Obese mice lost weight after being fed the microbe Akkermansia muciniphila, which appears to have a symbiotic relationship with the inner lining of the intestine.
MICHELLE D. MILLIMAN/SHUTTERSTOCK
The gut is home to innumerable different bacteria — a complex ecosystem that has an active role in a variety of bodily functions. In a study published this week in Proceedings of the National Academy of Sciences1, a team of researchers finds that in mice, just one of those bacterial species plays a major part in controlling obesity and metabolic disorders such as type 2 diabetes.
The bacterium, Akkermansia muciniphila, digests mucus and makes up 3–5% of the microbes in a healthy mammalian gut. But the intestines of obese humans and mice, and those with type 2 diabetes, have much lower levels. A team led by Patrice Cani, who studies the interaction between gut bacteria and metabolism at the Catholic University of Louvain in Belgium, decided to investigate the link.
Mice that were fed a high-fat diet, the researchers found, had 100 times less A. muciniphila in their guts than mice fed normal diets. The researchers were able to restore normal levels of the bacterium by feeding the mice live A. muciniphila, as well as ‘prebiotic’ foods that encourage the growth of gut microbes.
The effects of this treatment were dramatic. Compared with untreated animals, the mice lost weight and had a better ratio of fat to body mass, as well as reduced insulin resistance and a thicker layer of intestinal mucus. They also showed improvements in a host of other indicators related to obesity and metabolic disorders.
“We found one specific common factor between all the different parameters that we have been investigating over the past ten years,” says Cani.

Cani’s team has started unravelling the complicated mechanisms through which the bacterium may influence metabolism. Restoring normal levels of A. muciniphila led to increased intestinal levels of endocannabinoids, signalling molecules that help to control blood-glucose levels and maintain the gut’s defenses against harmful microbes.
Internal dialogue
A. muciniphila also seems to have a ‘dialogue’ with the cells of the intestinal lining and with the immune system, says Cani, sending a signal that affects the production of anti-microbial molecules, while increasing the production of mucus. It seems as if the bacterium is telling the host that it will take care of any invading harmful microbes in exchange for more food, he adds.
Cani “strongly believes” that A. muciniphila could one day be used to treat disorders such as obesity, diabetes and colitis in humans. “There is so much evidence in the literature that links this bacterium to human conditions,” he says.
Randy Seeley, an obesity researcher at the University of Cincinnati in Ohio, says that it is “ridiculously cool” that science can now link specific aspects of the microbiome to specific functions, and he is optimistic that the work will lead to useful treatments for humans, although that will take some time. “What we have to figure out is, what is the best way to change gut flora,” he says. “If you just toss bacteria in, they don’t stay.”
The fact that the immune system may be involved in the interaction between A. muciniphila and the body, Seeley adds, offers an intriguing possibility for another way to manipulate bacteria in the gut. “There will be drug targets that come out of that,” he says.
Nature
doi:10.1038/nature.2013.12975
References
1. Everard, A. et al. Proc. Natl Acad. Sci. USA http://dx.doi.org/10.1073/pnas.12194511

MEDICAL ADVICE DISCLAIMER: The information included on this site is for educational purposes only. It is not intended nor implied to be a substitute for professional medical advice. The reader should always consult his or her health care provider to determine the appropriateness of the information for their own situation, or if they have any questions regarding a medical condition or treatment plan. Reading the information on this website does not create a physician-patient relationship.

In China, cinnamon has been used to treat a variety of ailments such as headaches, loss of appetite, dyspepsia, the common cold, inflammation, wounds, nausea, and diarrhea as well as Diabetes Type 2.  After studying rodents, scientists felt cinnamon could possibly help through various mechanisms that are augmented with current diabetes medications.  After studying its effects in rodents, scientists believed cassia cinnamon extract may lower blood sugar and improve lipids via a number of mechanisms.  Human studies have shown mixed results. Some studies have shown no improvement and scientists felt improvement would  only occur when the  starting Hemoglobin A1C is>8 and the appropriate type of Cinnamon in appropriate doses must be used. Unfortunately, using cinnamon as a spice does not work.   Only cassia cinnamon available as pills, not as the spice, has been shown to have a significant effect on glycemic control.”Despite the mixed results coming from studies of cinnamon in type 2 diabetic patients, there is promise in its potential effects. Large, randomized, placebo-controlled studies of cinnamon need to be completed in order to fully evaluate its efficacy.”

