Category Archives: Diabetes

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

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

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

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The #1 Cause of Diabetes, According to Science - msnNOW

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

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

Pandemic tied to sharp rise in type 2 diabetes in kids

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

Immune cell "factories" work longer after mRNA vaccines

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

Following AstraZeneca with Pfizer shot boosts antibody response

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

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

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

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

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

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

Our Standards: The Thomson Reuters Trust Principles.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

The more information the better, he said.

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

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

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

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

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

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

Natalie J. Bellini

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

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

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

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

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Nick Jonas Kicks Off Diabetes 'Time in Range' Initiative - Healthline

Introduction

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Abbreviation: SCV, sensory conduction velocity.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

The authors report no conflicts of interest in this work.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Finerenone data:

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

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

Finerenone and SGLT2 Inhibitors Could Have Additive Effect on Kidney Protection

Cost of Diabetes:

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

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

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

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

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

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

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

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

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

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

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

Nick Jonas, #WhenInRange

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

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

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

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

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

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

MINNEAPOLIS Diabetes can raise the risk of Alzheimers disease more than sixfold, warns new research.

Good control of blood sugar protects against the devastating mental disorder, say scientists. Older patients who were admitted to the hospital for both high or low levels were over six times more likely to develop it.

The findings, published in the journal Neurology, are based on nearly 3,000 older people with Type 1 diabetes, the form not linked to obesity.

For people with diabetes, both severely high and low blood sugar levels are emergencies and both extremes can largely be avoided, says lead author professor Rachel Whitmer, of California University, Davis, in a statement. However, when they do occur, they can lead to coma, increased hospitalization and even death.

Diabetes is considered a risk factor for dementia by reducing blood flow to the brain. Experts estimate a third of cases could be prevented with simple lifestyle changes.

People with type 1 diabetes are living longer than before, which may place them at risk of conditions such as dementia, says Whitmer. If we can potentially decrease their risk of dementia by controlling their blood sugar levels, that could have beneficial effects for individuals and public health overall.

Type 1 diabetes is a chronic condition in which the pancreas cant produce enough of the glucose-controlling hormone insulin. It usually starts in childhood.

The study analyzed episodes of high or low blood sugar resulting in hospital emergencies, hyperglycemia and hypoglycemia, respectively. The latter can lead to unconsciousness, and the former to cardiovascular disease and blindness.

Participants admitted at some point for both complications were up to six times more likely to develop dementia years later. Those who suffered just one of the extremes were also more prone.

Researchers tracked 2,821 participants, with an average age of 56, for seven years. Of those, 335 (12 percent) and 398 (14 percent) had a history of severe high and low blood sugar, respectively, and 87 (three percent) both. Over the study, 153 cases of dementia were diagnosed about five percent of the population.

The risk more than doubled and rose by 75 percent among those with high or low blood sugar events, respectively. And it soared more than six times for those who experienced both compared to peers who had neither, after accounting for age, sex and ethnicity.

Our findings suggest exposure to severe glycemic events may have long-term consequences on brain health and should be considered additional motivation for people with diabetes to avoid severe glycemic events throughout their lifetime, adds Whitmer.

She points out participants only counted as having dementia if they had been diagnosed. Many cases go undiagnosed, suggesting the risks may be even higher.

Severe glycemic events can occasionally occur in the more common Type 2 form, caused by unhealthy diets and lack of exercise.

SWNS writer Mark Waghorn contributed to this report.

Read more:
Type-1 diabetes patients may be more than 6 times as likely to develop dementia - Study Finds

Managing type 2 diabetes can feel like a full-time job. And, like many demanding roles, it can lead to burnout that makes it hard to stay on track.

Theres never a break, says Tami Ross, RD, a certified diabetes care and education specialist and the author of What Do I Eat Now?: A Guide to Eating Well with Diabetes or Prediabetes.

Keeping up with everything that diabetes requires, including monitoring blood sugar levels and going to regular doctor appointments, can be exhausting. Add on everyday stressors, the pandemic, and other chronic conditions, and you can easily start feeling depleted and defeated.

While diabetes burnout is common, there are ways to recover from it. Keep reading to learn about the warning signs of burnout and what to do about it.

Even though theres no standard definition for diabetes burnout, it usually involves feeling frustrated and exhausted from the daily demands of managing the condition, according to a 2019 article from the American Journal of Nursing.

