Recent clinical trial data have led to new guidelines on managing heart failure with reduced ejection fraction, which promise to add years of life for people with the condition, many of whom also have diabetes. The need to adopt the Four Pillars of these new guidelines without delay was under discussion at the recent ADA conference, as Dr Susan Aldridge reports.

Speaking at the American Diabetes Association (ADA) Scientific Sessions this summer, Dr Patricia Campbell, Heart Failure Lead at Southern Trust Northern Ireland, reviewed best practice in diagnosis and treatment of people with heart failure with reduced ejection fraction (HFrEF). ”It’s important in the patient’s heart failure journey that they’re diagnosed early and accurately,” she says. “In the UK, 80% of patients are diagnosed when they’re already in hospital with an acute decompensated heart failure episode. This really is suboptimal, because heart failure is persistent and progressive. The pressure and volume overloads during acute decompensation drive cardiac remodelling, reduce contractile function and cause progression of the disease. So, after each episode, the patient never quite gets back to their previous level of functioning.”

On the other hand, we do know that optimisation of medical therapy early in the journey can prevent multiple hospitalisations and slow disease progression. “So, if there’s one message to take home from today it’s ‘think about BNP’. You guys [in your diabetes clinics] are looking after patients that I haven’t met yet, but they do have risk factors for heart failure. So, if someone has vague symptoms and you’re not sure what they’re related to, think about measuring their BNP.”

The Four Pillars of heart failure therapy

Most people with heart failure will already be on ACE inhibitors and beta blockers. However, the so-called Four Pillars of medication recommended in the most recent heart failure guidelines from the American Heart Association and other organisations are: angiotensin-receptor blockers/neprilysin inhibitors (ARNI, e.g. sacubitril/valsartan), beta blockers, mineralocorticoid receptor antagonists (MRA) and SGLT-2 inhibitors. Most of these have level A evidence for their efficacy in heart failure. For instance, the most recent trials on SGLT-2 inhibitors – DAPA-HF and EMPEROR-Reduced – show a 25% reduction in death or hospitalisation for heart failure with a number needed to treat of 21 over an 18-month follow-up. “In cardiovascular terms, that is an extremely low number needed to treat and therefore high-quality value medicine.” Dr Campbell says. 

She warns against clinical inertia. “You might think ‘I’ve got a patient in my practice with heart failure and they’re doing fine, so I’m not inclined to change anything’. Intuitively, we know that if a patient is newly diagnosed, or admitted to hospital, they are not stable and that warrants a change in therapy. We tend to think any stable heart failure is not at risk, but that is false. They are at risk of a decompensation episode if they have intercurrent illness, a new arrhythmia or atrial fibrillation, and are then at risk of sudden cardiac death.  These medicines are shown to reduce death or hospitalisation for heart failure, so we have to overcome our clinical inertia, even in the stable heart failure patient.”

Why these Four Pillars? Because each of these medicines acts on a different pathophysiological pathway – their mechanisms are independent and additive and their benefits are incremental. “So, the goal has changed from the last guidelines and it is now to implement as many of them as possible as quickly as possible,” says Dr Campbell. 

If you’re still not sure, because your patient is fine and they haven’t been in hospital in a few years, there is still a reason to change. Dr Campbell pointed to recent trial data, comparing comprehensive with conventional treatment, which showed that for a 55-year-old patient who is not particularly symptomatic, comprehensive treatment gave an extra 8.3 years of event-free survival, while a 65-year-old enjoyed an extra 6.3 years. “We are doing our patients a disservice if we are not maximising their medicines,” she says.

Implementing the Four Pillars

There are three changes to the way heart failure medication should be managed, according to the new guidelines. First, speed matters. “We have been too slow in introducing lifesaving therapies in the past, because we were doing it systematically according to the appearance of trial data,” Dr Campbell noted. Second, prioritise initiation of the Four Pillars and up-titrate afterwards. And third, there is no fixed or preference for the sequence of introducing these medications. “So, we are moving away from the approach that was vertical, step-wise, with titration to full dose of each drug before adding the next. It was chronological – based on order of completion of trials and assuming the most effective and well-tolerated treatments were developed first. This delays initiation of life-saving treatments that are immediately beneficial.”

For there is data from the CHARM-HFrEF trials on ARBs and from EMPHASIS-HF on MRAs that show the benefits start early, within two to four weeks. “These benefits happen, even when patients are in the early stages of being up-titrated. Even if you’re on tiny doses of an ARB or MRA, you’re still getting benefit. The same is true with SGLT-2 inhibitors. So, give the four pillars of care as soon as possible, and then up-titrate.”

She also suggests ignoring conventional sequencing and instead do these three steps. First, give the beta blocker and SGLT-2, then the ARNI and finally the MRA. This should all be achievable within three to four weeks, with up-titration to follow. This is in contrast to conventional sequencing, which takes six months or more.

Having said this, implementation should be individualised and adapted to the patient in front of you, according to their symptoms, functional status, renal function and comorbidities. “Also, you really should be getting these medications initiated before discharge from hospital after acute heart failure,” Dr Campbell advises. “It’s a time when you’ve got so many vital signs in front of you – lab results, and so on  – whereas we know in the real world there are multiple problems, such as patients not getting seen quickly enough after discharge or not often enough thereafter.”  

Barriers to implementation

Doctors worry that SGLT-2 inhibitors reduce estimated glomerular filtration rates (eGFR), for patients with heart failure often also have chronic kidney disease. It is the slight dip in eGFR on initiation that is the source of this concern. However, in the longer term, SGLT-2 inhibitors actually reduce the underlying decline in eGFR that occurs with chronic kidney disease. We also know from DAPA-HF and EMPEROR-Reduced that they reduce the risk of end-stage kidney disease and renal or cardiac death.

The presence of hyperkalaemia is also not a reason for not initiating these therapies, because both MRAs and dapagliflozin have been shown to reduce it. And when it comes to blood pressure, Dr Campbell notes that “A lot of heart failure patients won’t have a good, robust blood pressure, but SGLT-2 inhibitors are self-titrating in that those with lowest blood pressure get the lowest blood pressure drop and those with the highest blood pressure get the highest drop and this equalises out over time. So, low blood pressure should not be a reason not to start MRAs, SGLT-2 inhibitors and beta blockers.” Finally, SGLT-2 inhibitors have also been shown to have benefit for patients who are frail, so again, don’t hold back from using them in this group either. 

For more on this topic, enrol on the following EASD e-Learning courses:

Any opinions expressed in this article are the responsibility of the EASD e-Learning Programme Director, Dr Eleanor D Kennedy.

The cost-of-living crisis being experienced around the world is not just about energy and food prices. It also encompasses access to healthcare and affordability of therapies. According to findings presented at the recent ADA Scientific Sessions, these costs are hitting people with heart failure hard, particularly those in lower socioeconomic classes, who are already disproportionately affected by the condition. Dr Susan Aldridge reports.

