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Friday, April 19, 2024
Diabetes

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No fewer than 63,958 Nigerians died of diabetes and its complications in 2019, out of 2.7 million living with the non- communicable disease (NCD) in the country.

It has also been predicted that there would be a 143 per cent increase in prevalence of the chronic disease between 2019 and 2045, that is, there would be 3.861 million more Nigerians (6.5 million) to live with the condition if nothing is done to stop the trend.

These figures were disclosed by a panel of experts during “Novo Nordisk World Diabetes Day Webinar (Nigeria)” held to mark the World Diabetes Day (WDD) 2020 at the weekend.

To check the situation, the experts, among other recommendations, urged the Federal Government to conduct a national prevalence study on diabetes and other non-communicable diseases and to strengthen the primary health care centres to be able to screen, diagnose and treat the disease.

The theme for the WDD 2020, “The Nurse and Diabetes”, is meant to raise awareness around the crucial role that nurses play in supporting people living with diabetes.

The panel of experts include: Consultant Physician/ Endocrinologist, Lagos State University Teaching Hospital (LASUTH), Prof. Anthonia Ogbera; Consultant Physician/ Endocrinologist, Enugu State University Teaching Hospital (ESUTH) and Vice President, Diabetes Association of Nigeria (DAN), Dr. Ejiofor Ugwu; Senior Nursing Officer/Diabetes Educator, EKO HOSPITAL Lagos, Mrs. Adekunbi Ayanrinde and Senior Diabetes Nurse, Educator, ISN products Nigeria Limited, Mrs. Cynthia Ozoalor.

Ogbera, in a paper on the strategies to reduce the rising burden of diabetes in Nigeria, said the disease killed more people than COVID-19, Human Immuno-deficiency Virus (HIV) and other diseases. She raised the alarm that the burden of the disease is rising in the country, but expressed regret that the focus in disease control in Nigeria and other Sub Saharan African countries is on communicable and infectious diseases, leaving NCDs patients to suffer. “So there should be a shift in focus,” Ogbera said.

According to the endocrinologist, Nigeria ranks next to South Africa on the continent as worst affected countries with 2.7 million people living with the disease. “Diabetes is a lifelong condition so there must be a life long follow up,” she said.

On how to stem the tide, Ogbera recommended: “Scale up screening and diagnosis.

Once people are told they have diabetes they run to tertiary and secondary facilities. It should not be so. The PHC centres should be scaled up. We should keep on educating the public. Patients should be treated with a target.

“We need to conduct national prevalence study. We do not have any factual data. The only one done in 1990 showed the prevalence was 2.2 per cent when we were just 90 million people in Nigeria. There should be access to medical education. The message is to strengthen PHC to be able to detect and manage diabetes.”

Ugwu recommended adoption of holistic approach and multi-disciplinary measures involving different experts in the healthcare industry, including doctors, nurses, pharmacists, dieticians, physiotherapists and others.

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A recent study reveals that losing fat without reducing muscle mass results in a significantly lower risk of heart failure in people with type 2 diabetes.

In the United States, around 1 in 10 people have diabetes, and 90–95% of them have type 2 diabetes. Type 2 diabetes usually develops after age 45. Estimates suggest that by 2045, 700 million adults worldwide will have this condition.

Type 2 diabetes usually begins as insulin resistance. This is a condition wherein the body’s cells no longer react to the insulin the pancreas produces to control blood sugar.

Genetics, ethnicity, and advancing age all play a role in the development of insulin resistance and diabetes. However, excess weight, a lack of exercise, an unhealthful diet, and smoking may be driving factors in its occurrence.

Once doctors diagnose this condition, the primary treatments they advise generally include taking medications and making certain lifestyle changes, such as losing weight and improving the diet.

As diabetes nearly doubles the risk of death due to heart disease or stroke and increases the risk of having heart failure by a factor of two in males and five in females, many researchers are focusing on preventing these and similar health complications for those with diabetes.

Heart failure, or congestive heart failure, occurs when the heart muscle does not pump the blood adequately. This leads to a buildup of fluid in the lungs or legs, or sometimes both.

Heart failure has a number of potential causes. For example, after a heart attack (when the heart muscle sustains damage due to a lack of oxygen), the muscle is weak and cannot pump well.

Heart failure can also occur due to type 2 diabetes. This is as a result of direct harm to the heart muscle from raised blood sugar and systemic inflammation associated with the condition.

One prevention strategy includes weight loss for people with overweight or obesity. However, not much is known regarding what type of weight loss has the most impact on reducing the risk of diabetes-related heart issues.

The study

To investigate this further, researchers at the University of Texas Southwestern Medical Center (UTSW) in Dallas analyzed data from the Look AHEAD study.

This is a randomized trial investigating weight loss due to intensive lifestyle intervention, consisting of healthful eating and increased physical activity versus support and education alone in people with type 2 diabetes.

The UTSW research, which appears in the journal Circulation, received funding from the National Heart, Lung, and Blood Institute, the Texas Health Resources Clinical Scholars Program, and the National Institutes of Health (NIH).

The researchers selected 5,103 people from the Look AHEAD study who did not have heart failure at the beginning of the study. The participants also had sufficient baseline measurements needed for prediction equations to estimate how much fat mass and lean (muscle) mass they had.