Diabetes burnout affects more than just your emotional health, though. It can also impact your ability to control your diabetes. In a 2018 study, more than a third of adults with type 2 diabetes pointed to burnout as a barrier to following treatment plans.

Universally, people with diabetes burnout become overwhelmed by the demands of living with diabetes and [are] tired of managing their condition, says Andrea Newcom, RD, a diabetes care specialist and health coach at Omada Health.

Identifying diabetes burnout can be tricky because its unique to the individual, says Shahzadi Devje, RD, a certified diabetes educator.

The length, severity, and signs of diabetes burnout not only vary between people, but also within the same individual. One episode of burnout may look different from another, depending on whats going on in your life.

While there arent standard measurement tools for the condition, diabetes burnout may include psychological symptoms, like:

Changes in the way youre managing the condition may also be warning signs of diabetes burnout. You may have the condition if you find yourself:

Symptoms of diabetes burnout can also be physical. The stress-related condition is linked to sleep changes, headaches, body aches and pains, and more frequent bouts of illness, says Devje.

Although symptoms may overlap, diabetes burnout and depression are not the same thing.

[W]ith diabetes burnout, these feelings are specific to diabetes, says Ravi Kavasery, MD, the medical director of quality and population health at AltaMed Health Services.

With depression, however, the sadness, frustration, and hopelessness pervade all areas of your life, Kavasery says. According to a 2014 study, about 20 to 30 percent of people with diabetes experience depressive disorders.

If you think you may have depression or diabetes burnout, talk with a healthcare professional to figure out the root of the problem and ways to cope.

While it might not be possible to get rid of the daily demands of managing diabetes, there are ways to beat burnout from the condition. Here are some tips on recovering from diabetes burnout.

When youre feeling burnt out, you might be tempted to push through, ignore your feelings, or bash yourself for not following through with treatment plans.

Yet the first step in managing burnout is accepting its presence including the emotions that come from it. Journaling can be a helpful tool to explore your feelings in a judgment-free space.

Talking with a doctor or healthcare professional about your burnout symptoms can feel uncomfortable or even upsetting. However, Kavasery says its important to remember that youre not doing anything wrong.

We all need support in different ways, and sometimes our individualized care plans stop working for us, he says.

When talking with a healthcare professional, be honest about the ways diabetes burnout is affecting your life. That way, you can work together as a team to address the problem and find solutions that work for you.

Counteract burnout symptoms by getting strategic about whats causing them to begin with.

Ask yourself: What about diabetes management is stressing you out? What in particular is making it harder to focus on your health?

If the problem is an unrealistic diabetes management plan, like exercise goals that dont fit into your busy schedule, talk with your healthcare team about alternative solutions.

Your goals and targets must be relevant and fit within your lifestyle [so they dont] feel like a continued burden, Devje says.

Trying new techniques to manage your diabetes can be a helpful way to feel re-inspired and alleviate burnout.

Breathe new life into your old ways of managing the condition, says Sabrina Romanoff, PhD, a clinical psychologist. She suggests trying new diabetes-friendly recipes if your go-to meals have you stuck in a rut.

Other ideas include switching up your exercise routine by walking different routes, signing up for online or in-person fitness classes, or rediscovering your favorite childhood sport.

Another way to address diabetes burnout is by finding ways to connect with other people with the condition. Building relationships with those who truly get you gives you the opportunity to share your hardships and successes, says Ashley Ellis, PharmD, a diabetes educator and the clinical director at Compwell.

Consider tapping into a diabetes support group, either in person or virtually, to exchange tips and tools for managing diabetes and fighting burnout.

A vacation from the office can often help cure work-related burnout. Likewise, a short, safe vacation from the things you do to control diabetes may also help you feel less burnt out, Ross says.

Ross suggests talking with your healthcare team about how to safely take a few days off to help restore your energy. That might mean resting instead of going through your normal exercise routine, or checking your blood glucose levels slightly less often for 1 to 2 days.

If you know someone with diabetes who seems to have the symptoms of diabetes burnout, you may be able to help them find some relief. Here are ways to show your support,

Genuinely connect with your loved one by stating your concern and desire to support them. Romanoff suggests saying, It looks like things have been challenging for you recently. Whats been on your mind, and what can I do to help?

Give your loved one space to express their frustration and sadness, Ellis says. You can also show empathy by recognizing the immense effort and energy required to manage a complicated condition, Devje adds.

Enjoy active adventures together with the intention of having fun, rather than talking about and dealing with diabetes.

Helping them take a break from thinking about the condition can remind them that diabetes doesnt have to prevent them from enjoying their life.