MEDICAL ADVICE DISCLAIMER: The information included on this site is for educational purposes only. It is not intended nor implied to be a substitute for professional medical advice. The reader should always consult his or her health care provider to determine the appropriateness of the information for their own situation, or if they have any questions regarding a medical condition or treatment plan. Reading the information on this website does not create a physician-patient relationship.

By Marilynn Marchion: Eating fish is good for your heart but taking fish oil capsules does not help people at high risk of heart problems who are already taking medicines to prevent them, a large study in Italy found.

The work makes clearer who does and does not benefit from taking supplements of omega-3 fatty acids, the good oils found in fish such as salmon, tuna and sardines.

Previous studies have suggested that fish oil capsules could lower heart risks in people with heart failure or who have already suffered a heart attack. The American Heart Association recommends them only for people who have high levels of fats called triglycerides in their blood, says the group’s president, Dr. Donna Arnett of the University of Alabama at Birmingham.

Fish oil capsules failed to prevent flare-ups of atrial fibrillation, a common heart rhythm problem, in a large study in 2010.

The new study was led by the Mario Negri Institute for Pharmacological Research in Milan. It tested 1 gram a day of fish oil versus dummy capsules in 12,513 people throughout Italy. They had not suffered a heart attack but were at high risk of having one because of diabetes, high blood pressure, high cholesterol, smoking, obesity or other conditions. Most already were taking cholesterol-lowering statins, aspirin and other medicines to lower their chances of heart problems.

Researchers at first planned to compare the rate of death, heart attacks and strokes in the two groups, but these were less frequent than anticipated. So they started measuring how long it was before people in either group suffered one of these fates or was hospitalized for heart-related reasons. After five years, the rate was the same — about 12 percent of each group had one of these problems.

“They’re very high-risk people and so the level of other treatments was very high,” Arnett said. “When you’re being aggressively treated for all of your other risk factors, adding fish oil yielded no additional benefits.”

Results are published in Thursday’s New England Journal of Medicine. Makers of fish oil supplements helped pay for the study.

Eating fish is known to help protect against heart disease, and the Heart Association recommends it at least twice a week.

“People who choose to eat more fish are more likely to eat heart healthier diets and engage in more physical activity,” and studies testing the benefit of supplements may not be able to completely adjust for differences like these, said Alice Lichtenstein, director of the cardiovascular nutrition lab at Tufts University in Boston.

The results do show that people can’t rely on a pill to make up for a bad diet, she said.

“It is sort of like breaking a fish oil capsule over a hot fudge sundae and expecting the effect of the calories and saturated fat to go away,” she said.

___

Online:

Fish oil: http://nccam.nih.gov/health/omega3/introduction.htm

Journal: http://www.nejm.org

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MEDICAL ADVICE DISCLAIMER: The information included on this site is for educational purposes only. It is not intended nor implied to be a substitute for professional medical advice. The reader should always consult his or her health care provider to determine the appropriateness of the information for their own situation, or if they have any questions regarding a medical condition or treatment plan. Reading the information on this website does not create a physician-patient relationship

May 3, 2013 — In a promising development for diabetes treatment, researchers have developed a network of nanoscale particles that can be injected into the body and release insulin when blood-sugar levels rise, maintaining normal blood sugar levels for more than a week in animal-based laboratory tests. The work was done by researchers at North Carolina State University, the University of North Carolina at Chapel Hill, the Massachusetts Institute of Technology and Children’s Hospital Boston

“We’ve created a ‘smart’ system that is injected into the body and responds to changes in blood sugar by releasing insulin, effectively controlling blood-sugar levels,” says Dr. Zhen Gu, lead author of a paper describing the work and an assistant professor in the joint biomedical engineering program at NC State and UNC Chapel Hill. “We’ve tested the technology in mice, and one injection was able to maintain blood sugar levels in the normal range for up to 10 days.”

When a patient has type 1 diabetes, his or her body does not produce sufficient insulin, a hormone that transports glucose — or blood sugar — from the bloodstream into the body’s cells. This can cause a host of health effects. Currently, diabetes patients must take frequent blood samples to monitor their blood-sugar levels and inject insulin as needed to ensure their blood sugar levels are in the “normal” range. However, these injections can be painful, and it can be difficult to determine the accurate dose level of insulin. Administering too much or too little insulin poses its own health risks.