Data on the participants’ weight and waist circumference were available at the beginning of the study and over a 4-year period. The team also noted hospitalizations for heart failure over a 12-year time frame.

During the trial’s 12-year follow-up, 257 study participants were hospitalized for heart failure treatment.

In the Look AHEAD study, scientists used a scanning technique called dual-energy X-ray absorptiometry (DXA) to determine body composition in a subset of about 1 in 5 of the participants. These participants also had information recorded on factors such as height, weight, waist circumference, and ethnicity.

This meant that the researchers could validate existing equations that predict the proportion of fat mass and lean mass from these factors, which are simple to collect compared with the much more complicated process of conducting a DXA scan.

The researchers’ analysis of the subset of participants with DXA scans provided a new equation specific to this study group. They applied this new equation to the remaining participants without a DXA scan to accurately predict their fat mass and lean mass.

This revealed that adults in the study who had lost weight were less likely to develop heart failure if they lowered their fat mass and waist circumference. However, losing lean mass did not change their risk.

The investigators note that although the risk of heart failure decreased in those who lost body fat and reduced their waist circumference, the study data showed no significant reductions in heart attack risk.

The team also considered the participants’ ejection fraction (EF) ratio. This is a measurement of the amount of blood leaving the heart with each contraction.

The data showed that reducing body fat mass by 10% resulted in a 22% lower risk of heart failure with preserved EF ratio and a 24% lower risk of heart failure with reduced EF ratio.

“Our study suggests that simply losing weight is not enough. We may need to prioritize fat loss to truly reduce the risk of heart failure.” – Study co-author Dr. Kershaw Patel, a cardiologist at Houston Methodist Hospital in Texas

Supporting evidence

A study from May this year, which appears in the journal Circulation Research, compared obesity phenotypes, diabetes, and cardiovascular diseases.

The comparison suggests that some people who have a healthy weight or overweight but an excess amount of fat deposits around the internal organs and under the skin have a higher risk of diabetes and heart disease.

The researchers say that it is not possible to determine the risk of cardiovascular disease and type 2 diabetes based on body mass index (BMI) alone — mostly because body composition is so diverse.

They suggest that since excessive amounts of fat tissue largely define cardiovascular risks, reducing body fat is critical for prevention.

Implications and limitations

The results of the UTSW study suggest that for people with diabetes who also have overweight, losing weight, in general, may not be adequate to reduce heart health risks.

If further studies replicate these findings, it could confirm that losing weight by shedding visceral fat from around the organs — rather than losing muscle mass — is a key factor when it comes to reducing the risk of heart failure in type 2 diabetes.

The study authors also say that further investigation is necessary to determine if building or maintaining muscle in addition to losing fat mass would be even more effective in reducing the risk of diabetes-related heart failure.

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A trial suggests that in patients who are no longer responding to metformin, taking a combination of two newer drugs is safe and yields clinical benefits for at least 2 years.

Insulin helps regulate the amount of glucose circulating in the blood. In type 2 diabetes, the body does not produce enough insulin, its cells no longer respond effectively to the hormone, or both.

In the long term, high blood glucose levels can cause a wide range of debilitating and potentially life threatening complications. These include high blood pressure, damage to organs such as the heart and kidneys, nerve damage, and blindness.

According to the Centers for Disease Control and Prevention (CDC), type 2 diabetes affects more than 30 million individuals in the United States and accounts for 90–95% of all cases of diabetes.

Type 2 diabetes used to be called adult-onset diabetes because it mostly affects people over the age of 45. But in recent decades, rates of type 2 diabetes in children, teenagers, and young adults have increased in the U.S.

Lifestyle changes can control or even reverse the condition. Doctors also prescribe drugs to stabilize patients’ blood glucose levels.

The first-line treatment is metformin, but in some patients, the drug’s efficacy can decline over time, necessitating alternative treatments.

Drug combination

A clinical trial called DURATION-8 investigated a combination of two newer drugs — exenatide and dapagliflozin — in patients whose blood glucose levels did not respond to metformin.

Initially, the trial lasted 28 weeks, but it was later extended to 52 weeks. The results suggest that the combination was safe and continued to be more effective than either drug alone.

In addition to stabilizing blood glucose levels, the drug combination was associated with lower blood pressure and body weight.

The researchers report in the journal Diabetes Care that the drug duo remained safe and effective 2 years (104 weeks) after treatment began, following a second extension of the trial.

“Many therapies in diabetes management are short-lived, which is why it is useful to test for long-term effect,” says first author Dr. Serge Jabbour, director of the division of endocrinology and the Diabetes Center at Thomas Jefferson University in Philadelphia, PA.

Exenatide belongs to a class of drugs called glucagon-like peptide-1 receptor agonists, which work by promoting insulin secretion, reducing the release of glucose from the liver, and increasing the feeling of fullness after a meal.

Dapagliflozin belongs to a class called sodium-glucose cotransporter-2 inhibitors, which boost the amount of glucose that is excreted in urine.

“These two classes work synergistically to help control a type 2 diabetes patient’s glucose levels and other measures associated with diabetes,” says Dr. Jabbour. “We can now feel more confident about prescribing these medications long term.”

AstraZeneca, which makes branded versions of both drugs, funded the study. The company also played a role in designing the study, gathering the data, and evaluating it.