Diabetes burnout can make it difficult to acknowledge all the hard work that goes into controlling the condition.

Ross recommends praising your loved one for the things theyre doing well, such as following diet recommendations or getting exercise. This can provide them a much-needed confidence boost.

Once you recover from diabetes burnout, find ways to keep it at bay. Here are some tips on preventing diabetes burnout.

When prioritizing your health, making achievable goals can help set you up for success. That might mean moving your body for 10 minutes after every meal or taking a brisk walk during your lunch break, Ellis says.

Small wins can help build your confidence, so you can achieve even bigger goals over the long term.

Stress can trigger or exacerbate burnout, so its important to develop ways to cope. Here are some ways to reduce stress, according to the Centers for Disease Control and Prevention (CDC):

For many people, food goes beyond a source of nourishment by preserving family traditions, special memories, culture, and identity, Devje says.

Being told to revamp your diet to manage diabetes and remove culturally significant foods can reduce the joy of eating and create a negative, fearful relationship around food, she says.

If your diabetes management plan includes making changes to your diet, consider connecting with a dietitian or other healthcare professional about ways to continue incorporating culturally relevant foods into your meals.

Technology can make it easier and even more fun to build healthy habits. Try apps for cooking, exercise, meditation, or other self-care practices to add excitement into your daily life.

Diabetes burnout is a common experience that can leave you feeling frustrated, exhausted, and unmotivated to stick to your treatment plan.

However, there are ways to recover from diabetes burnout and prevent it from coming back. You may find relief by joining a diabetes support group, trying new recipes and types of physical activity, or taking a brief, safe break from your routine.

If youre experiencing symptoms of diabetes burnout that are making it difficult for you to manage the condition, talk with a healthcare professional about ways to cope.

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Diabetes Burnout: 6 Ways to Find Relief - Healthline

Psoriasis and diabetes are two distinct conditions that are common comorbidities for each other. This means that people with psoriasis have an increased risk of developing type 2 diabetes. Researchers do not fully understand the mechanisms behind this link, but evidence suggests that inflammation may play a role.

Research into psoriasis and diabetes and the connection between them is still ongoing. However, scientists currently believe that inflammation from psoriasis may cause insulin resistance, which can lead to type 2 diabetes.

It is important to treat both conditions and try to prevent potential complications. Making certain lifestyle changes can also sometimes be effective in reducing the risk of comorbidities or minimizing the symptoms of both conditions.

In this article, we discuss the connection between psoriasis and type 2 diabetes, the prevalence of comorbidities, and the treatment options.

Psoriasis is a skin condition in which the immune system mistakenly overreacts and attacks healthy tissue, causing skin cells to build up too quickly for the body to shed them. As a result, inflamed raised areas of skin with white or silvery flakes called plaques may appear anywhere on the skin. Psoriasis may also affect other areas of the body, such as the nails and scalp. In some cases, inflammation affects the joints, resulting in psoriatic arthritis.

The medical community defines psoriasis as an autoimmune condition in which the immune system starts working too much in response to certain triggers. Factors that can increase the risk of psoriasis include infections, medications, smoking, and obesity.

Diabetes is a condition that impairs the bodys ability to process blood sugar. There are two main types of diabetes: type 1 and type 2.

In type 1 diabetes, which is also known as juvenile diabetes, the body is unable to produce the hormone insulin because the immune system attacks the cells that carry out this function. In type 2 diabetes, the body either does not produce enough insulin or becomes resistant to it. This is the most common type of diabetes, and it has strong links with obesity.

Evidence indicates a clear link between psoriasis and type 2 diabetes. People with psoriasis have a higher risk of developing several metabolic conditions, including type 2 diabetes.

Researchers are still studying the exact reason for the connection, but evidence suggests that a few factors may play a role.

A 2019 study highlights that psoriasis is associated with systemic inflammation. This includes inflammation in multiple organ systems, which may explain the increased risk of metabolic disorders such as diabetes. The research also indicates that there may be metabolic genetic links between the two conditions.

Another possible link is that psoriasis contributes to diabetes by increasing insulin resistance. A 2018 study on mouse and human skin indicates that skin inflammation from psoriasis can result in insulin resistance, which is a risk factor for type 2 diabetes.

A 2020 study suggests that diabetes and psoriasis also share similar mechanisms that drive disease. Together, the conditions may lead to more cell and tissue damage, creating a vicious cycle.

