Your Brain and Diabetes

This content originally appeared on diaTribe. Republished with permission.

By Brett Goerl and Matthew Garza

Recent studies have shown a link between brain diseases like Alzheimer’s and Parkinson’s and diabetes.  Unfortunately, these conditions are becoming more common as our population grows older. Find out more and ways to improve brain health.

What are neurodegenerative diseases?

The term “neurodegenerative diseases” refers to a range of diseases in which the cells in our brains break down and can no longer perform their designated functions associated with movement or mental ability, according to the EU Joint Programme – Neurodegenerative Disease Research. The most common neurodegenerative diseases that affect people with diabetes are mild cognitive impairment (MCI) and dementia, which includes Alzheimer’s disease.

As we age, it is completely normal for our memory, thinking, and judgment to slightly decline. However, MCI occurs when our mental abilities decline faster than expected and begin to interfere with our daily lives. Age is by far the biggest risk factor for MCI, but diabetes, smoking, high blood pressure and cholesterol, obesity, and depression can further increase a person’s risk of developing MCI.

In around 10-15% of cases each year, the mental decline seen in MCI may progress further, making it difficult for us to carry out a healthy and happy life. When this happens, it is called dementia. The two most common types of dementia that affect people with diabetes are Alzheimer’s disease (AD) and vascular dementia.

While the symptoms of AD and vascular dementia are similar, they are caused by two different processes that occur in our brains. AD is thought to be caused by the abnormal build-up of proteins in the brain. One protein is “amyloid,” which clumps together in spaces around brain cells. The other protein is “tau,” which get tangled up inside brain cells. Vascular dementia, on the other hand, occurs when the blood vessels in our brain become narrow or start to bleed. This reduces the brain’s ability to get the oxygen it needs to keep brain cells healthy and for the brain to function properly. In both cases, brain cells become damaged, leading to a wide range of problems such as memory loss, worsened judgment, and personality changes.

AD is the most common form of dementia in the US, making up 60-70% of dementia cases. In the US, an estimated 5.4 million people of all ages are affected by AD, and one in eight people 65 years and older suffer from it. Considering the 14.3 million adults aged 65 and older in the U.S. who have diabetes, and it is easy to see why Alzheimer’s disease and diabetes are two of the most common diseases of aging. And recent research has suggested that they may be linked in various ways.

How do neurodegenerative diseases like Alzheimer’s and vascular dementia relate to diabetes? 

We often think of diabetes as a problem with our metabolism since the lack of insulin (in type 1 diabetes) or insulin resistance (in type 2 diabetes) affects our body’s ability to maintain normal blood glucose levels. However, our brain consumes the most glucose compared to any other organ in our body. While the brain accounts for roughly 2% of our body weight, it uses almost 20% of the sugars we eat or release from our body’s stores.

An increasing amount of research shows that people with AD and other forms of dementia experience insulin resistance in the CNS (central nervous system, which includes the brain and the spinal cord), similar to what people with type 2 diabetes experience in other areas of the body, such as the muscles, the liver, and the fat. Scientists have yet to determine exactly what the relationship between diabetes and AD or other forms of dementia may be caused by, but there are a few theories that have been proposed.

  • One of these theories focuses on brain insulin resistance, which is when brain cells stop responding normally to insulin, leading to problems related to the ways our brain cells communicate, use energy, and fight infection.
    • Insulin receptors can be found in many areas of the brain, where they are involved with brain cell growth, communication, and survival. While insulin levels are lower in the brain than in the bloodstream, all the insulin that makes its way to the brain comes from the same insulin produced in the pancreas – it crosses over what is known as the blood-brain barrier (or BBB). This barrier prevents unwanted things from the bloodstream from entering the brain. However, injected insulin does not cross the BBB. The reduced transport of insulin across the BBB may be why brain insulin levels are lower when the body experiences insulin resistance (such as in pre-diabetes and type 2 diabetes) and in diseases such as AD.
    • Insulin in the brain is known to help control our metabolism in certain other organs of the body, like the liver and fat tissue. The hypothalamus, the part of our brain that controls hunger, thirst, and emotions, is highly sensitive to levels of insulin in the brain. The association between type 2 diabetes and brain health may be due to problems with insulin’s actions in the hypothalamus, increasing a person’s likelihood of developing whole-body insulin resistance.
  • Diabetes also increases the risk for damaged blood vessels, leading to heart disease and stroke. Damaged blood vessels can starve the brain of oxygen, leading to cognitive decline and vascular dementia.
  • Diabetes disrupts how our bodies produce amylin, a hormone related to insulin that helps our bodies digest food. People with obesity and pre-diabetes often have high amounts of amylin, some of which can circulate and cross into the brain. Studies have shown that amylin can interact with the same protein deposits in the brain known to cause AD.
  • Experiencing hyperglycemia for long periods of time can degrade the myelin sheath (a protective layer that surrounds your neurons). This leads to issues in how your nerves send and receive signals to your body. It can also lead to your brain cells dying.

