After learning that the venom of a Gila monster lizard contained hormones that can regulate blood sugar, Daniel Drucker started wondering why. And could the venom somehow help treat diabetes?

Drucker is a scientist and endocrinologist at the University of Toronto who has dedicated his career to understanding the universe of hormones in the body, which do everything from regulating appetite to helping with digestion. His curiosity about the Gila monster led to a call with a zoo in Utah. In 1995, Drucker had a lizard shipped from Utah to his lab and began experiments on the deadly venom.

Ten years later, a synthetic version of a hormone in the venom became the first medicine of its kind approved to treat type 2 diabetes. Known as a GLP-1 (for glucagon-like peptide-1) receptor agonist, the medicine set off a cascade of additional venom-inspired discoveries.

After doctors noticed mice and humans on the drug for diabetes appeared to lose weight, they began to consider its use in obesity science. In June 2021, another effective treatment, this one for obesity, got Food and Drug Administration approval. Called semaglutide and marketed as Wegovy, it also takes its structure from the lizards venom.

If this origin story sounds outlandish, consider the history of obesity treatments. Over the years, people have turned to extreme and unlikely interventions to try to lose weight, from jaw wiring, laxatives, and vagotomies to lap band operations and fen-phen, a miracle diet drug that was ultimately recalled.

The new treatment a once-weekly injectable from Novo Nordisk, a Danish pharmaceutical company that has hired many leading diabetes and obesity scientists as consultants is poised to safely help many people with health-threatening obesity, physicians and researchers say. It may even illuminate some of the mysteries around how appetite works in the first place.

Its phenomenal, says Michael Krashes, a diabetes and obesity investigator at the National Institutes of Health. Semaglutide is a big step forward we finally have something thats reliable and able to produce sustained effects over time, adds Ivan De Araujo, a neuroscientist who studies brain-gut interactions at Mount Sinais Icahn School of Medicine. Neither scientist is affiliated with Novo Nordisk.

Doctors who treat obesity patients told Vox they wished they had a treatment option like semaglutide years ago, and patients described the drug as life-altering.

Yet many people with obesity may not seek out semaglutide, and doctors may not prescribe it to them not only because of the dangerous history of weight loss medications, but also because of a persistent bias and stigma around a disease that now afflicts nearly half of Americans. Obesity is still widely viewed as a personal responsibility problem, despite scientific evidence to the contrary. And history has shown that the most effective medical interventions, such as bariatric surgery currently the gold standard for treating obesity often go unused in favor of dieting and exercise, which for many dont work.

Theres also a practical challenge: Health insurers dont typically cover obesity medications, says Scott Kahan, an obesity doctor and professor at Johns Hopkins Bloomberg School of Public Health and the George Washington University School of Medicine. Medicare explicitly excludes weight medications, Kahan, who consults with Novo Nordisk, says. And most insurers follow what Medicare does.

The new drug certainly wont be a cure-all for obesity, Krashes adds. You are not taking a 280-pound person and making them 130, he points out, though reductions that are enough to improve health outcomes are typical. Drucker, who began consulting with Novo Nordisk and other drug companies after his reptilian discovery, agrees that its a starting point for obesity: It will only scratch the surface of the problem in the population that needs to be healthier.

But semaglutide is the most powerful obesity drug ever approved, he adds. Drugs that will produce 15 percent body weight loss we did not have that before in the medical therapy of obesity. With additional, potentially more effective GLP-1 receptor agonists coming online in the future, were at the beginning of a promising new chapter of obesity therapeutics. A look at the fascinating science of how the medication works could also go a long way to changing how Americans think about this disease.

We have to thank the lizard for that, Drucker says.

To understand how semaglutide causes some people to eat less, its helpful to understand what hormones do. Theyre the bodys traveling messengers: Manufactured in one area, they move to another to deliver messages through receptors molecules that bind to specific hormones in distant organs and cells.

The gut makes dozens of hormones, and many of them travel to the brain receptors that either curb appetite or stimulate it, Drucker explains. GLP-1 is one such gut hormone. Its unleashed in the gut in response to food and stimulates the pancreas to make more insulin after a meal, which lowers blood sugar. (GLP-1 is also made in the brain stem, where it may modify appetite.)

It sends a signal to our brain that says, You know, weve had enough to eat, says Drucker.

Enter semaglutide, one of a class of medicines the GLP-1-receptor agonists that imitate GLP-1, helping the body lower glucose (in the case of people with diabetes) and, researchers suspect, curb appetite (in the case of people living with obesity who may also have diabetes).

The precise way the drug works on obesity is still unknown, in part because scientists dont understand exactly how appetite works. But researchers generally agree that the drug harnesses the brains GLP-1 receptors to curb food intake. When researchers delete the GLP-1 receptors from the brains of mice, the drug loses its appetite-suppressing effects, says Krashes.

Obesity is primarily an issue of our brain biology, and the way its processing info about the environment we live in, says Randy Seeley, a University of Michigan researcher focused on obesity treatments, who also consults with Novo Nordisk.

With semaglutide, the idea is that were changing your brain chemistry for your brain to believe you should be at a lower weight, Seeley added.

This brain-based pharmacological approach is likely to be more successful than diet and exercise alone, Seeley says, because the most important underlying part of somebodys weight has to do with how their brain operates, not a lack of willpower.

Some people with a higher body mass index are perfectly healthy and dont require any treatment. Semaglutide was only indicated by the FDA for patients who classify as clinically obese with a body mass index of 30 or greater or those who are overweight and have at least one weight-related health problem.

For the many people who have used it, it has proved safe and effective, according to the FDA. In weight loss clinical trials, semaglutide helped people lose about 15 percent of their body weight on average significantly more than the currently available obesity drugs and more than enough to improve health outcomes.

The drugs most common side effects nausea, diarrhea, constipation, and vomiting were mostly short-lived. De Araujo is finding that adverse reactions might be caused by how the drug differs from the naturally occurring peptide hormone: The hormone acts mostly locally and degrades quickly, while the medicine works mainly on the brain and is designed to stick around in the body. Thats where the nausea, vomiting probably derive from, De Araujo argues.

Patients who have tried semaglutide told Vox that it helped them manage their weight and relationship to food, and that their side effects were manageable and quickly resolved.

Jim Eggeman, a 911 operator in Ohio, said that before taking semaglutide, I could sit down and eat a large pizza, and now its one to two pieces at the most. He started on the drug for diabetes after a heart attack in December 2019 and lost 35 pounds, bringing his weight to 220.

Paula Morris-Kaufman, of Cheshire, UK, used the drug to address weight gain following cancer treatments. It helped her bring her weight back to a normal range, she says, and curb her habit of compulsive eating. If you give me a plate of food, I just eat a small portion of it and feel full really quickly.

Its possible that some of the benefits of treatment come in part from lifestyle changes, which were encouraged by the clinical trials. In many cases, patients on semaglutide also switched to a healthier diet when they started on the drug and added exercise to their routines. But study participants taking the drug still lost significantly more weight than those under the same conditions who received a placebo.

The need for additional interventions like diet and exercise is one reason why Kahan stops short of calling this drug a game changer. Its an incremental improvement over existing drugs, he says, and its still out of reach for many of the individuals who could benefit from it. The game changer description is not appropriate, because many people dont have access to these medicines.

Only about 1 percent of eligible patients were using FDA-approved medications for obesity in 2019, a study showed. The same is true for bariatric surgery, currently the most effective intervention for obesity, which can also drive type 2 diabetes into remission.

If someone walks into your office with heart disease and you as a physician dont try to treat it, thats malpractice, Seeley says. If somebody comes in with a BMI over 30 and you dont treat it, thats Tuesday. He thinks some of the hesitancy for treating patients with obesity medications comes from the history of dangerous weight loss drugs.

Ingrained biases about obesity have also made it harder for patients to get access, Kahan says. Obesity tends to be categorized as a cosmetic issue in health insurance policies, he says. In order to get coverage, employers have to explicitly decide to buy a rider and sign a contract to add weight management services and products to their insurance plans. Hed like to see obesity treatments covered by insurers in the same way diabetes and hypertension drugs are.

