes that help in everything from the absorption of nutrients to their dispersal through the bloodstream. It’s also designed to anticipate our eating patterns. Even before a meal, our bodies begin to turn on some of these genes and turn off others, preparing for the burst of sustenance – which is why we feel the pangs of hunger just before our lunch hour.

And while scientists have known that the food clock can be reset over time if a person changes their eating patterns, very little was known about how the food clock works on a genetic level.

Until now!  A new study by researchers at the University of California, San Francisco published in Proceedings of the National Academy of Sciences, is helping to reveal how this clock works on a molecular level. The study showed that normal laboratory mice given food only during their regular sleeping hours will adjust their food clock over time and begin to wake up from their slumber, and run around in anticipation of their new mealtime. But mice lacking a certain gene (PKCγ) are not able to respond to changes in their meal time and instead sleep right through it.

The work has implications for understanding diabetes, obesity and other metabolic syndromes because a desynchronized food clock may serve as part of the pathology underlying these disorders.

food_clock_3It may also help explain why night owls are more likely to be obese than morning larks,” says Louis Ptacek, MD, Distinguished Professor of Neurology at UCSF. “Understanding the molecular mechanism of how eating at the “wrong” time of the day desynchronizes the clocks in our body can facilitate the development of better treatments for disorders associated with night-eating syndrome, shift work and jet lag.”

All of which is potentially good news for this sleep-deprived, word-traveler, up-all-night-on-the-ambulance, always-on-a-diet blogger! SRxA-logo for web

Dance Away Diabetes

As anybody who’s been following the news over the last year or so will know, there is a growing epidemic among American children – type 2 diabetes.

It’s a problem that is both confronting and confounding more doctors, families, and health care professionals every day.

Until 15 years ago, type 2 diabetes was never seen in young people. Now it’s occurring with alarming frequency. And, type 2 diabetes appears to be more aggressive in young people between the ages of 10 and 17, putting them at great risk for life-threatening illnesses typically associated with seniors. Doctors know that a major risk factor is obesity. Beyond that, they are mostly in the dark.

Worse still, the standard treatment for type 2 diabetes in children is ineffective because metaformin – a drug which is effective in adults, has a high failure rate among children.

When it comes to preventing type 2 diabetes, more exercise and a healthier diet are key but doctors know young peoples’ habits are tough to change.

Which is why SRxA’s Word on Health was interested to learn of the “Dance for Health” program being pioneered by Professor Terri Lipman, a nurse practitioner and professor of pediatric nursing at the University of Pennslvania.  Dance for Health encourages children and adults to ward off the disease and hip-hop their way to good health.

Penn Nursing has partnered with Philadelphia’s Sayre High School and the Bernett Johnson Sayre Health Center to assess and improve physical activity among school-aged children, with the goal of lowering the risk for obesity.

Busting cool moves across a wooden gym floor, the Sayre High School dance team led children through one hour of dancing weekly for one month. Using pedometers, the research team found that the students averaged twice as many steps on days they danced.

At the same time, researchers noted that the children had elevated resting heart rates after exercise, indicating that they were not physically fit. Dance for Health aims to change that.

Dancing is not only free, culturally relevant, and fun,” says Dr. Lipman, “it is also an easily accessible way for children to lead a more active lifestyle. Through this program, we aim to promote to schools and healthcare providers the benefits of incorporating dance into children’s lives to improve their overall health.”

The partnership between Penn Nursing and Sayre High School has yielded other benefits. Dr. Lipman now hosts weekly evening dance classes for children and adults ages 5 to 91!

At the same time, they are educating the neighboring community, demographically at high risk for diabetes, about prevention through good nutrition, exercise, and recognition of warning signs. In addition to taking basic measurements such as weight, height, and waist circumference, the students also check for acanthosis nigricans, a darkening of the skin associated with obesity and diabetes.

