“Our Trials are Totally Different.” The Denise Faustman Interview

There’s no question that Dr. Denise Faustman does things differently.

Dr. Faustman’s research has won her avid fans and raised millions from donors, but it has also provoked significant pushback from major diabetes organizations. Dr. Faustman wears that repudiation like a badge of honor, proof that her work is disruptive and important.

A Maverick Approach

Dr. Faustman takes an unconventional approach. Her work, which is focused on the underlying immune response responsible for type 1 diabetes, has led her to a very old and inexpensive drug, a tuberculosis vaccine used widely in the developing world. It’s a treatment that may have been hiding in plain sight for generations.

Dr. Faustman’s immune intervention trials also concentrate on adults with long-standing type 1 diabetes. By contrast, virtually all of her peers have targetted patients with new-onset diabetes, or even patients that have yet to develop diabetes. This approach is generally considered more likely to succeed, because the targets of the interventions have not yet entirely lost their ability to secrete insulin. But in Dr. Faustman’s telling, it hasn’t accomplished much yet:

“Over the last 30 years, immune intervention trials in type 1 diabetes haven’t had very good outcomes. The important diabetes advances have been different versions of insulin and new forms of blood testing, but the immune intervention trials have been a very sad point. Nothing’s worked very well, no new treatments have been approved.”

“Our trials are totally different. They’re all in people that have had diabetes for decades.”

Dr. Faustman told me that a who’s who of diabetes experts has told that her approach is crazy, a response that has clearly tickled her contrarian side.

“We thought the need is to treat the people that actually have the disease. It sounds like a no-brainer, but keep in mind that nobody else is doing it!”

The decision to study patients with long-established diabetes, which was originally made well over a decade ago, was inspired in part by financial constraints: “we could not afford to do new-onset diabetic trials.” And focusing on an incredibly inexpensive generic drug meant that Dr. Faustman had no way of interesting large pharmaceutical companies and their very large R&D budgets.

“It’s a terrible drug to make money off of.”

BCG

The drug is BCG, the Bacillus Calmette–Guérin vaccine, which was first used a century ago in order to protect patients from tuberculosis. It is considered extremely safe, and is still administered to millions of infants annually, most prominently in the developing world.

BCG first piqued Dr. Faustman’s interest because it was “the only drug in animal models that has worked in established diabetic mice.” Exactly why it worked, though, still requires some unraveling. The results of her Phase I trial – results that were both celebrated and questioned – showed that patients receiving the vaccine experienced impressive improvements in glucose control without restoring insulin production or insulin sensitivity.

Most immune intervention drug trials involve the suppression of immune cells that are harming the body – in the case of type 1 diabetes, the T-cells that attack the pancreatic Beta cells. But the BCG vaccine works the opposite way, not by depleting the immune system, but by putting something else back in.

“BCG adds to the microbiome. It’s actually the tuberculosis organism, inactivated. So you’re putting back in, effectively, tuberculosis. When you revaccinate with this vaccine, the reason it takes a little while is that it gets to your bone marrow and actually resets your stem cells in your bone marrow.”

Why would you want tuberculosis in your bone marrow? Dr. Faustman referred to the hygiene hypothesis, the idea that many autoimmune and allergic diseases are caused at least in part by our excessively sanitary modern world. Myobacterium tuberculosis may have co-evolved with humans for thousands of years, and its absence may therefore trigger immune system dysfunction.

“The absence of this organism has allowed these rogue immune systems to take off and create all these autoimmune diseases. We’re just reestablishing this synergistic relationship to get immune tolerance.”

Because of its many possible effects, BCG has lately become “fashionable” in the research community, Dr. Faustman told me. The old vaccine is being evaluated as a treatment for other serious autoimmune diseases, and it has also been theorized to provide protection against the novel coronavirus that causes COVID-19.

But how does all that help with your blood sugar levels? Dr. Faustman believes that when BCG vaccine “retrains” the immune system, it also causes the immune system itself to begin utilizing large amounts of glucose in the bloodstream.

“What really happens is that their white blood cells now become the regulator of sugar, and have restored sugar transport. So there are underlying defects in type 1 diabetes in the use of the lymphoid system as a sugar regulator, and BCG restores that.”