Type 1 diabetes could be a risk factor for dementia for many of the same reasons as type 2 diabetes. In particular, the cardiovascular complications such as heart disease and stroke that are associated with type 1 diabetes could provide an explanation for its relationship with vascular dementia. Additionally, higher rates of cognitive dysfunction for those with type 1 diabetes could be related to frequent cases of hyperglycemia and hypoglycemia. Indeed, severe hypoglycemic and hypoglycemic events are associated with increased dementia risk for older adults with type 1 diabetes.

Is diabetes a risk factor for developing neurodegenerative disease? 

On average, people with diabetes experience slightly more cognitive difficulties associated with MCI across their lifespan, but experiencing cognitive difficulty does not mean you will eventually get diagnosed with dementia or AD. The prevalence of type 2 diabetes and neurodegenerative diseases, however, both increase with age, meaning it is more common for older people (65+ years) with type 2 diabetes to get diagnosed with vascular dementia or AD.

Data suggests that people with diabetes have a 73% increase in the risk of developing any type of dementia and 56% increase in the risk of developing AD compared to people who do not have diabetes. This makes diabetes one of the strongest risk factors for getting dementia aside from aging. Health measures like A1C, cholesterolhigh blood pressure(or hypertension), and eGFR are negatively impacted by diabetes and may also be associated with cognitive performance and neurodegenerative diseases.

  • In the ACCORD-MIND trial, the largest and most rigorous study on diabetes and the brain to date, higher A1C levels were associated with lower cognitive function in people with diabetes. Similarly, another study found that the risk for dementia increased as a person’s A1C level increased, regardless of whether or not the person had type 2 diabetes.
  • A recent analysis of over 100 studies found that higher levels of LDL cholesterol (known as “bad cholesterol”) was an independent risk factor for the development of AD.
  • High blood pressure in middle-aged people has been linked to future cognitive decline and dementia, and in particular, vascular dementia. This may be due to high blood pressure in the brain causing damage to blood vessels, such as small blockages and bleeding.
  • In a study on kidney health and dementia recently published recently, researchers found that lower rates of kidney filtration (as measured by eGFR) were associated with higher risk of onset of both vascular dementia and AD.

What about Parkinson’s Disease?

Parkinson’s Disease (PD) is another neurodegenerative disease associated with aging. In PD, the cells in your brain deteriorate and begins to affect a person’s ability to perform daily activities associated with movement. Symptoms can include tremors (rhythmic shaking), muscle stiffness and rigidity, and PD can even slow your movement in a process called bradykinesia. It can also lead to other symptoms not associated with movement such as disrupting sleep, constipation, anxiety, depression, and fatigue.

As with other neurodegenerative diseases, research has been conducted to identify if there is a link between diabetes and PD. In particular, one study from 2018 showed an association between the two conditions. The researchers looked at the English National Hospital Episode Statistics and Mortality Data from 1999-2011 and divided the data into two cohorts, those with type 2 diabetes (2,017,115 people) at the time of hospital admission and those without (6,173,208 people). It was found that those with diabetes had a 30% higher chance of developing PD than those without, and the younger a person was with diagnosed type 2 diabetes, the more likely their chance of developing PD.

Though researchers do not yet understand the exact way that diabetes and PD are related, they do have a few hypotheses. Namely, there is the chance that certain genetic abnormalities that lead to diabetes may also lead to PD; even if one of these conditions does not directly cause the other, people who have one may be more likely to also have the other. In addition, when diabetes and PD coexist in a person, they may create a more hostile environment in the brain, leading the neurodegenerative processes underway in PD to speed up and be more severe.

What are strategies to reduce the risk of developing a neurodegenerative disease?

There is evidence that leading a healthy lifestyle can reduce your risk of developing diabetes-related complications like dementia or PD. For example, heart attacks and stroke can increase the risk of developing vascular dementia; therefore, lifestyle modifications that help you maintain an ideal blood pressure and levels of cholesterol for your age and health status are important. This can be accomplished by exercising regularly and consuming a diet low in saturated fat, salt, and sugar.

Below are some other tips for improving brain health, which can go a long way in reducing the risk of neurodegenerative diseases like AD. The good news is that many of these strategies are also recommended for managing diabetes.

  • Take control of your blood glucose levels by aiming for a greater time-in-range (TIR). To learn more about time-in-range goals, click here.
  • Smoking is associated with higher rates of dementia. In a recent review, smokers were 40% more likely to develop AD than non-smokers. Given that people with diabetes are at an increased risk of developing dementia, smoking is likely to increase this risk further. If you smoke or experience nicotine addiction, talk to your healthcare professional about a plan to quit or cut back.
  • Keep blood pressure at the target discussed with your health care provider (which might be 130/80 mmHg or less, if you are at high risk of cardiovascular disease) by exercising regularly and eating a diet low in salt (aim for less than 2,300 mg of sodium each day)
  • Take your diabetes medications consistently and as directed by your healthcare team. Some early evidence shows that certain diabetes drugs, like GLP-1 receptor agonists, may be beneficial for brain health. In fact, exenatide, a GLP-1 receptor agonist, is currently in clinical trials for treating PD.
  • A very active area of research focuses on the dementia-preventing effects of having an active and stimulating mental life and rich social networks. Working to maintain an active and socially rich lifestyle could help prevent some of the effects of diabetes on dementia risk.