Study design

The researchers randomly assigned 695 adults with type 2 diabetes whose blood glucose was not adequately controlled by metformin to three treatment groups:

  • a weekly injection of exenatide and a daily oral dose of dapagliflozin
  • weekly exenatide and daily oral placebo
  • a weekly placebo injection and daily oral dapagliflozin

After 2 years, 431 patients remained in the trial. Most of the participants who dropped out did so because they did not want to sign up to an extension of the trial.

After adjustments for other possible contributing factors, those who received both drugs saw the greatest average reduction in their glycated hemoglobin (HbA1c) levels — a measure of the stability of blood glucose levels — compared with the start of the trial.

In patients who took both drugs, there were also improvements in blood glucose levels after fasting and 2 hours after eating, and reductions in body weight and systolic blood pressure.

The researchers report that patients tolerated well the combination of exenatide and dapagliflozin.

While patients experienced no episodes of major hypoglycemia (dangerously low levels of blood glucose), there were more episodes of minor hypoglycemia in patients who took both drugs compared with the other two experimental groups.

Conclusions

The authors conclude that the clinical benefits of taking both drugs were maintained for 2 years, with “no unexpected safety findings.” They continue:

“Further studies are needed to investigate whether the combination treatment effects observed in DURATION-8 could potentially extend to a reduced incidence of [cardiovascular] and renal events in patients with type 2 diabetes.”

The authors acknowledge that the relatively high proportion of patients who withdrew from the study after 1 year limits the “robustness” of its findings after 2 years.

Finally, they note that their findings may not apply to all patients. Treatment should be tailored to individuals and modified according to how well they progress.

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Doctors have warned that people in the United States may be drinking excessively as a way to cope with the COVID-19 pandemic.

In a new viewpoint article, two doctors have warned that more people in the U.S. may be turning to alcohol as a way of coping with the “myriad stressors” of the COVID-19 pandemic.

The article, published in the Journal of General Internal Medicine, proposes a series of interventions to try to minimize this behavior and better support people with alcohol use disorder.

Coping strategy

It is well documented that drinking alcohol is one way that people cope with stressful situations. For example, research has shown that in the U.S., people tend to drink more alcohol following terrorist attacks.

Furthermore, if a person has alcohol use disorder, they are more likely to use alcohol to cope with the stress of a traumatic event.

In this context, the current COVID-19 pandemic is a particular cause for concern. The authors of the current article point out that rather than being a single event, the effects of the COVID-19 pandemic are prolonged over time, potentially exposing people to ongoing trauma.

Further, the pandemic has caused various potential stressors that a person may cope with by drinking alcohol.

As well as the catastrophic effect on people’s health and the loss and grief experienced by many, the pandemic has also disrupted economies and social and cultural life, threatening people’s jobs, disrupting their interpersonal support structures, increasing barriers to health care, and forcing many people into isolation.

Before the pandemic, researchers had noted that people in the U.S. were tending to drink more. This was particularly the case for females.

Recent research suggests that people in the U.S. increased their alcohol consumption in the early phase of the pandemic. This is in line with similar findings from studies in the United Kingdom and Australia.

Alcohol health effects

This matters because well-documented links exist between increased alcohol consumption and adverse health outcomes.

As the National Institute on Alcohol Abuse and Alcoholism point out, alcohol consumption can change mood and behavior, damage a person’s heart, liver, and pancreas, increase the risk of several types of cancer, and weaken a person’s immune system.

Research has also linked excessive alcohol consumption to mental health disorders, such as anxiety and depression, which may worsen during the pandemic.

Consequently, it is important to encourage people to find alternative coping strategies in response to the stressors of the pandemic. Effective support should also be available for people experiencing the effects of increased alcohol consumption or people with alcohol use disorder.

Interventions

The authors of the present study offer various suggestions for interventions that may help reduce people’s dependence on alcohol during the pandemic. Other suggestions focus on better preparing clinical services to support people with substance abuse issues.

According to Dr. Shelly F. Greenfield, director of the Alcohol, Drug, and Addiction Clinical and Health Services Research Program at McLean Hospital in Belmont, MA, “[i]ncreasing identification of harmful alcohol use in patients and intervening early are key components of addressing this problem.”

“In addition, recognition of the problem from policymakers could lead to changes in federal regulations — such as we have seen with telehealth — and improvements in access to healthcare,” she notes.

The authors suggest that public health messaging should raise awareness of the potential for increased drinking during the pandemic, as well as giving advice on alternative coping strategies for the stressors of the pandemic.

They also suggest that primary care practitioners should offer increased screening for alcohol use disorder when people contact primary care services.

Technologies, such as telehealth — that enable clinical information to pass between doctors and individuals at a distance — may also be valuable for people who are isolating or where the pandemic has forced a reduction in the enrolment for some face-to-face clinical services.

Finally, the authors highlight that ensuring people have access to health insurance to cover medical treatment costs is crucial. This is particularly important given the number of people who depend on work-place health insurance and the significant number of people who have lost their jobs during the pandemic.

Co-author Dr. Dawn E. Sugarman, a research psychologist in the Center of Excellence in Alcohol, Drugs, and Addiction at McLean Hospital, notes that:

“We hope this article will call attention to the pandemic’s effects on alcohol use and offer mitigating approaches to this under-recognized public health concern.”