The Effect

“It’s definitely a game-changer. Our hope, based on the early results, is that it will lower your A1c 10-15%, stably. You can use less insulin, and have better blood sugar control.”

It is, however, a slow process:

“It takes a number of years to have its metabolic and immune effects. We know we need to follow these patients for 3-5 years to get the maximal effect. But it’s got good durability. It’s quite permanent.”

The nine patients that originally received the BCG vaccine for the Phase I trial are still checking in with Dr. Faustman’s lab every six months, and she says that they continue to enjoy dramatic improvements in glucose management.

“Everyone wants to know if we have any [trial participants] off insulin. We have one person off insulin. Normally when he’s on a fairly low dose of insulin his A1c is in the normal range. When he goes off insulin, he no longer goes into DKA, but he goes up to around 7.2%.

“Is it gonna last twenty years? Thirty years? We don’t know yet.”

Sample Size

One of the chief concerns that other experts have raised with Dr. Faustman’s work is the tiny sample used in her Phase I trial: a mere nine patients received the BCG vaccine.

Dr. Faustman is completely unphased by this criticism, arguing that the statistical significance of her results speaks for itself.

“A p-value of .05 is as statistically significant in a sample of 10 as it is in a sample of 200,000. The only difference is, in the sample of 10, everybody responded, and the magnitude of the response was large.

“If you have to design big trials, you have small effects and unresponsive groups. And that’s what you’re seeing in the [rest of the] diabetes community.”

The criticism of her work by major diabetes authorities, particularly ADA and JDRF, doesn’t seem to have phased her, although she admits that it has slowed down the pace of her trials. She quoted one of her most significant boosters, the late Lee Iococca, a rockstar among American executives as the CEO of Chrysler during the 1980s. Iacocca told her, “I love it when they’re shooting the cannons at me. It means I’ve got something good.”

Dr. Faustman continued: “If they didn’t think it was competitive, it wouldn’t matter to them. The fact that they shot their cannons, to issue statements that were not truthful, it shows that it mattered to them a lot, that it was threatening to them.” She believes that the criticism set forth by the ADA and JDRF in a remarkable joint letter was not only misguided but dishonest.

Don’t Do It Yourself

Referring to the BCG vaccine’s long history of safety, Dr. Faustman suggested that there was little downside to her proposed intervention.

I felt an uncomfortable comparison to some of the pandemic era’s health controversies, in particular to the arguments advanced by many in favor of poorly investigated COVID-19 treatments such as hydroxychloroquine and ivermectin. I asked her what she would say to readers that are ready to go get the BCG vaccine themselves, before it’s been evaluated by the FDA. It’s a question she deals with constantly.

About once a month, Dr. Faustman gets a call from a physician, asking confidentially where one might acquire BCG of the correct strain. Sometimes it’s pharmacies attempting to fulfill a prescription, sometimes it’s the patients (or parents) themselves.

“Everyone’s trying to do it in the closet because it’s a safe drug, right? People try to do it all the time. But you should really wait until we get the right strain and the dosing. What we try to say is that if you get vaccinated with the wrong strain of BCG, we’re not sure, when we give you the right strain, that it’s gonna work.”

The BCG vaccine may be easy to come by in countries where it is used frequently, but there’s no telling what strain you’d get and what the effects would be.

For patients that are very eager about BCG, Dr. Faustman recommends registering for one of her clinical trials.

Timeline to Treatment

There’s already a phase II trial underway, which will test the BCG vaccine in adults with long-standing type 1 diabetes. This expands the study size from 9 to over 200; Dr. Faustman expects that good results in a much larger cohort will finally resolve the criticism and controversy that has dogged her for years.

Meanwhile, her lab is beginning its first trial of children with type 1 diabetes.

In an ideal world, she told me, the phase II trial for adults would be followed by phase III, an even larger study which she would then present to the FDA for evaluation. In a best-case scenario, the approved drug could be administered to regular patients in “five to eight years.”

“We’re moving as fast as we can.”

Source: diabetesdaily.com

The PROTECT Study

This content originally appeared on Beyond Type 1. Republished with permission.

By Makaila Heifner

Let’s face it, there are a lot of research studies out there, and we mean… a lot. But one you should definitely know about is The PROTECT Study. Especially if you or a loved one was recently diagnosed with type 1 diabetes (T1D).

