This comes after the surge in the numbers of children dying from the bacterial throat infection strep A earlier this month. It’s safe to say that following the Covid-19 pandemic, we’re all on edge when it comes to infectious illnesses, especially ones which are highly contagious.
So, we asked the experts for the lowdown how to know if you have a simple cold, strep A or Covid infection.
What is strep A?
“Strep A is a type of bacterium found in the throat and on the skin,” explains GP and director of Cosmedics Dr Ross Perry. “Group A streptococcus (GAS) is a common bacterium that lots of us carry it in our throats and on our skin and it doesn’t always result in illness.” So why the focus on it? Well, the concern is two-fold. Firstly, strep A bacteria can lead to more serious infections in rare cases.
Duncan Reid, pharmacist at Pharmacy2U, explains: “Streptococcus A (strep A) are a group of bacteria that cause scarlet fever and respiratory and skin infections such as strep throat and impetigo. Scarlet fever is usually a mild illness, but it is highly infectious. Symptoms of scarlet fever are a sore throat, headache and fever, along with a fine, pinkish or red body rash with a sandpapery feel. On darker skin, the rash can be more difficult to detect visually but will have a sandpapery feel.” Secondly, we’re currently seeing a steep rise in cases.
Why is there so much strep A around this year?
“We have seen a huge rise in cases since September,” says Dr Perry. “According to Dr Susan Hopkins (the chief medical advisor for the UK Health Security Agency) it is thought that this is due to greater social mixing than pre-pandemic, and the fact that children were less exposed to the bacterial infection during lockdown.”
This has led to a sharp uptick in cases, particularly among primary school children and several deaths have sparked concern among parents and the general public. It is important to remember, however, that for the majority of people, a strep A infection will be a mild illness.
“Outbreaks of group A strep do happen every few years,” Dr Zoe Watson, GP locum and founder of Wellgood Wellbeing, reassures us. “The current surge in cases actually still isn’t as high as the last outbreak in 2018, but the current levels are certainly higher than usual for this time of year, so experts are worried this may continue to rise. Currently, there is no evidence that a new strain group A strep is circulating. The increase is most likely related to high amounts of circulating bacteria and increased social mixing after relaxation of social distancing rules.”
How do you catch strep A?
“Strep A is spread through contact with droplets from an infected person when they talk, cough or sneeze,” explains Reid. “Some people can have the bacteria present in their body without feeling unwell or showing any symptoms of infections, and while they can pass it on, the risk of spread is much greater when a person is unwell. It is still possible to infect others for up to three weeks.”
As with any other infectious illness, it’s especially important to be thorough with handwashing, using a tissue to catch coughs and sneezes and staying away from others if you’re unwell – steps we’re all used to, after the last couple of years.
What are the symptoms of strep A?
You may not even know you have a strep A infection, but if you do become unwell, the chances are you’ll suffer from cold-like symptoms. “For some people, strep A may show no symptoms, but others can be very unwell with symptoms such as a high temperature, sore throat, swollen tonsils, temperature, skin rash and earache,” explains Dr Perry.
How can I tell if I have Covid, flu, strep A or a cold?
As the symptoms of all three are closely linked and extremely common in winter, it can be tricky to tell the difference. Children get three times as many colds per year than adults, so Reid advises: “It’s important to remember that most will have a common seasonal virus, which can be treated by keeping hydrated, and with paracetamol.”
Is it a cold?
“At this time of year, viral infections are very common and prevalent,” reassures Dr Perry. “A simple cold is a viral infection of the nose and throat and normally short-lived and harmless. You can expect a cold to last seven to 10 days, sometimes a little longer depending on lifestyle. The main symptoms of a cold will be runny nose, sore throat, congestion, raised temperature, fatigue, muscle aches and a mild cough.”
Flu is everywhere this year. Some symptoms are similar to those of a cold, including having a cough and sore throat, but others include high temperature, aching muscles, headaches and loss of appetite. In fact, it sounds a lot like Covid…
What about Covid?
“It is more common to have other symptoms present if it is Covid,” explains Dr Perry. “You’re more likely to have a cough, loss of smell and fever, fatigue and muscle aches, so if you feel it is more than just a cold, it’s best to take a Covid test to be sure.”
Or strep A?
Strep A generally presents as a prolonged sore throat with an accompanying rash, which feels like sandpaper, or strawberry tongue where white lumps appear. Look out for any problems breathing and swallowing and worsening symptoms which last longer than a couple of days and show no sign of improvement.