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Over the years, scientists have demonstrated an association between red and processed meats and cancer. However, they are still unpicking the mechanisms that drive this relationship.

The authors of a recent study, which appears in BMC Medicine, argue that at least part of the answer might lie in an immune interaction.

Nutrition and dietary habits play pivotal roles in a wide range of health conditions, including type 2 diabetes, obesity, cancer, hypertension, and cardiovascular disease.

Red meats and processed meats have each received a fair amount of attention in this regard. Both have been implicated in cancer risk, but how they exert their influence is up for debate. As the authors of the latest study explain:

“Although various mechanistic explanations have been proposed, [such as a] high energy/fat diet, N-nitroso, nitrates, nitrites, heme iron, [and] compounds produced by gut microbiome or during cooking, none seems to be specific to red meat or dairy.”

A role for antibodies?

The authors point to tentative evidence that N-glycolylneuraminic acid (Neu5Gc) might be a risk factor for colorectal cancer.

Neu5Gc is a carbohydrate, or sugar, present in foods derived from mammals, and it is abundant in red meat and dairy. It occurs at low levels in some fish but is absent from poultry.

Humans cannot synthesize Neu5Gc, but when we consume it, small amounts accumulate on cell surfaces. When immune cells encounter this nonhuman material, it triggers the production of anti-Neu5Gc antibodies. Studies have shown that humans have a wide range of these antibodies.

Scientists have also found evidence that long-term exposure to these antibodies promotes inflammation and cancer in animal models. However, they have yet to identify any clear effect of eating mammalian products on levels of these antibodies.

As these anti-Neu5Gc antibodies travel around the body, they bump into Neu5Gc on cell surfaces, sparking inflammation. Experts believe that this, in turn, exacerbates cancer, because cancer cells tend to have higher levels of Neu5Gc on their surfaces.

In one study, researchers demonstrated an association between levels of circulating Neu5Gc antibodies and colorectal cancer risk. However, the level of antibodies was not associated with red meat intake.

Now, the latest study has set out to unpick the relationship between a person’s diet and their levels of Neu5Gc once and for all.

Diet and Neu5Gc

In the study, a group of scientists — most from Tel Aviv University, in Israel, or the Sorbonne Paris Cité Epidemiology and Statistics Research Center, in Bobigny, France — took data from the NutriNet-Santé survey. This extensive survey conducted in France aims to investigate the complex relationships between nutrition and health.

The authors of the present study took data from 16,149 adults, all of whom had registered a minimum of six dietary records.

Meanwhile, the researchers calculated the amount of Neu5Gc in a wide range of common foods. Using this data, they constructed what they refer to as the “Gcemic index,” which ranks food according to levels of Neu5Gc —specifically, the Neu5Gc content in each food relative to the amount measured in beef.

Next, the researchers analyzed blood samples from 120 participants with at least eighteen 24-hour dietary records; they noted the levels of anti-Neu5Gc antibodies in the serum.

“We found a significant correlation between high consumption of Neu5Gc from red meat and cheeses and increased development of those antibodies that heighten the risk of cancer,” explains corresponding author Dr. Veder Padler-Karavani, of Tel Aviv University.

“For years, there have been efforts to find such a connection, but no one did. Here, for the first time, we were able to find a molecular link thanks to the accuracy of the methods used to measure the antibodies in the blood and the detailed data from the French diet questionnaires.”

Now, combining earlier knowledge and the data provided by the new study, the theory becomes more solid: Consuming mammal products, such as red meat and dairy increases the amount of Neu5Gc on cell surfaces. In turn, this increases the level of circulating anti-Neu5Gc antibodies.

With an increase in these antibodies comes an increase in inflammation, which might raise the risk of exacerbating certain medical conditions, such as cancer.

It is worth noting that the immune response described above is unlikely to be the only link between red meat and cancer.

The authors also mention other factors, including the high fat content in meat and mutagens — chemical compounds that cause irreversible changes in cellular genetic material — such as heterocyclic amine, which is produced when meat is cooked at high temperatures.

In the future, the researchers hope that their Gcemic index will become a tool to assess the amount of Neu5Gc in a person’s diet. This might help design personalized recommendations for at-risk individuals.

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New research conducted in mice has shown how coxsackievirus B type 4 — an enterovirus, a virus transmitted through the intestines — may be able to trigger diabetes in people who have the virus.

A new study has shown a possible mechanism for triggering diabetes in people who have coxsackievirus B type 4 (CVB4), a type of enterovirus.

The research, published in the journal Cell Reports Medicine, may also be valuable in exploring whether SARS-CoV-2, the virus at the heart of the current pandemic, can trigger diabetes.

Diabetes

According to the Centers for Disease Control and Prevention (CDC), diabetes is an ongoing health condition that affects how a person’s body transforms food into energy.

As a person consumes food and drinks, their blood sugar increases. Their pancreas then produces the hormone insulin, which enables cells to access this blood sugar.

However, a person with diabetes may not be able to either make good use of insulin (type 2 diabetes) or produce enough of it (type 1 diabetes).

Type 2 diabetes is by far the most common form of diabetes, accounting for approximately 90–95% of all cases of diabetes in the adult population.

The American Diabetes Association consider both types of diabetes to be caused by a combination of genetic and environmental factors.