The PROTECT Study aims to understand how the investigational medicine, teplizumab, works in children and young adults who have recently been diagnosed with T1D, as well as assessing if there are any side effects while taking the medication. This treatment is still being evaluated in clinical studies and has not been approved by the FDA for treating T1D. In previous studies of high-risk individuals, teplizumab was shown to delay the onset of T1D an average of nearly 3 years (35 months).

Who Is Eligible for the Study?

This study will include 300 children and adolescents in clinics across the United States, Canada, and Europe that meet the following criteria:

  1. Age 8-17 years old
  2. Diagnosed with T1D in the previous 6 weeks
  3. Positive for 1 of 5 T1D autoantibodies (test to be done as part of the study) 4. Ability to produce a minimum amount of your own insulin (test to be done as part of the study)
  4. Otherwise generally healthy, with no other significant medical conditions, recent or history of infections, or taking medicines that might interfere with teplizumab

If you meet all the criteria, the next step is to visit a study clinic, where the study team will:

  • Discuss the study in more detail and explain what participation would mean for you or your child.
  • Talk through the potential benefits and risks of being involved in the study.
  • Ask questions and carry out medical tests to determine whether you or your child are right for the study and the study is right for you or your child.

If you and/or your child are interested in potentially participating in the PROTECT study, click here to find a study clinic near you.

Before the study begins, you/and your child must agree to and sign an Informed Consent Form which explains the study in detail, any potential risks or benefits of participation, as well as your rights and responsibilities as a participant of the study.

All study-related treatment and care will be provided to eligible patients without charge; however, patients will not receive any compensation for their participation in the study. Patients who decide to participate are able to withdraw from the study at any time for any reason.

Participants do not have to change their primary doctors as the study provides short-term study-related care only. Patients are encouraged to tell their regular doctors about taking part in a clinical research study. Some medicines are prohibited to take while part of the study so a patient’s doctor may want to contact the study physician to request additional information.

How Does It Work?

If you/or your child are selected to be part of this study, you/your child will be placed in one of two groups, either the teplizumab group or the placebo group (meaning you/your child will receive no treatment). Deciding who will be placed in each group is chosen at random by a computerized system, and neither you/your child nor the study doctor will know which treatment group you/your child was placed in. This is done so that results from the different groups can be handled the same way.

Over the duration of the study, you/your child will receive 2 courses of study medicine given by intravenous (IV) infusion. The IV infusion usually lasts about 30 minutes and will be given daily over 12 days on 2 separate occasions, 6 months apart.

The study will last just over a year and a half (the study reports the study will last up to 84 weeks) and require 36 study clinic visits, including the initial screening, treatment courses, and observation periods.

During visits to the study clinic, you/your child will be asked several questions and perform a series of study-related medical tests. These tests are done in order to understand how the treatment is affecting you/your child and how well the body is responding to the medication.

Identifiable information (for instance, name or address) will not be accessible to anyone who is not directly part of this study; additionally, The Sponsor (the company carrying out the study) will not have access to any personal information that is submitted through the study’s website.

Why?

The treatment works by interfering with the cells that destroy the insulin-producing beta cells in the pancreas. If the treatment successfully interferes with these cells (T cells) patients who are taking teplizumab may be able to continue producing their own insulin and reduce their need for insulin injections, have better control over their blood glucose, and experience fewer complications from T1D.

Visit theprotectstudy.com to learn more about PROTECT.

Source: diabetesdaily.com

The Top Tips for Your Best A1c Yet

Tip 1: Protein – Including some protein, whether plant or animal-based, at every meal, will help with satiation and with post-meal glucose spikes.

Tip 2: Movement – Consistent physical activity and movement each day will help increase your insulin sensitivity. Any type of exercise or movement is suitable!

Tip 3: Portion Sizes – Knowing what and how much you’re eating will help reduce guesswork with insulin dosing or food tracking.

 

Ben Tzeel a registered dietitian, certified strength and conditioning specialist, joins Diabetes Daily to discuss nutrition, ways of eating, and getting the most out of your diabetes management tools and tactics. He is the owner of Your Diabetes Insider, an online nutrition and fitness coaching business that focuses on individuals living with diabetes. He has lived with type 1 diabetes since he was seven years old.