Since many people will have either no symptoms with strep A infections or feel cold or flu-like, the experts agree it is important to keep an eye on any worsening or persistent symptoms. “In rare cases, the group A bacteria can pass into the bloodstream, causing an illness known as invasive group A strep (iGAS),” explains Dr Perry. “Invasive disease happens when the bacteria get past your body’s immune defences. This can happen when you are already ill or are on treatments, such as some cancer therapies that affect your immune system.”
While still uncommon, there has been an increase in invasive group A strep cases this year, particularly in children under 10, as seen in the news headlines. According to Dr Perry, warning signs of invasive disease include a fever of above 38°C and severe muscle aches.
“You should monitor a rising temperature, particularly in children if they go over 39°C and for babies over 38°C,” advises Dr Perry. “Check for an accompanying rash which feels like sandpaper, or strawberry tongue where white lumps appear, any problems breathing and swallowing and worsening symptoms which prolong after two days and show no sign of improvement. Seek medical advice immediately from your GP and NHS 111 out of hours if you’re concerned.”
How is it treated?
“In general, a group A strep infection starts off as minor, or ‘non-invasive’ but can become more serious, or ‘invasive’ when the bacterium is able to infect areas where it is not usually found, such as the blood and the lungs,” explains Dr Watson. “This can happen if it’s not treated with antibiotics in a timely manner or if the infection simply becomes too overwhelming for the body to cope with, even with antibiotics on board.”
The good news is that when caught early enough, strep A responds well to antibiotic treatment. “Treatment with antibiotics will help you get better quicker, reduce the chance of serious illnesses, such as pneumonia,” advises Reid. “It also makes it less likely that you’ll pass the infection on to someone else.”
The advice is clear: trust your judgment when it comes to a poorly child. If you’re concerned, seek prompt medical attention and remember that, thankfully, strep A outbreaks do tend to be short-lived.
The evasive BA.5 omicron variant is driving up Covid cases and hospitalizations as it spreads rapidly across the United States—but despite deaths remaining lower compared to earlier waves, experts tell Forbes there are still plenty of reasons to remain cautious and warn Americans against letting their guard down too soon.
While Covid-19 cases and hospitalizations have been on the rise in most states in recent weeks and jumped 20% nationwide over the past fortnight, deaths have risen only modestly and have hovered around 300-400 a day since April. Driving the new wave is BA.5, an omicron offshoot that has a “superpower to cause reinfection” and can evade immunity from vaccination and previous infection, even from other omicron variants, Dr. Peter Chin-Hong, an infectious disease expert at the University of California, San Francisco, told Forbes.
The disconnect reflects the fact that vaccines and past infections still provide strong protection against serious illness and death for BA.5 as well as there being more options available to treat early disease like Pfizer’s Paxlovid. Chin-Hong said there are still plenty of reasons to avoid infection, not least because Covid can still cause severe symptoms “even if you don’t end up in the hospital” and symptoms can “last for weeks.”
Infection also carries the risk of “long Covid”—lingering and sometimes debilitating symptoms that can persist for months or years—and early evidence suggests this is more likely the more times you get infected. Avoiding infection also helps safeguard people around you who may have less protection against serious disease like children, the elderly and those with weakened immune systems, Dr. Stuart Turville, a virologist at the University of New South Wales in Australia, told Forbes.
Increasingly transmissible variants of omicron have surged across the U.S. this year. BA.5, the most infectious form of the virus yet, rapidly spread and became the dominant variant in early July. It now accounts for an estimated 78% of cases, according to the Centers for Disease Control and Prevention and community transmission has spiked. Concerns over BA.5, as well as the related BA.4, prompted officials to direct vaccine makers to target the variants in updated shots and the Biden Administration announced new plans to tackle its spread.
Officials and experts say it is especially important to ensure strong protection against serious disease by keeping up-to-date on vaccinations, including booster shots. Despite the appeals of public health officials and being available for many months, booster uptake in the U.S. is poor. Fewer than half of fully vaccinated people have received their first booster dose and fewer than 30% of those who have and are eligible for a second have taken up the offer, according to CDC data.