Both conditions are also associated with similar risk factors, such as obesity, metabolic disorders, cardiovascular disease, and renal disease. The authors of a 2017 article also suggest that psoriasis may actually be an independent risk factor for diabetes.

Diabetes and psoriasis are common comorbidities for each other, meaning that they often both affect the same person. Evidence notes that both conditions are fairly common in the United States, with more than 8 million people having psoriasis and more than 34 million people having diabetes.

Although little information is available on the prevalence of comorbid psoriasis and diabetes, research suggests that the prevalence of type 2 diabetes among people with mild or severe psoriasis is roughly 37.4% and 41%, respectively. This finding indicates that the risk of developing diabetes may increase with the severity of psoriasis.

There is currently no cure for either psoriasis or diabetes. Instead, treatments focus on managing the condition.

For psoriasis, treatments aim to reduce symptoms by decreasing inflammation, stopping skin cells from growing as quickly, removing scales, and avoiding potential triggers of flare-ups.

For diabetes, treatments aim to keep blood glucose levels stable and at a healthy level through a combination of diet, exercise, and synthetic insulin.

In people with both conditions or other comorbidities, doctors may adjust the treatment approach to avoid complications. For example, if a particular treatment method for psoriasis will affect another health condition that the person has, doctors may recommend other treatments.

Home remedies, which center around lifestyle changes, are an important part of managing both psoriasis and diabetes.

Along with other health benefits, eating a well-balanced diet can help a person better control their diabetes and prevent potential complications. Likewise, eating well can help lessen the severity of psoriasis symptoms. Certain dietary choices may also help lower the likelihood of comorbidities developing and reduce inflammation in the body.

Regular exercise keeps the body healthy, and it may also play a role in helping people manage both diabetes and psoriasis. Regular exercise can reduce stress and boost the immune system, which may help with psoriasis. It may also help with diabetes by keeping blood glucose levels within target ranges.

People can also use regular exercise to help control other risk factors for these disorders. For instance, it can help a person manage their weight.

Steps such as eating a nutritious diet and engaging in regular exercise can also help a person manage their weight. As obesity is a risk factor for both conditions, maintaining a moderate weight is an important step to reduce the risk.

Stress is a potential trigger for psoriasis flare-ups, and it can also make it difficult for a person to control their blood glucose levels. Therefore, finding ways to reduce stress may help manage these conditions.

The most effective stress management techniques may vary among individuals, but common approaches include:

Other lifestyle adjustments that may benefit health and potentially reduce the symptoms of psoriasis and diabetes include limiting alcohol, stopping smoking, and getting adequate sleep.

A doctor should work with a person who has psoriasis, type 2 diabetes, or both conditions to help them manage and control the symptoms. A person may also benefit from seeing a dermatologist for skin issues or an endocrinologist for a diabetes treatment plan.

Working with primary care doctors and specialists to help control and manage these conditions may increase a persons quality of life.

Anyone who notices any troubling symptoms or potential complications should consult a doctor.

Psoriasis and diabetes are common comorbidities for each other, meaning that people with psoriasis are much more likely than other people to develop type 2 diabetes. Both conditions have similar risk factors and involve the immune system and inflammation.

Correctly managing both conditions is important to promote good health and reduce the risk factors for other comorbidities. Through treatments and lifestyle changes, people may be able to control both conditions and prevent potential complications.

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Psoriasis and diabetes: What is the connection? - Medical News Today

It was only about 24 hours after the shock of my lifetime: My freshly-turned 6-year-old daughter was in the hospital, diagnosed with type 1 diabetes (T1D).

There was so much to learn. And yet, one thing kept floating to the top of my mind. As selfish as I felt, I had to let it out to the endocrinologist sitting there explaining to me how to handle a vial of NPH insulin.

Never mind that, I said, tears welling up in my eyes, How are we ever going to ski again?

That endo, who happened to be an avid skier himself, put down whatever he was showing me, took a breath, looked me in the eye and made this promise:

You will ski, Moira, and so will your whole family. And youll do it the same way you did before this. Ill guide you. Youll see. Diabetes need not take away or even greatly alter the activities your family loves.

Flash forward 6 weeks later, and I was in Vermont at Okemo Mountain Resort, dropping my newly diagnosed itty-bitty kid off at ski school for the day.

How did it go? Ill save sharing a very telling outcome with you until the end of this story (youll want to hear it!). But in short: He was right.