Source: diabetesdaily.com

Global Survey on Do-it-Yourself Artificial Pancreas System (DIYAPS)

By Saskia Wolf, Communication and Dissemination Manager, OPEN

Please support a research study by and for people with diabetes!

At the moment, OPEN is conducting a GLOBAL SURVEY and needs the support of the Diabetes Online Community; this means we need YOUR support. If you are a person with diabetes or a parent/caregiver of one, please participate, whether you are using a DIYAPS or not! More Information is provided on the OPEN website, as well as FAQs and tutorials: https://open-diabetes.eu/open-survey

We all know that diabetes is difficult to live with. It’s all on you to keep yourself alive, and to avoid the chronic effects that won’t present for many years. And no, it’s not easy to just “be disciplined” and keep your blood glucose in a healthy range!

People with diabetes sometimes need help, but not in a paternalistic sense that interferes with daily life. Besides a supportive healthcare professional team and loving family and friends, what does help look like?

For many years, proprietary medical devices were the only help people with diabetes had to manage their condition. Continuous glucose monitors and insulin pumps took a lot of the burden (and pain) away from managing diabetes, but they had limitations. Devices couldn’t talk to each other and had to be manually set; this “open loop” system lacked automation.

Because of these unmet needs, patients developed their own closed-loop systems. Yes, patients — software developers, engineers and other tech-savvy people as part of the #WeAreNotWaiting movement. They created algorithms, made devices talk to each other, and ended up with an automated insulin delivery system that automatically adjusts insulin delivery based on glucose levels to prevent going too high or low. These systems are free and open-source; despite the challenges in building them, the number of people using a “Do-it-Yourself Artificial Pancreas System” (DIYAPS) is steadily increasing.

Users of these systems report tremendous improvements not only in their HbA1c levels, but also in their quality of life. They can finally get a break from managing their diabetes, as well as sleep through the night without CGM alarms or fear of their glucose levels getting too low. But are these systems as life-changing as they sound? What are the barriers for people to build their own systems?

Some healthcare professionals are skeptical; scientists prefer academic studies to social media posts, and thus far most studies have only had small cohorts. There was a need for a concerted research project, led by scientists, clinicians, and users of a DIYAPS alike. This was the genesis of the OPEN Project EU.

The OPEN Project has received funding from the EU Horizon 2020 RISE program to investigate various aspects of DIYAPS, working directly with patients and healthcare professionals. Please visit our website for further information on the project, our team and our publications, follow us on Twitter and visit our Facebook page (@OPENDiabetesEU) and subscribe to the newsletter.

Thank you very much!

Source: diabetesdaily.com

Did a Virus Trigger Your Type 1 Diabetes?

Type 1 diabetes is an autoimmune disease– that is, a disease resulting from the immune system attacking the body. In the case of type 1 diabetes, the immune system mistakenly attacks the beta cells in the pancreas that produce insulin, and without insulin-producing beta cell function, one develops type 1 diabetes, and quickly. Researchers still are not 100% sure what causes type 1 diabetes, but many believe that a virus can “trigger” the body into attacking itself, resulting in disease.

Why does this happen? When a virus invades the body, the immune system starts to produce a response to fight the infection. T-cells are central to recognizing and fighting off the virus. However, if the virus has some of the same antigens as the pancreatic beta cells (in the case of type 1 diabetes), the T cells sometimes actually start attacking the body’s own beta cells. Once all of the body’s beta cells have been destroyed, type 1 diabetes is developed and diagnosed.

It can take more than a year for the body’s T-cells to destroy the majority of the beta cells, but that original viral infection is hypothesized to be a trigger in the development of type 1 diabetes.

A recent study showed that kids exposed to enteroviruses are more likely to develop type 1 diabetes. Enteroviruses are a group of viruses that usually cause mild symptoms, similar to that of the common cold. Certain strains, such as the poliovirus or hand, foot, and mouth disease, can cause more serious complications.

Researchers in Finland tested more than 1,600 stool samples from 129 children who had recently developed type 1 diabetes and 282 children without diabetes for enterovirus RNA (a marker of previous exposure to infection). They found a significant difference: 60% of the control group showed signs of prior infection (without diabetes), versus 80% of the group with type 1 diabetes.