That will require a shift in mindset, Drucker says. We would never blame other individuals for developing high blood pressure or cardiovascular disease or cancer, he says. Its widely known that those conditions are driven by complex biological determinants, including genes, as well as environmental factors. Obesity is no different.

When Drucker started in endocrinology in the 1980s, he didnt have many tools to help patients. With the addition of semaglutide, there are multiple surgical options and drugs for obesity and diabetes. The challenge now is helping those who would benefit gain access.

I would be delighted if no one needed GLP-1 for diabetes and obesity, Drucker says. That might be possible in a food landscape that didnt nudge people toward the overeating and poor diet that leads to these chronic conditions. But for now, we have new options that are safe, appear to reduce complications, and are very effective. ... We shouldnt just throw up our hands and say theres nothing we can do.

Originally posted here:
New obesity drug semaglutide is safe and effective for weight loss and diabetes - Vox.com

Walmart is seeking to bring everyday low prices to medical care.

They announced the launch of a version of insulin that will be less expensive to people who do not have health insurance or struggle to afford the cost of life-saving drugs.

These products will save customers between 58% to 75% off the cash price of branded analog insulin products, which translates to a savings of up to $101 per branded vial or $251 per package of branded FlexPens, said the company in a new release this week.

Starting this week, Walmart will be selling its own private-label version of analog insulin (a newer, more reliable form of the drug) to anyone who has a prescription. Called ReliOn NovoLog, it will also be available at Sams Club in mid-July.

The insulin will cost about $73 for a vial or about $86 for a package of pre-filled insulin pens.

RELATED: 100 Years After First Diabetes Breakthrough, Canadian Scientists Believe Theyve Found a Cure

We know many people with diabetes struggle to manage the financial burden of this condition, and we are focused on helping by providing affordable solutions, said Dr. Cheryl Pegus, executive vice president, Walmart Health & Wellness. We also know this is a condition that disproportionately impacts underserved populations.

With ReliOn NovoLog insulin, were adding a high-quality medication for diabetes to the already affordable ReliOn line of products and continuing our commitment to improve access and lowering cost of care.

RELATED: Could Electromagnetic Fields Treat Diabetes? These Scientists Think So

ReliOn products include private label, lower priced versions of blood glucose monitors, lancets, and other diabetes management essentials.

According to CNBC, US lawmakers have scrutinized diabetes drug companies in the past, like Eli Lilly and the French company Sanofi, for increasing prices over the last two decades, leading Sanofi to roll-out a limited price reduction program.

Walmart worked directly with manufacturer Novo Nordisk to reduce costs.

POPULAR: Excited Scientists Make Type-2 Diabetes Breakthrough With First-Ever Glimpse At How Protein Behind Disease Works

This price point, we hope, will improve and hopefully revolutionize the accessibility and affordability of insulin, said Dr. Cheryl Pegus, Walmarts executive vice president of health and wellness.

SAVE Your Friends Some Money By Sharing This on Social Media

See original here:
Walmart Unveils Low-Priced Insulin to Diabetes Patients Who Can't Easily Afford it - Good News Network

Global Type 1 Diabetes Drugs Market 2021-2025 The analyst has been monitoring the type 1 diabetes drugs market and it is poised to grow by $ 2. 83 billion during 2021-2025, progressing at a CAGR of almost 6% during the forecast period.

New York, July 05, 2021 (GLOBE NEWSWIRE) -- Reportlinker.com announces the release of the report "Global Type 1 Diabetes Drugs Market 2021-2025" - https://www.reportlinker.com/p06102922/?utm_source=GNW Our report on the type 1 diabetes drugs market provides a holistic analysis, market size and forecast, trends, growth drivers, and challenges, as well as vendor analysis covering around 25 vendors.The report offers an up-to-date analysis regarding the current global market scenario, latest trends and drivers, and the overall market environment. The market is driven by the growing prevalence of type 1 diabetes and feasibility of early diagnosis of type 1 diabetes. In addition, the growing prevalence of type 1 diabetes is anticipated to boost the growth of the market as well.The type 1 diabetes drugs market analysis includes the product segment and geographic landscape.

The type 1 diabetes drugs market is segmented as below:By Product Long-acting insulins Rapid-acting insulins Pre-mixed insulins Non-insulin drugs

By Geography North America Europe Asia ROW

This study identifies the expected launch of novel products as one of the prime reasons driving the type 1 diabetes drugs market growth during the next few years.

The analyst presents a detailed picture of the market by the way of study, synthesis, and summation of data from multiple sources by an analysis of key parameters. Our report on type 1 diabetes drugs market covers the following areas: Type 1 diabetes drugs market sizing Type 1 diabetes drugs market forecast Type 1 diabetes drugs market industry analysis

This robust vendor analysis is designed to help clients improve their market position, and in line with this, this report provides a detailed analysis of several leading type 1 diabetes drugs market vendors that include Astellas Pharma Inc., AstraZeneca Plc, Biocon Ltd., Bristol-Myers Squibb Co., Eli Lilly and Co., MannKind Corp., Novo Nordisk AS, Actiza Pharmaceutical Pvt. Ltd., Sanofi SA, and Viatris Inc. Also, the type 1 diabetes drugs market analysis report includes information on upcoming trends and challenges that will influence market growth. This is to help companies strategize and leverage all forthcoming growth opportunities.The study was conducted using an objective combination of primary and secondary information including inputs from key participants in the industry. The report contains a comprehensive market and vendor landscape in addition to an analysis of the key vendors.

The analyst presents a detailed picture of the market by the way of study, synthesis, and summation of data from multiple sources by an analysis of key parameters such as profit, pricing, competition, and promotions. It presents various market facets by identifying the key industry influencers. The data presented is comprehensive, reliable, and a result of extensive research - both primary and secondary. Technavios market research reports provide a complete competitive landscape and an in-depth vendor selection methodology and analysis using qualitative and quantitative research to forecast the accurate market growth.Read the full report: https://www.reportlinker.com/p06102922/?utm_source=GNW

About ReportlinkerReportLinker is an award-winning market research solution. Reportlinker finds and organizes the latest industry data so you get all the market research you need - instantly, in one place.

__________________________

Story continues

Read the rest here:
The Global Type 1 Diabetes Drugs Market is expected to grow by $ 2.83 billion during 2021-2025, progressing at a CAGR of almost 6% during the forecast...

Chances are, you know someone with diabetes, that not-so-sweet disease most associated with sugar. Maybe it's your sister, aunt or best friend. Or perhaps you have it. If so, you're in good companyHalle Berry, Tom Hanks and Nick Jonas are among the celebrities that also struggle with diabetes, along with more than 100 million Americans who live with diabetes or prediabetes, according to the Centers for Disease Control and Prevention.

In fact, it's one of the most common conditions in the United States, and the numbers are growing. Diabetes has become the 7th largest cause of death in the United States. And the 10 states with the highest rates of type 2 diabetes are in the South. It's not surprising then that the South has its own moniker for the disease: "the sugar."

So you probably think the cause of diabetes is pretty self-evident, right? It's the sugar! Think again. This sweet science report reveals the actual #1 cause. Read onand to ensure your health and the health of others,don't miss these Sure Signs You Have "Long" COVID and May Not Even Know It.

View original post here:
The #1 Cause of Diabetes, According to Science - msnNOW

The ultrastructural morphology exhibited by the 2019 Novel Coronavirus (2019-nCoV), which was identified as the cause of an outbreak of respiratory illness first detected in Wuhan, China, is seen in an illustration released by the Centers for Disease Control and Prevention (CDC) in Atlanta, Georgia, U.S. January 29, 2020. Alissa Eckert, MS; Dan Higgins, MAM/CDC/Handout via REUTERS.

June 28 (Reuters) - The following is a roundup of some of the latest scientific studies on the novel coronavirus and efforts to find treatments and vaccines for COVID-19, the illness caused by the virus.