If you are 65 years of age or older and have memory concerns or other cognitive complaints (i.e., brain fog, depression, personality change), talk to your healthcare provider about getting a cognitive assessment. Learn more here.

Source: diabetesdaily.com

Michelle L. Litchman Focuses on Diabetes Program Accessibility for People Who Are Deaf

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

By Kayla Hui, MPH

Michelle L. Litchman, PhD, FNP-BC, FAANP, FADCES, assistant professor at the college of nursing at the University of Utah and medical director for Diabetes One-Day Education and Care Program at the Utah Diabetes of Endocrinology Center, was selected as a Betty Irene Moore Nurse Fellow. The fellowship is designed to develop nurse leaders and innovators who are making an impact in health care. Each fellow receives $450,000 over their fellowship tenure, including an extra $50,000 for their home institution. For Dr. Litchman, her project will focus on diabetes program accessibility for people who are deaf.

“This is really important to me because I have six family members who are deaf, including my mom. And so I’ve actually witnessed how some deaf people don’t receive the health care that they need,” Litchman tells Beyond Type 1.

Having type 2 diabetes is associated with a higher risk for hearing loss, according to a 2019 research study. For folks with pre-diabetes with blood glucose levels higher than normal, there was an associated 30 percent rate of hearing loss compared to individuals with normal blood sugar.

Barriers to Diabetes Program Accessibility

Litchman says that one of the challenges of current programs is that sign language interpreters are not always offered or available. She adds that when interpreters are available or offered, they are not always certified in communicating health information. “You need a medical interpreter, having someone that’s certified and also really knowledgeable about the medical terminology and space,” Litchman says.

Coupled with not having sign language interpreters available in the healthcare setting, Litchman stresses that health information is not always communicated in the language spoken by the patient who is deaf. “In a situation where there’s somebody who is deaf, you have to be providing that information directly to that person in their primary language,” Litchman explains. “There’s an assumption that people who are deaf also know English. For many, their primary language is actually sign language.”

Over the next three years, Litchman will design diabetes programs with language in mind and a focus on language deprivation–when children are not exposed to sufficient linguistic stimuli during the critical periods of language acquisition. According to Litchman, some parents do not teach their children sign language. “If they’re not taught sign language, they’re relying on reading lips. It actually deprives them of a lot of language, reading lips [has] only about 30 to 40 percent accuracy.”

Research shows that patients who are deaf or hard of hearing experienced poorer direct child-caregiver communication. Continuous exclusion from family communication was associated with a higher risk for chronic health outcomes.

“People may have home sign language, American sign language, reading lips, relying on captions,” Litchman says. Because the language used varies for each person, Litchman will leverage language deprivation research to inform her diabetes programming. “My work has some peer support threads. So I am hoping when we do these sessions, there’ll be group sessions where they can lean on one another for tips and tricks on how to make things work in their life,” Litchman explains. “I think a lot of us hope to improve outcomes related to diabetes, helping people feel like they can self manage, have the information, feel like they also have a group of people that they can lean on,” Litchman shares.

Source: diabetesdaily.com

Asian Isn’t a Monolith: Why More Specific Data Matters in Diabetes Research

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

By Kayla Hui, MPH

In the United States, diabetes affects 20 percent of the Asian American population, but that broad statistic doesn’t paint the whole picture. Despite being the fastest-growing racial group in the United States, health outcomes are often categorized by broad racial and ethnic categories, which limits our understanding of how diabetes truly impacts individual ethnic groups within the Asian diaspora. Disaggregated data—showing how diabetes impacts people from more specific origins—could help us better understand how to support and treat individual groups within the Asian American Pacific Islander communities.

“Asian Americans have 50 different ethnicities. Putting 50 ethnicities into one Asian American and Pacific Islander (AAPI) group—that is a fallacy,” H. Chris Hahm, PhD, MSSW, professor at the Boston University School of Social Work and lead researcher for the Epi Asian American Women’s Action In Resilience Empowerment (AWARE) study tells Beyond Type 1. According to the Pew Research Center, the majority of the 20 million Asians that live in the U.S. have roots that trace back to at least 19 countries in East Asia, Southeast Asia, or the Indian subcontinent.

Hahm says that because each ethnic group differs significantly across a variety of factors such as educational attainment, culture, and income level, having disaggregated data is imperative when trying to study diabetes among ethnic groups across the Asian diaspora.