The results also showed that children who developed type 1 diabetes were exposed to the enterovirus more than a year before their diabetes diagnosis; taking this lag time into account, the researchers proved that children with diabetes are exposed to three times more enteroviruses than children without diabetes.

vaccine against enterovirus

A vaccine against enteroviruses may help prevent type 1 diabetes. | Photo credit: Adobe Stock

Researchers are hopeful about current trials, showing vaccines against enteroviruses could potentially prevent 30-50% of new cases of type 1 diabetes, but not all infections can be prevented.

Jessica Dunne, PhD, director of discovery research at JDRF, is excited by the current research. “Enteroviruses are not the only trigger for diabetes, so it’s important to note that even if we prevented all enterovirus infections we probably wouldn’t be able to prevent all cases of type 1 diabetes. I think it would go a long way,” Dunne said.

Clearly, other genetic and environmental facts are at play in the development of type 1 diabetes, but a growing amount of research is pointing to a virus as a common trigger. Other studies have shown that pregnant mothers with antibodies from enteroviruses go on to have children who develop type 1 diabetes.

Not every virus can trigger this reaction ending in disease. The virus must have antigens that are similar enough to the antigens in beta cells (and thus could easily be confused by the immune system); those viruses include:

  • B4 strain of the coxsackie B virus
  • German measles
  • Mumps
  • Rotavirus

There is even new, mounting evidence that the current COVID-19 (SARS-CoV-2 virus) pandemic could be triggering a new wave of type 1 diabetes diagnoses now and into the future.

There is still much debate in the medical community over the exact cause of type 1 diabetes, and most researchers believe it to be a mix of genetics and environmental factors, but the theory of enterovirus-triggered diabetes is gaining support from physicians and researchers alike. There is still much to be explored in the development of type 1 diabetes, but research like this is promising for the eventual development of a vaccine to help prevent new type 1 cases worldwide. Understanding viruses and their connection to the immune system can help unravel the medical mystery of type 1 diabetes without an apparent cause.

What was your experience when you were diagnosed with type 1 diabetes? Were you extremely sick with a viral illness, several months or even years before diagnosis? Do you think a virus could have triggered your diabetes? Share this post and comment with your story, below! We love hearing from our readers.

Source: diabetesdaily.com

UK Study Under Review Finds People With Type 1 Diabetes More at Risk to Die of COVID-19 Than People With Type 2 Diabetes

There’s a large UK study (2 million people) under peer review that’s gaining traction on social media. Why? Because it defies our – already overtaxed mental states – of what’s possible.

Covid-19: people with type 1 diabetes more likely to die than those with type 2.” This is how The Guardian, among other publications, headlined it.

NHS (United Kingdom National Health Service) research reports that people with type 1 diabetes are at 3.5x higher risk for death if they get COVID-19 than people without diabetes. In contrast, people with type 2 diabetes are twice as likely to die as people without diabetes.

Surprised? I was. And even though the research is currently being reviewed, and nothing’s yet been proven, the data has a strong statistical basis.

If you’re curious what all this means, I can share with you information I’m privileged to have access to. I am part of a team of global diabetes experts – MDs, researchers, scientists, heads of the university, and hospital departments. The group was formed a few months ago under the leadership of Professor Itamar Raz, diabetologist and former head of Israel’s national diabetes health policies and Guang Ning, Head of Shanghai Clinical Center for Endocrine and Metabolic Disease.

The team is digesting a barrage of information, sharing their expertise and experiences and brainstorming prevention and treatment guidelines that they can safely, and quickly, recommend to health professionals and the public.

Unnerved by The Guardian article, I reached out to the group immediately. Philip Home, Emeritus Professor at Newcastle University, UK responded within an hour. It was 10:30 PM in the UK.

Here’s what I can tell you with the proviso, as Home emphasizes, that currently this research presents an interpretation of the data, which is dependent on a rapidly changing situation in the UK. This means its application to other people, in other circumstances, is not easy – medicine is as much art as it is science. And, it’s hard to know whether there have been any population and/or calculation errors. For instance, some people with type 2 diabetes on insulin may have been incorrectly counted as type 1s.

Below (in italics) is a summary from my email exchange with Professor Home.

Those Not Necessarily at Higher Risk:

This comment is currently a hypothesis, but we do think people who have no evidence of vascular damage, no retinopathy, no albuminuria (including microalbuminuria) and no cardiovascular disease, are likely not at greater risk to be hospitalized or die if they get COVID-19 than people without diabetes.