The social determinants of health are extremely important and are tied to outcomes. This is as true in heart failure as in other chronic conditions. Speaking at the American Diabetes Association’s (ADA) conference this summer, Dr Shahzeb Khan, Duke University School of Medicine, pointed to a study of hospitalisation for heart failure (HHF) in young adults from 2004 to 2018, which showed an increase over this time. “Of particular interest is that 50% of these hospitalisations occurred in households in the lowest quartile of household income,” he says.

There was also a relationship between living in a ‘food desert’ and recurrent HHF and all-cause hospitalisations. A food desert is a low-income area with limited access to healthy foods. Another study showed that 63% of choices about healthy food and beverages are mediated by expenditure, so a healthy lifestyle is seen by many as a privilege.

Many health conditions are disproportionately clustered in poorer regions, Shahzeb says. But when it comes to healthcare, patients of lower socioeconomic status are more likely to face health inequalities and to have comorbidities. They have fewer interactions with primary care and are more likely to ‘end up’ in secondary care.   

Socioeconomic status and heart failure

A study looking at more than 40,000 patients from the Swedish Heart Failure Registry found that Class 4 heart failure was twice as common in the lowest compared with the highest socioeconomic class.

“What was even more worrisome is that patients of lower socioeconomic class had a 15% lower use of heart failure devices and medical therapies,” says Shahzeb. “They also had a higher comorbidity burden, including diabetes. And, although they were more likely to have heart failure, they were less likely to be admitted to hospital with it and receive an implantable cardiac defibrillator or anticoagulants.”

He was involved in another study on differences between rural and urban regions in mortality from heart failure, ischaemic heart disease and stroke, using the Centers for Disease Control and Prevention database. “Our study showed that people from rural areas had a much higher mortality from heart failure compared with people from metropolitan areas,” he says. “This can be linked to multiple factors, including access to healthcare, financial constraints and lower levels of health education.”  

There has been a very recent study of the global disparities in prescription of guideline-recommended drugs for heart failure with reduced ejection fraction. It covered more than 8000 patients hospitalised for acute heart failure in 44 countries. A lower proportion of patients in lower- and middle-income countries were on guideline-recommended therapy and, to make matters worse, they were also on lower doses. “This study clearly shows that that improved access to medicines, globally, is direly needed,” says Shahzeb.

Turning to heart failure in the USA, one study showed that one in six patients forgo or delay care, with more than half of these saying they do so because of cost. These patients are, unsurprisingly, more likely to appear in an emergency room and actually end up with higher annual inpatient and total healthcare costs. There are very similar findings for atherosclerotic cardiovascular disease, where one in two families of non-elderly patients with the condition have difficulty in paying medical bills.

Financial toxicity

Shahzeb went on to describe a study of healthcare spending by families with large employer coverage between 2003 and 2018. “This shows that out-of-pocket spending is rising steadily and has increased by 67% over that period. Patients with heart failure and their families are experiencing very large out-of-pocket healthcare expenses.” The study found that one in seven families with a member who has heart failure – and as many as one in four low-income families with a member who has heart failure – experience so-called ‘financial toxicity’. This means spending over 20% of their post-subsistence income on healthcare expenses per year. The main contributors to this out-of-pocket spending are insurance premiums and medications costs. “Therefore, financial toxicity represents an additional challenge for families of patients with heart failure, especially those on low incomes,” Shahzeb concludes.

“There is a huge difference in the best therapy available and the best therapy actually being delivered,” he continues. A US study on sacubitril/valsartan, which is now recommended for management of patients with heart failure found that, despite FDA approval, less than 3% of heart failure patients were taking it within the first 18 months. This may be associated with out-of-pocket costs, for this drug costs far more than other heart failure medications. 

Meeting the challenge  

“Now that we know that socioeconomic status has a huge impact on heart failure outcomes, we need to assess cardiologists’ knowledge, attitudes and practices on cost discussions and cost-conscious care,” says Shahzeb. “There is a lack of evidence on the quality of cost discussions between patients and physicians and, even in the guidelines, there is very little on how to conduct these discussions.”

He has some pilot study-based descriptive data on patients’ views and goals on cost discussions for heart failure treatment and says: “They may feel uncomfortable discussing costs with their physicians. We have very little information on patient perspectives on how to conduct such complex discussions.”

He is therefore working on the development and validation of a heart failure-related financial navigation programme for recently diagnosed patients. This includes one-to-one discussions, financial education, budget worksheets and appropriate counselling. There will also be research on financial toxicity and, ultimately, Shahzeb hopes that patient contributions to high-value therapies can be minimised. Addressing the socioeconomic aspects of heart failure, including costs, should hopefully improve outcomes.

Any opinions expressed in this article are the responsibility of the EASD e-Learning Programme Director, Dr Eleanor D Kennedy.

It’s an increasingly popular way to lose weight and improve health, but which intermittent fasting method should we be prescribing to patients with overweight and obesity? This question was addressed at the ADA’s latest conference. Lisa Buckingham reports.

As we battle the obesity pandemic, intermittent fasting (IF) has been cited as a potentially valuable tool. But what do we mean by intermittent fasting? And with several versions available, which is likely to be most effective and sustainable for people with overweight and obesity?

Speaking at the American Diabetes Association’s scientific sessions this summer, Krista Varady, professor of nutrition at the University of Illinois, USA, defined IF as an umbrella term that covers several types of eating pattern. Alternate-day fasting (ADF) – 500 calories on fast days and whatever you want on feast days; the 5:2 diet – two 500-calorie fast days per week and five feast days; and, by far the most popular, time-restricted eating (TRE) – an eating window of, say, eight hours and fasting for 16 hours.

Professor Vardy’s team did a trial on ADF, which investigated whether fasting plus aerobic exercise can treat non-alcoholic fatty liver disease (NAFLD). The trial design included an ADF group, which ate 600 calories on fast days; an exercise group that exercised five times per week for 60 minutes at moderate intensity; an ADF plus exercise group and a control group of usual diet. It was a three-month study and adherence was excellent. Participants had a liver-fat percentage of around 17%.

In the ADF plus exercise group, liver fat was significantly reduced (-5.5%) versus the exercise group (-1.3%) and control (-0.2%), but was not significant versus ADF alone (-2.3%). Bodyweight was significantly reduced in the combination group (-4.6%) versus exercise and control groups, but not versus ADF (-5.1%).

For liver enzymes, ADF plus exercise saw alanine aminotransferase (ALT) reduced versus control only. Aspartate aminotransferase (AST) remained unchanged. The combination group also saw promising changes in indicators of glycaemic control – fasting glucose, insulin, insulin resistance and waist circumference were reduced versus control only.

Overall, she said, they didn’t see much difference between the combination group and the ADF group, but the results of the combination were still positive.

With regard to ADF, Professor Varady said she is often asked whether people overeat on feast days. From their research, the answer is no. People typically eat only 10% (200 kcal) more than baseline, and report that they become more in touch with their hunger and fullness cues. It’s this inability to overeat on the feast days that leads to the weight loss.