For type 1 diabetes, scientists believe that viruses are one aspect of these environmental factors.

In particular, research suggests that enteroviruses — a family of viruses that can cause a variety of diseases with “neurologic, respiratory, skin, and gastrointestinal” symptoms — may be key viral triggers for type 1 diabetes.

However, scientists are not yet sure exactly how this triggering function occurs.

Complex chain of events

In the present study, the researchers wanted to better understand how enteroviruses may trigger type 1 diabetes.

To do so, they used mice that had been grafted with human pancreatic cells with CVB4, as well as human and mouse insulin-producing cells that also had the virus.

After conducting various experiments with these infected cells, the researchers identified a complex chain of events that may account for the trigger of diabetes.

The researchers observed that CVB4 infection induced downregulation of URI, a protein that controls various cellular functions. This downregulation triggered a cascade of molecular events.

This in turn resulted in the silencing of the gene Pdx1, which governs the function of beta cells in the pancreas. These beta cells produce insulin.

As Dr. Nabil Djouder, a researcher at the Spanish National Cancer Research Center and the lead author of the study, explains, “Pdx1 silencing causes the loss of the identity and function of the beta cells, which become more like alpha cells, in charge of increasing blood glucose levels, and hence leading to hyperglycemia and subsequent diabetes, independently of any immune reactions.”

Helping to corroborate their findings, the researchers also noted that mice with diabetes that overexpressed the URI protein were more tolerant of blood sugar changes.

Finally, the researchers noted a correlation between the expression of URI, Pdx1, and viral particles in pancreata from people with diabetes. For the scientists, this suggests a causal relation between human diabetes and enteroviruses.

A prevention strategy?

As well as helping make clear the mechanism behind the viral triggering of diabetes, the study also raises the possibility of using antiviral therapies alongside drugs that inhibit the silencing of Pdx1 to prevent and treat diabetes.

The researchers demonstrated that DNA methyltransferase inhibitors, which inhibit a protein involved in the silencing of Pdx1, reinstated Pdx1 expression and glucose tolerance in diabetic mice.

The scientists believe that their study may also have implications for the COVID-19 pandemic. Dr. Djouder explains, “Similarly to our investigations on enteroviruses, some recent clinical observations have associated SARS-CoV-2, the virus responsible for COVID-19, to diabetes in infected patients.”

“Since the receptor of SARS-CoV-2 is present in beta cells, it would be interesting to study if this virus also alters URI function and silences the expression of Pdx1 to affect beta cell function, promoting diabetes.” – Dr. Nabil Djouder

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New research reveals how gum disease might exacerbate inflammation elsewhere in the body. The findings help explain associations between gum disease and several other conditions that involve excessive inflammation.

In gum disease, or periodontitis, bacteria in dental plaque provoke an attack by the immune system. This triggers inflammation, which over time, erodes the soft tissue and bone supporting the teeth.

According to the Centers for Disease Control and Prevention (CDC), almost half of adults over 30 in the United States have periodontal disease.

Research suggests that it contributes to a wide range of other conditions in which chronic inflammation plays a role. The long list includes arthritis, heart disease, diabetes, cancer, respiratory disease, and dementia.

However, the mechanism linking these conditions to periodontal disease has been unclear until now.

Experiments by researchers in the Faculty of Dentistry at the University of Toronto, Canada, have revealed that gum disease primes blood cells called neutrophils, which then overreact to infection elsewhere in the body.

The neutrophils, which are part of the body’s innate immune defenses, release signaling molecules called cytokines that exacerbate inflammation.

“It’s almost as if these white blood cells are in second gear when they should be in first,” says the study’s senior author, Prof. Michael Glogauer. “The [neutrophils] are much more likely to release cytokines much more quickly, leading to negative outcomes.”

The results appear in the Journal of Dental Research.

Systemic immune response

When the researchers induced periodontal disease in mice, it led to a proliferation of neutrophils in the animals’ bone marrow, suggesting a widespread or “systemic” immune response.

By contrast, mice with peritonitis — an infection of the peritoneum, the membrane lining the abdomen — had increased numbers of neutrophils in their blood close to the site of infection.

However, mice that already had periodontal disease when they developed peritonitis had a significantly greater number of neutrophils at the infection site.

After further investigation, the researchers found that neutrophils from animals with gum disease and peritonitis had molecular markers in their outer membranes indicating they were “primed” to cause inflammation.

However, the mice with peritonitis but not gum disease did not have neutrophils primed in the same way.

To determine whether similar immune changes occur in people, the scientists asked healthy volunteers not to brush or floss their teeth for 3 weeks. This led to gingivitis, a mild form of gum disease.

When the scientists analyzed blood samples from the participants in the lab, they found neutrophils primed to cause inflammation, just like those in their earlier animal experiments.

After the volunteers went back to brushing and flossing their teeth, the neutrophils in their blood returned to their previous, less reactive state.

The authors conclude:

“Together, these results demonstrate that periodontal tissue inflammation has systemic effects that predispose toward an exacerbated innate immune response. This indicates that [neutrophils] can respond synergistically to simultaneous and remote inflammatory triggers and therefore contribute to the interaction between [periodontal disease] and other inflammatory conditions.”