Further, if one’s blood sugar is also well managed, A1c under 7.5%, they are probably at no greater risk of getting COVID-19 in the first place than someone without diabetes.

Those at Higher Risk for Poorer Outcomes:

People who have type 1 diabetes who show evidence of vascular damage, should they get COVID-19, would be at higher risk of severe outcomes including hospitalization and death. The risk for vascular damage is higher the longer you’ve had diabetes, particularly if glucose levels have been high.

Further, if you have poor glucose management you may be at greater risk to contract the virus.

People can check with their health professionals whether their markers that indicate vascular damage are in range, that includes CRP, HDL cholesterol, triglycerides, and liver enzymes (ALT). They can also check if they have any albumin leakage through the kidney. Also, they can check with their eye professional whether they have any retinal damage.

Understanding that this is a vascular issue and that vascular damage increases risk for comorbidities such as cardiovascular disease, I better understand why it’s possible someone with longer duration type 1 diabetes, who gets COVID-19, may be at higher risk for worse outcomes than someone with type 2 diabetes.

What else can you do now to protect yourself should you get COVID-19? First, don’t panic. As Home says, the data is not yet in. Second, use this time to build your nutritional and metabolic health. In other words, follow the common recommendations:

  1. Do your best to keep your blood sugar in target range
  2. Eat as healthily as you can – vegetables, whole, not processed foods, some fruit, dairy if you can tolerate it, beans, seeds, nuts, healthy fats
  3. Be active, even if you’re in lockdown

Like everyone, diabetes or no diabetes, wear a mask when out in public, stay six feet away from others and wash, wash, wash your hands. My personal prescription includes using those clean hands to then pour a glass of antioxidant-rich red wine.

Note: I wish to gratefully acknowledge Professor Home who responded to my query immediately, answered my questions, lowered my stress level and helped me interpret the medical data.

Source: diabetesdaily.com

Advancements in Treatment: The Use of Adjunctive Therapies in Type 1 Diabetes

This content originally appeared on diaTribe. Republished with permission.

By Paresh Dandona and Megan Johnson

Read on to learn about the research around GLP-1, SGLT-2, and combination therapy use in type 1 diabetes. Dr. Paresh Dandona is a Distinguished Professor and Chief of Endocrinology at the University of Buffalo, and Megan Johnson is a fellow on his team

For people living with type 1 diabetes, new treatments are finally on the horizon. The University at Buffalo (UB) Endocrinology Research Center is helping to revolutionize the treatment of this condition. Among the most promising new therapies are two non-insulin medications currently used in type 2 diabetes, SGLT-2 inhibitors and GLP-1 receptor agonists.

SGLT-2 inhibitors, such as Farxiga, act the kidney to help the body excrete more glucose in the urine. Meanwhile, GLP-1 receptor agonists like Victoza work in several different ways: increasing the body’s natural insulin production, decreasing the release of the glucose-raising hormone glucagon, slowing the emptying of the stomach, and curbing excess appetite. Some people with type 1 diabetes take these medications as an addition to insulin treatment as an “off-label” drug. To learn more about off-label, check out the article: Can “Off Label” Drugs and Technology Help You? Ask Your Doctor.

Why consider these medications?

In people without diabetes, the body is constantly releasing more or less insulin to match the body’s energy needs.  People with type 1 diabetes do not make enough insulin on their own and have to try to mimic this process by taking insulin replacement – but it isn’t easy.

People with type 1 diabetes often have fluctuations in their blood sugars, putting them at risk for both low blood sugars (hypoglycemia) and high blood sugars (hyperglycemia). Many individuals are unable to manage their blood sugars in a healthy glucose range with insulin alone. In fact, less than 30% of people with type 1 diabetes currently have an A1C at the target of less than 7%.

Can GLP-1 agonists be safely used in type 1 diabetes?

Over the past decade, the endocrinologists at the University at Buffalo and other research groups have been conducting studies to see whether GLP-1-receptor agonists can safely be used in type 1 diabetes.