The new, injectable nano-network is composed of a mixture containing nanoparticles with a solid core of insulin, modified dextran and glucose oxidase enzymes. When the enzymes are exposed to high glucose levels they effectively convert glucose into gluconic acid, which breaks down the modified dextran and releases the insulin. The insulin then brings the glucose levels under control. The gluconic acid and dextran are fully biocompatible and dissolve in the body.

Each of these nanoparticle cores is given either a positively charged or negatively charged biocompatible coating. The positively charged coatings are made of chitosan (a material normally found in shrimp shells), while the negatively charged coatings are made of alginate (a material normally found in seaweed).

When the solution of coated nanoparticles is mixed together, the positively and negatively charged coatings are attracted to each other to form a “nano-network.” Once injected into the subcutaneous layer of the skin, the nano-network holds the nanoparticles together and prevents them from dispersing throughout the body. Both the nano-network and the coatings are porous, allowing blood — and blood sugar — to reach the nanoparticle cores.

“This technology effectively creates a ‘closed-loop’ system that mimics the activity of the pancreas in a healthy person, releasing insulin in response to glucose level changes,” Gu says. “This has the potential to improve the health and quality of life of diabetes patients.”

Gu’s research team is currently in discussions to move the technology into clinical trials for use in humans.

Journal Reference:

Zhen Gu, Alex A. Aimetti, Qun Wang, Tram T. Dang, Yunlong Zhang, Omid Veiseh, Hao Cheng, Robert S. Langer, Daniel G. Anderson. Injectable Nano-Network for Glucose-Mediated Insulin Delivery. ACS Nano, 2013; : 130502161653001 DOI: 10.1021/nn400630x

MEDICAL ADVICE DISCLAIMER: The information included on this site is for educational purposes only. It is not intended nor implied to be a substitute for professional medical advice. The reader should always consult his or her health care provider to determine the appropriateness of the information for their own situation, or if they have any questions regarding a medical condition or treatment plan. Reading the information on this website does not create a physician-patient relationship.

New mouse model confirms how type 2 diabetes develops May 3, 2013 in Diabetes Researchers at Lund University in Sweden have developed a new mouse model that answers the question of what actually happens in the body when type 2 diabetes develops and how the body responds to drug treatment. Long-term studies of the middle-aged mouse model will be better than previous studies at confirming how drugs for type 2 diabetes function in humans.  “The animal models for type 2 diabetes studies that have previously existed have not been optimal because they use young mice. Our idea was to create a model that resembles the situation in the development of type 2 diabetes in humans. We generally get the disease in middle age when we start to put on weight and live a more sedentary, and more stressful, life. Our new middle-aged mouse model has enabled us to study long-term physiological effects of the development and treatment of type 2 diabetes in a completely new way”, said Bilal Omar, one of the researchers behind the study. What the Lund researchers have done is to feed normal mice fatty food over a long period from the age of eight months, i.e. middle age, until the end of their natural lives at the age of two. The mice become overweight, and develop high blood sugar levels and reduced insulin release, as expected before the onset of type 2 diabetes. “Throughout the period we were able to study the process that leads to the development of type 2 diabetes with a lifestyle like that of people predisposed to the condition”, said Bilal Omar. In the study, the researchers could confirm that fatty foods lead to inflammation in the islets of Langerhans in the pancreas, which produce insulin. Researchers have seen inflammation in the islets in people with type 2 diabetes, but in Bilal Omar’s view, it is only with the new mouse model that it can really be confirmed. Inflammation in these islets is an important risk factor for type 2 diabetes. “What was so interesting and exciting was that the mice that were treated with DPP-4 inhibitors, a class of drugs used for type 2 diabetes, did not develop inflammation and they maintained good insulin production. They were still obese, but had normal blood sugar, were otherwise healthy and lived longer”, said Bilal Omar. Researchers have worked for decades and on many fronts to understand the causes and course of diabetes. Models of different diseases are therefore an important tool for the development of new and better drugs, and a requirement to develop the best possible drugs is to understand what is happening on a physiological level. “The goal is to design drugs and treatments which, if they can’t cure the disease, can at least give the patient a better quality of life for several years”, said Bilal Omar. “Another aspect of our findings is that the inflammation in the islets was caused by a high-fat diet. Even if it is too early to draw parallels with the diet of humans, it makes it doubtful whether a high-fat diet over a long period should be recommended, as in the LCHF diet”, said Professor Bo Ahrén, another of the researchers behind the study. More information: Omar, B. et al. Enhanced β-cell function and anti-inflammatory effect after chronic treatment with the dipeptidyl peptidase 4 inhibitor vildagliptin in an advanced age diet induced obesity mouse model, Diabetologia, May 2013. link.springer.com/… 5-013-2927-8 Journal reference: Diabetologia search and more info website Provided by Lund University search and more info website

