Following pharmaceutical company Eli Lilly’s much-lauded move to cut US prices for its insulin products, US President Joe Biden is calling on other drugmakers to make similar reductions for the vital medication.
According to Euronews, Lilly is directly slashing its insulin prices by about 70%, since many patients cannot access discounts, and is capping consumer costs at US$35 (R635) a month.
Biden is driving a push for cheaper insulin, signing a law that capped insulin at US$35 a month for senior citizens on Medicare, and urged companies to lower prices on their own. “For far too long, American families have been crushed by drug costs many times higher than what people in other countries are charged for the same prescriptions,” Biden said.
“Insulin costs less than US$10 to make, but Americans are sometimes forced to pay over US$300 for it. It’s flat wrong”.
Biden has called for a national cap on insulin prices, but his current Act does not extend to that.
A Lilly press release revealed that the price of Humalog® (insulin lispro injection) 100 units/mL (Lilly’s most commonly prescribed insulin) and Humulin® (insulin human) injection 100 units/mL by would be cut by 70%. This price change would take effect around the end 2023. Lilly also said it would cut the price for the generic Lispro to US$25 a vial starting in May. In South Africa, a Humulin® 10mL vial costs R525.28, or US$28.08, according to Health-e’s medicine price registry.
Lilly CEO David Ricks said his company was bringing the changes as not all patients could benefit through discounts through insurers or pharmacy benefit managers.
“We are driving for change in repricing older insulins, but we know that 7 out of 10 Americans don’t use Lilly insulin. We are calling on policymakers, employers and others to join us in making insulin more affordable,” said Ricks. “For the past century, Lilly has focused on inventing new and improved insulins and other medicines that address the impact of diabetes and improve patient outcomes. Our work to discover new and better treatments is far from over. We won’t stop until all people with diabetes are in control of their disease and can get the insulin they need.”
Since insurers and pharmacies will take a while to implement the price cuts, Lilly will immediately cap monthly out-of-pocket costs at $35 for people who are not covered by Medicare’s prescription drug programme.
Child obesity is linked to increased risk of developing diabetes in adulthood, both autoimmune forms of diabetes and different forms of type 2 diabetes, according to a new study in the journal Diabetologia. The risk of developing the most insulin-resistant form of diabetes is, for example, three times as high in children with obesity.
Diabetes affects ~7% of the adult population and is one of the world’s fasted growing diseases. It has traditionally been divided into two subgroups – type 1 and type 2 diabetes – but research suggests that this is a simplification.
In 2018, a Swedish study identified five subgroups of adult-onset diabetes, characterised by auto-immunity, severe insulin deficiency, serious insulin resistance, overweight and advanced age.
One way the researchers say that the relevance of these subgroups can be highlighted is to examine if the influence of known risk factors for diabetes differs between the proposed diabetes types.
“Our study is one of the first attempts to find this out,” says the study’s first author Yuxia Wei, doctoral student at Karolinska Institutet. “Childhood obesity has been linked to several chronic diseases, but has never been studied in relation to the recently proposed diabetes subgroups.”
Wanted to investigate the effect of child obesity
The purpose of the present study was therefore to see if the effect of childhood obesity differs. The researchers used a method called Mendelian randomisation, which uses genetic information to study the correlation between an environmental risk factor and disease risk while taking into account the impact of other risk factors.
Basing their analysis on genetic data from over 400 000 UK Biobank participants, the researchers compared children who considered themselves larger than other children with children who rated their weight as normal.
The results showed that overweight/obesity in childhood was linked to a 62% higher risk of autoimmune diabetes, a doubling of the risk of diabetes characterised by insulin deficiency, almost a tripling of the risk of the most insulin-resistant form of diabetes and a seven-times higher risk of the form of diabetes primarily characterised by overweight.
“Our analyses show that children who are larger than others are more likely to develop four of the five proposed new subgroups of adult-onset diabetes,” says Wei. “In other words, obesity in childhood seems to be a risk factor in effectively all types of adult diabetes, with the exception of age-related diabetes. This underscores how important it is to prevent obesity in children since it can have lasting effects on their future health.”
The study was a collaboration among researchers at Karolinska Institutet, Bristol University (UK) and Sun Yat-Sen University (China).