More variants. It is inevitable that SARS-CoV-2, the virus that causes Covid-19, will evolve and spawn new variants over time. Another omicron offshoot, BA.2.75—inexplicably and successfullydubbed “Centaurus” by the internet—has already caught the eye of virologists. The variant is spreading rapidly in India, has been detected across Europe and North America and shows signs of evading immunity.
Little data is available and it’s not clear whether BA.2.75 causes more severe disease. It’s also not clear whether it would be able to take over from BA.5 “as the ruler of the roost,” Chin-Hong explained, as they haven’t had a chance to directly compete with each other as yet.”
A great deal. Data collection and surveillance is poor compared to earlier on in the pandemic. Individual testing is down, genomic surveillance is reduced and evidence suggests cases could be vastly higher than official figures state. Conversely, hospital figures are inflated and reflect routine testing upon admission, which catches many “incidental” infections from people seeking care for other problems.
There is a lot to be understood about the newer omicron variants as well, experts say. BA.5, as well as other more recent omicron offshoots like BA.4 and BA.2.75, are relatively new pathogens that are infecting or reinfecting large numbers of people in the community, Turville explained, which makes it hard to provide absolute and definitive answers. “As with most things with SARS CoV-2, it is a large bag of unknowns,” he added.
Turville told Forbes the decoupling of deaths from cases shows the longer term effects of vaccination and exposure to the virus. It’s a “maturing immunity to SARS-CoV-2 in general” which has taken off the “edge of disease severity,” he added.
While cases are growing—and likely undercounted—it’s worth noting that they are a long way from the earlier omicron peak in January. In July, there were around 100,000-120,000 cases reported on average compared to more than 800,000 in mid January.
So far there is no evidence that this variant causes more serious illness. And infectious disease experts say that even though new infections are on the rise, the impact of BA.5 is unlikely to be on the scale of the surge we saw last winter — in part because the country is better equipped to manage it.
The U.S. is averaging about 300 deaths a day, compared to 3,000 last winter. Dr. Anna Durbin, a professor at the Johns Hopkins University School of Medicine, says the combination of prior infections and vaccinations is still protective, and COVID-19 treatments are better.
“Most people have some underlying immunity that is helpful in fighting the virus,” she explains. “We have antivirals … And I think that because of that … we’re not seeing a rise in deaths. And that’s very reassuring. It tells me that even this virus, even BA.5, is not so divergent that it is escaping all arms of the immune system.”
She adds that new booster shots specifically targeting omicron — which could roll out as soon as this fall — should also be helpful in preventing serious illness and deaths.
There are steps you can take to reduce your exposure to the virus, like masking up in crowded indoor spaces. Here’s how to step up your mask game.
The nervous and immune systems are tightly intertwined. Deciphering their chatter might help address many brain disorders and diseases.The brain is the body’s sovereign, and receives protection in keeping with its high status. Its cells are long-lived and shelter inside a fearsome fortification called the blood–brain barrier. For a long time, scientists thought that the brain was completely cut off from the chaos of the rest of the body — especially its eager defence system, a mass of immune cells that battle infections and whose actions could threaten a ruler caught in the crossfire.
In the past decade, however, scientists have discovered that the job of protecting the brain isn’t as straightforward as they thought. They’ve learnt that its fortifications have gateways and gaps, and that its borders are bustling with active immune cells.
A large body of evidence now shows that the brain and the immune system are tightly intertwined. Scientists already knew that the brain had its own resident immune cells, called microglia; recent discoveries are painting more-detailed pictures of their functions and revealing the characteristics of the other immune warriors housed in the regions around the brain. Some of these cells come from elsewhere in the body; others are produced locally, in the bone marrow of the skull.
By studying these immune cells and mapping out how they interact with the brain, researchers are discovering that they play an important part in both healthy and diseased or damaged brains. Interest in the field has exploded: there were fewer than 2,000 papers per year on the subject in 2010, swelling to more than 10,000 per year in 2021, and researchers have made several major findings in the past few years.
No longer do scientists consider the brain to be a special, sealed-off zone. “This whole idea of immune privilege is quite outdated now,” says Kiavash Movahedi, a neuroimmunologist at the Free University of Brussels (VUB). Although the brain is still seen as immunologically unique — its barriers prevent immune cells from coming and going at will — it’s clear that the brain and immune system constantly interact, he adds (see ‘The brain’s immune defences’).