Read more at: http://medicalxpress.com/news/2013-05-mouse-diabetes.html#jCp

MEDICAL ADVICE DISCLAIMER: The information included on this site is for educational purposes only. It is not intended nor implied to be a substitute for professional medical advice. The reader should always consult his or her health care provider to determine the appropriateness of the information for their own situation, or if they have any questions regarding a medical condition or treatment plan. Reading the information on this website does not create a physician-patient relationship.

A newly discovered hormone – betatrophin – could revolutionize the treatment of type 2 diabetes
It could halt the development of the condition
In mice the hormone was shown to increase the number of insulin-producing beta cells up to 30-fold

By Fiona Macrae Science Correspondent

PUBLISHED: 11:00 EST, 25 April 2013 | UPDATED: 18:47 EST, 25 April 2013Diabetics could be freed from the need to inject themselves by the development of a once-a-year drug

Millions of diabetics could be freed from having to inject themselves several times a day by a once-a-year drug.

Scientists have discovered a hormone which can boost the number of insulin-making cells by up to 30-fold.

This would ‘dramatically’ improve treatment for type 2 diabetes. This form of the condition, often triggered by weight gain, is becoming more common in the obesity crisis.

Researchers from Harvard University believe the betatrophin hormone may even have the power to halt type 2 diabetes in its tracks.

‘It could eventually mean that, instead of taking insulin injections three times a day, you might be able to take this hormone once a week or once a month, or in the best case, maybe once a year,’ they said.

In patients with type 2, or adult-onset diabetes, cells in the pancreas do not make enough insulin, a hormone vital to the conversion of sugar into energy. Insulin they do make does not work properly.

Initially, the condition is often controlled with a stringent diet and exercise regime. But many patients will suffer worsening health over time, eventually needing tablets or insulin injections.

Seeking an alternative to simply giving insulin, the US researchers looked for a way of boosting its production in the body.

This led them to a hormone which they christened betatrophin.

Given to mice, it raised the number of insulin-producing beta cells by up to 30-fold, reported the journal Cell.

In addition, the ‘enormous’ number of new cells only made insulin when needed, which should lead to more natural blood sugar levels and better health.
Given to mice, the new hormone raised numbers of insulin-producing beta cells up to 30-fold

Given to mice, the new hormone raised numbers of insulin-producing beta cells up to 30-fold

Researcher Professor Doug Melton said the discovery had left him so excited that he could hardly sleep. He added: ‘Our idea is relatively simple.

‘We would provide this hormone, the type 2 diabetic will make more of their insulin-producing cells and this will slow down, if not stop, the progression of their diabetes.’ Drug firms have already seized on the breakthrough and the hormone could be tested on people in just three years.

However, the need to show it would be safe and effective in large numbers of people means it is a decade away from the market.

Yesterday’s Daily Mail reported how just one 12oz can of sugary drink a day can raise the risk of type 2 diabetes by a fifth.

Complications of high blood sugar include heart disease, blindness, and nerve and circulatory damage.

It is thought that one in 20 Britons has diabetes, with type 2 making up 90 per cent of the cases.

The US work may also be useful in treating type 1 diabetes, which typically develops in childhood or adolescence.

MEDICAL ADVICE DISCLAIMER: The information included on this site is for educational purposes only. It is not intended nor implied to be a substitute for professional medical advice. The reader should always consult his or her health care provider to determine the appropriateness of the information for their own situation, or if they have any questions regarding a medical condition or treatment plan. Reading the information on this website does not create a physician-patient relationship.

Read more: http://www.dailymail.co.uk/health/article-2314762/End-diabetes-jab-Scientists-insulin-boosting-hormone-away-daily-injections.html#ixzz2RhX7Y5v9
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An anti-fat bias refers to the prejudicial assumption, whether conscious or subconscious, of personality and behavioral characteristics based solely on the visual assessment of a person’s corpulence. Heavier people are narrowly perceived as being indolent, inept, weak willed and unmotivated, or irresponsible.