For example, a research study, published in Diabetes Care, looked to understand the prevalence of type 2 diabetes among the U.S. South Asian communities when compared with four racial and ethnic groups: African Americans, white, Latinos, and Chinese Americans. In the study, South Asians include individuals originating from India, Pakistan, Nepal, Sri Lanka, and Bangladesh. While the study did not disaggregate based on ethnicity, after factoring in educational attainment, family income, and tobacco use, it was able to find that South Asians had a statistically significant higher age-adjusted prevalence of diabetes when compared to the aforementioned four groups.

The study also found that South Asians were significantly more likely to be insulin resistant and less likely to have responsive beta cell function, meaning the body could not compensate for the insulin resistance on its own. Data such as this helps us further understand that diabetes may develop differently among different groups and a one-size-fits-all approach to treatment is likely inadequate.

Poverty, a social determinant of health and diabetes, also differs by ethnic group. Hahm adds that grouping Asians together despite their varying levels of difference can be harmful when trying to understand the health disparities of different ethnic communities. “When you’re in poverty, you’re more likely to develop [type 2] diabetes or heart disease,” Hahm says. “That’s why it is really important to have disaggregated data.” As an example, 39.4 percent of Burmese Americans and 20 percent of Native Hawaiians and Pacific Islanders live in poverty; both fall within groups that experience higher rates of type 2 diabetes than other Asian subgroups. These correlations could point toward clues that could help better treat individual communities with a whole-person approach.

“Creating that visibility is the power of disaggregated data when it is meant to advance health equity. It is the basis for systemic change and empowerment of groups that have often not been heard,” Angela Glover Blackwell, JD, founder in residence at PolicyLink says in a report.

Unfortunately, having research studies solely focused on one ethnic group becomes challenging given the small amount of research funding allocated to studying the health of Asian Americans. Funding by the National Institutes of Health (NIH) only allocated 0.17 percent of the total NIH budget toward Asian Americans and Pacific Islanders (AAPI) from 1992 to 2018.

“AAPI researchers have a difficult time getting funded,” Hahm states. She adds that funding is so integral to a researcher’s career that without it, researchers wouldn’t get to continue studying their passions. “If you don’t get tenure, that means you are much more likely to go to other teaching universities,” Hahm explains. “This means your research is almost over.”

A report by PolicyLink titled Counting a Diverse Nation: Disaggregating Data on Race and Ethnicity to Advance a Culture of Health found that racial and ethnic health disparities and inequities can only be eliminated if quality data is available. By having disaggregated data by ethnicity, it can help track problems and underlying social determinants which can be used to create culturally-tailored approaches to medicine and public health.

Hahm hopes that more disaggregated research focused on ethnic Asian American groups can bring Asian American issues to the forefront, changing them from invisible to visible, and catalyzing a change in health outcomes for all Asian ethnic groups.

Source: diabetesdaily.com

Teplizumab: Can We Delay the Onset of Type 1?

This content originally appeared on diaTribe. Republished with permission.

By Dr. Francine Kaufman

Provention Bio’s new injectable drug was recommended by an FDA committee for approval on May 25, 2021. Studies show that teplizumab can delay, for people at risk for type 1, the onset of the condition for two years or more. Learn what happened at the FDA meeting and what might come next.

Rarely does one get to witness the potential for an entirely new therapeutic or preventive drug to come onto the medical horizon. But that is the threshold we have now reached with the possible approval by the U.S. Federal Drug Administration (FDA) of the first drug that attempts to delay the onset of type 1 diabetes (T1D) ­– teplizumab.

Some questions remain to be seen: whether there is enough data, whether the data is sufficiently compelling, and whether the risk-to-benefit ratio is favorable enough for the FDA to grant teplizumab’s approval. To address these issues, the FDA convened an Endocrinologic and Metabolic Drugs Advisory Committee Meeting (EMDAC) on May 27, 2021.

What is teplizumab?

Teplizumab is a drug (specifically, an anti-CD3 monoclonal antibody) that binds to cells in the immune system called T-cells (these are the body’s infection-fighting cells). Scientists hope that teplizumab will change the types of T-cells in a person’s body so that autoimmunity – or the destruction of body tissue by ones’ own immune system – is decreased. This would reduce the self-destruction of the insulin-producing cells of the pancreas, called beta-cells, that leads to T1D.

What’s next for teplizumab?

The FDA now has to determine if teplizumab can truly help beta-cells survive. This will show the “effectiveness” or “efficacy” of the drug. The FDA also must determine if teplizumab is safe or if there are too many side effects (the “safety” of the drug).

How did we get here?

The drug manufacturer, Provention Bio Inc., applied to the FDA to approve teplizumab as a way to delay the onset of T1D in high-risk individuals. Even before Provention Bio’s TN-10 clinical trial, other studies were conducted with different forms of this type of medication.

Macrogenics (the previous company to own teplizumab) evaluated whether anti-CD3 could be used at the onset of T1D to preserve some of the insulin producing beta-cells.  If people with T1D could still make some insulin on their own, in addition to the insulin they needed to take, diabetes management could be made easier, with less hyperglycemia, lower A1C levels, and less risk of diabetes complications. However, the data did not show sufficiently strong outcomes needed for the FDA to approve anti-CD3 for new-onset diabetes. Perhaps it was simply too late in the diabetes process for this type of drug to make a significant difference. So, the focus turned to prevention – and to “delaying” the onset of T1D.