Cytokine storms and COVID-19

The researchers caution that their work had some limitations. In particular, they would like to repeat their experiments in other models of periodontal disease, both in mice and nonhuman primates.

In addition, it remains unclear whether inflammation caused by neutrophils primed in this way contributes to worse outcomes in inflammatory conditions, such as heart disease.

According to one study, COVID-19 may be such a condition. In severe infections, an immune overreaction or “cytokine storm” can lead to vascular collapse, respiratory failure, and problems with other organs, such as the kidneys.

“There is evidence out there that patients with periodontal disease may be much more likely to have negative outcomes with COVID-19,” says Prof. Glogauer. “Neutrophils are the cells that are at prime risk of causing cytokine storms. That’s the exact cell we show is primed in people with periodontal disease.”

A recent article in the journal Medical Hypotheses proposes that screening for periodontal disease could help identify people at high risk of developing severe COVID-19 infections.

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Scientists have proposed a new therapy for type 2 diabetes. If proven effective, the therapy could help some people discontinue insulin treatment.

Scientists have proposed a new therapy for the treatment of type 2 diabetes, with a proof-of-concept study showing positive initial results. If effective, the therapy may mean that some people can stop taking insulin treatment.

The authors of the research presented their findings at UEG Week Virtual 2020, a conference organized by United European Gastroenterology, a professional nonprofit organization for specialists in digestive health.

Type 2 diabetes

According to the National Institute of Diabetes and Digestive and Kidney Diseases, a person may have type 2 diabetes when their blood sugar is too high.

People gain blood sugar, or blood glucose, mainly from the food they eat. Insulin helps cells access this glucose to use as energy. However, for a person with type 2 diabetes, either their body does not make enough insulin or their cells do not respond to insulin correctly.

This then means that the glucose in their blood increases, which can lead to complications of diabetes, such as heart and kidney disease, visual impairment, and loss of sensation in the limbs. The higher the blood glucose over time, the higher the risk of these complications.

According to the Centers for Disease Control and Prevention (CDC), about 1 in 10 adults in the United States have diabetes, and 90–95% of these individuals have type 2 diabetes.

Doctors typically recommend lifestyle changes, such as being more physically active and eating a more healthful diet, to treat type 2 diabetes, as well as medications to manage a person’s blood pressure and blood glucose levels.

Insulin treatment may be necessary if a person is unable to maintain their blood sugar at normal levels. This treatment can take the form of injections, pens, pumps, or inhalers. It encourages the cells in a person’s body to absorb more blood sugar.

However, people’s perception of the side effects of insulin treatment can be quite pronounced. As a result, doctors may be less likely to prescribe insulin, and, when they do, people may not take it regularly.

Consequently, therapies that can avoid these perceived side effects may be valuable in ensuring that people keep up with their prescribed treatment and avoid risking serious health issues.

Proof of concept

In this context, the researchers behind the present study used a novel technique that scientists first reported using in humans in 2016. Based on those preliminary results, it seemed promising.

The technique is called duodenal mucosal resurfacing (DMR). The duodenum is the first part of a person’s small intestine. DMR involves lifting the mucosal layer of the duodenal to allow the ablation of the revealed area using heated water — a process that removes the cells in the targeted area.

The researchers who developed the DMR technique were trying to replicate the positive impact that bariatric surgery (gastric bypass) has on blood sugar levels with a less invasive technique.

Studies of how bariatric surgery improves blood sugar control have concluded that there is a direct effect from the duodenum in addition to the weight loss that results from bariatric surgery.

DMR can take place in an outpatient setting and is minimally invasive. It involves an endoscope catheter to gain access to the duodenal.

The direct effect of the small intestine on glucose control appears to come from the presence of intraepithelial lymphocyte T cells. These are nestled between the gut cells involved in the absorption of nutrients from food.

Mice without these cells are protected from obesity and heart disease, even when eating a high fat diet.

These intraepithelial lymphocytes reduce the amount of a gut hormone called GLP-1. Therefore, in the current study, the researchers added regular doses of a GLP-1 agonist called liraglutide on day 14.

They did so to counteract the reduced amount of this essential lean, antidiabetic hormone. The study participants also received lifestyle counseling to help reduce their blood sugar levels.

The study involved 16 participants with type 2 diabetes receiving insulin treatment. Of the participants who received the DMR therapy with liraglutide, 12 (75%) were able to stop using insulin and maintain their blood sugar control after 6 months.

Promising initial results

The study participants also saw a variety of benefits to their metabolism.

The participants’ HbA1c readings, which determine a person’s glucose control, had all reduced to below 7.5%. After 12 months, this fell further to 6.7%.

Those who responded to the treatment saw a reduction in their body mass index from an average of 29.8 kilograms per square meter (kg/m2) before the study started to 25.5 kg/m2 12 months after the study. Fat in the participants’ livers reduced from 8.1% to 4.6% after 6 months.

Even for the participants who still needed insulin, the required amount reduced from an average of 35 units per day to 17 units per day after 12 months.

According to Dr. Suzanne Meiring, a researcher at the Amsterdam University Medical Center, the Netherlands, and co-lead of the study,

“A single endoscopic DMR ablation with GLP-1 drugs and lifestyle counseling can lead to discontinuation of insulin therapy in a subset of patients with type 2 diabetes while improving their blood glucose control and overall metabolic health.”