This shift in attitude is widespread in the community, says Leonardo Tonelli, chief of the neuroendocrinology and neuroimmunology programme at the US National Institute of Mental Health in Bethesda, Maryland. In his experience, almost every neuroscientist who reviews grant proposals for the agency accepts the connection, he says, although many still need to catch up with the latest discoveries in neuroimmunology, which have started to reveal the underlying mechanisms.
The rush to understand how the brain and immune system knit together has prompted a wealth of questions, says Tony Wyss-Coray, a neuroimmunologist at Stanford University in California. “How important is this in normal brain function or disease? That is a very hard question to answer.”
More than two decades ago, when neuroimmunologist Michal Schwartz had just set up her laboratory at the Weizmann Institute of Science in Rehovot, she couldn’t stop asking herself an unpopular question: could it really be true that the brain is completely cut off from immune protection? “It was completely axiomatic that the brain cannot tolerate any immune activity — everyone thought that if you have any immune activation, this was a sign of pathology,” she says. “But it didn’t make sense that tissue that is so indispensable, like the brain, cannot enjoy the benefit of being assisted by the immune system.”
The idea that the brain was off limits to the immune system took root decades earlier. In the 1920s, the Japanese scientist Y. Shirai reported that when tumour cells were implanted in a rat’s body, the immune response destroyed them, but when placed in the brain, they survived — indicating a feeble or absent immune response. Similar findings followed in the 1940s.
Most scientists also thought that the brain lacked a system for ferrying immune molecules in and out — the lymphatic drainage system that exists elsewhere in the body — even though such a system was first described in the brain more than two centuries ago. The prevailing view, then, was that the brain and the immune system lived largely separate lives. The two were thought to collide only under hostile circumstances: when immune cells went rogue, attacking the body’s own cells in diseases such as multiple sclerosis.
So when, in the late 1990s, Schwartz and her team reported that after an acute injury to the central nervous system, two types of immune cells, macrophages and T cells, protected neurons from damage and supported their recovery, many scientists were sceptical. “Everyone told me, you’re absolutely wrong,” Schwartz recalls.
Since those early experiments, Schwartz’s team and others have amassed a large body of evidence showing that immune cells do, indeed, have a significant role in the brain, even in the absence of autoimmune disease. Researchers have shown, for example, that in mice engineered to lack an immune system, neurodegenerative diseases such as motor neuron disease (amyotrophic lateral sclerosis) and Alzheimer’s disease seemed to progress more rapidly, whereas restoring the immune system slowed their progression. Scientists have also revealed a potential role for microglia in Alzheimer’s disease.
More recently, scientists have shown that immune cells at the brain’s edges are active in neurodegenerative diseases. After examining the cerebrospinal fluid of people with Alzheimer’s, Wyss-Coray and his colleagues found evidence of a rise in numbers of T cells in the brain’s fluid-filled borders5. The expansion of these immune-cell populations suggests that they might have a role in the disease, Wyss-Coray says.
But whether immune cells hurt or help the brain is an open question. In their studies of Alzheimer’s and other neurodegenerative disorders, Wyss-Coray and his colleagues suggest that the immune system could be damaging neurons by releasing molecules that boost inflammation and trigger cell death. Others have suggested that T cells and other immune cells could instead be protective. For example, Schwartz’s group has reported6 that in mouse models of Alzheimer’s, boosting the immune response leads to a clearance of amyloid plaques — a pathological hallmark of the disease — and improves cognitive performance.
It’s now becoming clear that the brain’s margins are immunologically diverse: almost any type of immune cell in the body can also be found in the area surrounding the brain. The meninges — the fluid-filled membranes that wrap the brain — are an “immunological wonderland”, says Movahedi, whose work focuses on macrophages in the brain’s borders. “There’s so much happening out there.”
Some residents are exclusive to the frontiers. In 2021, Jonathan Kipnis, a neuroimmunologist at Washington University in St. Louis, Missouri, and his colleagues reported7 that there is a local source of immune cells: the bone marrow of the skull.
When they explored how the bone marrow mobilizes these cells, Kipnis and his colleagues demonstrated8 that, in response to an injury to the central nervous system or in the presence of a pathogen, signals carried in the cerebrospinal fluid were delivered to the skull bone marrow, prompting it to produce and release these cells (see ‘Private protectors’).
What role these locally produced immune cells have remains to be seen, but Kipnis’s group thinks that they might have a gentler role than immune cells from elsewhere in the body, regulating the immune response rather than being primed to fight. Kipnis says that this distinction, if true, has implications for treatment. In diseases such as multiple sclerosis, he says, symptoms could perhaps be improved by preventing immune cells from other parts of the body from coming in. By contrast, with a brain tumour, he adds, “you want the fighters”.