Another study that they did five years ago asked whether fasting or daily calorie restriction is better for weight loss. It was one of the first studies on IF and – at 12 months – remains one of the longest: six months of weight loss followed by six months of weight maintenance. They had an ADF group, a calorie-restriction (CR) group and control of usual diet.

ADF and CR subjects lost the same amount of weight (6%) by month six, and this weight loss was maintained by month 12. ADF and CR also had similar effects on body composition, with one not being better than the other in terms of fat mass lost.

Professor Varady moved on to discuss time-restricted eating (TRE). This tends to be more popular than ADF, she said, as it’s easier to achieve, although the weight loss is not as high. When to place the eight-hour window is another question she’s often asked and the answer is that it’s healthier to place it earlier in the day as our bodies are more insulin sensitive in the mornings. However, starting the window at, say, 8 am was found to result in high dropout rates in trials because you can’t eat after 4 pm.

She pointed out that it’s still a very new field with little data behind it. She and her team did a three-month trial of TRE, with a window of eating from 10-6, to look at whether it actually works for weight loss versus a control group of usual diet with no timing restrictions. Adherence was very high.

Participants lost 2.6% bodyweight versus control. It’s easier to stick to than ADF, said Professor Varady, but weight loss is slower. However, the most interesting finding was that eating within an eight-hour window reduced energy intake by 350 kcal without calorie counting, simply because you have fewer hours in which to eat. The average American eats within a 14-hour window.

Finally, she drew attention to their work looking at whether a shorter eating window produces more weight loss. This trial compared a four-hour window (3-7 pm) with a six-hour window (1-7 pm), with a control of usual diet with no timing restrictions.

Participants lost the same amount of weight (3.2%), but the four-hour group lost it slightly faster than the six-hour group. Both groups saw similar reductions in fasting insulin (15%) and insulin resistance (20%), with no change in fasting glucose. No changes were seen in blood pressure or in lipids, but Professor Varady attributed this to the participants being in the healthy range at baseline.

An interesting point was raised about diet quality. One of the trial reviewers asked if the diet was of sufficiently high quality to make it safe if when people are eating in such a short window of time. After looking into this, the researchers found that diet quality was not compromised – people ate less of everything but it was in the same proportions as unrestricted eating.

For physicians that would like to prescribe these diets, Professor Varady provided some practical considerations and lessons from their research. Firstly, there is an adjustment period – it takes about 10 days to adjust to the new meal regimen and it’s worth letting patients know that those first days might be challenging. They may also experience headaches, but these subside when enough water is taken on. Secondly, patients can exercise and many feel a boost of energy while fasting, so there’s no need to change routine. Lastly, alcohol is permitted in moderation during the eating window with TRE, and on the feast days during ADF.

They are not suitable for children under 12, pregnant women, adults over 70 and people with eating disorders.

As for which diet to choose, Professor Varady said that it’s up to the person and what fits their lifestyle. She summarised that ADF is harder to follow and you need to count calories, but it has a faster weight loss of about 10-15 lb in three months. TRE is easier to follow with no calorie counting but has a slower weight loss of 5-10 lb in three months.

Studies have not extended beyond 12 months so it’s hard to say whether it works for long-term weight maintenance and more long-term data is needed.

For more on diet and lifestyle interventions in diabetes, enrol on the following EASD e-Learning module:

Any opinions expressed in this article are the responsibility of the EASD e-Learning Programme Director, Dr Eleanor D Kennedy.

Falls and fractures are more common among people with diabetes, with osteoporosis likely the underlying cause. Bone health, therefore, was under discussion at the ‘complications compendium’ session at the recent American Diabetes Association (ADA) Scientific Session. Dr Susan Aldridge reports back.

The World Health Organisation defines osteoporosis as a ‘systematic skeletal disease characterised by low bone mass and microarchitectural deterioration of bone tissue, with a consequent increase in bone fragility and susceptibility to fracture.’ Addressing the ADA session, Dr Rodrigo Valderrabano of Brigham and Women’s Hospital, who has an interest in bone metabolism, noted his appreciation of that emphasis on bone quality, because it’s important in the context of diabetes. He went on to note the high toll exacted by post-fracture morbidity and mortality. For 25% of people are institutionalised after a hip fracture, 40% are confined to a wheelchair, 60% have no recreation, while the mortality rate for women is 20% and up to 40% for men. 

Earlier research has shown that fractures can occur in those with normal bone density, which is particularly important for people with diabetes. Type 1 diabetes is 

associated with low bone density for a number of reasons – for instance, if children get it early in life, they don’t develop their peak bone density. In type 2 diabetes, however, bone density is actually elevated, as was seen in findings from Women’s Health Initiative. “This was so curious when we discovered this,” says Rodrigo. “It would be expected to reduce fracture risk, but there is a wealth of data showing that both type 1 and type 2 diabetes are associated with higher fracture risk at all sites.”

Underlying mechanisms

There are multiple hormonal interactions that could contribute to mechanisms of bone fragility in diabetes –  feeding back from the pancreas to maturation of osteoblasts and also from osteoblasts to the pancreas. Also, when there is longstanding hyperglycaemia, the person may develop end-stage glycation end products, which can attach to hydroxyapatite in bone and decrease bone turnover. Furthermore, there can also be a reciprocal relationship, with low levels of bone turnover biomarkers being associated with insulin resistance and incident diabetes.

“It’s also well known that diabetes is associated with an increased rate of falls, which may be modulated by microvascular complications, and this risk is extremely high in those treated with insulin,” Rodrigo adds. Unpublished data on 220,000 people in Taiwan shows that the number of fractures increases with age and the number of microvascular complications. “So, if you see someone in clinic with complications, even if their bone density is normal, you should still consider them at high risk for falls and fractures. Lower the bar for osteoporosis treatment.”

The Taiwan study also shows that fracture risk increases with HbA1c – 8 to 9% was associated with a 24% increased risk and 9 to 10% with a 41% increased risk of hip fractures. So, aim for an HbA1c below 8%, to reduce the risk of fracture.

Bone health should also be a consideration when selecting diabetes medications. Sulphonylureas and insulin increase the risk of falls and fractures, probably because they increase the risk of hypoglycaemia. Thiazolidinediones also increase the risk, maybe because they shift differentiation of mesenchymal stem cells towards adipogenesis and away from osteogenesis. Of the SGLT-2 inhibitors, dapagliflozin does not affect bone turnover markers or bone mineral density, but canagliflozin is associated with bone loss and an increased risk of hip fracture. “This is a drug you might not want to use in someone with fractures or known osteoporosis,” Rodrigo warns. 

Assessing bone health in diabetes

Rodrigo says it’s a good idea to go through the FRAX (fracture risk assessment tool) algorithm, which gives the 10-year probability of a fracture, at least occasionally with people who have diabetes and initiate osteoporosis treatment accordingly. 

“The effect of type 2 diabetes is actually similar to that of rheumatoid arthritis (RA) in FRAX,” he advises. “So one potential strategy would be to just click the RA button in FRAX and get a better estimation of the risk of someone with type 2 diabetes.”