With some planning, testing, tweaking and a whole lot of faith, we merged right back into our active ski lives, hitting up resorts all over America, savoring both powder and sun days and most of all: sharing the activity that was and still is for us a vital family bond.

Its a lot to think about: sending your child (or anyone) with T1D off for a day of heart-pumping activity thats sure to have an impact on blood sugars.

For us, since skiing was a family activity before T1D joined our lives (both my children started at around age 2. I like to tell people I only had kids so I could ski with them. Its only kind of a joke), our goal was to return to how we did it before T1D.

That meant dropping my child at ski school for the day, heading off for my own high-level ski fun and then a post-ski-school late afternoon family ski session.

Fortunately, our endo felt it was important to show my daughter (and me) that diabetes didnt control us; that rather, we could fit diabetes in around the things we love to do.

It was important to me because I wanted my child to learn from pros. Because I wanted my child to experience the friend-making and group-skiing vibe that is such a vital part of the skiing experience all your life. Because, frankly, I wanted to go do some grown-up skiing for at least part of our ski days.

And because I wanted my child to know and see that she could and would be safe and fine doing things without me hovering.

In other words: My reasons had more to do with growing an engaged skier than they did with diabetes. Thats how, our endo told me, it should be.

Natalie Bellini, diabetes care and education specialist (DCES) and endocrinology nurse practitioner at R & B Medical Group in the Buffalo New York region, told DiabetesMine that our decision was a solid one.

I think all things with managing T1D is never saying no. Its learning how to adjust so we can say yes, she said.

Which brings me to my first tip: Do a practice trip with just you and your child with T1D to work out both your nerves and the kinks. By heading up with just my daughter for a weekend (and leaving my other child and husband behind) I was able to cut down what I had to worry about, pack, keep track of, and manage, freeing up my headspace to take this on.

My first step in setting up the practice trip is a must-do that Bellini suggests: a planning call or meeting with the endo or diabetes educator.

Its important here to point out that no one can simply list out how to tweak insulin dosing for a ski trip in a general way. As we all know, diabetes is individual; everyone seems to have their own unique reaction to just about everything we do.

Some people go higher in cold weather sports. Some people have adrenaline spikes that self-correct later. Some people need much less insulin while skiing.

Most experts advise those going out for the first time to err on the side of needing less insulin. Our endo suggested I cut back my daughters long-acting insulin first by about 30 percent and then see. Today, for those on multiple daily injections (MDI), that would mean cutting the long-acting the night before. For those using an insulin pump, a temp basal program can be set that morning.

Your healthcare team will help you make that decision.

We recommend to everyone cutting back basal by 30 to 50 percent, and then simply checking blood sugars every couple of hours, Bellini said.

The goal with new skiers, with or without diabetes, is to have an amazingly wonderful day skiing It is not to have a perfect blood glucose day, but to learn from the glucose is so that the next time you go out its more predictable, she advises families.

Next, its smart to call the ski school ahead of time.

It is helpful for a parent to reach out so that we are aware of the dates and can be prepared to greet them, Kurt Hammel, Childrens Programs assistant manager at Deer Valley Resort in Utah, told DiabetesMine.

Their goal in speaking with parents, he said, is both to understand the childs needs ahead of time, give parents an outline of the day (as well as foods to be served at any snacks or meals while in ski school) and most of all, he said, to also reassure them that we can provide a safe experience.

Some parents consider asking for a private instructor so they can focus on their childs diabetes needs. For us, since my goal was for my child to have a full ski life experience, sending her to group ski school worked best.

Ski resorts usually cannot promise which instructor you have ahead of time, since they usually build up the groups, the morning of the ski day or the night before. But I did have a time when my daughter was little that a ski resort decided to assign an instructor to her ahead of time and work the groups around that.

It was Killington Mountain Resort in Vermont and the reason was amazing: They had an instructor with T1D. It was very much serendipity, but you never know what you may get from speaking to them ahead of time.

Our endo helped us hone in on what we expected from a ski school. We expected the instructor to be willing to carry glucose tabs in their pocket (even though our daughter had some in her pocket too). We expected them to keep an eye on her, knowing just the basics. We instructed them that if she said she felt low not to stop and check and assess, but rather to encourage her to just eat fast-acting carbs.

When she was little, we did ask them to always have her ride the lifts with an instructor.

Most of all, we expected them to teach her how to ski in a professional and positive way.

First, we had to figure out what she needed to carry and what could be left in the base lodge. For a ski program that returns to the same base area, its easy enough to put most of the diabetes gear in a locker or storage basket (most ski areas have such options).