“Many patients with type 2 diabetes are very happy to be able to discontinue insulin therapy, since insulin therapy comes with weight gain and hypoglycemic events.”

Further research needed

It is important to note that this is a very small proof-of-concept study. The researchers presented it as a conference paper, and, therefore, few details are available in the public domain for scrutiny.

The intervention combined two innovative treatments. No details of any side effects of the two treatments (DMR and GLP-1 agonist) are available. While promising, there is a need for larger trials to confirm the results.

Importantly, precisely how and why the therapy appears to work is not yet clear.

The scientists believe that it may work because the mucosal cells that the DMR therapy affects undergo changes in response to unhealthful diets that can promote insulin resistance.

“Based on the results of this study, a large international randomized controlled trial, called Revita T2Di Pivotal, will soon start to further investigate its effectiveness in greater numbers,” says Dr. Meiring.

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79397416 Image credit: Rolf Bruderer/Getty Images

Researchers have uncovered new clues to the mystery of how the gut’s nervous system affects glucose metabolism in the rest of the body. Their findings could lead to new treatments for type 2 diabetes.

Type 2 diabetes causes the body’s cells to become less sensitive to signals from insulin, the hormone responsible for regulating levels of glucose in the blood.

This low sensitivity is called insulin resistance, and it keeps the cells from absorbing the extra glucose that enters the bloodstream after a meal.

Over time, high concentrations of glucose in the blood damage tissues all over the body, causing complications such as heart disease, vision loss, and kidney disease.

The Centers for Disease Control and Prevention (CDC) estimate that more than 30 million people in the United States have type 2 diabetes.

Changes to the diet, exercise, and other aspects of life can improve symptoms and even reverse the condition in some people. Drugs are also available to treat type 2 diabetes, but they can cause side effects such as nausea and diarrhea.

Another drawback to some antidiabetic drugs is that they have to be injected.

Discovering oral treatments that are not only effective but also free of side effects is therefore a priority for diabetes researchers.

Now, a group of scientists, many affiliated with the French National Institute of Health and Medical Research, or INSERM, in Toulouse, believe that they are a step closer to developing such a treatment. They have published their findings in the journal Gut.

Friendly bacteria

This latest research builds on previous work suggesting that fat, or lipid, molecules produced by “friendly” gut bacteria can improve blood glucose metabolism.

These lipids are thought to influence the gut-brain axis — the vital two-way communication between the brain and the gut’s highly developed nervous system, also known as the enteric nervous system or “second brain.”

In type 2 diabetes, communication between the gut and brain appears to break down. As a result, after a meal, the brain fails to send signals to the liver, muscles, and fat tissue telling them to absorb more glucose from the bloodstream. This, in turn, leads to insulin resistance.

Normally the duodenum, the first part of the small intestine, signals to the brain, which involves a relaxation of the smooth muscles in its lining. In individuals with type 2 diabetes, however, these muscles are permanently contracted, or hypercontractile, so the signal is never sent.

The researchers believe that friendly gut bacteria are the key to reversing hypercontractility and restoring healthy glucose metabolism.

Nutrients that feed friendly bacteria are called prebiotics. In particular, carbohydrates called fructooligosaccharides (FOS) are known to promote the growth of bacteria that improve glucose metabolism through the production of various lipids.

However, the identity of these lipids has remained unknown until now.

Key lipids

To find out more, the researchers fed mice a special diet supplemented with FOS. Then, they compared the contents of their colons with those of mice that did not receive supplementary FOS.

The team discovered that the only lipid with significantly increased levels in the colons of the FOS mice was a lipid called 12-HETE.

When they fed 12-HETE to diabetic mice, the lipid not only reduced duodenal hypercontraction but also improved the mice’s blood glucose levels.

To explore whether these results applied to humans, the scientists analyzed biopsies from the duodenums of people with type 2 diabetes who had received antidiabetic treatments and those of healthy volunteers who had not.

They found that there was 38% less 12-HETE in the duodenums of the people with diabetes, compared with the healthy volunteers. The researchers acknowledge that this finding was not statistically significant, but also point to the small numbers of volunteers in their study.

Finally, they showed that 12-HETE reduces muscle contraction in the duodenum by boosting the signal from a nerve receptor called the mu-opioid receptor. This restored communication between the gut and the brain.

Intimate relationships

This study is one of the latest to reveal intimate relationships between the bacteria in the human gut, known collectively as the microbiota, and our health.

The scientists are optimistic that their work will inspire new treatments, which could either boost production of 12-HETE in the gut or involve taking the lipid orally, as a supplement.

In their paper, the researchers conclude:

“Using a combination of nutritional and pharmacological approaches, we have identified a new mode of communication between gut microbes and the host. In addition, we have identified novel targets and their mechanisms of action in rodents, and possibly in humans. The identification of specific targets […] to treat [type 2 diabetes] and its comorbidities represent a groundbreaking solution to develop medications without side effects.”

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608924839 Image credit: Govinda Haribol/EyeEm/Getty Images

Researchers have worked out how to use electromagnetic fields to treat mice with type 2 diabetes.

Scientists have discovered that they can successfully treat type 2 diabetes in mouse models by exposing the rodents to electromagnetic fields.

