The associations are exhibited as cumulative relative risks over 0-3 lag days with the 75th percentile of ambient temperature distribution as the reference (22.6°C). The blue lines are the effect estimates and the gray shaded areas are the 95% confidence interval. CREDIT Department of Global Health Promotion, TMDU
n extreme heat events, people with diabetes had a greater risk of being hospitalized for complications related to hypo- or hyperglycemia (i.e., low or high blood glucose levels)
The global effects of climate change have been demonstrated to extend beyond the environment to many other areas, including human health, particularly concerning different health conditions. People with diabetes are at higher risk of requiring hospitalization during unusually hot days (termed ‘extreme heat events’), as the body is more likely to become dehydrated and have difficulty balancing the concentration of components in the blood. Now, researchers in Japan have revealed an additional risk for people with this condition by identifying a link between extreme heat events and the likelihood of hypo- and hyperglycemia–related emergency hospitalizations.
“It is important that the physiological implications of extreme heat on individuals with metabolic disorders, such as diabetes, are well understood,” explains first author Keitaro Miyamura of Tokyo Medical and Dental University (TMDU). “This can be accomplished by examining outcomes about extreme heat events and using a sophisticated model that accounts for the fact that ultimate effects may occur after heat events.”
To do this, the research team applied a distributed lag non-linear model (a model for estimating exposure-time-response function) to a dataset consisting of nationwide data for hypo- and hyperglycemia–related emergency hospital admissions from 2012–2019, as well as ambient temperature data from weather stations in each prefecture. Relative risk was determined for 2 levels of heat events (standard and extreme). “Relative risks for standard and extreme heat effect on emergency hospitalization for hypoglycemia were 1.33 and 1.65, respectively, and similar risks were found for hyperglycemia. In most regions, the higher the temperature, the higher the relative risk,” says lead author Takeo Fujiwara.
The model, which took into account a time delay of up to 3 days, showed that the impacts of climate change on health may not always be obvious. These findings will provide policymakers with information about subtle or latent health effects that may need to be considered in environmental or health care policies. This is particularly important since the effects of climate change will only increase in the foreseeable future.
The risk of type 2 diabetes (T2D) is more than halved by weekly injections of new obesity drug semaglutide, according to new research being presented at the annual meeting of the European Association for the Study of Diabetes (EASD) in Stockholm, Sweden (19-23 Sept).
Semaglutide was recently approved in the US as an obesity treatment1 and has been provisionally approved to treat obesity in England.2
“Semaglutide appears to be the most effective medication to date for treating obesity and is beginning to close the gap with the amount of weight loss following bariatric surgery,” says Dr W. Timothy Garvey, of the Department of Nutrition Sciences, University of Alabama at Birmingham, Birmingham, AL, USA, who led the research.
“Its approval was based on clinical trial results showing that it reduces weight by over 15% on average, when used together with a healthy lifestyle programme.
“This amount of weight loss is sufficient to treat or prevent a broad array of obesity complications that impair health and quality of life and is a game changer in obesity medicine.”
Obesity is known to increase the risk of T2D at least six-fold and Dr Garvey and colleagues were interested in whether semaglutide could reduce this risk.
To learn more, they carried out a new analysis of the data from two trials of semaglutide.
In STEP1, participants (1,961) with overweight or obesity received an injection of 2.4mg of semaglutide or a placebo weekly, for 68 weeks.
STEP4 involved 803 participants with overweight or obesity. All received weekly injections of 2.4mg semaglutide for 20 weeks. They then either remained on semaglutide or were switched to placebo for the next 48 weeks.
Participants in both trials received advice on diet and exercise.
The researchers used Cardiometabolic Disease Staging (CMDS) to predict the participants’ risk of developing T2D in the next 10 years.
CDMS has been previously shown be a highly accurate measure of T2D risk and is calculated using a formula which factors in a patient’s sex, age, race, BMI and blood pressure, as well as blood glucose, HDL cholesterol and triglyceride levels.
In the STEP1 participants receiving semaglutide, 10-year risk scores for T2D decreased by 61% (from 18.2% at week 0 to 7.1% at week 68).
This compares to a 13% reduction in risk score for those given the placebo (17.8% at week 0 to 15.6% at week 68).
Risk scores mirrored weight loss, which was 17%, on average, with semaglutide vs 3% with placebo.
At the start of the trial, risk scores were higher in the participants with pre-diabetes than in those with normal blood sugar levels. However, semaglutide reduced the risk by a similar amount in both groups.
In the STEP 4 participants, the largest decreases in risk scores were seen in the first 20 weeks (from 20.6% at week 0 to 11.4% at week 20). In those who continued receiving semaglutide, the risk score decreased further to 7.7% but, in those who were switched to placebo, it rose to 15.4%.
This indicates that sustained treatment with semaglutide is needed to maintain the reduction in T2D risk
Dr Garvey says: “Semaglutide reduces the future risk of diabetes by over 60% in patients with obesity – this figure is similar whether a patient has prediabetes or normal blood sugar levels.