Pandemic tied to sharp rise in type 2 diabetes in kids

Hospitalization rates for children with newly diagnosed type 2 diabetes rose sharply during the pandemic, two hospitals reported at the American Diabetes Association Scientific Sessions, held virtually this year. At Our Lady of the Lake Children's Hospital in Baton Rouge, Louisiana, children with newly diagnosed type 2 diabetes accounted for 0.62% of inpatients from March through December 2020, up from 0.27% the year before. Those numbers are low, "but just the fact that this rate has more than doubled over the past year is ... significant," said Dr. Daniel Hsia of Pennington Biomedical Research Center in Baton Rouge. Children hospitalized in 2020 had more severe diabetes, with higher blood sugar and more dehydration, than children admitted in the prior year, he said. At Children's National Hospital in Washington, DC, cases of new-onset type 2 diabetes in children increased 182% from 2019 to 2020 - and the children were sicker than in previous years, a separate team reported. Most of these children at both hospitals had not previously had COVID-19. Social distancing measures may have kept children from having regular physical activity and contributed to weight gain, and also kept parents from taking them for routine medical care, all of which may have contributed to more severe illness, researchers speculated. "Our study reinforces the importance of maintaining a healthy lifestyle for children even under such difficult circumstances" Hsia said in a statement. (https://bit.ly/2T4HsV6)

Immune cell "factories" work longer after mRNA vaccines

The tiny "factories" in lymph nodes that churn out antibody-producing B cells to fight infections, called germinal centers, were still functioning to hold COVID-19 at bay for months after people received the mRNA vaccine from BioNTech and Pfizer (PFE.N), according to a new study. After most vaccines, germinal centers last only a few weeks. "Germinal centers are the key to a persistent, protective immune response," said Ali Ellebedy of Washington University School of Medicine in St. Louis, who coauthored a report on Monday in Nature. "Germinal centers are where our immune memories are formed. And the longer we have a germinal center, the stronger and more durable our immunity will be because there's a fierce selection process happening there, and only the best immune cells survive." Researchers studied cells from germinal centers in armpit lymph nodes of 14 recipients of the Pfizer/BioNTech vaccine. Three weeks after the first dose, all 14 had germinal centers that were still generating B cells. B-cell production "expanded greatly" after the second shot and stayed high, they reported. Eight of 10 people biopsied 15 weeks after the first dose, still had functioning germinal centers. "We're still monitoring the germinal centers, and ... in some people, they're still ongoing," Ellebedy said. "This is truly remarkable." The same effect is likely also true for Moderna's O> mRNA vaccine, the researchers believe. Ultimately, immune cells called T cells are what sustains the germinal centers' work after they disappear. The researchers plan next to investigate the magnitude and durability of T cell responses after mRNA COVID-19 vaccines. (https://go.nature.com/3jr3WtZ)

Following AstraZeneca with Pfizer shot boosts antibody response

Giving a dose of the Pfizer/BioNTech COVID-19 vaccine four weeks after an AstraZeneca (AZN.L) shot produces better immune responses than a second dose of AstraZeneca's, Oxford University researchers said on Monday. In a study of 830 older adults, mixed two-dose schedules of AstraZeneca and Pfizer vaccines produced higher concentrations of antibodies against the coronavirus that a full schedule of the AstraZeneca shot. The most effective approach two doses of Pfizer/BioNTech mRNA vaccine - produced levels of antibodies about 10 times higher than two doses of the AstraZeneca vaccine, the researchers reported on Friday in a Lancet preprint. However, the AstraZeneca shot followed by a Pfizer jab induced antibody levels about as high as two Pfizer/BioNTech doses. Giving the Pfizer shot first, followed by AstraZeneca's, was not as successful. That combination yielded antibody levels higher than two AstraZeneca shots but lower than two doses of the Pfizer vaccine. There were no new safety issues uncovered in the study. Matthew Snape, the Oxford professor behind the trial, said the findings could be used to give flexibility to vaccine rollouts but were not significant enough to recommend a broad shift away from clinically approved schedules. (https://bit.ly/3xXX37B)

COVID-19, not Pfizer's vaccine, tied to Bell's palsy

The Pfizer/BioNTech vaccine has not been linked with a higher risk for the facial nerve paralysis known as Bell's palsy, but COVID-19 itself does increase the risk, suggest two separate studies published on Thursday in JAMA Otolaryngology-Head and Neck Surgery. One study involved 110 people in Israel who received the Pfizer vaccine, including 37 in whom the characteristic facial droop developed on average nine days after the first dose or 14 days after the second. After accounting for underlying risk factors for Bell's palsy, the researchers concluded the vaccine itself did not increase the risk. Furthermore, they found, rates of Bell's palsy had not gone up during the vaccine rollout. In the second study, researchers compared Bell's palsy rates among roughly 348,000 patients with COVID-19 and roughly 63,500 people who had been vaccinated against the coronavirus. The Bell's palsy risk was nearly seven times higher in those with COVID-19, they found. "Our data suggest that rates of facial nerve palsy are higher in patients who are positive for COVID-19, and this incidence exceeds the reported incidence of Bell's Palsy with the COVID-19 vaccine," said Dr. Akina Tamaki of University Hospitals Cleveland Medical Center, who coauthored that study. "Taken together, it supports that the vaccine is safe from a facial nerve paralysis standpoint." (https://bit.ly/2Tiw6wx, https://bit.ly/3hgiEBu, and https://bit.ly/3y3mi8A)

Open https://tmsnrt.rs/3c7R3Bl in an external browser for a Reuters graphic on vaccines in development.

(Corrects first item to reflect updated diabetes figures from Children's National Hospital, changes more than doubled to rose sharply)

Reporting by Nancy Lapid, Megan Brooks, Marilynn Larkin and Alistair Smout; Editing by Bill Berkrot

Our Standards: The Thomson Reuters Trust Principles.

The rest is here:
Pandemic tied to spike in diabetes in children; type of immune response lasts months after Pfizer/BioNTech vaccine - Reuters

Singer and actor Nick Jonas, who lives with type 1 diabetes and uses a continuous glucose monitor (CGM) himself, is throwing his celebrity status behind a new global effort promoting Time in Range as a powerful metric for modern diabetes management.

The big idea is to spread awareness among people with diabetes (PWDs) everywhere that focusing on Time in Range (TIR) can help them keep their glucose levels steadier and improve quality of life. It is fundamentally a more useful metric than the longstanding gold standard A1C, which only indicates a mathematical average.

This celebrity campaign kicked off June 24 just before the start of the American Diabetes Associations annual meeting, with Jonas and diabetes orgs like Beyond Type 1, JDRF, and several others signing on with San Diego based CGM-maker Dexcom to lead the effort.

Its all part of a growing push to make CGM technology a standard of care that healthcare professionals will use regularly to better monitor daily, weekly, and monthly glucose level patterns and make decisions based on that data.

Its time to kick-start the conversation here around the importance of Time in Range and how it makes peoples lives better, Jonas said on a press call with diabetes advocates, announcing the new initiative.

Advocates have long been fighting to prioritize TIR because it gives people a sense of how often they are staying within the desired, healthy glucose range.

This is different than the traditional A1C lab test that only provides an average of glucose levels over the prior 3 months, but doesnt reflect change or variability. So, two people with an A1C of 6.7 percent could have very different management profiles, where one has the coveted flatline, but the other person has highly variable glucose levels with frequent hypoglycemia. Or someone could have an ideal A1C level of 6 percent, but it only reflects a middle point between 3 months of severe high and low blood sugars.

TIR, on the other hand, uses continuous glucose monitor (CGM) results to show the amount of time a PWD stays within the desired range, expressed in an average of hours and minutes over any period of days, weeks, or months.

The Beyond A1C movement spearheaded by the diaTribe Foundation can now take a victory lap, with increasing recognition of TIR as a new established parameter for doctors to evaluate blood glucose control in PWDs.

A global consensus of diabetes experts define the target range as 70 to 180 mg/dL, and the new International Consensus on Time in Range recommends that patients should stay within that range at least 70 percent of the time.

Increasing research shows that glucose variability may play nearly as large a part in poor diabetes outcomes as do the glucose levels themselves. TIR helps PWDs and doctors identify variability far more efficiently than A1C.