The TN-10 trial compared teplizumab to a placebo in 79 people with type 1 diabetes ranging in age from eight to 49 years. Teplizumab was given by intravenous infusion (IV) for 30 minutes over 14 days. To assure that study participants and research staff did not know who received teplizumab or the placebo, the placebo was given through IV in the same manner.

After two years, 43% of those given teplizumab developed clinical diabetes compared to 72%  of participants in the placebo group. The health outcomes between the treatment and placebo groups were significant and in favor of teplizumab, but the number of people in the trial was small (only 79 people). Similarly, TN-10 showed teplizumab to be safe, but it is hard to be sure about both the short- and long-term safety profile of the drug. Provention Bio is asking the FDA to allow teplizumab to be approved for children and adults who are at risk for (but do not yet have) diabetes. Because of this, understanding the safety and effectiveness of the drug is even more important.

What happened at the FDA meeting?

The EMDAC panel was asked to analyze the data and provide a recommendation on teplizumab, but the final decision, as always, rests with FDA. The panel was composed of 17 highly regarded endocrinologists, rheumatologists, cardiologists, biostatisticians and mathematical statisticians, a consumer representative, and a patient representative. All panelists agreed that teplizumab showed benefit to the participants of the TN-10 study by delaying the onset of diabetes by two years. However, there was concern about some of the data from prior studies on teplizumab which did not reveal a significant effect on glucose management in people with new-onset T1D.

The panel focused on safety concerns, mainly in terms of long-term risks. The data from TN-10 and the five previous studies in those with newly diagnosed T1D showed higher rates of diabetic ketoacidosis, viral infections, and cytokine release syndrome (which causes flu-like symptoms) in the anti-CD3 groups than in the placebo groups. There were also three total deaths in the treatment groups and none in the placebo groups. The EMDAC panel agreed that long-term surveillance studies would be required to better understand how safe this treatment is, if approved by the FDA.

Although five previous studies were submitted as evidence about teplizumab, the manufacturing and the rate at which the drug was cleared from the blood stream are not the same as what has been seen with the teplizumab under FDA review. This brings up the concern that the prior studies don’t truly support the present submission. The panel also agreed that if the FDA approved teplizumab, it could only be indicated for use in people with the same characteristics as those evaluated in TN-10 – people over the age of eight, with a family history of T1D, and similar glucose profiles. Since about 80% of people who develop T1D have no affected relative, the target population for the drug would be smaller than the actual number of people it could help, at least to begin with, though this could be reconsidered once more safety data is available.

Of the 17 EMDAC panel members, 10 voted in favor and seven voted against recommending FDA approval of teplizumab for the delay of T1D.

What does this mean in the diabetes community?

During the Open Public Hearing that helped influence the EMDAC’s decision, diabetes community leaders and organizations provided input, shared perspectives, and advocated for approval. The experts talked compellingly about the benefit of a two-year delay in diabetes diagnosis and what that would mean with regards to health. Several endocrinologists described the burdens of managing diabetes despite improvements in medications and technology, and the unmet needs that are still present in type 1 treatment regimens. The speakers included:

  • JDRF CEO Dr. Aaron Kowalski
  • Dr. Mark Atkinson (University of Florida)
  • Dr. Louis Phillipson (University of Chicago)
  • Dr. Jeff Hitchcock (Children with Diabetes)
  • Dr. Jeremy Pettus (University of California San Diego)
  • Dr. Jennifer Sherr (Yale University)
  • Dr. Korey Hood (Stanford University)
  • diaTribe founder Kelly Close (Close Concerns) and Jackie Tait (dQ&A), who detailed input from a survey by dQ&A on 1,078 people with T1D.

These speakers were supported by 187 letters posted to the FDA, as well as a dQ&A survey of 1,078 adults with T1D. Survey participants reflected upon how a two-year delay before needing to start insulin would have affected their life with diabetes.

Now it is in the hands of the FDA. If approved, teplizumab would become the first disease-modifying, preventive drug for T1D, and it could have the potential to change the paradigm of how the condition is managed. Stay tuned as we aim to keep you updated on this drug’s journey through the FDA approval process.

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

Will Insulin in a Pill Soon Become a Reality?

Since insulin was first discovered and isolated for therapeutic use nearly 100 years ago, most everyone with insulin-dependent diabetes has had to rely on exogenous insulin, given in the form of injections, whether via an insulin pump or multiple daily shots every single day of their lives (inhalable insulin was approved by the FDA in 2014, but its use is not widespread).

While research and development have come a long way in that time, the reality for millions (and over 7 million people in the United States alone) has been thousands upon thousands of invasive injections, oftentimes causing scarring, bruising, and pain. However, that may be about to change.

Researchers from the New York University in Abu Dhabi have successfully developed a pill using nanomaterial layers that disseminate insulin in rats safely without being destroyed by their stomach acids. This could be life-changing for the millions of people around the world who rely on insulin to live.