For diabetics, the makeup of insulin doses – governed by the proportion of insulin molecule clusters present – are crucial for effective treatment. Getting too little or too much insulin can lead to hyperglycaemia or hypoglycaemia. A new study appearing in Communications Biology has discovered that though it is not a danger to patients, an assumption underlying the design of insulin preparations is well off the mark.
The absorption of insulin in the body is controlled by how insulin molecules assemble themselves in clusters. Whereas a single molecule provides rapid action in the body, clusters of six molecules – known as hexamers – are long-acting. For decades, it has been assumed that insulin assembles with a certain distribution of molecular clusters of either one, two or six molecules. Pharmaceuticals have been designed based upon this assumption – but now researchers have discovered that this important point has been wrong for years.
“It is now apparent to us that we’ve gotten things wrong by 200 percent. There are only half as many single molecules in insulin compared to what we thought. Conversely, there are far more six-molecule clusters than we assumed. These experiments were not on animals but were performed on a microscope slide and one should be careful how to interpret their direct application to humans,” says study lead author Professor Nikos Hatzakis of the University of Copenhagen.
He adds: “However, our results may mean that when we believe to be administering a certain dose, it may mean that insulin behaves in a different way than expected and that even better insulin therapeutics can be developed.”
This means that insulin taken by diabetics may not be getting absorbed as expected. Though the researchers stress that it is not outright dangerous for patients, there is potential for designing more precise medicines.
From a crude model to detailed view
“Insulin preparations have only gotten better and better over the years, and a great many diabetics are well regulated. However, the development of insulin preparations has been based on a certain assumption about how the molecules assemble. With the crude standard model, this process was never been appreciated at a detailed level. That’s what we can do,” says the study’s other lead author, Professor Knud J. Jensen, of the Department of Chemistry.
“This doesn’t mean that current insulin medications are bad or that patients have been medicated wrongly. But we now have a basic understanding of how insulin behaves and how much could be available to the body as rapid-acting medication. We now have the right method for providing us with accurate figures. We hope that the industry will use this or a similar tool – both to check current insulin preparations and to develop new ones,” adds Nikos Hatzakis.
The research results were achieved through a mix of chemistry, machine learning, simulations and advanced microscopy. The Department of Chemistry researchers began by directly observing the process in which each insulin molecule joins forces with other molecules to assemble into clusters. This allowed them to see how fast each cluster forms. The researchers looked at about 50 000 clusters.
Knowing the exact distribution of different clusters in a given amount of insulin is fundamental when developing medications that need to have either short- or long-acting effects in the body:
“The clustering of insulin is incredibly important for how preparations work. Because the difference between a rapid- and slow-acting insulin preparation is dependent upon how quickly the molecules assemble in clusters and how quickly they disassemble. Access to highly advanced equipment makes it relatively simple and fast to gain insight into exact concentrations, knowledge that at the same time, is also quite sophisticated,” says lead author Freja Bohr, a PhD fellow in Nikos Hatzakis’ research group at the Department of Chemistry.
Improving insulin preparations
In addition to the different distribution of molecular clusters, the observations also show that cluster formation is a much more complex process than once presumed. The clusters can both grow and shrink at far more different intervals than previously supposed.
“Without being able to say exactly how just yet, this should make it possible to expand the number of ways in which preparations are designed. This could lead to an insulin with a different effect profile that reduces the fluctuations in patients’ blood sugar – which remains a major challenge,” says Freja Bohr.
Health activists demonstrating in Cape Town for a rise in the tax on sugary drinks were disappointed by Finance Minister Enoch Godongwana’s announcement in his Budget speech that the tax would be frozen for two years. Godongwana said this was “due to the difficult operating environment for the sugar industry from the impact of flooding and social unrest.”
The tax on sugary drinks was first introduced in 2018 to reduce consumption. The tax is imposed on drinks with more than 4g of sugar per 100ml. Research from the University of the Witwatersrand in 2021 showed that it has been effective in reducing the consumption of sugar-sweetened drinks.
HEALA, a coalition of organisations focused on nutrition, organised a flash mob in the Cape Town city centre ahead of the Finance Minister’s Budget Speech on Wednesday, advocating for an increase in the sugary drinks tax. They want the tax to be increased from 11% to 20%, following the guidance of the World Health Organisation.
The flash mob was part of HEALA’s “Less Sugar, More Life” campaign, and featured school pupils from Cape Town in a dance.