It simply better reflects how peoples lives are being impacted by diabetes, including things like fear of hypoglycemia overnight, losing control and not being able to safely manage our own actions, or the stress and mental burdens we experience when eating foods that make our blood sugars rise dramatically and impact our moods.

Yet, most PWDs on insulin are not yet using TIR or dont discuss it with their healthcare provider (HCP). In the press announcement, Dexcom published results of a survey based on their internal company data from November 2020, that found:

Jonas, who co-founded the nonprofit Beyond Type 1, has openly talked about using the Dexcom CGM for years. He starred in a high-profile Superbowl ad for Dexcom in February 2021, and with that, has probably done more to raise the profile of diabetes among a younger generation than any celebrity ever.

DiabetesMine was fortunate to interview him a few times over the years following his diagnosis as a teenager in 2005 especially once he teamed up with Dexcom.

Now, hes using his platform to promote this TIR initiative to both promote the Dexcom CGM and further his mission to show people that its possible to live a healthy, active, productive life with diabetes.

The campaign site When In Range went live on June 24, with a variety of infographics, materials, and videos to explain TIR and help people achieve it through different technologies and treatments.

On the morning of this collaborations announcement, a group of diabetes advocates were invited to join a brief online call with Jonas to hear him discuss it. DiabetesMine posed a question about where A1C results fit into this new campaign. Many believe that A1C and TIR can complement each other, and thats what Jonas responded with when asked the question.

The more information the better, he said.

Of course, a key question for all on the Jonas call was about access and affordability of CGM technology.

Its no secret that pricing and accessibility are major barriers to CGM use necessary to efficiently monitor TIR and many who have a medical need for this technology cant afford a CGM.

Im very aware, as all of us on this call are of the need for access and that growing conversation is a priority for us all, in the U.S. and globally, Jonas said. He recognized that his Super Bowl ad upset some people for that reason, but emphasized that raising awareness about diabetes on a mass scale helps lay the foundation for change. I think that helps the bigger conversation about this need for access around the world, he said.

While CGM is the most common tech used to track TIR, there are ways to monitor it using traditional fingerstick meters with a digital platform to analyze the data. That method certainly doesnt generate as much glucose data on a continuous basis, but it can be helpful in showing broader patterns and management trends.

TIR is already included in the standards of care released by the American Diabetes Association (ADA), American Association of Clinical Endocrinologists (AACE), and other diabetes medical groups. Thats making it more of a focus for clinicians to talk with their patients about, whether for in-person or virtual visits. And its certainly a metric being integrated into many diabetes devices and mobile apps, for PWDs to view regularly.

TIR was a big topic at the ADAs annual Scientific Sessions in late June 2021. Multiple diabetes experts in a variety of presentations highlighted the importance of TIR as they discussed latest research findings and management, complications that can materialize despite ones A1C result, and even policy implications from looking at TIR rather than just A1C.

Natalie J. Bellini

One of those experts presenting on TIR at the conference was Natalie J. Bellini, a New York endocrine nurse practitioner and certified diabetes care and education specialist (CDCES), who is part of the Time in Range Coalition created by the diaTribe Foundation, aiming to make TIR the primary glucose metric for diabetes care going forward.

I think the new global media movement will help propel the conversation between patients and providers, she told DiabetesMine. Patients who are referred to our practice using CGM do not all come in with medical records discussing TIR. I think we, as clinicians, need to use the tools we have to help patients reduce the risks of hyper and hypoglycemia by increasing awareness and analyzing data in a way that helps them address their personal time in range.

She notes that therapy goals resulting from TIR data could include things like urgency in reducing hypoglycemia or prebolusing to reduce postprandial spiking, followed by changes to insulin pump settings or increased or decreased basal insulin, changes insulin to carb or sensitivity factors, etc. These are very fundamental and critical elements of managing diabetes on a daily basis.

Time in range has given us a new tool to improve patient outcomes by opening discussions around insulin dosing, insulin timing, specific behaviors, other medications, stress, and all kinds of other factors we were not able to do before, Bellini said. Patients and clinicians alike need to adopt it into their vernacular. We also need more randomized controlled studies that help link time in range, time below range, and time above range to outcomes [but] those are expensive and take a long time.

Read the rest here:
Nick Jonas Kicks Off Diabetes 'Time in Range' Initiative - Healthline

Introduction

The increase in the size of the global aging population and the prevalence of type 2 diabetes mellitus (T2DM) have led to grave individual, societal, and financial burdens associated with diabetes-related cognitive dysfunction.1,2 Studies have indicated that individuals suffering from diabetes have a 1.5-to-2.5-times increased risk of cognitive decline,3 and the dementia progression cannot be reversed once clinical symptoms occur.4 Thus, early diagnosis is beneficial for delaying disease progression and improving prognosis.

Diabetic peripheral neuropathy (DPN) occurs in up to 50% of patients with type 2 diabetes,5 and can lead to disability and amputation; therefore, it is associated with poor quality of life and high mortality.68 However, the relationship between DPN and cognitive impairment is not clear. One study observed no significant differences in cognitive function between patients with and without DPN,9 whereas a follow-up study found that DPN carried a 1.61-times higher risk of the development of mild cognitive impairment (MCI).10 Therefore, assessing the clinical features of cognitive decline in patients with DPN merits investigation.

Olfactory tests have potential utility for screening for MCI,11 as olfactory impairment is related to neurodegenerative diseases and T2DM.11,12 Typically, olfactory dysfunction occurs at 48 years before the diagnosis of Parkinsons disease,13 and low scores in olfactory tests suggest an increased probability of a diagnosis of Alzheimers disease over the subsequent 25 years.14 We previously revealed that the olfactory threshold scores were lower in patients with T2DM than in people not suffering from T2DM, and that alterations in olfactory behavior occurred before clinically measurable cognitive decrements in T2DM.15 The application of magnetic resonance imaging (MRI) and functional MRI (fMRI) have confirmed the reductions in odor-induced brain activation and the weakened functional connectivity (FC) in the olfactory network in patients with T2DM.15,16 However, alterations in the olfactory network of patients with DPN have not been investigated.

In the present study, we evaluated the cognitive function, olfactory behavior, and activation of olfactory-related brain functions in healthy controls (HCs), T2DM patients without DPN, and T2DM patients with DPN. This allowed us to explore the clinical features of cognitive decline and the role of olfactory-circuit alterations on cognitive dysfunction in T2DM patients with DPN.

This study was carried out from August 2017 to August 2019 at Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School. The HCs and patients with T2DM were recruited. T2DM was diagnosed according to the criteria set by the World Health Organization/International Diabetes Federation. The data of 100 individuals (64 T2DM patients and 36 HCs) matched for age, sex, and educational level were analyzed. The inclusion criteria were patients: (i) aged from 40 to 75 years; (ii) right-handed; and (iii) with over 6 years of education. The exclusion criteria were patients: (i) with neurological and psychiatric disorders, anxiety or depression; (ii) with a history of frequent hypoglycemic episodes, cerebrovascular disease or cardiovascular disease, corticosteroid treatment, abnormal thyroid function, alcohol/substance abuse, infections or cancer; (iii) with nondiabetic peripheral neuropathies: cervical spine and lumbar disease, connective tissue disease, inflammatory neurologic diseases, or exposure to peripheral neurotoxicity of chemicals; (iv) with nasal diseases affecting olfactory function (eg, allergic rhinitis, acute/chronic sinusitis, deviated nasal septum, or nasal polyposis); (v) without the ability to undergo olfactory tests or MRI; (vi) with excessive head movement during fMRI (>2.5 rotation or >2.5 mm shift and image artifacts).

A system from Nihon Kohden (Tokyo, Japan) was used for electromyographic measurements of the nerve conduction velocity (NCV) by a very experienced technician. The skin temperature of the patients was stabilized to approximately 31C at a room temperature of 24C. The NCV was assessed on both sides: median nerve (motor and sensory), ulnar nerve (motor and sensory), common peroneal nerve (motor), tibial nerve (motor), and sural nerve (sensory). Nerve conduction was considered abnormal if 3 of the tested NCVs were reduced below the reference value specific to the Chinese population.17 Abnormalities of nerve conduction and the symptoms or signs of neuropathy were used to confirm DPN.6 The DPN symptoms included neuropathic sensory symptoms, mainly in the legs, feet, or toes, as well as numbness, prickling, burning, or aching pain. DPN signs included symmetrical reduction in distal sensation or decreased/absent ankle reflexes.