“Imagine being able to take insulin in a pill instead of injecting it a couple of times a day,” said first author Farah Benyettou, a research scientist in the Trabolsi Research Group at the New York University in Abu Dhabi. “The insulin was loaded in a system that protects it from the acidic environment of the stomach. Once in the body, the system can sense the blood sugar level and can release the loaded insulin on demand.”

A pill form of insulin has the potential to radically change the daily management of diabetes for the better: It would make treatment easier for children and people with a fear of needles, safer for both patients and clinicians in hospital and clinic settings, more effective, and patient-friendly.

Nearly 30% of people with diabetes rely on insulin injections, and while it might not be for everyone, this revolutionary advancement would be the first of its kind in the world.

Other attempts at orally administering insulin have been made in the past but faced roadblocks in the gastrointestinal tract, where stomach acids and bile quickly destroy insulin and any effectiveness it has.

This is different from common type 2 diabetes drugs like Metformin that aren’t insulin but simply improve the efficacy of insulin that their body already makes.

The research team in Abu Dhabi thinks it has solved the problem of the insulin-destroying stomach bile issue by encapsulating insulin within nCOF nanoparticles in a capsule that is resistant to such acids but responsive to sugar, reacting quickly when it senses blood glucose in the body is rising but survives the dangerous journey down the G.I. tract to reach the bloodstream.

This new advancement also has the potential to reduce or eliminate low blood sugars, as the release of insulin shuts off as soon as it senses blood sugars have fallen. This creates a helpful feedback loop and prevents an overdose of insulin, which for many, is an almost a daily occurrence on injections, where people are constantly walking a balance beam to prevent both high and low blood sugars in a world of stress, meals, exercise, and normal everyday living.

While this is all excellent news, it’s important to remember that the study’s success was only observed in rats, and human bodies are very different. The team will next test different nanomaterials to see what may be appropriate for human trials, and potentially, widespread market availability.

“Our revolutionary technology developed at NYUAD will dramatically improve the well-being of diabetic patients worldwide in a very simple and straightforward way,” says senior author Ali Trabolsi, an associate professor of chemistry at the New York University in Abu Dhabi.

While taking a daily insulin pill may is far from a functional cure, managing diabetes could become easier than ever, especially if the threat of low blood sugars is greatly reduced or eliminated.

The team hopes that diabetes management can soon be a lot less stressful, painful, and dangerous for the millions of people around the world who currently rely on insulin.

Source: diabetesdaily.com

New Study Shows Greater Risk for Severe COVID-19 Among People with Diabetes

This content originally appeared on diaTribe. Republished with permission.

By Eliza Skoler

New results from the CORONADO study reveal that one in five people with COVID-19 and diabetes die within 28 days of hospital admission. The main predictors of severe illness are older age and diabetes complications. 

In May, the CORONADO study revealed that one in ten people with COVID-19 and diabetes died within seven days of hospital admission. Read our early article on the study here.  New findings from the same study show that one in five people with COVID-19 and diabetes died within 28 days of hospital admission.

In the spring of 2020, the study followed 2,796 people with diabetes in France for 28 days after being admitted to the hospital for COVID-19. The analysis looked at rates of death and rates of discharge from the hospital during the 28-day period. The results revealed that after 28 days, 50% of individuals had been discharged and 21% of individuals had died (29% were still hospitalized). The analysis also looked at other factors in the study population:

  • Average age was 70 years old
  • About 40% had long-term microvascular (such as eye or kidney) or macrovascular (such as heart or leg) complications; 11% had heart failure
  • 78% had high blood pressure
  • Almost two thirds were men
  • 88% had type 2 diabetes, and 12% had type 1 diabetes

Older age, diabetes complications (especially heart disease and high blood pressure), difficulty breathing, use of anticoagulant (blood thinning) medication, and biological markers of inflammation were associated with a lower chance of hospital discharge. Similarly, older age, longer duration of diabetes, and a history of microvascular complications were associated with severe illness and poor outcomes from COVID-19 infection. On the other hand, younger age and metformin use were associated with leaving the hospital by the end of 28 days. As discussed in a previous article, while metformin use was associated with a more favorable health outcome, it was not shown to cause better health. Overall, the factors associated with death were the mirror-opposite of those associated with hospital discharge.

Long-term blood sugar management (measured by A1C) was not found to affect COVID-19 outcomes, though high plasma glucose levels at the time of hospitalization were strongly associated with death. Because glucose levels may be tied to COVID-19 outcomes, careful diabetes management remains important for preventing severe illness.

People with diabetes do not have a higher risk of getting COVID; rather, they are more likely to experience severe illness and worse outcomes if infected with COVID-19. It remains important for people with diabetes, as well as their contacts and loved ones, to do everything possible to stay healthy and safe: get vaccinated as soon as you can, continue to social distance, and wear one (or two!) masks in public. To learn more, read “What You Should Know About COVID-19 Vaccines and Diabetes” and “COVID Variants, Double Masks, Diabetes, Oh My!