Our partnership with Sayre has opened the door to a strong relationship with residents of the community around Penn,” says Dr. Lipman. “It has allowed us to work with individuals, schools, and community groups to fight diabetes together.”

Do you know of any similar initiatives?  Ballroom Dance for bulimics?!? Samba for stroke?!? Share your stories with us.

The Peak Time for Everything

Not enough hours in your day?  So much to do…so little time?  If you’re anything like me, these will be familiar expressions.

And in which case, you should be interested to learn that maybe, just maybe, you could pack more into each day if you did everything at the optimal time?

A growing body of research suggests that paying attention to your body clock, and its effects on energy and alertness, can help pinpoint the different times of day when it’s best to perform at specific tasks.

Most people organize their time around everything but the body’s natural rhythms.

But workday demands such as commuting, social events and kids’ schedules inevitably end up clashing with the body’s natural circadian rhythms of waking and sleeping.

And as difficult as it may be to align your schedule with your body clock, it may be worth a try, because there are significant potential health benefits.

Disruption of circadian rhythms has been linked to problems such as diabetes, depression, dementia and obesity.

When it comes to doing cognitive work, for example, most adults perform best in the late morning, says Dr. Steve Kay, a professor of molecular and computational biology at the University of Southern California.  As body temperature starts to rise just before awakening in the morning and continues to increase through midday, working memory, alertness and concentration gradually improve. Taking a warm morning shower can jump-start the process.

The ability to focus and concentrate typically starts to slide soon thereafter. Most people are more easily distracted from noon to 4 p.m.

Alertness tends to slump after eating a meal, and sleepiness tends to peak around 2 p.m.  But you may want to rethink taking a nap at your desk.  It turns out, somewhat surprisingly, that fatigue may boost creative powers.

For most adults, problems that require open-ended thinking are often best tackled in the evening when they are tired. According to a 2011 study when students were asked to solve a series of two types of problems, requiring either analytical or novel thinking, their performance on the second type was best when they were tired.

Mareike Wieth, an assistant professor of psychological sciences at Albion College in Michigan who led the study says, “Fatigue may allow the mind to wander more freely to explore alternative solutions.”

Of course, not everyone’s body clock is the same. Morning people tend to wake up and go to sleep earlier and to be most productive early in the day. Evening people tend to wake up later, start more slowly and peak in the evening.

Communicating with friends and colleagues online has its own optimal cycles, research shows. Sending emails early in the day helps beat the inbox rush.  6 a.m. messages are most likely to be read.

Reading Twitter at 8 a.m. or 9 a.m. can start your day on a cheery note. That’s when users are most likely to tweet upbeat, enthusiastic messages, and least likely to send downbeat tweets steeped in fear, distress, anger or guilt.

Other social networking is better done later in the day. If you want your tweets to be re-tweeted, post them between 3 p.m. and 6 p.m., when many people lack energy to share their own tweets and turn to relaying others’ instead. And posts to Facebook  at about 8 p.m. tend to get the most “likes,” after people get home from work or finish dinner.

When choosing a time of day to exercise, paying attention to your body clock can also improve results. Physical performance is usually best, and the risk of injury least, from about 3 p.m. to 6 p.m.

Muscle strength tends to peak between 2 p.m. and 6 p.m. as does lung function which is almost 18% more efficient at 5 p.m. than at midday.

Is there a best time to eat? Experts suggest limiting food consumption to hours of peak activity to keep from packing on pounds.  Perhaps we are not only what we eat, we are when we eat!

Apples, Pears & Risk of Death

Are you an apple or a pear? Could your big belly shorten your life?

Conventional wisdom tells us that the shape of our body and where we store fat can drastically alter our health outlook. For example, apple shapes – people who carry their weight around their middles – have long been thought to have a higher risk for heart disease and type 2 diabetes, when compared to the general population. But recent research suggests that this risk might be overstated and that excess fat anywhere on the body raises disease risk equally.

Body mass index (BMI), the most commonly accepted measure of obesity, has long been criticized because it doesn’t take into account body composition. Because it only uses height and weight, it can classify muscular people as overweight or obese.