“We don’t even notice how much sugar we are drinking in sugary drinks and it’s harmful to our health. I want other young people to know that it’s dangerous,” said one of the dancers, Enkosi Stofile.
“The announcement by the Finance Minister, coupled with ineffective increases on other health taxes such as alcohol and tobacco, is a direct attack on the lives of millions of people at risk of serious health conditions such as diabetes, cardiovascular diseases and cancer,” said Nzama Mbalati, HEALA’s Programmes Manager.
Mbalati said there was no rationale for the decision to maintain the rate of tax on sugary drinks. “This decision is not in the interest of ordinary people. Instead, it puts profits ahead of people.”
About 10 000 new cases of diabetes are reported in South Africa each month, according to the International Diabetes Federation. Up to 70% of women and 39% of men are obese or overweight. Sugar is a cause of obesity and tooth decay, and is linked to a range of other non-communicable diseases. The national budget for 2023, tabled by Godongwana in parliament today, includes a R200-million reduction in health spending this year.
Before the budget speech, News24 reported that the South African Sugar Association said 6000 jobs could be lost if the tax was increased. SASA also said 9,000 jobs had already been lost since the levy was introduced.
However, in the aftermath of a fraud scandal at Tongaat Hulett, South Africa’s largest sugar producer, in 2018, 5,000 workers were served with retrenchment letters.
Disclosure: Community Media Trust does work for HEALA. GroundUp was once a project of Community Media Trust and still has a close relationship with Community Media Trust.
Excess weight or obesity raises mortality risk by between 22% to 91%, a significantly higher rate than previously believed, while the mortality risk of being slightly underweight has likely been overestimated, according to new research published in the journal Population Studies.
The analysis of nearly 18 000 participants counters prevailing wisdom that excess weight boosts mortality risk only in extreme cases, and it also challenges the use of body mass index (BMI) to investigate health outcomes due to its inherent biases. After accounting for those biases, it estimates that about 1 in 6 deaths in the US are related to excess weight or obesity.
“Existing studies have likely underestimated the mortality consequences of living in a country where cheap, unhealthy food has grown increasingly accessible, and sedentary lifestyles have become the norm,” said author Ryan Masters, associate professor of sociology at CU Boulder. “This study and others are beginning to expose the true toll of this public health crisis.”
Challenging the obesity paradox
While numerous studies show that heart disease, high blood pressure and diabetes (which are often associated with being overweight) elevate mortality risk, very few have shown that groups with higher BMIs have higher mortality rates.
Instead, in what some call the “obesity paradox,” most studies show a U-shaped curve: Those in the “overweight” category (BMI 25–30) surprisingly have the lowest mortality risk. Those in the “obese” category (30–35) have little or no increased risk over the so-called “healthy” category (18.5–25). And both the “underweight” (< 18.5) and extremely obese (> 35) are at increased risk of death.
“The conventional wisdom is that elevated BMI generally does not raise mortality risk until you get to very high levels, and that there are actually some survival benefits to being overweight,” said Masters, a social demographer who has spent his career studying mortality trends. “I have been suspicious of these claims.”
He noted that BMI, which doctors and scientists often use as a health measure, is based on weight and height only and doesn’t account for differences in body composition or how long a person has been overweight.
“It’s a reflection of stature at a point in time. That’s it,” said Masters, noting that Tom Cruise (at 170cm and an extremely muscular 91kg at one point), had a BMI of 31.5, famously putting him in the category of “obese.” “It isn’t fully capturing all of the nuances and different sizes and shapes the body comes in.”
Taking these nuances, Masters accessed data from the National Health and Nutrition Examination Survey (NHANES) the from 1988 to 2015, analysing 17 784 people, including 4468 deaths.
He discovered that a full 20% of the sample characterised as “healthy” weight had been in the overweight or obese category in the decade prior. When set apart, this group had a substantially worse health profile than those in the category whose weight had been stable.
Masters pointed out that a lifetime carrying excess weight can lead to illnesses that, paradoxically, lead to rapid weight loss. If BMI data is captured during this time, it can skew study results.
“I would argue that we have been artificially inflating the mortality risk in the low-BMI category by including those who had been high BMI and had just lost weight recently,” he said.
Meanwhile, 37% of those characterised as overweight and 60% of those with obese BMI had been at lower BMIs in the decade prior. Notably, those who had only recently gained weight had better health profiles.