Source: diabetesdaily.com

Metformin May Reduce Your Risk of Death from COVID-19 Infection

This content originally appeared on diaTribe. Republished with permission.

By Eliza Skoler

The use of metformin – the most common initial medication for people with type 2 diabetes – was associated with a lower rate of mortality from COVID-19 among people with diabetes in a study in Alabama, confirming five previous studies.

Do you take metformin? It’s the first-line therapy used to lower glucose levels in people with type 2 diabetes. A recent study found that metformin use was associated with a lower rate of COVID-related death among people with type 2 diabetes. Since people with diabetes are at increased risk for severe illness from COVID-19, including hospitalization and death, the relationship between metformin and COVID outcomes in this report may be of interest to many people around the world who take the medication.

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The study looked at the electronic health data from 25,326 people tested for COVID at Birmingham Hospital in Alabama, including healthcare workers, between February and June of 2020. Of those tested, 604 people were positive for COVID-19 – and 239 of those who were positive had diabetes. These results showed that the odds of testing positive for COVID were significantly higher for people, particularly Black people, with certain pre-existing conditions, including diabetes. This does not mean people with diabetes are more likely to get COVID-19, only that people with diabetes were more likely to test positive at this hospital.

Importantly, the study found an association between metformin use and risk of death – the study reported that people who were on metformin before being diagnosed with COVID-19 had a significantly lower chance of dying:

  • People taking metformin had an 11% mortality (or death) rate, compared to 24% for those with type 2 diabetes not on metformin when admitted to the hospital.
  • This benefit of metformin remained even when people with type 2 diabetes and kidney disease or chronic heart failure were excluded from the calculations. This is important because people with kidney or heart disease are often advised against taking metformin. By removing this population, it helps to support the notion that metformin may be involved in this difference.
  • Body weight and A1C were not associated with mortality among people with diabetes taking metformin. This suggests that the association of metformin use with reduced COVID-related deaths was not due to the effects of the medication on weight or glucose management.

The data suggest that being a person with diabetes who takes metformin may provide some level of protection against severe COVID-19 infection among people with diabetes. Other studies have shown similar results, though it is not known whether metformin may itself reduce COVID-related deaths among people with type 2 diabetes. The authors discussed some previously reported effects of metformin beyond lowering glucose levels, such as reducing high levels of inflammation (the body’s natural way of fighting infection), which has been described as a risk factor in severe COVID infection. Severe infection with COVID-19, resulting in hospital admission, can lead to damage to the kidneys and decreased oxygen supply to the body’s tissues – and in these circumstances, serious side effects of metformin can occur.

“Given that COVID leads to higher mortality rates and more complicated hospital courses in people with diabetes, it is important to consider whether specific diabetes medications can provide some relative degree of protection against poor COVID outcomes,” said Dr. Tim Garvey, an endocrinologist at the University of Alabama at Birmingham. “This study adds to growing evidence that people with type 2 diabetes treated with metformin have better outcomes than those not receiving metformin.”

Dr. Garvey also cautioned: “Of course, these case-control studies show associations and do not rise to the level of evidence that might be found by a randomized clinical trial. For example, people with diabetes not treated with the first-line drug, metformin, may have a larger number of diabetes complications or longer duration of disease compared with people not on metformin – which could explain the more severe outcomes. In any event, we advocate for early administration of COVID-19 vaccines and other protective measures for people with diabetes.”

Professor Philip Home, a professor of diabetes medicine at Newcastle University in the UK, agreed, saying, “Multiple studies have now addressed the issue of whether metformin and insulin use are associated with better or worse outcomes in people with diabetes who contract COVID-19. In line with previous literature on other diseases, it was expected that people on metformin would do better, and people on insulin worse, than people with diabetes not using these medications. This is confirmed.”

Home continued: “It is believed to happen because people using metformin are younger and have better kidney function than those not taking the medication, while those on insulin tend to have other medical conditions. The good news is that if you have type 2 diabetes and are taking metformin, you are likely to be fitter than if you have type 2 diabetes and do not take the medication – but there is no evidence that metformin itself will make a difference to your outcome if you do get COVID-19. So, get vaccinated as soon as possible!”

To learn more about metformin, read “Everything You Always Wanted to Know About Metformin, But Were Afraid to Ask.”

Source: diabetesdaily.com

How Racial Bias Impacts Health Outcomes

COVID-19 is killing black Americans at three times the rate of white Americans. But it is not just COVID-19. Four hundred years of systematic discrimination has created systems that leave black people with dramatically worse health outcomes than others. Many living with diabetes have faced discrimination in their lifetime. Diabetes still poses barriers to getting fair treatment in our society, whether in school or work, exclusion from sports teams, or mismanagement in the hospital setting. All too often, living with diabetes as a person of color will compound these barriers.

Studies have shown that there are systemic, negative biases against people of color embedded in our healthcare system. This is layered on top of inequitable social determinants of health that people of color face, leading to poorer health outcomes, additional complications, and earlier deaths.