So a father-son team of researchers from New York have come up a new tool – the A Body Shape Index (ABSI).

This formula takes into account waist circumference (WC), BMI, and height.

In a study of  more than 14,000 adults, above average ABSIs correlated with a higher risk of premature death — even when adjusted for risk factors like smoking, diabetes, hypertension, and cholesterol. Regardless of age, gender, BMI, and ethnicity, elevated death rates were found for both high and low BMIs and WCs.  This led the researchers to conclude that both measures are inaccurate for predicting premature death risk.

Measuring body dimensions is straightforward compared to other most medical tests, but it’s been challenging to link these with health,” says researcher Nir Krakauer, assistant professor in the department of civil engineering at the City College of New York.

The bottom line of all this?  It’s not just belly fat that can kill you, excess pounds anywhere can have an adverse effect on health.

However, before you throw in the towel or start ordering your coffin, other studies suggest you shouldn’t worry if have a bit of junk in the trunk!  According to new research from Oxford University, fat in the thighs and buttocks might actually help protect you from metabolic disease and a Danish study even found that people with thin thighs have a greater risk of premature death.

What’s your body shape, and how do you feel about it? We look forward to hearing from you.

Diabetes Drug may Repair Injured Brains

Here’s a good brain teaser for a Wednesday.  What do an old diabetes drug, brain injury and Alzheimer’s Disease have in common?

Here’s some clues to help you solve the riddle.

(i)           Metformin is a widely used treatment for type II diabetes

(ii)          An increasing proportion of people with Alzheimer’s Disease also have diabetes

(iii)         Hyperinsulinemia (excess levels of insulin in the blood) may enhance the onset and progression of neurodegeneration

Have you solved it?  If so, congratulations!

If not, the answer, according to data just published in the journal Cell Stem Cell is that the former may hold the clue to treating the latter.

In other words, the study suggests that metformin, an anti-diabetes drug first discovered in the 1920’s, is able to help activate the mechanism that signals stem cells to generate brain cells.

Principal investigator, Freda Miller, a Professor from the Department of Molecular Genetics at the University of Toronto
says “If you could take stem cells that normally reside in our brains and somehow use drugs to recruit them into becoming appropriate neural cell types, then you may be able to promote repair and recovery in at least some of the many brain disorders and injuries for which we currently have no treatment.”

The research involved laboratory experiments using both mouse and human brain stem cells, as well as learning and memory tests performed on live mice given the drug.

Miller and her colleagues started by adding metformin to stem cells from the brains of mice, then repeated the experiment with human brain stem cells generated in the lab. In both cases, the stem cells gave rise to new brain cells.

They then tested the drug in lab mice and found that those given daily doses of metformin for two or three weeks had increased brain cell growth and outperformed rodents not given the drug in learning and memory tasks.

In the key experiment, mice were forced to learn the position of a platform hidden under the surface of a water-filled maze and then asked rapidly to learn a new position.

Mice were injected with either metformin or saline for 38 days. On days 22 through 38, they learned the initial position of the platform, which provided an escape from the water-filled maze.  Then the platform was moved to the opposite side of the maze, and the animals were asked again to learn its position. In both tasks, the mice learned the platform positions with equivalent speed.

But when they were put back in the maze – this time with the platform removed – control mice spent more time searching for it in the original position, while the metformin-treated animals preferentially looked in the new region.

The implication  is that metformin helped the mice form their new memories of the second platform position. Further analysis showed that their enhanced ability was paralleled by an increase in the number of  neurons.

In a separate study researchers have shown that metformin can increase lifespan and delay the onset of cognitive impairment in a mouse model of Huntington’s disease.

Taken together, these findings raise the possibility that metformin’s ability to enhance neurogenesis might have a positive impact in some nervous system disorders.