“The health and mortality consequences of high BMI are not like a light switch,” said Masters. “There’s an expanding body of work suggesting that the consequences are duration-dependent.”
By including people who had spent most of their life at low-BMI weight in the high-BMI categories, previous studies have inadvertently made high BMI look less risky than it is, he said.
When he looked at differences in fat distribution within BMI categories, he also found that variations made a huge difference in reported health outcomes.
Exposing a public health problem
Collectively, the findings confirm that studies have been “significantly affected” by BMI-related bias.
When re-crunching the numbers without these biases, he found not a U-shape but a straight upward line, with those with low BMI (18.5–22.5) having the lowest mortality risk.
Contrary to previous research, the study found no significant mortality risk increases for the “underweight” category.
Previous studies attributed 2 to 3% of UA adult deaths to high BMI, but his study estimates an eight times higher rate.
Masters said he hopes the research will alert scientists to be “extremely cautious” when making conclusions based on BMI. But he also hopes the work will draw attention to what he sees not as a problem for individuals alone to solve but rather a public health crisis fuelled by an unhealthy or “obesogenic” environment in the US.
“For groups born in the 1970s or 1980s who have lived their whole lives in this obesogenic environment, the prospects of healthy aging into older adulthood does not look good right now,” he said. “I hope this work can influence higher-level discussions about what we as a society can do about it.”
Because of their illness, patients with chronic medical conditions may experience self-stigma, or negative beliefs, emotional reactions, and behaviours towards themselves. New research published in the Journal of Diabetes Investigation found a link between self-stigma and glycated haemoglobin (HbA1c) in adults with type 1 diabetes.
The study included 109 adults in Japan with type 1 diabetes who completed questionnaires that generated scores based on a self-stigma scale. Although the findings support a link between self-stigma and sub-optimal HbA1c, additional studies are needed to show whether this is a causal relationship.
“We focused on this issue through clinical experiences with people with type 1 diabetes, whose glycaemic management improved markedly by social supports of eliminating diabetes-related stigma. Although the finding of an association between self-stigma and HbA1c is significant, further longitudinal research is required to determine whether self-stigma leads to sub-optimal HbA1c,” said corresponding author Yukiko Onishi MD, PhD, of the Institute of Medical Science, Asahi Life Foundation, in Tokyo. “This research does support and highlight the importance of eliminating self-stigma when treating people with type 1 diabetes.”
People with diabetes who experience periods of hypoglycaemia, a common event in those new to blood sugar management, are more likely to have worsening diabetic eye disease. Now, researchers say they have linked such low blood sugar levels with a molecular pathway that is activated in hypoxic cells in the eye.
The research, involving human and mouse eye cells and intact retinas grown in a low glucose environment in the laboratory, as well as mice with low glucose levels, was published in Cell Reports.
“Temporary episodes of low glucose happen once or twice a day in people with insulin-dependent diabetes and often among people newly diagnosed with the condition,” says Akrit Sodhi, MD, PhD, Johns Hopkins Medicine professor. Low glucose levels can also occur during sleep in people with non-insulin dependent diabetes. “Our results show that these periodic low glucose levels cause an increase in certain retinal cell proteins, resulting in an overgrowth of blood vessels and worsening diabetic eye disease,” adds Sodhi.
Up to a third of diabetic patients will develop diabetic retinopathy, which is characterised by the overgrowth of abnormal blood vessels in the retina.
Sodhi says the current study suggests that people with diabetic retinopathy may be particularly vulnerable to periods of low glucose, and keeping glucose levels stable should be an important part of glucose control.
For the study, the researchers analysed protein levels in human and mouse retinal cells and intact retinas grown in an environment of low glucose in the laboratory, as well as in mice that had occasional low blood sugar.
In human and mouse retinal cells, low glucose levels triggered a cascade of molecular changes that can lead to blood vessel overgrowth. First, the researchers saw that low glucose caused a decrease in retinal cells’ ability to break down glucose for energy.
When the researchers focused on Müller glial cells, which are supportive cells for neurons in the retina and rely primarily on glucose for energy production, they found that the cells increased the expression of the GLUT1 gene, which makes a protein that transports glucose into cells.