Many fail to be empathetic to their plight – coldly assuming if heavier people respected themselves more or had ambition they wouldn’t have allowed themselves to get so large or go so long being overweight.

Kimberly A. Gudzune, MD, an assistant professor in the Division of General Internal Medicine at the Johns Hopkins University School of Medicine, led the study of 39 primary care physicians and 208 of their patients – focusing on bonding and empathy between the two.

Although overweight patients received the same amount of time, treatment, and advice, some doctors were found to have an implicit anti-fat criticism, and established less of an emotional rapport with heavier patients – regardless of the medical topic being discussed.

“If you aren’t establishing a rapport with your patients, they may be less likely to adhere to your recommendations to change their lifestyles and lose weight,” Gudzune reinforced.

It was suggested doctors respected obese patients less due to the assumption they (patient) should be doing more to help themselves lose weight. This negative attitude was conveyed through verbal and non-verbal cues during patient-treatment encounters.

Researchers suggest physicians should be more encouraging and supportive, as obese patients who are already frustrated about their body issues, would likely be more permissive to the idea of a weight-loss plan and counseling if approached in a positive, relatable manner.

In prior research, people were found to be less trusting of their overweight doctors. Sara Bleich, an obesity and health policy researcher at the Johns Hopkins Bloomberg School of Public Health in Baltimore, conducted a survey of 358 adults.

Participants were given hypothetical scenarios in which they were to interact with a normal weight, overweight or obese doctor. People were asked how comfortable they would feel talking with that doctor about health concerns and the physician’s credibility.

Ranking on a scale from one to five – five being highest – study participants rated their trust level as 4.0 toward an average weight doctor, 3.4 for an overweight doctor. Obese physicians received the lowest score of a 3.3.

Similarly, the likelihood of following the doctor’s advice was rated: average 3.9, overweight 3.5, and obese 3.5. The results, which demonstrated a noteworthy weight bias against the medical professionals, were published in the International Journal of Obesity.

In both respects, patient care ultimately suffers.

First, your eyes are bigger than your stomach!

A saying I often heard as a child. But, I have to admit my mother was right. And I’m not alone in being woefully inaccurate when it comes to eyeballing food portions.
But how many of us would cheerfully admit that? We tend to gloss over the truth, or worse, eat unconsciously. I’ll offer below some practical ways to aid portion control, but before I go there, a reminder of the most important element, awareness.
You can’t change anything you’re not aware of! How many of you have eaten large portions because it’s on your plate, or because it tastes good? Be honest here!
If there were hands up in response, I’d guess around 90% of you recognize your tendency to do so.
When a typical restaurant in America serves portions EIGHT times the size of the nutritional recommended portion, we’re all in trouble. Why? Because that becomes the norm through familiarity, frequency and reinforcement.
Add in our appallingly poor visual recall (being able to accurately replicate the size of any object or portion) and we grow increasingly unable to serve up only enough to fill us, rather than ending up overeating.

1. Be aware of how you calculate a portion of food.

Investigate next time before you eat. Remember to think about portion size.
How do you measure it-by the serving spoonful, plateful, piece of meat or fish, eyeball it?
Does it differ by using different size plates, whether you name it a meal or snack?
Do you tend to simply divide up the amount of food cooked by the number of people eating?

TIP- Don’t trust your accuracy if eyeballing the portion size. Chances are you’ll be way off. Use a utensil that offers the same serving size every time.

TIP- Pay attention to the quantity, don’t just ladle it out. Experiment with how much you need before feeling full. recall how much you filled the plate last time, and how much you were able to eat before feeling full.
Paying attention to your actions increases the possibility you’ll be able to judge it better next time.

TIP-Switch out dinner-size plates for smaller plates or bowls.

2. What are your beliefs regarding the amount of food?

Were you brought up to clean your plate regardless?
Do you see larger portions correlating with giving love, caring or being generous?
Is food a stand-in for something else?

In particular, do you have the good healthy habit of serving small portions, with opportunity to have seconds if still hungry? Most of us haven’t given took much thought to this aspect of eating, a multiple times daily activity! In fact, it’s so frequent that we often zone out when eating.

TIP- Understand what food means to you beyond the obvious.
Serve small portions with full awareness and encouragement to return for more if still hungry. With sensible sized first portions, seconds are good manners, not greed! Knowing seconds are OK will avoid deprivation.