Miller’s team is already planning a pilot study to test metformin in young patients with acquired brain damage, either as result of treating a childhood brain tumor or from a traumatic head injury.

We will report back to you with results, as they are published.

FDA Ad Study: Clarifying the Confusion

As a public health agency, the FDA encourages the communication of accurate health messages about medical conditions and treatment.  One way the pharma industry does this is through non-branded disease awareness communications. These are aimed at either the general public or health care practitioners and discuss a particular disease or health condition, without making mention of any specific drug.  Usually, they encourage consumers to seek, and health care practitioners to provide, appropriate treatment for the particular disease state.

This is helpful for under-diagnosed and under-treated diseases such as depression, hyperlipidemia, hypertension, osteoporosis, and diabetes. Some research has shown that consumers prefer disease awareness advertising. It’s considered more informative and less persuasive than full product advertising.

The pharma industry likes it too.  Disease awareness communications are not subject to the regulations and restrictions mandated by the FDA for prescription drug advertising.

But now, the FDA is concerned that disease awareness ads might confuse consumers. According to a Federal Register notice issued on June 20, the agency wants to know whether the public can distinguish between product claims and disease information, and how different types of information impact comprehension.

So worried in fact,  the Agency has planned a study entitled, “Experimental Study: Disease Information in Branded Promotional Material” to look into those questions.

The study will examine print ads for three conditions – COPD, lymphoma and anemia.

4,650 American adults will be divided into three groups and asked to review the ads electronically.

  • One group will see information about the disease that avoids discussion of disease outcomes the drug has not been shown to address i.e.  “Diabetes is a disease in which blood sugar can vary uncontrollably, leading to uncomfortable episodes of high or low blood sugar.”
  • Other participants will see disease information that mentions consequences of the disease that go beyond the indication of the advertised product, such as, “Untreated diabetes can lead to blindness, amputation, and, in some cases, death.”
  • A third group will see drug product information only.

Disease information will be presented in different ways. For example, on alternating paragraphs, on separate pages or in different fonts and colors from product claims.

Specifically the study will address whether or not consumers are able to distinguish between claims made for a medication and general disease information when they see an advertisement for a drug.  For example, if an ad for a drug that lowers blood glucose, mentions diabetic retinopathy do consumers  think the drug will prevent the affliction, even if no direct claim is made?

The Agency says: “If consumers are able to distinguish between disease information and product claims in an ad, then they will not be misled by the inclusion of disease information in a branded ad. If consumers are unable to distinguish these two, however, then consumers may be misled into believing that a particular drug is effective against long-term consequences.”

SRxA’s Word on Health looks forward to seeing the results. Given that warning letters have been issued in the past over ads that contain mixed messages, this is an opportunity for the FDA to revisit its stance toward such advertising, reduce consumer confusion and, most importantly, learn how best to disseminate useful health information.

The biggest-selling drug in 2018 will be…

EvaluatePharma, a UK based company specializing in pharma and biotech analysis has been gazing long and hard into its crystal ball.

Having scrutinized the world’s leading 3,500 pharmaceutical and biotech companies they have come up with a list of what, they believe, will be the top 10 selling drugs in 2018.

  1. Januvia       (diabetes) – $9.7 billion
  2. Humira        (arthritis) – $8.2 billion
  3. Avastin        (cancer) – $7.5 billion
  4. Enbrel          (arthritis)  – $7.2 billon
  5. Revlimid     (myelodysplastic syndrome) – $6.75 billion
  6. Prevnar 13  (pneumococcal vaccine) – $6.72 billion
  7. Rituxan         (cancer) – $6.3 billion
  8. Lantus           (diabetes) – $5.9 billion
  9. Remicade     (arthritis) – $5.8 billion
  10. Advair            (COPD)  – $5.7 billion

Surprised?  No conventional molecules, no cholesterol lowering agents, no blood pressure meds and not a single new drug among the top ten.  However, they predict the #11 best seller will be GS-7977 – the much anticipated oral hepatitis C drug from Gilead Sciences .