Trabecular Bone Score (TBS) is a newer technology – it’s a software that gets laid onto the regular DEXA (bone density) scan to try to assess the bone quality. “As of last year, this was approved by insurance here, so we’ll see it pop up more and more,” Rodrigo says. To illustrate, he showed two spine scans with very similar bone densities but the bone quality, as revealed by TBS, was very different and you could see holes in the bone in the person with a low TBS. “People who have low TBS [tend to] fracture more, independently of bone density. This has been looked at in people with diabetes and it does a better job than bone density.” He advises using TBS with FRAX, to give a better idea of fracture risk. And, as it’s software, you can go back and apply it to existing bone scans.

“We should have a lower bar for osteoporosis testing,” Rodrigo concludes. “Ask your person with diabetes to stand up in front of you. If it takes them longer than just a few seconds, that’s someone who might be going to have trouble with falls and fractures. And why not consult your friendly neighbourhood ‘bonehead’ [bone health specialist]? There’s sure to be one lurking around your institution.”

Any opinions expressed in this article are the responsibility of the EASD e-Learning Programme Director, Dr Eleanor D Kennedy.

The impact of sedentary behaviour in pregnancy and how to address it was a hot topic at the ADA’s latest conference. Lisa Buckingham reports.

Light-intensity physical activity (PA) and its health benefits is a growing area of research.  Compared with formal exercise and moderate/vigorous-intensity exercise, it’s a topic we have much to learn about, according to Dr Sylvia Badon, perinatal epidemiologist at the Kaiser Permanente Northern California Division of Research. Her presentation at the American Diabetes Association’s (ADA) Scientific Sessions in June centred on sedentary behaviour, 24-hour movement and diabetes in pregnancy.

Sedentary behaviour is how a large proportion of people spend their days and Dr Badon began by defining it as any waking behaviour characterised by an energy expenditure of 1.5 metabolic equivalents of task (METs) or less while in a sitting, reclining or lying posture. It’s distinct from inactivity, which is activity that doesn’t accumulate enough to be classed as light-intensity PA.

With regard to sedentary behaviour during pregnancy, research suggests that it has adverse effects on glucose metabolism. It also shows that pregnant individuals tend to be more sedentary than the general adult population, which is important to bear in mind when considering interventions, said Dr Badon. On average, they spend between seven and 18 hours a day being sedentary and the few studies that look at how this pans out across pregnancy suggest there may be an increase in sedentary behaviour as the pregnancy progresses.

Several studies have looked at how total time spent being sedentary impacts risk for gestational diabetes (GDM). Dr Badon highlighted a piece of research from 2022, which showed that the more time spent sitting in the early to mid-pregnancy stage, the higher the risk of GDM.

There have also been studies that looked at the impact of sedentary behaviour in pregnancy on glucose metabolism outside the context of GDM. This research finds that higher levels of sedentary behaviour is associated with higher fasting glucose, higher fasting insulin and higher insulin resistance as measured by HOMA-IR.

Sedentary recommendations

As a result of this and other work showing negative impacts on cardiometabolic outcomes, the World Health Organisation (WHO) and other bodies added targeting sedentary behaviour in pregnancy to their recommendations. For example, the WHO recommends limiting the amount of time spent being sedentary, and says that the time that would have been spent being sedentary should be replaced with physical activity of any intensity (including light intensity) because it provides health benefits.

Here, Dr Badon showed a pie chart of a day to illustrate that the 24-hour day is a limited period of time and we can’t pull extra hours out of it when we discuss increasing beneficial movement – therefore, behaviour change is about replacement of one behaviour for another. Recommendations include not only replacing sedentary behaviour with light-intensity PA but also including some moderate to vigorous-intensity PA.

Activity and glycaemia

But if these specific behaviour-replacement recommendations are carried out, are they associated with better glucose metabolism during pregnancy? To try to answer this, her team used data from an RCT conducted in pregnant individuals with pre-pregnancy overweight and obesity who were randomised to either a lifestyle intervention or a usual-care control group. They attended the study clinic at 8-15 weeks, where they self-reported on measures such as sleep and also wore an accelerometer to create an average 24-hour movement profile. At 29-38 weeks, the researchers used blood tests and other measures of glucose metabolism.

In the control group, participants spent an average of 8.1 hours sleeping, almost nine hours in sedentary behaviour, 6.4 hours of light PA and just over half an hour of moderate to vigorous- intensity PA. This meant that they were meeting recommendations (Dr Badon reminded the audience that people who volunteer for these types of trial are quite different to the general population).

They then used a compositional data analysis approach to look at all of the movements in the 24-hour day, account for the correlation between them and model (through isotemporal substitution modeling) how specific behaviour replacements might impact later cardiometabolic biomarkers, specifically glucose and insulin.

They found that replacing up to 30 minutes of sedentary behaviour with light or moderate to vigorous-intensity PA was not associated with predicted changes in glucose in late pregnancy. The results were similar for insulin and insulin resistance. However, she points out that this was an observational study in a very specific population.

Behaviour replacement

When we think about controlled lab experiments when studying PA, Dr Badon said, we have a sedentary control group. However, when we use cross-over studies where the same individual comes in and does different types of PA, we begin to understand what happens when one behaviour truly is replacing another.

She used an example of research from 2001, in which 20 women with GDM came in and, on the first day, consumed a standard breakfast. They then sat down for two hours and their fasting glucose was measured at one and two hours. The following day, they consumed breakfast and then took a leisurely walk at their own pace followed by sitting for the next hour. This was therefore a direct behaviour replacement. In the walking group, there was a decrease in the one-hour post-prandial glucose (5.35 mmol/l compared with 6.02 mmol/l in the sitting group). It remains to be seen whether this can be replicated in less controlled environments at the population level.

Additional research needs to be done, she concluded, to understand 24-hour movement replacements and glucose metabolism in pregnancy in both individuals with GDM and those with normal glucose tolerance, how these behaviour replacements may change across pregnancy, and whether other specific replacements may be more or less beneficial in pre-pregnancy diabetes management.

In the post-presentation questions, the issue of sleep and timing of sleep was raised, and Dr Badon said that it’s an extremely important missing piece in the 24-hour movement space. There is a lot to be explored on the relationship between waking behaviour and sleep, and how chronotype, timing of sleep and timing of physical activity play their part.

For more on the topics raised in this article, enrol on the following EASD e-Learning courses:

Any opinions expressed in this article are the responsibility of the EASD e-Learning Programme Director, Dr Eleanor D Kennedy.

Thanks to the GLP-1 receptor agonists and newer, related drugs, it’s now possible to go beyond the traditional glucocentric model of diabetes treatment and address obesity too. The implications of this new approach, and the latest findings on anti-obesity medication, were under discussion at the recent ADA conference, as Dr Susan Aldridge reports.

Given that 86% of people with type 2 diabetes are also overweight or obese*, Dr Ivania Rizo of the Boston Medical Center suggests a new treatment paradigm driven by the overlap between type 2 diabetes, obesity and cardiovascular disease. “We can now go beyond a glucocentric model of care, where the management of obesity is not a competitor, but an addition,” she told delegates at the recent American Diabetes Association Scientific Sessions.