3. Familiarize yourself with your particularly ingrained eating habit.

For myself, the habit of something sweet for dessert was difficult to let go of. Although nothing to do with hunger I’d still crave the taste after eating. Once diagnosed with Type 2, understanding that the craving would have to cease, I ‘weaned’ myself off it by finding something minty to finish off the meal. Mint tea, sucking a mint or even minty gum all worked. After that flavor permeated my taste buds, I felt no craving for anything sweet.
An alternative was to return to the European habit of my younger years, finish the meal with cheese!

TIP-Find flavors that satisfy but discourage cravings for harmful foods to end the meal on. Mint or something savory works.

4. Learn to differentiate between the different types of hunger.

There are 7 types of hunger through the senses that can all lead to eating if we don’t differentiate them.
Olfactory hunger (smelling food being cooked).
Visual hunger (walking past a bakery and seeing scones).
Emotional hunger (feeling disappointed, abandoned, sad).
Cognitive hunger (thinking when to eat).
Auditory hunger (hearing someone prepare dinner).
‘Mouth’ hunger (the desire for pleasurable sensations like hot, crunchy etc).
Stomach or physical hunger (your tummy is rumbling).

Of the 7, only the last one, physical hunger, should be attended to.

TIP-See if you can identify all the types of hunger. Resolve to try only to feed stomach hunger.

With the other 6 types, unless your mind clings to the idea, remove the stimulus if possible.
For example, if going by the bakery evokes visual hunger, you’ll walk past it in 30 seconds and your mind will be thinking of something else by then.
With auditory hunger, choose to replace the sounds of food being prepared with something else, like music.

5. Practice being kind and forgiving to yourself.

No need to be unkind to yourself or overly harsh. Judging yourself is not helpful, even if it’s automatic. Treat yourself with kindness and patience,knowing this is a really hard habit to change. Accept the reality you won’t succeed at times, then return again and again to the practice. Everytime you return is success, not failure.

TIP-Be as kind to yourself as you would like others to be.

6. Allow yourself to eat 4-6 smaller meals/snacks daily.

You’ll end up eating the same amount overall, but split it up. That way, there’ll be less time in between meals/snacks, and you won’t feel so ‘stuffed’ from overeating. The habitual activity of thinking about and preparing or eating will increase, so no deprivation or sense of loss.

TIP-Serve the usual quantity, but split it onto 2 plates, putting one in the fridge for later. Pay attention to see if you feel actual physical hunger after the smaller portion.

It was a revelation for me to realize I won’t starve by eating less, but actually feel more comfortable!

7. Devise your own unique way of cutting back on the amount of food. Share it with us for the benefit of others. Listen out for others to appreciate your suggestion. You’ll feel really good about yourself having helped another.

TIP-Feel good about yourself by sharing what works for the benefit of others.

Josie Levine PhD is a psychotherapist, health coach, consultant and writer to those wanting to improve their health and lifestyle. Her blog is http://mindfullymanagingdiabetes.com. To receive her latest post, click here.

Josie Levine, Ph.D.

CMAJ April 15, 2013 First published April 15, 2013, doi: 10.1503/cmaj.121950

© 2013 Canadian Medical Association or its licensors
All editorial matter in CMAJ represents the opinions of the authors and not necessarily those of the Canadian Medical Association

From the Department of Epidemiology (J.-Y. Min), Institute of Health and Environment, Seoul National University, Seoul, Republic of Korea; and the Department of Occupational and Environmental Medicine (K.-B. Min), Ajou University School of Medicine, Suwon, Republic of Korea.

Kyoung-Bok Min, E-mail mink1999@ajou.ac.kr

Abstract

Background: Connecting peptide (C-peptide) plays a role in early atherogenesis in patients with diabetes mellitus and may be a marker for cardiovascular morbidity and mortality in patients without diabetes. We investigated whether serum C-peptide levels are associated with all-cause, cardiovascular-related and coronary artery disease-related mortality in adults without diabetes.

Methods: We used data from the Third Nutrition and Health Examination Survey (NHANES III) and the NHANES III Linked Mortality File in the United States. We analyzed mortality data for 5902 participants aged 40 years and older with no history of diabetes and who had available serum C-peptide levels from the baseline examination. We grouped the participants by C-peptide quartile, and we performed Cox proportional hazards regression analysis. The primary outcome was all-cause, cardiovascular-related and coronary artery disease-related mortality.