“Sustained treated is required to maintain the benefit.
“Given the rising rates of obesity and diabetes, semaglutide could be used effectively to reduce the burden of these chronic diseases.”
A new study published in Diabetologia (the journal of the European Association for the Study of Diabetes [EASD]) finds that there is a widening gap in diabetes-related mortality between urban and rural areas in the USA, and that reductions in mortality rates are seen predominantly in urban areas have been mainly limited to female and older patients while outcomes in male and younger individuals worsened. The research was led by Dr Mamas A. Mamas, of Keele University UK, and colleagues.
Diabetes is one of the most widespread chronic diseases and a leading cause of global mortality, estimated by the World Health Organisation to result in more than 1.5 million deaths per year. While the diabetes-related mortality rate has decreased in high-income countries such as the USA, this trend may not apply equally to all groups or across all regions.
Rural populations may have an increased risk of developing DM, and often have less access to healthcare and receive a lower quality of service provision than their counterparts in urban areas. Age and ethnic background also affect both the risk of developing DM and the likelihood of dying from the disease.
The authors analysed 20 years of data from the US Centers for Disease Control and Prevention (CDC) Wide-Ranging ONline Data for Epidemiologic Research (CDC WONDER) Multiple Cause of Death database which recorded the cause of death of every US resident who died in the period 1999-2019. Each death certificate recorded a single underlying cause with up to 20 additional factors, as well as demographic data such as age, sex and ethnicity, and deaths were grouped by county to calculate Age-Adjusted Mortality Rates (AAMRs) per 100,000 population for urban and rural areas.
Between 1999 and 2019 there were 1,572,536 deaths (80% in urban counties) where diabetes was given as the underlying cause and 5,025,745 deaths (again 80% in urban counties) with diabetes as a contributory factor.
The team found that the AAMR of diabetes patients was higher in rural areas across all age, sex, and ethnicity groups and over the 20-year period of the study there was no statistically significant change in the AAMR of diabetes as the underlying or contributing cause of death in rural areas.
By contrast, urban areas saw a significant decrease in the AAMR of diabetes as the underlying (−17%) and contributing (−14%) cause of death over the same time period. As a result, the urban-rural diabetes-related mortality gap has tripled in the USA, rising from 2.0 to 6.8 deaths per 100,000 population for diabetes as the underlying cause, and from 6.8 to 24.3 deaths per 100,000 population for the disease as a contributing factor, with the main impact being felt by male patients and those under-55 years old.
In both urban and rural areas, AAMRs were higher in males and saw a significantly smaller decrease than in females leading to a widening of the male-female diabetes mortality gap. Among under-55s there was an increase in diabetes-associated AAMRs over the time period which was larger in rural (+59% underlying, +65% contributing) than urban (+15% underlying, +14% contributing) populations. This contrasted with the over-55s who experienced a decrease in AAMRs in urban (-21% underlying, -16% contributing) residents and no statistically significant change (-5% underlying, +4% contributing) in rural areas.
Ethnicity was also linked to mortality with American Indian and Black individuals having substantially higher diabetes-related AAMRs than Asian and White patients, and within each ethnic group, rural living was associated with higher mortality. For example, in rural areas, the mortality amongst Black patients remained similar between 1999 and 2019, whereas it decreased by 28% in urban areas. Diabetes-related AAMRs in 2019 were twice as high in Black patients compared to White patients, in both rural and urban settings.
The team note: “Our finding of an increasing gap in diabetes outcomes is in agreement with previous studies that reported greater improvements in blood pressure and cholesterol control for urban adults with diabetes than for those in rural areas over the last two decades.” They add: “These differences remained significant even after multiple adjustments for ethnicity, education, poverty levels and clinical characteristics.”
The observed increases in mortality among the under-55s may be linked to the increasing prevalence of type 2 diabetes, particularly in adolescents and young adults. Early-onset of the condition is typically more aggressive and has a higher rate of premature complications, and previous research has found that glucose control is worse in younger individuals with the disease. Since male patients are more likely to be diagnosed at an early age, this may explain the widening male-female mortality gap observed in both urban and rural populations.
The authors highlight that successful management of diabetes and the control or prevention of associated complications requires medical expertise that may be unavailable or difficult for rural populations to access. Patients in these communities are also less likely to have their primary care delivered by physicians, and they have been further impacted by the disproportionate closure of rural hospitals.
The urban-rural divide is inextricably linked to social determinants of health including education, economic resources, psychological stress and access to preventive healthcare. The authors say: “Healthcare equity, expansion of Medicaid, and telemedicine initiatives that extend access to specialty care may mitigate some of the rural–urban disparities in mortality. However, the ultimate solutions may lie in economic and policy interventions that broaden our focus from treating disease to preventing it.”