The Diabetes Control and Complications Trial (DCCT) led to a very glucocentric model of care, but older diabetes drugs cause weight gain.  “GLP-1 receptor agonists really did change the landscape,” says Ivania. “Importantly, they act on the brain to reduce appetite and food cravings and lower the preference for energy and fat dense foods.” There are now five GLP-1 receptor agonists available and the amount of weight loss achievable with them has steadily improved over time – from 1-3% with exenatide, to approximately 3-4% with liraglutide, more with semaglutide and higher doses of dulaglutide – and, now, even more with tirzepatide.

Semaglutide was evaluated in the SUSTAIN clinical trial programme and showed more reduction of HbA1c and weight than comparators. Earlier this year, the SUSTAIN FORTE trial showed that semaglutide 2 mg is more effective than the 1 mg dose in helping people lose 10% of their body weight. There have also been seven randomised controlled trials of GLP-1 receptor agonists that show reduction in three-point MACE (major adverse cardiovascular events – cardiovascular mortality, non-fatal myocardial infarction and non-fatal stroke).

Beyond GLP-1 receptor agonists

“There is now Intense interest in developing molecules with dual or triple agonist action – against GLP-1 and GIP (glucose-dependent insulinotropic peptide) and/or glucagon – using the complementary actions of gut hormones,” Ivania says. GLP-1 and GIP are the two main gut hormones responsible for the amplification of insulin after oral nutrition, but people with type 2 diabetes have an impaired response to both. The dual agonist tirzepatide, approved by the FDA for type 2 diabetes earlier this year, restores this response by activating the gut hormone receptors in sequential fashion – GIP after GLP-1. And, according to the SURPASS-2 trial, it reduces HbA1c and body weight even more than semaglutide.

There are other dual agonists on the horizon now, such as cotadutide, a dual GLP-1 and glucagon receptor agonist which, at a higher dose, is superior to liraglutide in reducing HbA1c and weight. Cotadutide also has the extra advantage of reducing markers of non-alcoholic fatty liver disease (NAFLD). 

Anti-obesity medications

“Anti-obesity medications are truly underutilised,” says Ivania. “There is a large unmet need in obesity, compared with type 2 diabetes. For 8% of the population has type 2 diabetes and 86% of them receive anti-diabetes medication. But half the population has obesity and only 2% of them are being treated with anti-obesity medication.”

Returning to type 2 diabetes, a stepwise approach to obesity management with medication can be considered. So, GLP-1 agonists/dual agonists or SGLT-2 inhibitors could be used alongside metformin and lifestyle in a patient-specific way. And there are also anti-obesity medications that could be added to the treatment toolbox. Tirzepatide is not yet approved for the treatment of obesity, although it is the first investigational drug to deliver more than 20% weight loss in a clinical trial, so the best choice is semaglutide. Other options include phentermine/topiramate, naltrexone/bupropion and liraglutide. The STEP-8 trials of liraglutide 3 mg versus semaglutide 2.4 mg in people without diabetes, but with overweight or obesity, showed that the latter produces substantially more weight loss. Ivania starts her own patients on liraglutide and then switches to semaglutide, if necessary. And now there is cagrilintide, the first long-acting amylin analogue for weight management, given once a week, which can be used with semaglutide for significant weight loss.   

So, in conclusion, diabetes and obesity are complex diseases that progress over decades. Double-digit weight loss addresses both insulin resistance and obesity. “We need to go beyond the glucocentric model to address weight-centric goals too,” Ivania says. “A combination of agents with complementary modes of action is essential in diabetes and weight management, and we also need equitable access to these medications.” 

For more on obesity and diabetes, enrol on the following EASD e-Learning modules:

*Daousi C, Casson IF, Gill GV, MacFarlane IA, Wilding JPH, Pinkney JH. Prevalence of obesity in type 2 diabetes in secondary care: association with cardiovascular risk factors. Postgrad Med J. 2006 Apr;82(966):280-4.

Any opinions expressed in this article are the responsibility of the EASD e-Learning Programme Director, Dr Eleanor D Kennedy.

Bariatric surgery can lead to health benefits in type 2 diabetes that go way beyond weight loss and remission. The latest findings in this area were presented at the recent ADA conference, making a strong case for using surgery to tackle diabetes and obesity. Dr Susan Aldridge reports.

Addressing the American Diabetes Association (ADA) Scientific Sessions in June, Dr Ricardo Cohen, bariatric surgeon and Director of the Center for Diabetes and Obesity at the Oswaldo Cruz German Hospital, São Paulo, Brazil, said: “Obesity management is not the future for treating diabetes, it’s the present.” He went on to discuss the role that bariatric/metabolic surgery can play in weight loss and management in type 2 diabetes.

The DiRECT trial showed that those who lost the most weight (through diet) were the ones who were more likely to achieve at least glucocentric remission, with HbA1c less than 6.5%. For lower amounts of weight loss, the numbers achieving this decrease. There’s also now a lot of data that show double digit weight loss will prevent cardiovascular events and mortality. “It’s clear that this double digit weight loss is what we need to pursue for diabetes treatment,” Ricardo says.

But clinical trial findings reveal that many participants need additional interventions to maintain this all-important weight loss. Once the diet stops, there is a strong tendency to put the weight back on. Surgery, however, shifts the satiety/meal size curve so the individual doesn’t want to eat so much.   “We need a long-term intervention and this is what I’m here for – to show the benefits of surgery,” he says. “I have no doubts that surgery is great for weight loss and glycaemic control.”

These long-term benefits are confirmed by the follow-up studies. The Swedish Obese Subjects (SOS) study is the most ‘squeezed’ in the bariatric literature, with 90 sub-studies. In one of these, with over 20 years of follow-up, surgery was associated with sustained loss of around 27% of body weight. Gastric bypass was associated with the greatest weight loss. The participants having surgery also enjoyed longer life expectancy that was linked to the amount of weight loss. In another study, 51% of those having gastric bypass surgery were still in diabetes remission after 12 years, compared with just 4% of those on medication.

Furthermore, it looks as if the numbers that could benefit from surgery might be greater than previously thought. A meta-analysis of 94,000 patients in 94 studies shows that those below and above a body mass index (BMI) of 35 reached same rate of glucocentric remission, with 71% achieving an HbA1c below 7% without medication. “So, even in patients with BMIs from 30 to 35, the benefits of surgery are greater than those achieved by medical treatment,” says Ricardo. 

Beyond weight loss and remission  

Bariatric surgery involves more than just weight loss. There are changes in gut microbiota, glucose transport, intestinal glucose metabolism, gastrointestinal nutrient sensing and gut hormones. So, it is not surprising to see other health benefits following surgery. The Diabetes Surgery Study showed improvement in blood pressure at five years, while the STAMPEDE (Surgical Therapy and Medications Potentially Eradicate Diabetes Efficiently) study led to both five- and 10-year improvements in blood pressure, LDL and HbA1c, and a recent trial by Geltrude Mingrone and his team showed a reduction in macro- and microvascular diabetes complications after surgery.  