Results: The mean serum C-peptide level in the study sample was 0.78 (1 standard deviation 0.47) nmol/L. The adjusted hazards ratio comparing the highest quartile with the lowest quartile was 1.80 (95% confidence interval [CI] 1.33–2.43) for all-cause mortality, 3.20 (95% CI 2.07–4.93) for cardiovascular-related mortality, and 2.73 (95% CI 1.55–4.82) for coronary artery disease-related mortality. Higher C-peptide levels were associated with increased mortality among strata of glycated hemoglobin and fasting serum glucose.

Interpretation: We found an association between serum C-peptide levels and all-cause and cause-specific mortality among adults without diabetes at baseline. Our finding suggests that elevated C-peptide levels may be a predictor of death.

MEDICAL ADVICE DISCLAIMER: The information included on this site is for educational purposes only. It is not intended nor implied to be a substitute for professional medical advice. The reader should always consult his or her health care provider to determine the appropriateness of the information for their own situation, or if they have any questions regarding a medical condition or treatment plan. Reading the information on this website does not create a physician-patient relationship.

Abbott is voluntarily recalling its FreeStyle InsuLinx blood glucose meters in the United States due to a malfunction that could lead to a delay in the identification and treatment of severe hyperglycemia or incorrect treatment being given, which could potentially lead to serious injury or death.

The problem is occurring at extremely high blood glucose levels of 1024 mg/dL and above, says the company. When this happens, the FreeStyle InsuLinx Meter will display and store in memory an incorrect test result that is 1024 mg/dL below the measured result. For example, at a blood glucose value of 1066 mg/dL, the meter will display and store a value of 42 mg/dL (1066 mg/dL – 1024 mg/dL = 42 mg/dL).

The company is notifying all registered users, healthcare professionals, pharmacies and distributors where the FreeStyle InsuLinx Meter is sold. Abbott estimates that there are approximately 50,000 active FreeStyle InsuLinx Meter users in the United States. Upon identifying the issue, Abbott notes it promptly developed and implemented an update to the meter.

This move follows a similar recall, last month, by the LifeScan unit of Johnson & Johnson, which voluntarily recalled almost 2 million of its OneTouch Verio blood glucose meters because they malfunctioned at extremely high blood glucose levels.

Customers who are using the FreeStyle InsuLinx meter should immediately take one of the following actions to address this issue with their meter, Abbott says:

They can access a software update to resolve the issue at www.freestyleinsulinx.com/swupdate. This update will allow them to maintain settings and historical data on their meter.

Customers can contact Abbott Diabetes Care Customer Service at 1-866-723-2697 to expedite return and replacement of their FreeStyle InsuLinx meter at no charge. Replacements are available, and Abbott will send meters to customers immediately upon request.

The company is advising that the current FreeStyle InsuLinx meter may be used until customers are able to update the meter software or until a requested replacement meter arrives. But if patients experience symptoms that are not consistent with their readings, they should contact their healthcare professional and follow his or her treatment advice. Although blood glucose levels at 1024 mg/dL and above are very rare, if they do occur they are a serious health risk and require immediate medical attention, Abbott stresses.

“Our first priority is to safeguard the health and safety of patients,” said Heather Mason, senior vice president, diabetes care, at Abbott. “We are committed to ensuring that our customers are able to continue to test their blood glucose with confidence, and we initiated this voluntary recall to ensure our products continue to meet the highest standards of quality and safety. We regret any inconvenience this action may cause.”

No other Abbott blood glucose meters are affected by this issue.

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To date, there has been 1 reported patient incident in the United States that may be related to this specific issue. The patient sought medical treatment and was diagnosed with hyperglycemia, treated, and released. It has not been determined that the FreeStyle InsuLinx meter was the cause, the company notes.

Outside the United States, there have been no patient incidents reported related to this specific issue.

The FreeStyle InsuLinx meter is also available in Australia, Belgium, Canada, France, Germany, Israel, Italy, the Netherlands, Spain, Switzerland, and the United Kingdom. Customers in these countries can get more information about how to address this issue by visiting www.freestyleinsulinx.com/swupdate.

Abbott has notified the US Food and Drug Administration and all relevant healthcare authorities in the other countries and is working with the individual regulatory agencies around the world where the affected products have been sold.

Additional information about this recall can be found at https://www.abbottdiabetescare.com/press-room/2013/2013-c.html or by calling 1-866-723-2697.

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