The Mini-Mental State Examination (MMSE) and Montreal Cognitive Assessment (MoCA; Beijing Version) were used to evaluate general cognition.18 A MoCA score of 1925 was regarded as evidence of mild cognitive impairment. Multiple cognitive subdomains were also assessed. The 16-word Philadelphia Verbal Learning and Wechsler Memory Scale tests Trail Making Test (Parts A and B), Animal Naming Test, Boston Naming Test, Stroop Color-Word Test (Parts I, II and III), and Digit Span Test (forward and backward) were conducted to evaluate episodic memory, information-processing speed, word fluency, executive function, and working memory. All tests needed approximately 60 minutes to complete in a fixed order.

Olfactory tests were carried out using the Olfactory Function Assessment by Computerized Testing (OLFACTTM) with a system from Osmic Enterprises (Cincinnati, OH, USA), as described previously.16 The olfactory tests were computerized and standardized. The olfactory threshold test was conducted using a series of binary dilutions of an n-butanol solution in light mineral oil. The scores indicated the sensitivity of participants to detect odors, and the values ranged from 1 to 13.5. The olfactory identification test and memory test had two tasks: task A had 10 odors, while task B had the same 10 odors as task A, as well as 10 new odors. Participants were exposed to the odors and were required to identify each one from four pictures in the two tasks. In task B, they also had to indicate whether each odor was new or old. Participants had a 10-min break between tasks A and B.

Clinical data were collected using a standardized questionnaire that included information on demographics, T2DM duration, alcohol consumption and smoking, history of stroke, and family history of T2DM, as well as measurements of height, weight, waist circumference, hip circumference, and resting blood pressure. Patients with T2DM underwent a 100 g standard meal test. Individuals without previously diagnosed T2DM were subjected to a 75 g oral glucose tolerance test after an overnight fast of at least 8 h. Plasma concentrations of glucose, insulin, and C-peptide were measured upon fasting and 2 h after glucose ingestion. Concentrations of glycosylated hemoglobin (HbA1c), total cholesterol (TC), triglyceride (TG), high-density lipoprotein-cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C) were also measured.

Our previous study utilized the odor-induced fMRI paradigm,15 which consists of 12 trials. Every trial comprised 30 seconds of odorless fresh air and 6 seconds of odor stimulation with lavender oil (Givaudan Flavors, East Hanover, NJ, USA). Four gradually increasing concentrations of oil (0.032%, 0.10%, 0.32%, and 1.0%) were diluted in 1,2-propanediol (SigmaAldrich, Saint Louis, MO, USA) to offset the effect of brain habituation. Each concentration was used three times, alternating between fresh air and lavender scent. Throughout the fMRI, the technician asked participants to keep breathing and press the button once they smelled the lavender scent.

Image data were acquired on a 3.0T MRI scanner (Achieva 3.0T TX, Philips Medical Systems, The Netherlands) with an 8-channel head coil. T1-weighted images were acquired with TR/TE=9.7 ms/4.6 ms, FA=8, FOV=256 mm 256 mm 192 mm, voxel size= 1 mm 1 mm 1 mm. Functional MRI was acquired with a gradient-echo planar imaging sequence scan, TR/TE=2300 ms/30 ms, FA=90, FOV=192 mm 192 mm 140 mm, slice thickness = 4 mm, voxel size=3 mm 3 mm 4 mm, with 230 repetitions for resting-state fMRI and 222 repetitions for odor-induced fMRI.

Statistical Parametric Mapping (SPM12, Wellcome Trust Centre for Human Neuroimaging, London, UK) was used to preprocess the fMRI data. SPM12 was undertaken in six distinct steps. In step 1, the first six images of the task scan and the first 10 images of the resting state scan were discarded to remove fluctuations in the initial transit signal. In step 2, spatial realignment was done to remove head movements: shift <3 mm and rotation <3. Step 3 consisted of co-registration with the T1-weighted high-resolution anatomical image. Step 4 was spatial normalization to the brain template of the Montreal Neurological Institute. Step 5 was spatial smoothing with an 8-mm Gaussian smoothing kernel. Step 6 was linear detrending and temporal band-pass filtering (0.010.08 Hz) to eliminate high-frequency noise and low-frequency drift.

Brain activation during the olfactory-stimulation tasks was estimated using a general linear model. Each participant had three conditions in the fMRI task: fresh air, scent, and rest. Contrasts were made between every two conditions. We chose several olfactory-related regions as our regions of interest (ROI); these covered the hippocampus, bilateral parahippocampus, piriform cortex, amygdala, insula, and orbitofrontal cortex in the Automated Anatomical Labeling templates and Brodmann areas 28 and 34 (entorhinal cortices). The total cluster size was 5029 voxels. Differences in activations between groups were estimated as beta values.

FC was computed using a seed-based correlation analytical method. Seed regions were selected as brain regions that showed significantly different activation during olfactory stimulation in patients with DPN when compared with patients not suffering from DPN. We then extracted the time series of the signal in the seed regions and used these time series to generate voxel-wise FC maps.

Data for continuous variables are presented as the mean standard deviation and dichotomous variables as percentages. One-way analysis of variance (ANOVA), followed by Dunnetts test, was conducted for continuous variables. Pearson chi-square was performed for dichotomous variables. Independent-samples t-tests were used to compare the duration in both diabetes groups. Partial correlation analyses, controlled for age, sex, and educational level, were conducted to analyze the association of the NCV with olfactory behavior and cognitive function. Differences were considered statistically significant when P was < 0.05. These analyses were undertaken with SPSS v20.0 (IBM, Armonk, NY, USA).

DPABI (v4.1_190725) was used to analyze the fMRI data. Differences in brain function were determined using voxel-based independent-sample t-tests for odor-induced brain activation and seed-based FC of the resting state between two groups. Correction of the significance threshold was based on Gaussian random field (GRF) theory, with a voxel level of P < 0.001 and a cluster level of P < 0.05.

Structural equation modeling (SEM) using SPSS Amos version 24 was conducted to determine the interrelationships of nerve conduction, the olfactory system, and cognitive function. The mean- and variance-adjusted maximum likelihood test statistic (MLMV) was performed for the SEM, given its robustness for data with non-normal distribution. Root mean square error of approximation (RMSEA; good if 0.08); normal fit index (NFI > 0.90); comparative fix index (CFI >0.90); and TuckerLewis index (TLI >0.90) were used to assess the global structural fitness of the model.

Overall, 100 individuals matched for age, sex, and educational level were analyzed: 36 T2DM patients without DPN (NDPN group), 28 T2DM patients with DPN (DPN group), and 36 HCs. The T2DM patients had higher HbA1c levels, fasting and two-hour plasma glucose levels, waist circumference, and waist-to-hip ratios, and lower postprandial C-peptide levels when compared with the HCs. The DPN group had higher HbA1c levels than the NDPN group. No significant differences were noted in the TG or TC levels. The motor conduction velocity (MCV) of the median nerve, ulnar nerve, common peroneal nerve, and tibial nerve and the sensory conduction velocity (SCV) of the median nerve, ulnar nerve, and sural nerve were slower in the DPN patients than in the NDPN cases and HCs (Table 1).

Table 1 Demographics, Clinical and Metabolic Characteristics, Cognitive Assessment Scores, and Olfactory Test Scores of T2DM Patients by DPN Status

The MMSE, MoCA score, memory, processing speed, working memory, and executive function were all significantly lower in the DPN patients than in the HCs. Compared with the NDPN group, the DPN group had a significantly lower score for memory (155.215.2 vs 142.0 20.0, p= 0.042) and a longer time required for the processing speed test (102.337.9 vs 134.269.2, p=0.004) (Table 1).

Olfactory behavior, including odor identification and memory, was decreased in the DPN patients compared with the NDPN patients. The DPN group had a significantly lower score than the HCs for the olfactory threshold and odor identification and memory (Table 1).