While there is much observational evidence to show that surgery reduces hypertension, the GATEWAY (Gastric Bypass to Treat Obese Patients With Steady Hypertension) study’s primary endpoint was a reduction of at least 30% in the medication needed to maintain a blood pressure of 140/90 mmHg. At 36 months, this was reached in 73% of patients on surgery versus 11 % on medication. And 35% in the surgical arm actually achieved remission of their hypertension (blood pressure of 130/80 mmHg, without hypertension medication), versus none of those in the medication arm of the trial.   

Bariatric surgery also helps with kidney disease. Ricardo was involved in the MOMS (Microvascular Outcomes after Metabolic Surgery) trial, which looked at the effect of surgery versus usual care on early stage chronic kidney disease (CKD) in patients with type 2 diabetes and obesity. Those in the usual care arm were allowed GLP-1 receptor agonists and SGLT-2 inhibitors, which no doubt contributed to their relatively good outcomes. The primary endpoint was remission of CKD, with a urinary albumin creatinine ratio of 30 mg/g or less, which was achieved in 84% in the surgery arm and 56% in the usual care arm.   Those in the surgery arm also needed less insulin and less oral diabetes medication. Finally, quality of life was better in almost all domains following surgery. 

There have also been many studies showing reduction in mortality after surgery, mainly involving gastric bypass. One of these also showed decreases in atrial fibrillation, nephropathy, coronary artery disease, cerebrovascular disease and heart failure. “By operating on 13 patients, one life can be saved,” Ricardo says. Surgery has also led to greater survival in patients with a prior myocardial infarction. “There have only been two papers on this, but I think we can say that metabolic surgery can reduce the likelihood of a secondary coronary event – and it’s safer than a heart bypass,” he adds.  

Finally, in earlier studies, the endpoint was always glucocentric remission of type 2 diabetes, without medication. Ricardo now suggests that this is ‘old fashioned’ and that adjuvant pharmacotherapy should be provided, as in oncology where surgery, radiotherapy and chemotherapy may all be employed. “Some surgeons think that surgery is a miracle on its own – and I was one of them. But now I think it is best to combine our efforts. “

In summary, according to Ricardo, the overall treatment strategy in type 2 diabetes should be self-directed lifestyle change first – showing the patient how they can start their journey to diabetes control. Then comes professionally directed lifestyle change. Then add medications. “We currently have very powerful medications, like tirzepatide and semaglutide. If patients don’t respond to medications, then do surgery. This is our weight-centred approach to diabetes. The best thing is combining both surgery and medication, which will lead our patients to the best outcomes available.”

For more on the topics covered in this article, enrol on the following EASD e-Learning courses:

Any opinions expressed in this article are the responsibility of the EASD e-Learning Programme Director, Dr Eleanor D Kennedy.

Counselling and pharmacotherapy can each of them aid weight loss in people with obesity. So what happens when you combine the two? Lisa Buckingham reports on the case for pairing these interventions, as presented at the ADA’s 82nd Scientific Sessions.

“Why would you consider this pairing?” asked Dr Scott Kahan, director of the National Centre for Weight and Wellness, and faculty director at Johns Hopkins Bloomberg School of Public Health, addressing the American Diabetes Association’s (ADA) recent conference. The answer is that losing weight is hard – even if you lose weight, physiology pushes back, and even if you fight through the physiological counter-regulatory changes, you need to continue indefinitely. Combination therapy, he said, almost always leads to more weight loss and other improved outcomes.

Dr Kahan highlighted a paper that showed patients losing about 10% of their bodyweight in three months on a medically monitored diet. The participants were then followed for a year. There was some weight regain, as expected, but the study also tested a range of counter-regulatory hormones at three months and then again at a year. At both intervals – even after a year, when some weight had been regained – the participants’ satiety hormones were still significantly lower and their primary hunger hormone (ghrelin) was still elevated.

Some people can keep weight off just with behavioural counselling, but even if you can fight through this and keep it up indefinitely, he said, the fact remains that more weight loss is (usually) better (within reason) in terms of comorbidities. Once we’re into the 10% and above range, we see more benefit over the smaller percentages of weight loss, such as improvement in sleep apnoea, long-term cardiovascular outcomes and quality of life.

To begin the case for combination therapy, he drew a comparison with the evidence for depression treatment. Counselling can be very effective – as can medication – but dozens of studies have shown that when you combine the two, you get much more benefit.

In obesity, there are numerous examples of combination therapy’s effectiveness. However, before outlining the counselling/medication combination, he showed papers looking at combining two medications. For example, one paper showed that with a modest dose of phentermine, you get weight loss of about 7%and topiramate of about 9%. When you combine a half-dose of both of them, you get considerably more weight loss more than either of them alone at double doses.

Data in support of pairing behavioural therapy and pharmacotherapy goes back many decades. He cited one example of sibutramine (no longer on the market). The drug alone didn’t give much benefit; the drug plus basic lifestyle counselling gave more benefit (double the weight loss); those two plus meal replacement gave even more.

Another paper showed that more intensive behavioural counselling plus sibutramine resulted in greater weight loss than basic counselling and sibutramine, showing a gradation of effect.

With regard to the new medications that have been approved in the past decade, he first highlighted a trial using naltrexone/bupropion. Patients got intensive behavioural counselling and achieved 7.5% weight loss. When combined with the medication, they achieved almost 50% more weight loss.

In a comparable study of the same medication, but with less intensive, usual-care counselling, both groups achieved less weight loss compared with the other trial.

Another example was liraglutide combined with intensive behavioural counselling, which resulted in about double the weight loss compared with the counselling alone.

The same group also did another study that Dr Kahan felt better reflects what happens in clinical practice. Both groups had a medically monitored diet for 14 weeks, resulting in about 6% weight loss. At that point, they were randomised to either placebo and ongoing counselling, or the medication plus counselling. With just the counselling, they kept off the weight or lost a little bit more, but with the medication as well, they kept the weight off better and lost even more weight.

A third study involving liraglutide used a medically monitored diet for two months, after which participants were randomised to either basic counselling with a placebo, exercise counselling, the medication, or exercise counselling with the medication. Again, a gradation of outcomes was seen – the more intensive the intervention, the better the outcomes. At a year, one in three of the combination group were keeping off 20% of their bodyweight. This is bariatric-surgery-level weight loss, said Dr Kahan, but without surgery.

It doesn’t need to be one thing or the other, or even a combination to start with but they can be sequentially added as indicated.

He moved on to discuss a key point – obesity is significantly undertreated and that applies to every modality of treatment. His data was specific to the USA, but he explained that less than 1% of eligible people with obesity who have Medicare are given intensive behavioural therapy (IBT); roughly 1% receive pharmacotherapy; 1.5% get bariatric surgery. He compared this to diabetes treatment where 85% of people with diabetes are getting the indicated treatments. This should be 100%, he said, but the comparison is still worlds apart from obesity treatment.