Not so surprising, given the obesity epidemic sweeping the western world that 2 of the front runners are diabetes drugs. Likewise, given the globally aging population – 3 are for arthritis.

#5 may be a surprise to many. Few people had ever heard of myelodysplastic syndrome before ABC news anchor Robin Roberts announced last week that she has the disease.  Still, it’s predicted number 5 status doesn’t mean that an epidemic is expected – it’s still relatively rare with only 10,000 or so new cases detected each year. Its lofty status on the list is more to do with the price. It costs a staggering $10,000 or so for a 28 day supply of the pills.

Other predictions from the EvaluatePharma World Preview 2018 report:

  • Worldwide prescription drug sales are forecast to total $885bn in 2018 an increase of 3.1% from 2011
  • Over $290bn of pharmaceutical sales are at risk from patent expirations between now and 2018
  • Pfizer was the top company for prescription drug sales in 2011, but  Novartis will top the list by 2018
  • Global pharmaceutical R&D spend forecast will grow by 1.5% per year to $149bn in 2018
  • Anti-coagulants (blood thinners) are set to record highest growth of major therapy categories to 2018

Interesting stuff. But the problem with such long term predictive models is that they are but a snapshot  trying to project out six years.

In reality, life is a movie, with a frequently changing plot. For example if J&J’s canagliflozin can reduce obesity and improve blood sugar levels better than Januvia then the projected No. 1 ranking is suspect, at best.

Insulin Patch Offers Hope of Needle Free Diabetes Management

Transdermal Specialties Inc. (TSI) is hoping to change the face, not to mention the abdomen, upper arm and thighs, of patients with diabetes.  The company’s new “Set IT And Forget IT” insulin delivery system will be unveiled at the American Diabetes Association’s 72nd Annual Scientific Meeting, June 9 -11, 2012 in Philadelphia.

Called the U-STRIP™, this breakthrough product is a programmable transdermal insulin patch which offers totally non-invasive insulin delivery for both Type-1 and Type-2 diabetic patients.

Using a patented alternating ultrasonic waveform process to enlarge the diameter of the skin pores, the U-Strip enables large molecule drugs, such as insulin, to permeate through the skin into the dermis and then into the blood stream. All without needles!

According to TSI, the key advantages of the U-Strip include:

  • Delivers insulin for both basal and bolus needs
  • Patches available in four different doses: 25, 50, 100 & 150 Units
  • Electronic delivery system tracks dosing history and glucose readings
  • Downloads data to physician for progress monitoring

12 clinical trials in over 125 diabetics have already been successfully completed. The company hopes to complete the last two clinical trials needed for FDA approval in the next 18 months.

The HPT- 6 trial will investigate whether the patch can reach the same glucose levels as a pump with less insulin, and will also compare the speed of delivery vs. injection to determine if the patch can be more effective in morning glucose reduction for those patients waking with high blood sugar levels.

The HPT-7 trial (slated for 2013) will focus on a real-world study of 500 Type-2 diabetics, who will conduct an at-home study to track their A1C levels. The A1C test measures average blood glucose control for the past 2 to 3 months.

The U-Strip represents a major advance in diabetes care” says Bruce K. Redding, Founder, President and CEO of TSI. “The insulin patch component offers a safe and painless alternative to injections with the promise of reduced side effects and improved insulin uptake efficiencies for the patient. The ultrasound actually reduces the quantity of insulin needed for effective glucose control and speeds the delivery over a pump or even direct injection. Improved patient monitoring and reporting of the Control Device enables better tracking of treatment programs and the new “Set-it and Forget-it”  function means more regular glucose control during both evening and daytime hours.

All of which sound like good news for the 27 million diabetics in the US, who eagerly await an alternative to injections. Over the years, various attempts, some more successful than others, have been made to capture this $3 billion market.

SRxA’s Word on Health will be keeping a watch on all diabetes developments and we’ll bring you further news as it happens.