Correlation analyses among patients with T2DM showed that memory had a positive association with the MCV and SCV of the ulnar nerve. Time spent in executive function and the processing speed test had a negative association with the MCV and SCV of the ulnar nerve. Higher olfactory identification and memory scores were correlated with faster SCVs of the median nerve (Table 2).

Table 2 Correlation of Neuropathy Parameters with Cognitive Assessment and Olfactory Behavior Test in Patients with Type 2 Diabetes

The olfactory-related regions of the brain were bilaterally activated after odor stimulation (Figure 1A and B). The independent-sample t-test showed reduced activation in the left frontal lobe in patients with DPN compared with that in the NDPN group (cluster size threshold: 51 voxels, with GRF correction, voxel level: P < 0.001, cluster level: P < 0.05,) (Figure 1CE). Positive associations were detected between activation of the left frontal lobe and sensory activation of the ulnar nerve and sural nerve (Figure 2).

Figure 1 Comparison of odor-induced brain activation in DPN and NDPN. Olfactory-related regions of the brain were activated after odor stimulation in DPN (A) and NDPN (B). Significantly decreased brain activation was demonstrated in DPN compared to NDPN (with GRF correction, voxel level: P < 0.001, cluster level: P < 0.05, cluster size threshold: 51 voxels) (C). value is decreased in the left frontal lobe in DPN (D and E). Independent sample t test. ***P < 0.001. L, left; R, right.

Figure 2 Associations between odor-induced brain activation and nerve conduction. Positive associations between the activation of the left frontal lobe and sensory nerve conduction of ulnar nerve (A) and sural nerve (B) in DPN group.

Abbreviation: SCV, sensory conduction velocity.

As shown in Figure 3, the independent-sample t-test revealed significantly decreased seed-based FC in the right insula in the DPN group compared with the NDPN group (cluster size threshold: 129 voxels, with GRF correction; voxel level: P < 0.001, cluster level: P < 0.05).

Figure 3 Comparison of seed-based functional connectivity in DPN and NDPN. The seed-based functional connectivity was shown in DPN (A) and NDPN (B). Significantly decreased brain functional connectivity was demonstrated in DPN compared to NDPN (with GRF correction, voxel level: P < 0.001, cluster level: P < 0.05, cluster size threshold: 129 voxels) (C). Seed-based functional connectivity with right insula is decreased in DPN (D and E). Independent sample t test. ***P < 0.001. L, left; R, right.

The path model (Figure 4) showed satisfactory model fit statistics, with CMIN/DF=1.510, CFI =0.971, NFI = 0.926, TLI =0.912, and RMSEA=0.071. The results show that the SCV of the median nerve is directly associated with the score for olfactory identification ( = 0.349, p = 0.006, 95% CI = 0.1080.563) and executive function ( = 0.266, p = 0.009, 95% CI = 0.449 0.067). The score for olfactory identification were negatively associated with the executive function consumption ( = 0.367, p = 0.002, 95% CI = 0.585 0.140). Given that there was a direct association between the SCV and executive function, the Sobel test of indirect effect confirmed that olfactory identification partially mediated the association between the SCV and executive function ( = 0.128, p = 0.003, 95% CI = 0.2780.039). Effect size calculations using MacKinnons formula (ie, the indirect effect: = 0.128 divided by the total effect: = 0.395) showed that the partial mediated percentage was 32% representing a small effect size according to Cohens guidelines.

Figure 4 Structual model among cognition, olfactory behavior and neuropathy parameters. Adjusted mediation model predicting executive function among diabetes with DPN. Analyses are adjusted for age, sex, and education. **p < 0.01, pathway.

We demonstrated that patients with DPN, when compared to those without DPN, suffered a decline in cognitive domains in memory and processing speed that correlated with the NCV. Moreover, the patients with DPN exhibited impaired olfactory behavior and decreases in activation in the left frontal lobe and in seed-based functional connectivity in the right insula. Furthermore, the results of the electrophysiological examination, combined with the observed olfactory behavior, could predict cognitive decline in T2DM patients.

Patients with DPN suffered a decline in the cognitive domains of memory and processing speed. Recently, several studies have reported results for cognition in T2DM patients.1 Diabetes-associated cognitive decrements have been reported to develop approximately 50% faster than those observed in normal cognitive aging.19 However, few studies have focused on cognition in DPN. Moreira and colleagues showed that cognitive impairment does not seem to have a relationship with the presence and severity of DPN; however, only a neurologic deficit scale (NDS) and a neurological severity score (NSS) were used for the diagnosis of DPN, while cognitive function was assessed using MMSE, the Trail Making Test (part A), the Trail Making Test (part B), and the Verbal Fluency TestAnimals.3 By contrast, we measured the SCV and MCV of the upper and lower limbs, as well as the general cognitive function and detailed cognitive domains. We demonstrated, for the first time, that patients with DPN had a worse cognitive memory function and processing speed than was observed in patients without DPN, and that the NCVs were related to several cognitive domains.

Olfactory dysfunction is viewed as a potential and early indicator for the diagnosis of neurodegenerative disorders,20 as it predicts incident mild cognitive impairment.21 In addition, reduced olfactory-threshold scores have been found in T2DM patients with apparently normal cognition,15 and Gouveri and colleagues found that olfactory dysfunction was associated with retinopathy.22 We have provided new evidence that patients with DPN had worse odor identification and poorer memory than patients who did not have DPN, and the DPN effects had a positive correlation with NCVs. Our use of computerized and standardized olfactory tests instead of Sniffin Sticks made our data more robust.

Emerging evidence from MRI and fMRI studies has shown an impact of DPN on the structure and function of the brain.23 People suffering from DPN who show lower gray-matter volume (globally and regionally) also walk more slowly and have greater variations in stride duration and/or longer support.24 Recent fMRI research has revealed an association between the poor functional performance in patients with DPN and greater activation in motor preparation regions.25 Similarly, MRI findings have revealed an involvement of the central nervous system, including dysfunction of somatosensory afferent pathways, in DPN.26,27 In addition, approximately 50% of patients with DPN can experience painful neuropathic symptoms, which are the most distressing symptoms of DPN.28,29 A number of central mechanisms, including central sensitization, changes in the balance of facilitation/inhibition within descending pathways, and increased thalamic vascularity, have recently been proposed based on experiments on neuropathic pain.23,30 The dorsal root ganglion has been considered as a treatment target for neuropathic pain because of its structure at the communication point in the transition from the peripheral to the central nervous system.31 However, few studies have focused on olfactory-related regions and functional connectivity. We have revealed a reduced activation in the left frontal lobe and a reduction in seed-based functional connectivity in the right insula in patients with DPN compared with those without DPN. These findings indicate a connection between the activation of olfactory neural circuits and DPN.

We observed that conduction in the ulnar nerve was correlated significantly with cognition and olfactory behavior in T2DM patients. Olfactory identification acted as a mediating factor in the effect of NCV on executive function, suggesting an involvement of olfactory function in the cognitive impairment in DPN. Peripheral nerves, including the trigeminal nerve, glossopharyngeal nerve, and vagus nerve, in addition to the olfactory nerve, are involved in the formation of the olfactory system.32 The olfactory neural circuits in the hippocampus are also connected with cognition, including memory processes.33 Our findings suggest that olfactory dysfunction may have a role in the pathogenesis of peripheral neuropathy and cognitive impairment, and that declines in olfactory capabilities could be indicators of cognitive decline in patients with DPN.

Our study had two main limitations. One was that the sample size was relatively small. Nevertheless, our patients were well matched for age, sex, and educational level, and we believe our study could provide insights into central changes in DPN patients. The second limitation was its cross-sectional design, which precludes any comments on the causal relationship between DPN and olfactory dysfunction in patients with DPN. Follow-up studies are warranted to ascertain the role of olfactory dysfunction in DPN and to determine if olfactory dysfunction could be an early sign of DPN and cognitive impairment.

This was the first study to demonstrate that patients with DPN had worse cognitive function in the domains of memory and processing speed compared to patients without DPN. Examinations of nerve conduction, combined with olfactory tests, might therefore aid in the early detection of cognitive impairment in patients with T2DM. Greater attention should be focused on screening for cognitive impairment in patients with DPN.