There are several reasons for this. The first is lack of training on obesity among primary care physicians and even specialists. The second is minimal insurance coverage for obesity treatment. And the last is perceived lack of time – doctors perceive that they have to solve the whole problem when they see the patient. It doesn’t need to be done all once, said Dr Kahan, because it’s a chronic condition and it’s something we can chip away at.

He also came back to the point about gradation of treatment – from basic counselling, which provides some benefit, up to intensive counselling plus medication for the most benefit. Whatever we can offer is going to be beneficial, he said. And more is generally better.

For more on obesity and diabetes, enrol on the following EASD e-Learning modules:

Any opinions expressed in this article are the responsibility of the EASD e-Learning Programme Director, Dr Eleanor D Kennedy.

Diabetes is one established risk factor for dementia among many others, so what kind of interventions can reduce risk? This question was addressed at the ADA’s latest conference. Lisa Buckingham reports.

Alzheimer’s disease (AD) and other dementias present a significant and growing health burden. In the USA, about a third of people will have dementia by age 85. There is therefore an urgent need for prevention strategies that can target high-risk groups – including those with diabetes – as there have been no new approved treatments since 2003. In a session on diabetes and dementia at the American Diabetes Association’s scientific sessions in June, Valory Pavlik, associate professor at Baylor College of Medicine, Texas, presented on lifestyle interventions for dementia prevention.

Professor Pavlik began by pointing out that AD is often used synonymously with dementia but that it’s important to distinguish between the clinical syndrome and underlying pathology. AD is a pathological diagnosis and there are other pathologies that also cause dementia. An AD diagnosis begins with a diagnosis of dementia from cognitive or behavioural symptoms and then progresses to probable AD if criteria, such as a clear-cut history of worsening and no evidence of other types of dementia (such as vascular or Lewy Body), is identified.

Non-modifiable risk factors include age, family history, apolipoprotein E (APOE) genotype, other genetic risk factors and possibly education (in that it has already been completed by the time you start looking at risk factors in middle age).

She highlighted the importance of APOE – if you have one e4, you have a 25% chance of developing AD by the time you’re 85; if you have two copies of this gene, you have a 45% chance.

Modifiable risk factors

With regard to modifiable risk factors, she began with a 2020 evidence-based review and meta-analysis of 243 prospective studies and 153 randomised controlled trials. It showed that diabetes is an established risk factor for dementia, along with depression, high homocysteine levels (hyperhomocysteinemia), stress and brain trauma. These all have a high level of evidence. Protective factors have a slightly lower level of evidence. They include exercise, healthy dietary patterns, early life education, vitamin C and small weight loss, although cognitive activity falls into green.

The Lancet Commissions also published evidence-based recommendations for the prevention of dementia in 2020. They found that if you follow the guidelines, you reduce your risk of dementia by 40%. Those that reduce pathological damage include minimising diabetes, treating hypertension, stopping smoking and reducing midlife obesity. Those that reduce pathological damage and increase and maintain cognitive reserve include frequent exercise, reducing occurrence of depression and avoiding excessive alcohol, and those that just do the latter are treating hearing impairment, maintaining frequent social contact and attaining a high level of education.

How are type 2 diabetes and AD linked?

The hypothesised mechanisms for the role of type 2 diabetes in AD include insulin resistance, oxidative stress/mitochondrial dysfunction and hyperglycaemia – these are thought to contribute to amyloid pathology. Diabetes also contributes to tau phosphorylation. There is no evidence that insulin resistance or hyperglycaemia promotes amyloidogenesis.

Professor Pavlik moved on to look at evidence for lifestyle interventions to prevent cognitive decline, leading to AD and related dementias (ADRD). There is much observational study evidence that supports the role of lifestyle change in protecting cognition. It can target multiple potential disease pathways and it’s known to prevent/control ADRD risk factors, particularly diabetes.

She referred back to the Diabetes Prevention Programme (DPP) research. Lifestyle intervention was equivalent to metformin in achieving glucose control. Achievement of behavioural goals was good – people lost weight, maintained it and increased physical activity. Compliance with metformin drifted down over time. In the follow-up looking at cumulative incidence of diabetes, lifestyle outperformed metformin and placebo. There is, therefore, very good evidence that physical activity and dietary changes can prevent diabetes, she said, which would then go a long way towards preventing some of the dementia that we see.

With regard to exercise alone, she looked at a 2001 meta-analysis that looked at the effects of exercise on glycaemic control and BMI in type 2 diabetes. The results showed that the effect of exercise on HbA1c (an improvement) doesn’t rely on weight loss, exercise intensity or exercise volume.

Can this reduction in HbA1c prevent dementia? The results of the ACCORD-MIND trial said no, so we don’t have evidence that glycaemic control itself improves cognitive function. Before moving on, she pointed out a study showing that exercise in people who already have dementia is helpful – it improved cognition a moderate amount.

What role for diet?

When it comes to diet, mostly observational data shows that polyunsaturated fatty acids, antioxidants (vitamins A, C and E) and polyphenols are neuroprotective. Folate is important for preventing hyperhomocysteinemia (one of the risk factors for dementia mentioned earlier). The diets that give you this combination of nutrients are the Mediterranean diet, the DASH diet and the MIND diet used in the US POINTER trial. All have high intakes of fish, olive oil, leafy green vegetables, legumes, fruit and nuts, and reduced meat and saturated fats.

The thinking behind designing interventions to prevent cognitive decline is to include multiple modalities. The FINGER trial in a Finnish population was the first to show a significant treatment effect from a multi-modal intervention to protect cognition.

It was a two-year study of lifestyle intervention versus usual care (regular health advice), with over 1000 participants aged 60-77. Lifestyle intervention comprised nutrition (a heart-healthy diet), exercise (strength training and aerobic exercise), cognitive training (memory and reasoning exercises) and vascular risk monitoring.

After two years, they saw a significant difference in cognition between the control and intervention group, with the intervention group scoring more highly. They also saw a significant improvement in functional ability, which was graded by the number of chronic disease risk factors. The more a person had, the better their functional status improved with intervention. They concluded that a multi-domain intervention could improve or maintain cognitive function in at-risk elderly people from the general population.

Lastly, Professor Pavlik outlined the US POINTER trial, which is sponsored by the Alzheimer’s Association and has almost finished recruiting. It has been designed to find out if the results of the FINGER trial could be replicated in a heterogeneous cohort of older Americans who are at risk for cognitive decline and AD, to adapt it to fit American culture and to identify and develop a community-based infrastructure that could support a sustainable program if results were positive.

There are 2000 participants aged 60-79 who are at increased risk of cognitive decline from suboptimal lifestyle and cardiovascular status, and first-degree family history of significant memory impairment. They are randomly assigned to self-structured education via a workbook vs structured lifestyle intervention. The primary endpoint will be a composite score from memory, executive function and processing speed scores.