His team has also detected a network of channels that snake and branch over the surface of the brain, and which swarm with immune cells, forming the brain’s own lymphatic system9. These vessels, which sit in the outermost part of the meninges, give immune cells a vantage point near the brain from where they can monitor any signs of infection or injury.
In sickness and in health
As evidence builds for the involvement of immune cells during brain injury and disease, researchers have been exploring their function in healthy brains. “I think the most exciting part of neuroimmunology is that it’s relevant to so many different disorders and conditions and to normal physiology,” says Beth Stevens, a neuroscientist at Boston Children’s Hospital in Massachusetts.
Many groups, including Stevens’s, have found microglia to be important to the brain’s development. These cells are involved in pruning neuronal connections, and studies suggest that problems in the pruning process might contribute to neurodevelopmental conditions.
Border immune cells, too, have been shown to be essential in healthy brains. Kipnis, Schwartz and their colleagues, for example, have shown that mice that lack some of these cells display problems in learning and social behaviour10. Others reported11 in 2020 that mice that develop without a specific population of T cells in both the brain and the rest of the body have defective microglia. Their microglia struggle to prune neuronal connections during development, leading to excessive numbers of synapses and abnormal behaviour. The authors propose that during this crucial period, T cells migrate into the brain and help microglia to mature.
One big mystery is how exactly immune cells — particularly those around the borders — talk to the brain. Although there is some evidence that they might occasionally cross into the organ, most studies so far suggest that these cells communicate by sending in molecular messengers known as cytokines. These, in turn, influence behaviour.
Researchers have been studying how cytokines affect behaviour for decades, finding, for example, that cytokines sent out by immune cells during infection can initiate ‘sickness behaviours’ such as increased sleep12. They have also shown in animal models that alterations in cytokines — induced by depleting them throughout the body or knocking out specific cytokine receptors on neurons — can lead to alterations in memory, learning and social behaviours13. How cytokines travel into the brain and exert their effects remains an area of active study.
Cytokines might also be a link between the immune system and neurodevelopmental conditions such as autism. When Gloria Choi, a neuroimmunologist at the Massachusetts Institute of Technology in Cambridge, and her colleagues boosted cytokine levels in pregnant mice, they saw brain changes and autism-like behaviours in the offspring14.
Although these insights are tantalizing, much of the work on how immune cells, especially those in the borders, operate in the brain is still in its infancy. “We are very far away from understanding what’s happening in healthy brains,” Kipnis says.
A two-way street
Communication between the immune system and the brain also seems to go in the other direction: the brain can direct the immune system.
Some of these insights are decades old. In the 1970s, scientists conditioned rats to become immunosuppressed when they tasted saccharin, an artificial sweetener, by pairing it with an immunosuppressive drug for several days15.
In more recent work, Asya Rolls, a neuroimmunologist at Technion — Israel Institute of Technology in Haifa, and her team explored the link between emotion, immunity and cancer in mice. They reported16 in 2018 that activating neurons in the ventral tegmental area, a brain region involved in positive emotions and motivation, boosted the immune response and, in turn, slowed tumour growth.
Then, in 2021, her group pinpointed neurons in the insular cortex — a part of the brain involved in processing emotion and bodily sensations, among other things — that were active during inflammation in the colon, a condition also known as colitis.
By activating these neurons artificially, the researchers were able to reawaken the intestinal immune response17. Just as Pavlov’s dogs learnt to associate the sound of a bell with food, causing the animals to salivate any time they heard the noise, these rodents’ neurons had captured a ‘memory’ of the immunological response that could be rebooted. “This showed that there is very intense crosstalk between neurons and immune cells,” says Movahedi, who wasn’t involved with this work.
Rolls suspects that organisms evolved such immunological ‘memories’ because they are advantageous, gearing up the immune system in situations when the body might meet pathogens. She adds that in certain cases, they can instead be maladaptive — when the body anticipates an infection and mounts an unnecessary immune response, causing collateral damage. This pathway might help to explain how psychological states can influence the immune response, providing a potential mechanism for many psychosomatic disorders, according to Rolls.