The researchers found that, in response to low glucose, the cells increased levels of a transcription factor, hypoxia-inducible factor (HIF)-1α. This turned on the cellular machinery, including GLUT1, needed to improve their ability to utilise available glucose, preserving the limited oxygen available for energy production by retinal neurons.
However, in hypoxic environments, as occurs in the retinas of patients with diabetic eye disease, this normal, physiologic response to low glucose triggered a flood of HIF-1α protein into the nucleus.
This resulted in an increase in the production of proteins such as VEGF and ANGPTL4, which cause the growth of abnormal, leaky blood vessels – the key culprit of vision loss in people with diabetic eye disease.
The researchers plan to study whether low glucose levels in people with diabetes may impact similar molecular pathways in other organs, such as the kidney and brain.
Sodhi says the HIF-1α pathway may serve as an effective target for developing new treatments for diabetic eye disease.
Researchers have found that a class of older antipsychotic drugs could be a promising new therapeutic option for people with type 2 diabetes, helping fill a need among patients who aren’t able to take other currently available treatments. The drugs interact with the metabolic enzyme succinyl CoA:3-ketoacid CoA transferase (SCOT), preventing the muscles from using ketones for fuel.
“There is a growing need to find new therapies for type 2 diabetes,” says John Ussher, professor in the Faculty of Pharmacy & Pharmaceutical Sciences and lead author of the recent study published in the journal Diabetes.
Metformin is one of the most common therapeutics for type 2 diabetes, but about 15% of patients aren’t able to take it. Iinsulin secretagogues, another commonly used drug class, isn’t as effective for later-stage patients.
“For the patients who can’t take metformin, patients with late-stage diabetes where their beta cells aren’t working as well, when you’re trying to find new therapies or new combination therapies as the disease progresses, it becomes more important to find new drug classes that target new mechanisms so then you have more options to try and lower blood sugar in those individuals,” Ussher explains.
The mechanism Ussher and his team turned their attention to is SCOT, which is an enzyme involved in the body’s process of making energy from ketones. Using computer modelling to find drugs that could potentially interact with SCOT, they landed on an older generation of antipsychotic drugs, a drug class called diphenylbutylpiperidines, or DPBP for short.
Ussher and his team had previously found that a specific drug within this class called pimozide could be repurposed to help treat diabetes, but they’ve since expanded their focus to see whether more of the DPBP class could also be useful for treating the disease.
“We’ve tested three drugs now, and they all interact with this enzyme,” says Ussher. “They all improve blood sugar control by preventing the muscle from burning ketones as a fuel source.”
“We believe this SCOT inhibition is the reason these antipsychotics might actually have a second life for repurposing as an anti-diabetic agent,” he adds.
Developing a drug is a complicated, time-consuming and expensive process. It involves clinical trials to test the safety and efficacy of the drug, and can easily cost hundreds of millions of dollars. Not to mention, it can take years to go from development in the laboratory to use in the clinic or hospital. Repurposing an existing drug may help fast-track the process, Ussher notes.
“With something that’s an older drug which we used historically in humans that we no longer use, we know what the adverse effects are, we know in general that it’s safe,” he says.
Though clinical trials are still needed, repurposing a drug allows researchers to focus specifically on the efficacy and safety of the new intended use, offering a quicker and cheaper path to a new therapy.
“As you already have safety data, it somewhat accelerates the process,” says Ussher. “And from an economic standpoint, often because a lot of these drugs being pursued for repurposing are older, they’re off patent and cheaper.”
Repurposing is effective because it capitalises on a main characteristic of most drugs, ie not being restricted to just one target in the body. As Ussher explains, most drugs actually have numerous targets they can influence.
“That’s where repurposing comes in,” he says. “Can we identify the other targets that a drug may interact with, and by identifying those other targets, can this drug serve a purpose for a different disease?”
This is what Ussher’s lab did in recognising the DPBP drug class could target SCOT activity as well as the dopamine receptors it targets in its original intended use to treat psychosis.
Knowledge of these original targets can also provide valuable context when refining and improving the repurposed drug. Since DPBP drugs were originally antipsychotics, many of their potential side-effects such as drowsiness, dizziness or fatigue arise from their effects on their original target: the dopamine receptors in the brain. Ussher’s lab is planning to try creating a modified version of the drug class that doesn’t reach the brain and has fewer potential adverse effects.