The components of the lifestyle intervention are physical activity, nutrition, cognitive stimulation and health coaching. The nutrition aspect uses the MIND diet, which is prescriptive with specified servings of certain foods and foods to avoid altogether. The physical activity is intensive with aerobic exercise, resistance training and stretching/balance work. Three times a week, they will complete a web-based BrainHQ program for cognitive training. Watch this space…

For more on lifestyle interventions and diabetes, enrol on the following EASD e-Learning module:

Any opinions expressed in this article are the responsibility of the EASD e-Learning Programme Director, Dr Eleanor D Kennedy.

Food insecurity is prevalent across the globe, with far-reaching consequences for people’s health and well-being – consequences that can be significantly exacerbated for young people with diabetes. A session at last month’s ADA conference looked at how we might address them. Lisa Buckingham reports.

Food insecurity (FI) is defined as limited or uncertain availability of nutritionally adequate and safe foods or limited or uncertain availability to acquire acceptable foods in socially acceptable ways.

As part of a session on FI at the American Diabetes Association’s (ADA) 82nd Scientific Sessions, Professor Beth Cummings, paediatric endocrinologist at Dalhousie University and IWK Health, Canada, presented on the insights and struggles of caregivers of children with type 1 diabetes in food-insecure households.

Household food insecurity affects one in six children under 18 in Canada. In the general population, this has adverse health outcomes for them, such as higher rates of iron deficiency, asthma and hospitalisation, as well as adverse mental health outcomes including depression and anxiety (this affects adults too). This, in turn, results in higher healthcare costs for those families.

In 2008, Professor Cummings group hypothesised that the impacts of FI might be greater in households with a child with insulin-requiring diabetes, given the additional impact of diabetes costs and the need for extra focus on nutrition.

They found that children in FI households had an HbA1c 0.6% higher than those in food-secure households, were less likely to use pumps and more likely to require hospital admission for diabetes. Families also reported re-using needles and checking blood glucose less often to save money.

Her group then went on to get a clearer picture of the lived experience using a clinic-based, qualitative study of parents/caregivers of five to 17-year-olds with type 1 diabetes. For context, physician and hospital costs in Nova Scotia are publicly funded; medications and devices funding is variable; low-income families may get a small amount of extra diabetes food allowance; insulin is not administered by schools (no school nurses), so young children often require morning intermediate insulin, making it essential that their food intake matches insulin dose.

Broader factors that affected FI were high cost of healthy food, insufficient support, and unanticipated costs such as car breakdown. All participants reflected that after their child’s diagnosis of type 1 diabetes, financial balance was harder to maintain and that having a child with diabetes was a major contributor to their family’s FI. 

Healthy eating costs more

A new or heightened awareness of the importance of healthy food also came up. Foods that can fill children up, be bought in bulk and cost less money are often processed, nutritionally poor and not suitable.

This was not just a perception, said Professor Cummings, and drew attention to a study that compared a healthy thrifty food plan for a child with type 1 diabetes with a regular thrifty food plan, and found that the healthy plan cost 17% more.

Caregivers in the study also reported increased time and effort for shopping (label reading and calculating quantities) and food preparation. A major theme was the challenge of affording snacks to avoid or treat hypoglycaemia. Some said that pumps provided flexibility with sometimes skipping snacks along with reduced worry about lower quality carbohydrates because they could more easily deal with the resulting hyperglycaemia.

Another major theme was the sacrifices made to combat FI having a disproportionate impact on other family members to shield the child with diabetes. Participants reported sacrificing household needs, paying bills and transportation, buying fewer Christmas and birthday presents, cuts to their general grocery budget, other children in the family going without basic needs or nutritious food, and adults eating less so that the child with diabetes could eat more. The unequal distribution of food among siblings created unique emotional impacts.

The final theme was that caregivers perceive barriers to accessing usual supports to combat FI. Breakfast programmes were difficult to access because of the timing, administration and calculation of insulin dose. Regarding food banks, caregivers felt embarrassed or that other people were more needy, had concerns about the quality of food, and found it difficult to access them when they’re only open during working hours.

Family support

The positives and tips from families included: shopping as a family is helpful; routines and making lists reduces the burden; using reward points, discounts and credits; being on an insulin pump and other flexible dosing enabling them to buy inexpensive foods.

They also offered ideas on ways that they could be better supported, including better communication and tailored advice from clinics that specifically address their FI needs; subsidies for healthy food should be included on government health programmes; access to support groups with people who have similar experiences so that they can share knowledge/strategies; guides or cookbooks about making healthy meals on a budget.

All of this research points to the fact that, when addressing FI with services and programmes, the focus needs to include the whole family. If not, assessments will underestimate the impact of FI, said Professor Cummings.

Her summary included the need for diabetes professionals to identify food insecurity and advocate for improved family support.

Empowering children

Another presentation within the session, from Dr Enza Gucciardi from the School of Nutrition at Toronto Metropolitan University, discussed empowering children with type 1 diabetes and the impact of a virtual food skills programme on food literacy and diabetes self-management.

She discussed their screening initiatives, which consisted of four components: screening questions, awareness posters in clinic, a care algorithm and a community resource package.

The screening questions were:
Within the past three months…

  • Did you ever worry about whether your food would run out before you got the money to buy more?
  • Was there ever a time when the food you bought just didn’t last and you didn’t have money to get more?
  • Did you or others in your house cut the size of your meals or skip meals because there wasn’t enough money for food?

Next was their posters and a care algorithm, which she emphasised is a compassionate, empathetic and non-judgmental process – we are not here to examine and judge how people spend their money, she said. The algorithm and full toolkit can be seen here:

They also developed resource handouts, which should be tailored locally based on the resources available in the area. However, research shows that these often aren’t used and it begs the question whether a resource navigator would be a better option, someone who can help families navigate what’s available and check in with them.

Major takeaways from this pilot were that most people appreciated discussing FI issues and felt comfortable if there was a rapport with the clinician; some expressed fear of being stigmatised and were embarrassed to ask for help; some didn’t want to discuss it in front of their child, and time constraints in a busy clinic was a major barrier to screening and follow-up for dietitians.

Food literacy

Lastly, she covered their pilot Summerlunch+ At Home Programme, an eight-week food literacy programme of virtual cooking classes and hands-on learning with a focus on nutrition skills. It was adapted for children with type 1 diabetes, employed a whole-family approach and was designed to engage children and families. Children could also meet peers with diabetes. Some 14% of families taking part were food insecure.

To reduce barriers to participation, free meal kits were delivered to families containing the ingredients for the virtual classes so no travel costs were involved. The recipes were vegetarian and focused on healthy eating guidelines, along with guidance on snacks and low-carb substitutes. The content focused on self-efficacy, nutrition knowledge and food skills, and included quizzes and games. Parents were encouraged to participate and be involved.

They are still in the process of looking at outcomes, including acceptability and effect on glycemic control. However, feedback from families was positive. Children and youth need to manage diabetes effectively now in order to have a healthy and bright future, concluded Professor Gucciardi, regardless of the barriers they face. Services must be equitable to all, and she challenged the audience to assess the framework of accessibility to reduce the burden of using available services.

Any opinions expressed in this article are the responsibility of the EASD e-Learning Programme Director, Dr Eleanor D Kennedy.