It could also inspire therapies. Rolls and her team found that blocking the activity of those inflammation-associated neurons lessened inflammation in mice with colitis. Her group hopes to translate these findings to humans, and is examining whether inhibiting activity using non-invasive brain stimulation can help to alleviate symptoms in people with Crohn’s disease and psoriasis — disorders that are mediated by the immune system. This work is in the early phases, Rolls says, “but it’ll be really cool if it works”.
Other groups are exploring how the brain controls the immune system. Choi’s team is tracing out the specific neurons and circuits that modulate the immune response. One day, she hopes to be able to generate a comprehensive map of the interactions between the brain and immune system, outlining the cells, circuits and molecular messengers responsible for the communication in both directions — and connecting those to behavioural or physiological readouts.
One of the biggest challenges now is to tease apart which populations of cells are involved in these myriad functions. To tackle it, some researchers have been probing how these cells differ at the molecular level, by sequencing genes in single cells. This has revealed a subset of microglia associated with neurodegenerative disease, for example. Understanding how these microglia function differently from their healthy counterparts will be useful in developing treatments, Stevens says. They could also be used as markers to track the progression of a disease or the efficacy of therapies, she adds.
Researchers have already begun using these insights into the immune ecosystem in and around the brain. Schwartz’s team, for example, is rejuvenating the immune system in the hope of fighting Alzheimer’s disease. This work has opened up new avenues for therapeutics, particularly for neurodegenerative conditions, Schwartz says. “It’s an exciting time in the history of brain research.”
Here’s a look at diabetes, a disease that affects millions of people around the world. Diabetes is characterized by high levels of blood glucose resulting from defects in insulin production, insulin action, or both. The disease can lead to serious complications such as blindness, kidney damage, cardiovascular disease, limb amputations and premature death.
People with diabetes or certain other underlying medical conditions are more likely to become severely ill if infected with Covid-19, according to the CDC. Worldwide, the number of people living with the potentially fatal disease has quadrupled since 1980, to around 422 million, according to the World Health Organization (WHO).
There are several types of diabetes: Type 1, Type 2 and gestational diabetes. Prediabetes occurs when blood glucose levels are higher than normal but not yet high enough to be diagnosed as diabetes. Before developing Type 2 diabetes, people almost always have prediabetes. Research has shown that some long-term damage to the body may occur during prediabetes.
Type 1 diabetes develops when the body’s immune system destroys pancreatic beta cells, the only cells in the body that make insulin. This form of diabetes usually strikes children and young adults. Only 5-10% of people with diabetes have Type 1. Risk factors for Type 1 diabetes may be autoimmune, genetic or environmental. There is no known way to prevent Type 1 diabetes.
Type 2 diabetes occurs when the body does not produce enough insulin or the cells do not use insulin properly. Type 2 diabetes is the most common form of diabetes and in adults, it accounts for about 90% to 95% of all diagnosed cases of diabetes. It is associated with older age, obesity, family history, physical inactivity and race/ethnicity.
It is more common in African Americans, Latino Americans, American Indians, Asian Americans, Native Hawaiians and other Pacific Islanders. Type 2 diabetes in children and adolescents, although still rare, is being diagnosed more frequently.
Gestational diabetes is a form of glucose intolerance diagnosed during pregnancy. It affects about 4% of all pregnant women. A diagnosis of gestational diabetes doesn’t mean that a woman had diabetes before she conceived, or that she will have diabetes after giving birth.
Other types of diabetes result from genetic conditions, surgery, medications, infections and other illnesses. Such types of diabetes account for 1% to 5% of all diagnosed cases.
Frequent urination Excessive thirst Unexplained weight loss Extreme hunger Sudden changes in vision Numbness in hands or feet Tiredness Dry skin Slow healing wounds Frequent infections
Adults with diabetes have heart disease death rates about two to four times higher than adults without diabetes. The risk for stroke is two to four times higher among people with diabetes. People with diabetes are at high risk for high blood pressure.
Diabetes is the leading cause of new cases of blindness among adults aged 20-74 years. Diabetes is the leading cause of kidney failure. Between 60% and 70% of people with diabetes have mild to severe forms of nervous system damage or neuropathy.
May 15, 2022 – In its biannual Diabetes Report Card, the CDC notes a decrease in newly diagnosed cases of diabetes after almost two decades of continual increases. In 2019, the number of newly diagnosed US adults decreased from a high of 9.3 per 1,000 in 2009 to 5.9 per 1,000 adults.