Black People Have a Higher Rate of Diabetes

Black people are more likely to have diabetes. There are 4.9 million non-Hispanic African Americans aged 20 years or older who have diabetes in the United States, according to the CDC. They are 77% more likely to have diabetes than non-Hispanic Caucasians. Part of this trend may be genetic, but one’s environment and socioeconomic status play a significant role in the development of type 2 diabetes, especially in a society without a robust social safety net.  Among racial and ethnic groups, African Americans have the highest poverty rate at 27.4% (compared to Hispanics at 26.6% and whites at 9.9%). Additionally, 45.8% of young black children under the age of 6 live in poverty, compared to 14.5% of white children.

There are many factors that contribute to this, but a history of institutionalized racism (the legacy of slavery, redlining and Jim Crow laws) have largely prevented African Americans from cultivating intergenerational wealth (which for most Americans comes from buying and selling real estate), and breaking the cycle of poverty proves to be nearly impossible in most circumstances.

Poorer, segregated (de facto segregation) black neighborhoods are more likely to face food deserts (areas where there are few or no grocery stores), lack access to healthy foods (including fresh fruits and vegetables), families may lack access to reliable meals (especially in the summer, when schools are no longer serving children breakfast and lunch), and unsafe streets and a lack of green space (few or no public parks). Neighborhoods of lower socioeconomic status are all risk factors for obesity and the eventual development of type 2 diabetes. 

Black People Have Higher Rates of Complications and Death

Black children and families are more likely to develop diabetes, and when they do, they face graver health outcomes. One recent study found that black youth have an average HbA1c of 10.6% compared to 8.3% for their white peers, and black children are twice as likely as white children to die from diabetes. Blacks are also more likely to experience greater disability from diabetes complications such as amputations, blindness, kidney failure, and increased risk of heart disease and stroke. Diabetic retinopathy is 46% more prevalent in African Americans than non-Hispanic whites, and African Americans are at least 2.6 times more likely to have end-stage renal disease due to diabetes than Caucasians. Most telling: the premature death rates for blacks with diabetes are 27% higher than for whites with diabetes.

racism and diabetes

Photo credit: iStock

Racism Is Built into Our Healthcare System

Implicit bias plays a large role in the unfair treatment of black people in the health care setting. In 2005, the National Academy of Medicine released a study that found that “racial and ethnic minorities receive lower-quality health care than white people, even when insurance status, income, age, and severity of conditions are comparable.” This suggests that poverty and lower socioeconomic status does not account for the whole picture of poorer health outcomes in black people with diabetes.

The report continued, “…minority persons are less likely than white persons to be given appropriate cardiac care, to receive kidney dialysis or transplants, and to receive the best treatments for stroke, cancer, or AIDS. It concluded, “some people in the United States were more likely to die from cancer, heart disease, and diabetes simply because of their race or ethnicity, not just because they lack access to health care.” Simply put: people are dying at higher rates just because the color of their skin is darker.

One study of 400 hospitals in the United States showed that black patients with heart disease received older, cheaper, and more conservative treatments than white patients presenting with the same disease and symptoms. Black patients with diabetes have higher rates of amputations than white patients, even when less invasive interventions are available. Additionally, another study showed that physicians were more likely to prescribe pain medications to white patients, mistakenly believing that black people “feel less pain”.

COVID-19 is killing black Americans at three times the rate of white Americans.

Where Do We Go from Here?

Social determinants of health, physician and healthcare workers’ implicit bias and systemic racism in our healthcare system all contribute to higher rates of disease, complications, and death. Neighborhoods and schools remain dramatically segregated and unequally funded.

The United States has a two-tiered health care system that provides fantastic care to those who can afford private health insurance, and little to none to those who cannot (aside from Emergency Department visits). We, as a society, do not value or fund preventive health care as much as we should. We don’t prioritize feeding our babies healthy food, or making sure they have space and safety to exercise regularly. We step in with too little too late for those who need help the most. We are biased in our healthcare decisions and have not fought against institutionalized racism early or long or loud enough. Now is not the time to “not be racist”, but to actively dismantle institutionalized racism from the inside out.

We need more black physicians, and nurses, and emergency medical technicians. We need to put our dollars into segregated neighborhoods and schools and prevent diabetes before it devastates underserved communities even more. We need to listen to black patients in hospitals. We need to trust black people when they voice their health concerns. We need more black voices in the diabetes online community. We need to lift up the voices of black people.

We need to do more for those that we have failed for far too long. We have already lost so much, and we need to act before it is too late.

Source: diabetesdaily.com

How a Vitamin D Deficiency Affects Diabetes

This content originally appeared on Integrated Diabetes Services. Republished with permission. More studies are being done on the implications of vitamin D deficiency in persons with diabetes. As much as pharmacology and medical science are unlocking the impacts of different chemicals on our bodies, the basic vitamins on the side of our Flintstones bottles still […]
Source: diabetesdaily.com

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