DPN, diabetic peripheral neuropathy; T2DM: type 2 diabetes mellitus; magnetic resonance imaging (MRI); fMRI, functional magnetic resonance imaging; FC, functional connectivity; MCI, mild cognitive impairment; NCV, nerve conduction velocity; HbA1c, glycosylated hemoglobin; TC, total cholesterol; TG, triglyceride; HDL-C, high-density lipoprotein-cholesterol; LDL-C, low-density lipoprotein cholesterol; ROI, regions of interest; GRF, Gaussian random field; MCV, motor conduction velocity; SCV, sensory conduction velocity; NDS, neurologic deficit scale; NSS, neurological severity score; BMI, body mass index; WHR, waist-hip ratio; MMSE, Mini-Mental State Examination; MoCA, Montreal Cognitive Assessment. ANT, Animal Naming Test; AVLT, Auditory Verbal Learning Test; BNT, Boston Naming Test; DST, Digit Span Task; SCWT, Stroop Color and Word Test; TMT, Trail Making Test; WASI, Wechsler Abbreviated Scale of Intelligence; SEM, Structural Equation Modeling; RMSEA, Root Mean Square Error of Approximation; NFI, Normal Fit Index; CFI, Comparative Fix Index; TLI, TuckerLewis Index.

All procedures performed in studies involving human participants were in accordance with the ethical standards of the institutional research committee and with the 1964 Helsinki Declaration and its later amendments or comparable ethical standards.

The data that support the findings of this study are available from the corresponding author upon reasonable request.

Our survey was approved by the Ethics Review Committee of Drum Tower Hospital. The registered clinical trial number on ClinicalTrails.gov is NCT 02738671.

All participants provided written informed consent prior to their inclusion in the study.

The authors would like to thank all volunteers for their participation in this study and thank medical personnel from Department of Endocrinology and Department of Radiology, Drum Tower Hospital affiliated to Nanjing University Medical School, for their valuable assistance. Wenyu Ni and Zhou Zhang shared first authorship.

This work was supported by the National Natural Science Foundation of China Grant Awards (82000775, 82030026, 81970689, 81970704, 81770819, 81703294, 81800752, 81900787, and 81800719), the National Key Research and Development Program of China (2016YFC1304804 and 2017YFC1309605), the Jiangsu Provincial Key Medical Discipline (ZDXKB2016012), the Key Project of Nanjing Clinical Medical Science, the Key Research and Development Program of Jiangsu Province of China (BE2015604 and BE2016606), the Jiangsu Provincial Medical Talent (ZDRCA2016062), the Six Talent Peaks Project of Jiangsu Province of China (YY-086), the Scientific Research Project of the Fifth Phase of 333 Project of Jiangsu Province of China, the Fundamental Research Funds for the Central Universities (021414380444).

The authors report no conflicts of interest in this work.

1. Livingston G, Huntley J, Sommerlad A, et al. Dementia prevention, intervention, and care: 2020 report of the lancet commission. Lancet. 2020;396(10248):413446. doi:10.1016/S0140-6736(20)30367-6

2. Jia L, Du Y, Chu L, et al. Prevalence, risk factors, and management of dementia and mild cognitive impairment in adults aged 60 years or older in China: a cross-sectional study. Lancet Public Health. 2020;5(12):e661e671. doi:10.1016/s2468-2667(20)30185-7

3. Biessels GJ, Despa F. Cognitive decline and dementia in diabetes mellitus: mechanisms and clinical implications. Nat Rev Endocrinol. 2018;14(10):591604. doi:10.1038/s41574-018-0048-7

4. Livingston G, Sommerlad A, Orgeta V, et al. Dementia prevention, intervention, and care. Lancet. 2017;390(10113):26732734. doi:10.1016/S0140-6736(17)31363-6

5. Feldman E, Callaghan B, Pop-Busui R, et al. Diabetic neuropathy. Nat Rev Dis Primers. 2019;5(1):41. doi:10.1038/s41572-019-0092-1

6. Tesfaye S, Boulton AJ, Dyck PJ, et al. Diabetic neuropathies: update on definitions, diagnostic criteria, estimation of severity, and treatments. Diabetes Care. 2010;33(10):22852293. doi:10.2337/dc10-1303

7. Boulton AJM, Vileikyte L, Ragnarson-Tennvall G, Apelqvist J. The global burden of diabetic foot disease. Lancet. 2005;366(9498):17191724. doi:10.1016/S0140-6736(05)67698-2

8. Selvarajah D, Kar D, Khunti K, et al. Diabetic peripheral neuropathy: advances in diagnosis and strategies for screening and early intervention. The lancet. Diabetes & Endocrinology. 2019;7(12):938948. doi:10.1016/s2213-8587(19)30081-6

9. Moreira RO, Soldera AL, Cury B, Meireles C, Kupfer R. Is cognitive impairment associated with the presence and severity of peripheral neuropathy in patients with type 2 diabetes mellitus? Diabetol Metab Syndr. 2015;7.

10. Roberts RO, Knopman DS, Geda YE, et al. Association of diabetes with amnestic and nonamnestic mild cognitive impairment. Alzheimers Dement. 2014;10(1):1826. doi:10.1016/j.jalz.2013.01.001

11. Roberts RO, Christianson TJH, Kremers WK, et al. Association between olfactory dysfunction and amnestic mild cognitive impairment and alzheimer disease dementia. JAMA Neurol. 2016;73(1):93101. doi:10.1001/jamaneurol.2015.2952

12. Dintica CS, Marseglia A, Rizzuto D, et al. Impaired olfaction is associated with cognitive decline and neurodegeneration in the brain. Neurology. 2019;92(7):e700e709. doi:10.1212/wnl.0000000000006919

13. Mahlknecht P, Iranzo A, Hogl B, et al. Olfactory dysfunction predicts early transition to a Lewy body disease in idiopathic RBD. Neurology. 2015;84(7):654658. doi:10.1212/Wnl.0000000000001265

14. Devanand DP, Tabert MH, Cuasay K, et al. Olfactory identification deficits and MCI in a multi-ethnic elderly community sample. Neurobiol Aging. 2010;31(9):15931600. doi:10.1016/j.neurobiolaging.2008.09.008

15. Zhang Z, Zhang B, Wang X, et al. Altered Odor-Induced Brain Activity as an Early Manifestation of Cognitive Decline in Patients With Type 2 Diabetes. Diabetes. 2018;67(5):9941006. doi:10.2337/db17-1274

16. Zhang Z, Zhang B, Wang X, et al. Olfactory dysfunction mediates adiposity in cognitive impairment of type 2 diabetes: insights from clinical and functional neuroimaging studies. Diabetes Care. 2019;42(7):12741283. doi:10.2337/dc18-2584

17. Bronzino JD, ed. Electromyography Diagnosis and Clinical Application. Peoples Medical Publishing House; 2013.

18. Nasreddine ZS, Phillips NA, Bedirian V, et al. The montreal cognitive assessment, MoCA: a brief screening tool for mild cognitive impairment. J Am Geriatr Soc. 2005;53(4):695699. doi:10.1111/j.1532-5415.2005.53221.x

19. Preacher KJ, Hayes AF. Asymptotic and resampling strategies for assessing and comparing indirect effects in multiple mediator models. Behav Res Methods. 2008;40(3):879891. doi:10.3758/brm.40.3.879

20. Moreira RO, Soldera AL, Cury B, Meireles C, Kupfer R. Is cognitive impairment associated with the presence and severity of peripheral neuropathy in patients with type 2 diabetes mellitus? Diabetol Metab Syndr. 2015;7(1):51. doi:10.1186/s13098-015-0045-0

21. Doty RL. Olfactory dysfunction in neurodegenerative diseases: is there a common pathological substrate? Lancet Neurol. 2017;16(6):478488. doi:10.1016/s1474-4422(17)30123-0