They conclude: “A synchronised effort is required to improve cardiovascular health indices and healthcare access in rural areas and to decrease diabetes-related mortality.”
New knowledge about the link between infection during pregnancy and autism
Children of women with gestational diabetes and obesity may be twice as likely to develop attention-deficit/hyperactivity disorder (ADHD) compared to those whose mothers did not have obesity, according to new research published in the Endocrine Society’s Journal of Clinical Endocrinology & Metabolism.
The estimated number of children aged 3–17 years ever diagnosed with ADHD is 6 million, according to data from 2016-2019. A major risk factor for ADHD in children is maternal obesity. Roughly 30% of women have obesity at their first doctor’s visit during pregnancy, and this number increases to 47% in women with gestational diabetes. Excessive weight gain during pregnancy in this population is a risk factor for children developing ADHD.
“Our study found pregnant women with obesity and gestational diabetes had children with long-term mental health disorders such as ADHD,” said Verónica Perea, M.D., Ph.D., of the Hospital Universitari MutuaTerrassa in Barcelona, Spain. “We did not find this association when these women gained a healthy amount of weight during pregnancy.”
The researchers studied 1,036 children born to women with gestational diabetes. Thirteen percent of these children were diagnosed with ADHD. The researchers found children of women with gestational diabetes and obesity were twice as likely to have ADHD compared to those born to mothers without obesity.
The researchers only found this association in women with gestational diabetes, obesity and excessive weight gain during pregnancy. The researchers did not observe a higher risk of ADHD in children of women with gestational diabetes and obesity if the amount of weight these women gained during pregnancy was within the normal range.
“It’s important for clinicians to counsel their patients on the importance of healthy weight gain during pregnancy,” Perea said.
Study identifies key protein that drives rheumatoid arthritis damage
Scientists have identified a protein known as sulfatase-2 that plays a critical role in the damage caused by rheumatoid arthritis. A chronic disease in which the immune system attacks the body’s own joint tissues, rheumatoid arthritis affects an estimated 1.5 million Americans.
Published in the journal Cellular & Molecular Immunology, the discovery sheds new light on the molecular processes that drive inflammation seen in rheumatoid arthritis. It could also someday lead to improved treatment of the disease, which currently has no cure.
“Tumor necrosis factor-alpha—or TNF-alpha for short—is one of the main inflammatory proteins that drive rheumatoid arthritis and is targeted by many currently available therapies,” said senior author Salah-Uddin Ahmed, a professor in Washington State University’s College of Pharmacy and Pharmaceutical Sciences. “However, over time patients can develop a resistance to these drugs, meaning they no longer work for them. That is why we were looking for previously undiscovered drug targets in TNF-alpha signaling, so basically proteins that it interacts with that may play a role.”
Though sulfatases such as sulfatase-2 have been extensively studied for their roles in different types of cancer, Ahmed said no one had looked at how they might be involved in inflammatory or autoimmune diseases such as rheumatoid arthritis.
The research team first explored this idea using cells called synovial fibroblasts, which line the joints and keep them lubricated to ensure fluid movement.
“In rheumatoid arthritis, these normally quiescent cells get activated by TNF-alpha and other inflammatory molecules, and they take on this aggressive character,” said first author Ruby J. Siegel, a PhD graduate in the WSU College of Pharmacy and Pharmaceutical Sciences. “They are not dying when they should, and they proliferate in a way that is almost tumor-like, forming this massive synovial tissue that should not be anywhere near that size and at the same time activating proteins that destroy cartilage and bone.”
Using the joint-lining cells of rheumatoid arthritis patients, they removed sulfatase-2 from one group of cells before stimulating all cells with the inflammatory TNF-alpha. What they found was that cells lacking sulfatase-2 did not show the same exaggerated inflammatory response to TNF-alpha as cells that were left intact.
“Looking at sulfatases for their potential role in inflammation was an educated guess, but once we did we saw a very consistent pattern of increased sulfatase-2 expression throughout different tissues and samples we studied,” Ahmed said. “This tells us that TNF-alpha relies on sulfatase-2 to drive inflammation, because as soon as we removed sulfatase-2 the inflammatory effects of TNF-alpha were markedly reduced.”
Resulting from a series of experiments spanning four years, the researchers’ findings open the door to future animal studies to test the effectiveness of inhibiting sulfatase-2 to ease rheumatoid arthritis symptoms. This could someday lead to the development of new combination therapies that along with other inflammatory proteins would also target sulfatase-2 to prevent bone loss, cartilage damage and deformed joints. Such therapies could help address the shortcomings of currently available rheumatoid arthritis drugs, many of which come with significant side effects.
“These drugs shut off TNF-alpha in your whole body, but it does have important immune functions,” Siegel said, adding that patients who take these types of drugs are more susceptible to infection and have an increased risk of developing cancer with long-term use. She also noted that TNF-alpha inhibitors are not effective in all people and are not recommended for patients with certain other health conditions.
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