“For us, the excitement is that it looks like the entire family of these compounds interacts with this protein [SCOT] and can improve blood sugar control in type 2 diabetes.”
Researchers have unlocked a means to modify the function of an enzyme crucial to fat production, a finding could lead to more effective treatments for childhood obesity and cancer.
While the research, published in the Proceedings of the National Academy of Sciences, was in fruit fly larvae, the ability to alter the rates of lipid metabolism could have significant implications for human health, said Hua Bai, an associate professor of genetics, development and cell biology at Iowa State University.
“We’ve identified what’s basically a metabolic switch. It’s like the accelerator on a car,” he said.
The initial aim was investigating how ageing was affected by fatty acid synthase, an enzyme that plays a role in de novo lipogenesis, which is the process of turning excess dietary carbohydrates into fat. Typically, levels of fatty acid synthase rise and fall based on an animal’s cellular needs and diet.
Surprisingly, the researchers noticed that early in a fruit fly’s development, de novo lipogenesis increases without an accompanying boost in the expression of fatty acid synthase. That suggested there must be some other factor at play, Bai said.
After proteins such as fatty acid synthase are created based on genetic code, their function can be altered by one of several different types of post-translational modification. Bai’s team found one of those processes, acetylation, affected one of the 2540 amino acids that combine to make fatty acid synthase, changing how effective it was at producing fat.
In addition to its role in obesity, elevated levels of de novo lipogenesis are linked to cancer, so controlling it through a single amino acid could lead to highly targeted treatments, Bai said.
“Fine tuning the acetylation levels of fatty acid synthase would be a much more precise treatment than blocking the entire protein,” he said.
Though the findings may be applicable to humans, any medical application in humans is years away, he said.
“The potential is high, but further testing is needed in other animals,” he said.
A new study may help explain how excess weight can contribute to diabetes, which may lead to targeted treatment and prevention. The findings suggest that many people with elevated insulin levels, an early marker of diabetes risk, also have defects in an enzyme important to the processing of a key fatty acid from the diet. The research was published in the journal Cell Metabolism.
“Between 30 million and 40 million people in the United States have Type 2 diabetes, and another 90 million to 100 million have risk factors that make them likely to develop Type 2 diabetes in the future,” said senior investigator Clay F. Semenkovich, MD, at the Washington University School of Medicine in St. Louis. “Many at risk for diabetes have elevated levels of insulin, a hallmark of insulin resistance and a signal that means trouble may be brewing. If we could intervene before they actually develop diabetes, we might be able to prevent significant health problems – such as heart disease, chronic kidney disease, nerve damage, vision loss and other problems – in a great number of people.”
When there is excessive body fat, beta cells in the pancreas ae signalled to secrete more insulin. When insulin levels become elevated and remain high, the body can become resistant to insulin, and eventually the beta cells that secrete insulin can fail, leading to diabetes.
Studying human tissue samples, Washington University researchers found that the overproduction of insulin involves a process called palmitoylation. This is the process by which cells attach the fatty acid palmitate to proteins.
Thousands of human proteins can be attached to palmitate, but the researchers found that when this fatty acid isn’t removed from proteins in beta cells, diabetes is the end result. Examining tissue samples from people who were thin or overweight, and with and without diabetes, the researchers found that the people with diabetes were deficient in an enzyme that removes palmitate from beta cells.
“They hyper-secrete insulin because this process goes awry, and they can’t appropriately regulate the release of insulin from beta cells,” Semenkovich explained. “Regulating insulin release is controlled in part by this palmitoylation process.”
The research team also genetically engineered a mouse that was deficient in the APT1 enzyme, which is responsible for palmitate removal from proteins. The engineered mice went on to develop diabetes.
Because impaired APT1 function contributed to diabetes risk, the researchers worked with the university’s Center for Drug Discovery to screen and identify compounds that can increase the activity of the APT1 enzyme.
“We’ve found several candidate drugs, and we’re pursuing those,” Semenkovich said. “We think that by increasing APT1 activity, we might reverse this process and potentially prevent people at risk from progressing to diabetes.”
Although he said the new findings identifying APT1 as a target are an important step, Semenkovich explained that APT1 is only one treatment target among many.
“There are several ways that Type 2 diabetes may develop,” he said. “This enzyme is not the answer, but it’s an answer, and it appears we have some promising tools that might keep some people with prediabetes from developing diabetes.”