22. Conti MZ, Vicini-Chilovi B, Riva M, et al. Odor identification deficit predicts clinical conversion from mild cognitive impairment to dementia due to Alzheimers disease. Arch Clin Neuropsychol. 2013;28(5):391399. doi:10.1093/arclin/act032

23. Gouveri E, Katotomichelakis M, Gouveris H, Danielides V, Maltezos E, Papanas N. Olfactory dysfunction in type 2 diabetes mellitus: an additional manifestation of microvascular disease? Angiology. 2014;65(10):869876. doi:10.1177/0003319714520956

24. Tesfaye S, Selvarajah D, Gandhi R, et al. Diabetic peripheral neuropathy may not be as its name suggests: evidence from magnetic resonance imaging. Pain. 2016;157(Suppl 1):S7280. doi:10.1097/j.pain.0000000000000465

25. Manor B, Newton E, Abduljalil A, Novak V. The relationship between brain volume and walking outcomes in older adults with and without diabetic peripheral neuropathy. Diabetes Care. 2012;35(9):19071912. doi:10.2337/dc11-2463

26. Venkataraman K, Pun V, Mohamed AZ, et al. Altered motor and motor perceptual cognitive imagery task-related activation in diabetic peripheral neuropathy: insights from functional MRI. Diabetes Care. 2019;42(10):20042007. doi:10.2337/dc19-0746

27. Selvarajah D, Wilkinson ID, Gandhi R, Griffiths PD, Tesfaye S. Microvascular perfusion abnormalities of the Thalamus in painful but not painless diabetic polyneuropathy: a clue to the pathogenesis of pain in type 1 diabetes. Diabetes Care. 2011;34(3):718720. doi:10.2337/dc10-1550

28. Selvarajah D, Wilkinson ID, Fang F, et al. Structural and functional abnormalities of the primary somatosensory cortex in diabetic peripheral neuropathy: a multimodal MRI Study. Diabetes. 2019;68(4):796806. doi:10.2337/db18-0509

29. Griebeler M, Morey-Vargas O, Brito J, et al. Pharmacologic interventions for painful diabetic neuropathy: an umbrella systematic review and comparative effectiveness network meta-analysis. Ann Intern Med. 2014;161(9):639649. doi:10.7326/m14-0511

30. Saive AL, Royet JP, Plailly J. A review on the neural bases of episodic odor memory: from laboratory-based to autobiographical approaches. Front Behav Neurosci. 2014;8(16625153 (Print)). doi:10.3389/fnbeh.2014.00240

31. Tesfaye S, Kempler P. Painful diabetic neuropathy. Diabetologia. 2005;48(5):805807. doi:10.1007/s00125-005-1721-7

32. Liem L, van Dongen E, Huygen F, Staats P, Kramer JJ. The dorsal root ganglion as a therapeutic target for chronic pain. Reg Anesth Pain Med. 2016;41(4):511519. doi:10.1097/aap.0000000000000408

33. Landis BN, Scheibe M, Weber C, et al. Chemosensory interaction: acquired olfactory impairment is associated with decreased taste function. J Neurol. 2010;257(8):13031308. doi:10.1007/s00415-010-5513-8

Read more from the original source:
Nerve Conduction and Ofactory Tests in Type Two Diabetes | DMSO - Dove Medical Press

As part of our coverage of ADA 2021, Endocrinology Network has put together a curated list of the top most-viewed and most impactful pieces of data to come from this year's conference. Our list includes 5 topics of coverage, including how the cost of diabetes management is burdening progress, SURPASS program, a trio of FIDELIO-DKD analyses, exciting news surrounding semaglutide, and a review of data from the SCORED and SOLOIST trials.

Editor's note: Clicking on slides will link back to the article in reference. In the event multiple articles are featured within a slide, links to these articles can be found below the slideshow.

See below for links to each piece of content examining prespecified analyses of FIDELIO-DKD.

See below for links to both articles examining studies from Hui Shao, MD, PhD, focusing on the rising costs of diabetes management.

Finerenone data:

Background Insulin Use Does Not Impact Benefits of Finerenone in Diabetic Kidney Disease

Finerenone Provides Consistent Benefit, Irrespective of Background GLP-1 RA Use

Finerenone and SGLT2 Inhibitors Could Have Additive Effect on Kidney Protection

Cost of Diabetes:

Diminishing Cost-Effectiveness Hurting Case for New Glucose-Lowering Agents

Estimating the Impact of the Medicare Part D Senior Savings Model on Expenses for Insulin Users on Medicare

Read the original here:
ADA 2021: Top Data and Other Highlights from the American Diabetes Association's 81st Scientific Sessions - Endocrinology Network

Our Diabetes Online Community (DOC) consists of a tapestry of different perspectives on multiple platforms all connected by diabetes, in some way. Yet, there is an awakening these days that diverse voices are not always included in the mainstream as much as they should be.

We at DiabetesMine are committed to shining a light on those lesser-heard voices and critical topics as much as possible. Wed appreciate all of your help in this. Pleasereach outwith feedback, topic suggestions, or if youre interested in penning a guest post to share your as-yet-unheard story.

In that spirit, we bring you the latest edition of our monthly DOC Roundup, featuring topics and voices that caught our attention during the month of June 2021:

Celebrating dads is always a big part of June and those in the Diabetes Community are no exception! We appreciate this post from D-Dad Tom Karlya, who shares a heartfelt perspective on being a parent of a child with type 1 diabetes (T1D) and watching as they grow into adults and take on their own care.

Valuable and hugely important discussions on diversity, equity, and inclusion happened throughout June in the D-Community, as we marked Juneteenth once again. There were many BIPOC (Black, Indigenous, People of Color) voices sharing their stories and talking specifically about the need to do better in diabetes care and when it comes to peer support. It was also great to see a push to recognize the issue of inequities in disaster preparedness, as expressed by a group of BIPOC diabetes advocates. Please watch this video on the issue and fill out the survey to lend your voice to this effort.

June marked Pride Month as well, showcasing recognition and acceptance for our LGBTQ+ brethren. We loved this coming out story featured by JDRF, this shout-out from the Sugar Mommas Facebook group, and this rainbow decorated Dexcom sensor by @midnightbutterflyiris on Instagram, to name just a few.

The American Diabetes Associations 81st Scientific Sessions took place June 25 to 29. For the second year in a row, due to the COVID-19 crisis, this annual conference was completely virtual. It brought together more than 15,000 people from across the globe to talk about anything and everything in diabetes research as well as future technology and treatments. The main hashtag for this event is #ADA2021 and you can check out the full agenda and some of the materials at the ADAs online meeting site.

ICYMI, the DiabetesMine D-Data Exchange, took place a week before the Sci Sessions and brought many different topics of discussion on data, devices, and more. Be sure to check out the hashtags #DData, #DData2021, and #WeAreNotWaiting, as well as our DiabetesMine summary of the event here.

Nick Jonas, #WhenInRange

A global campaign focused on time in range for those with diabetes kicked off in mid-June, with celebrity actor Nick Jonas (who has T1D himself) and several others working with continuous glucose monitoring company Dexcom and multiple nonprofit diabetes orgs to promote this effort. You can learn more about this #WhenInRange initiative here.

Insulin pricing remains a hot button issue across the United States, particularly as we mark the 100th anniversary in 2021 of insulins discovery. Mississippi is one of the latest states to join in the effort trying to hold big Pharma and the middle-men of drug pricing accountable for outrageous and too often deadly insulin prices.

Diabetes jokes are a never-ending source of ire in the DOC, and this past month brought on a new hullabaloo from those trying to poke fun inappropriately at diabetes. The Beta Cell Podcast on Twitter (and other social media channels) was one outfit calling this out for discussion, initiating a thread that captured the frustration many of us experience when seeing people without diabetes trying to use it as a misguided point or make it a punchline.

We got an LOL from this post by Megan Cornelius, who is @pushupsnpumps on Instagram. She points out the EAT ALL THE CARBS phenom that hits so many of us with diabetes when low blood sugars strike. Thanks for the humor, Megan!

We share our favorites each month and would love to include yours, too. Please ping us viaemailor onFacebook,Instagram, orTwitter.

Read this article:
Around the Diabetes Online Community: June 2021 - Healthline