The research, which appears in the journal Cell Metabolism, opens the door to further studies confirming the findings and exploring whether the therapy could be suitable for use in humans.

Type 2 diabetes

According to the Centers for Disease Control and Prevention (CDC), more than 34 million people — approximately 1 in 10 — in the United States have diabetes. Of these individuals, the vast majority have type 2 diabetes.

Type 2 diabetes occurs when a person’s cells do not react to the hormone insulin properly. Insulin, which the pancreas produces, mediates the ability of a person’s cells to receive blood sugar.

In this situation, a person’s body can tell that their cells are not receiving blood sugar properly, and the pancreas produces more insulin in response. At a certain point, the pancreas cannot meet the insulin demand, and, as a consequence, blood sugar levels increase.

The CDC highlight that high blood sugar levels can cause various serious health conditions, including vision loss, kidney disease, and heart disease.

According to the National Institute of Diabetes and Digestive and Kidney Diseases, key approaches to treating type 2 diabetes include eating a more healthful diet and being more physically active.

There are also many medications that can help a person manage the symptoms of diabetes.

However, adherence to type 2 diabetes treatment is relatively low. Research has suggested that at least 45% of people with type 2 diabetes are unable to control their blood sugar levels effectively.

A range of factors may contribute to a person’s ability to keep diabetes symptoms in check, including the perceived difficulties around accessing and taking medications.

Chance discovery

In this context, the scientists behind the present study believe that they may have made a significant discovery in the form of an effective and accessible way of treating mice with type 2 diabetes using electromagnetic fields.

The discovery came about by chance. Sunny Huang, an M.D.-Ph.D. student at the University of Iowa (UI) Carver College of Medicine and the co-lead author of the study, needed access to mice to practice taking their blood and measuring their blood sugar levels.

Dr. Calvin Carter, a postdoctoral researcher in the same lab, let Huang borrow the mice that he was using in an experiment on how electromagnetic fields affect the brains of the animals.

According to Huang: “It was really odd because normally these animals have high blood sugar and type 2 diabetes, but all of the animals exposed to [electromagnetic fields] showed normal blood sugar levels. I told Calvin, ‘There’s something weird going on here.’”

This was especially unusual given that the researchers had either genetically modified the mice in question to give them diabetes or induced the disease by feeding them a 60% high fat diet.

“That’s what sparked this project,” Dr. Carter adds. “Early on, we recognized that if the findings held up, they could have a major impact on diabetes care.”

Diabetes remote control

Huang and Carter worked with Prof. Val Sheffield, professor of pediatrics and of ophthalmology and visual sciences at UI, as well as Dr. Dale Abel, chair of the UI Department of Internal Medicine and an expert on diabetes, to see whether it was possible to verify their findings.

They found that by combining static electric and magnetic fields that were 100 times the Earth’s natural levels and directing these at the mice, they were able to change the mice’s blood sugar levels.

Furthermore, they found that after 3 days of exposing the mice to these fields while they were sleeping, the mice’s insulin resistance had reversed.

In Dr. Carter’s words:

“We’ve built a remote control to manage diabetes. Exposure to electromagnetic fields for relatively short periods reduces blood sugar and normalizes the body’s response to insulin. The effects are long lasting, opening the possibility of an [electromagnetic field] therapy that can be applied during sleep to manage diabetes all day.”

Quantum biological phenomenon

Despite static electric and electromagnetic fields being an ever-present aspect of life on Earth, experts know little about their effects on biology.

Research in this area has primarily looked at animals’ directional instincts — for example, birds’ ability to migrate.

According to Dr. Carter, “[t]his literature pointed to a quantum biological phenomenon whereby [electromagnetic fields] may interact with specific molecules.”

“There are molecules in our bodies that are thought to act like tiny magnetic antenna, enabling a biological response to [electromagnetic fields]. Some of these molecules are oxidants, which are studied in redox biology, an area of research that deals with the behavior of electrons and reactive molecules that govern cellular metabolism,” he adds.

The team then reached out to Prof. Douglas Spitz and Prof. Gary Buettner, UI professors of radiation oncology, and Dr. Jason Hansen, of Brigham Young University, all of whom are experts in redox biology.

One such oxidant molecule that has a role in type 2 diabetes is superoxide. The researchers found that exposing this molecule to the combined static electric and magnetic fields that they were generating triggered its signaling.

However, the effect was only present in the liver and did not occur in the muscles.

This signaling led to an antioxidant response to rebalance the redox set point in the mice: the balance between oxidants and antioxidants.

The team then devised a way to confirm this effect. As Dr. Carter explains: “When we remove superoxide molecules from the liver, we completely block the effect of the [electromagnetic fields] on blood sugar and on the insulin response. The evidence suggests that superoxide plays an important role in this process.”

Human applications?

Looking ahead, a key question for the researchers is whether it is possible to replicate these findings in humans, as well as in mice. The lack of an increase in insulin sensitivity in skeletal muscle from this intervention may be important, given its importance in diabetic control in humans. If so, then scientists may be able to develop a noninvasive, effective treatment for type 2 diabetes.

The researchers have already taken a step along this path by confirming their findings using human cells in the laboratory.

To take things further, they intend to run the experiment using larger animals whose physiology is closer to that of humans. They also plan to explore in more detail the redox mechanism that seems to be at the heart of the phenomenon.

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