In her pocket always was fast-acting glucose thats easy to handle, something Bellini says is a must.

Whether pumping or on MDI, our endo suggested we leave the backup insulin, syringes, sites, and all that in the locker at the base, since none are ever as immediate a need as rapid-acting glucose.

If lunch was going to be in another spot, we would tuck an insulin pen into her jacket when she was on MDI. Pro tip: The closer to the skin the insulin is, the less chance of it getting too cold (freezing and become ineffective). But most closing pockets in a good ski jacket work. Think about it: If your body is warm, your jacket is keeping all things warm.

When pumping, we made sure to keep the tubing as close to the skin as possible, while also leaving the pump accessible.

If you use a meter, its not a bad idea to have that in a pocket, and in that case, any pocket will do. Pro tip: When your meter tells you it is too cold to work (and it will), simply tuck it into your underarm for about 30 seconds and *poof!* its back to working again.

If you are relying on a continuous glucose monitor (CGM) and reading results off a phone, make sure you keep both in an inside pocket and have someone carry a backup charger. We love the new Clutch backup charger, as its super thin and carries a good charge in case your phone runs down.

As for emergency glucagon, whatever kind you keep on hand, either tuck it in your childs coat and let the instructor know where it is, or ask the instructor to carry it. Most ski patrol folks are familiar with treating a severe low, but ask the ski school ahead of time to be sure. Instructors have the ability to get ski patrol to a spot quickly.

And what about following numbers and reacting to them? Your medical team can help you decide that. For us, the first few times out were about not reacting to any numbers unless it was necessary. In other words, if our daughter ran a bit high, they wanted me to let it sit, so we could see what happens over the entire day and use that data to come up with a long-term plan.

Had I tried those first few times to keep her in a tight range with lots of corrections, her medical team explained, theyd not be able to see how the activity impacted things over hours and hours.

I did try to swing by at ski school lunch time to see how she was doing when she was younger something that was easy to do since the resorts usually have a pretty tight daily plan around that.

And you probably will be guided to check extra often during the first overnights after skiing, both to see what happens and to make corrections if needed at night.

For those on hybrid closed loop systems like the Tandem Control-IQ, Bellini said the best plan to speak to your medical team about setting exercise mode throughout the day while skiing and leave that target on overnight. That reduces the risk of hypoglycemia all by itself, she said.

This is going to surprise parents newer to diabetes, but my top advice centers more on skiing and riding than on diabetes: Make sure that the instructors teaching your child are certified by the PSIA (Professional Ski Instructors of America).

Id assert that this is more important than having expertise in diabetes.

While the notion of someone who understands T1D being your childs instructor is of course soothing and may be inspiring to your child, the baseline is that you want to send your child out there to become a strong, smart, and well-trained skier.

Learning to ski and ride is a complicated and detailed process. Learning from someone not well-trained to teach skiing could draw the wrong lines on the ski blueprint in your childs mind. So, opt for a trained instructor and its OK to ask that question when exploring options.

I also suggest parents not assume their child can only ski with a chaperone. I love skiing as a family. But I also love that my kids grew up knowing that, when age appropriate, its a sport they can head off and savor on their own.

There are some donts though, and most of them follow donts for anyone who does not have diabetes as well.

Do not ski off-piste (off-trail) alone. Tell your children that, when skiing without ski school or you, they are not ever allowed to go off trail and into the woods alone. Its just not smart. Mishaps can happen to anyone, like getting lost or injured, breaking gear, etc.

I actually did not allow my children to go off-piste without me or their dad. Ever.

Also, do not expect the ski school to watch a CGM and react to that information. Actually, neither you nor the ski school needs to know trends all day. A few check-ins planned with your medical team should work well.

Back to where I started.

That first day of trying it all out at Okemo resort was nerve-wracking for me, but I soldiered through. After our late-day family ski time, my daughter and I were at the base, talking about heading to swim in the outdoor slope side pool.

A fluffy, movie-set-like snow began to fall and as we stood there, out of nowhere, my then-tiny little skier raised both hands toward the sky, looked up at that snow and yelled with joy: Kids with diabetes DO still have fun!

And that, my fellow D-parent, is the telling outcome. Her joy. Her satisfaction. Her seeing first-hand that this would not stop her.

To me, thats the most vital outcome of all.

See more here:
The Do's and Don'ts of Skiing with Type 1 Diabetes - Healthline