  • The first of these was published in 2011 and showed a decrease in A1C within just four weeks of GLP-1 agonist treatment. Importantly, people given GLP-1 agonists plus insulin also had much less variation in their blood sugars, as measured by continuous glucose monitors (CGM).
  • Another study involved 72 people with type 1 diabetes who took GLP-1 agonist or placebo (a “nothing” pil) in addition to insulin for 12 weeks. The GLP-1 group had decreases in A1C, insulin requirements, blood sugar fluctuations, and body weight. People in this group did report more nausea – a common side effect of GLP-1 agonists.
  • Since then, multiple studies, some involving over 1000 people and lasting up to 52 weeks, have shown that GLP-1 treatment in people with type 1 diabetes can reduce A1C and body weight, along with insulin dosages.

Many of these studies, but not all, have suggested that GLP-1 agonists can do this without increasing the risk for hypoglycemia or diabetic ketoacidosis (DKA). There is also some evidence that GLP-1 agonists can improve quality of life in type 1 diabetes.

Who should consider GLP-1’s?

The effects of GLP-1 agonists seem to be especially strong in individuals who are still able to make some insulin on their own, although it also works in people who do not.

In one notable study, researchers gave a GLP-1 agonist to 11 people with type 1 diabetes who were still able to produce some insulin. To get an estimate of insulin production, they measured levels of a molecule called C-peptide, which is produced at the same time as insulin. In these 11 individuals, C-peptide concentrations increased after GLP-1 treatment. By the 12-week mark, they had decreased their insulin dosage by over 60%. Incredibly, five people were not requiring any insulin at all. Even though the study was very small, the results were exciting, because it was the first study to suggest that some people with type 1 diabetes had sufficient insulin reserve and thus, could – at least temporarily – be treated without insulin.

Can SGLT-2 inhibitors be used in type 1 diabetes?

SGLT-2 inhibitors like Farxiga have also shown tremendous potential. In two large studies called DEPICT-1 and DEPICT-2, adults with type 1 diabetes were randomly assigned to take either placebo or SGLT-2 inhibitor in combination with insulin. Over 700 people from 17 different countries participated in DEPICT-1, and over 800 people with type 1 diabetes participated in DEPICT-2. At the end of 24 weeks, people taking dapaglifozin had a percent A1C that was lower, on average, by 0.4 compared to people who had received placebo, and it was still lower, by over 0.3, at 52 weeks. The number of hypoglycemic events was similar in both groups.

As with GLP-1 agonists, people taking SGLT-2 inhibitors had weight loss and decreased insulin requirements. People taking SGLT-2 inhibitor, however, did have an increased risk of diabetic ketoacidosis (DKA). If individuals consider this therapy, they should be cautious about not missing meals or insulin, and not drinking large amounts of alcohol, as these behaviors can lead to increased ketone production.

Several other research groups, in trials recruiting up to 1000 individuals, have seen similar results when using this class of medications.  Researchers have been conducting additional studies to try to determine how best to minimize the risks associated with them. Farxiga (called Forxiga in Europe) has now been approved as the first oral agent as an adjunct treatment for type 1 diabetes in Europe and Japan.

Promising Combination Therapy

Now, endocrinologists are also looking at whether GLP-1 agonist and SGLT-2 inhibitor combination therapy could increase the benefits of each of these treatments. A study conducted on a small number of people showed that GLP-1 agonists can help prevent ketone production, so it is theoretically possible that this medication could reduce the risk of DKA that was seen with SGLT-2 inhibitors.

In an early study involving 30 people with type 1 diabetes who were already on GLP-agonist and insulin were randomly assigned to take SGLT-2 inhibitor or placebo, as well. People who received both drugs saw an 0.7% reduction in A1C values after 12 weeks, without any additional hypoglycemia. People on the SGLT-2 inhibitor did make more ketones, though, and two individuals in the combination group experienced DKA. Larger studies are now being conducted to expand on these results and learn more about how to give these drugs safely. The hope is that non-insulin therapies will soon be approved for type 1 diabetes. By unlocking the potential of these therapies, we can do more than manage blood glucose levels – we can improve people’s lives.

Source: diabetesdaily.com

STUDY: Link Between Jaundice at Birth and Type 1 Diabetes Risk

An association between high bilirubin levels at birth and a higher risk for developing type 1 diabetes has been previously suggested. Now, a large study has further confirmed the association. According to the Centers for Disease Control and Prevention: Jaundice happens when a chemical called bilirubin builds up in the baby’s blood. During pregnancy, the […]
Source: diabetesdaily.com

Search

+